Contents - (4. UPFK) 23-27 Kasım 2011

Transcription

With Contributions of
INTRODUCTION and WELCOME
Dear Colleagues,
We are very proud to invite you and to have the honour to host you at the “4th International Congress on
Psychopharmacology” which will be held in Antalya on November 23-27, 2011 as the Turkish Association for Psychopharmacology
(TAP) Conference.
The theme of the congress is: “Innovations and continuity in psychiatry & psychopharmacology: better care for better
health.”
We haven chosen to combine two key concepts as the main theme of this conference: ‘Innovations” and “Continuity”. This
is simply to reflect the fact that the field of psychopharmacology has been progressing rapidly with very novel psychotropic
medications being launched faster then ever.
Furthermore, many patients with mental illness present with a wide-range of psychiatric and medical co-morbidities which
require the treating clinician to have an up-to-date knowledge of psychotropic medications to be able to provide effective and
optimal treatments. Therefore, “continuity” refers to the fact that there is a gap between evidence-based practice guidelines
and actual care in clinical practice for patients with mental illnesses, a lack of “continuity” of knowledge to be shared with the
clinician. One of the objectives of this conference is to fill this gap by our rich scientific programme!
This year’s conference will help participants and clinicians to be able to discuss and to gain insight into translating the latest
evidence-based research into actual clinical practice, to assess where new psychotropic medications fit into patient-centred
treatment strategies and to get direct guidance on the toughest clinical challenges to help patients presenting with complex
psychiatric needs.
This conference will be a wonderful opportunity, not only to present the results of your work, but also to meet, to
communicate and to discuss research issues with other colleagues from the field in a beautiful and sunny part of the World.
There is no doubt that the 4th International Congress on Psychopharmacology will provide a warm and an elite atmosphere
in Antalya for discussions, solutions, and practical suggestions about daily practice problems and issues. We hope that
this will an opportunity for you, to refresh, update, and expand your knowledge in the major and challenging domains of
psychopharmacology, biological psychiatry, neuroscience and neuroimaging, by contributions from Turkish and international
researchers and clinicians. The Congress aims to create an interactive platform, where all participants are encouraged to ask
questions and share their experiences about difficult and treatment resistant cases.
As always and as expected, the Congress will bring together scientists from Turkey and other internationally renowned
scientists to share experiences and ideas on the latest developments in psychopharmacology at the conference, symposia,
debates, bilateral and multilateral discussion sessions, and satellite symposia. This congress will also dedicate time to ‘meet the
specialist’ sessions and courses, which will be held by distinguished scientists in the field.
Furthermore, the traditional “The Poster Presentation Research Incentive Awards” will also be presented at the 4th
International Congress on Psychopharmacology to the top three posters selected by the jury.
The most exciting and novel aspect of this Congress is that it is the first International conference organized by TAP.
We will be hosting fellow Associations, and fellow participants who are part of these Associations, from all over the world
including Canada, Malaysia, India, The Czech Republic, Greece, China, Hungary, USA, The UK, Australia, Israel, Iran, Russia,
Germany, The Netherlands, and The Ukraine.
Furthermore, there will be joint symposia with International Fellow and Partner Associations at this meeting. It is hoped that
this will increase International research collaborations.
Abstracts of all the presentations submitted to the 4th International Congress on Psychopharmacology will be published in
the latest issue of the Bulletin of Clinical Psychopharmacology as a supplement. This will ensure that these presentations are
available to be accessed at the SCI-E.
We hope that the conference will be a fruitful and enjoyable experience for all participants and we are looking forward to
meeting you in beautiful and sunny Antalya, Turkey!
The 4th ICP Organizing Committee
Turkish Association for Psychopharmacology
4th International
Congress on Psychopharmacology
“Innovations and continuity in psychiatry &
psychopharmacology: better care for better health”
November 23-27, 2011
Antalya, Turkey
PROGRAM
www.psychopharmacology2011.org
COMMITTEES
CO-CHAIRS
Mesut ÇETİN
Oğuz KARAMUSTAFALIOĞLU
PROGRAM COMMITTEE MEMBERS
Cengiz Han AÇIKEL
Feyza ARICIOĞLU
Murad ATMACA
Glen BAKER (Canada)
Cengiz BAŞOĞLU
Alican DALKILIÇ (USA)
Rasim Somer DİLER (USA)
Serdar DURSUN (Canada)
Servet EBRİNÇ
Atila EROL
Ömer GEÇİCİ
Ali Saffet GÖNÜL
Hasan HERKEN
Numan KONUK
Samet KÖSE (USA)
David OSSER ( USA)
Haluk A. SAVAŞ
Tahir TELLİOĞLU (USA)
Tümer TÜRKBAY
Ömer YANARTAŞ
SECRETARIAT
TREASURERS
Yasin BEZ
Gökay ALPAK
Ayhan ALGÜL
M. Alpay ATEŞ
EXECUTIVE COMMITTE
İsmail AK
Lütfullah BEŞİROĞLU
Mustafa BİLİCİ
Sunar BİRSÖZ
Ömer BÖKE
M. Emin CEYLAN
Mecit ÇALIŞKAN
Murat DEMET
Nesrin DİLBAZ
H. Murat EMÜL
Cüneyt EVREN
Ömer GEÇİCİ
Erdal IŞIK
Fatih KARAASLAN
Nesrin KARAMUSTAFALIOĞLU
Nazmiye KAYA
Selim KILIÇ
Selçuk KIRLI
Erhan KURT
Ömer ÖZBULUT
Bengi SEMERCİ
Ümit Başar SEMİZ
Aytekin SIR
M. Zihni SUNGUR
M. Hakan TÜRKÇAPAR
Özcan UZUN
İlhan YARGIÇ
Ümit YAŞAR
Kazım YAZICI
Mustafa YILDIZ
COMMITTEES
ORGANIZING COMMITTEE
Nihat ALPAY
Rüstem AŞKIN
Ömer AYDEMİR
İbrahim BALCIOĞLU
Mustafa BAŞTÜRK
Erhan BAYRAKTAR
Meral BERKEM
Can CİMİLLİ
Ali ÇAYKÖYLÜ
Orhan DOĞAN
M. Kerem DOKSAT
Ali DORUK
Alaattin DURAN
Engin EKER
Hayriye ELBİ METE
Hüsnü ERKMEN
Ertuğrul EŞEL
Erol GÖKA
Mustafa GÜLTEPE
Hayrettin KARA
İsmet KIRPINAR
Işın Baral KULAKSIZOĞLU
Bekir Aydın LEVENT
Özgür ÖNER
Aytekin ÖZŞAHİN
Mücahit ÖZTÜRK
M. Kemal SAYAR
Sefa SAYGILI
Levent SEVİNÇOK
Vedat ŞAR
Cem ŞENGÜL
Lut TAMAM
Bilgen TANELİ
Ertan TEZCAN
Musa TOSUN
Tayfun TURAN
Raşit TÜKEL
Müfit UĞUR
Medaim YANIK
Yankı YAZGAN
Ayşegül YILDIZ
Salih ZOROĞLU
INTERNATIONAL SCIENTIFIC ADVISORY BOARD
Ercan ABAY
Mehmet Yücel AĞARGÜN
Fisun AKDENİZ
Tunç ALKIN
Köksal ALPTEKİN
Jules ANGST (Switzerland)
Zehra ARIKAN
Çiğdem AYDEMİR
Cahide AYDIN
Nazan AYDIN
İsmail Hakkı AYHAN
Glen BAKER (Canada)
David BALDWIN (UK)
Reha BAYAR
Oğuz BERKSUN
Mansur BEYAZYÜREK
Michel BOURIN (France)
Charles BOWDEN (USA)
Adnan CANSEVER
John COOKSON (UK)
Behçet COŞAR
Duran ÇAKMAK
Abdülkadir ÇEVİK
Ali Savaş ÇİLLİ
Ayşen ÇOŞKUN
Bülent ÇOŞKUN
Bill DEAKIN (UK)
Melissa DELBELLO (USA)
Yunus Emre EVLİCE
Max FINK (USA)
Guy GOODWIN (UK)
Başak ÖZÇELİK
Erol GÖKA
Peykan GÖKALP
Bahar GÖKLER
Ayça GÜRDAL KÜEY
Hatice GÜZ
David GREENBERG (Israel)
Çiçek HOCAOĞLU
İlkin İÇELLİ
Rene S. KAHN (The Netherlands)
Ayhan KALYONCU
Emine KILIÇ
Neşe KOCABAŞOĞLU
Stan KUTCHER (Canada)
Levent KÜEY
Lee Wei LIM (Netherlands)
Karl LOOPER (Canada)
Herbert MELTZER(USA)
Levent METE
Hasan MIRSAL
Nahit MOTAVALLI MUKADDES
Norbert MULLER (Germany)
Donald Hugh MYRICK (USA)
Ziad NAHAS (USA)
Andrew NIERENBERG (USA)
David NUTT (UK)
Jim Van OS (The Netherlands)
David OSSER (USA)
Timuçin ORAL
Süha ÖZAŞKINLI
Haluk ÖZBAY
Ayşegül ÖZERDEM
Fuat ÖZGEN
Mine ÖZKAN
Sedat ÖZKAN
Mine ÖZMEN
Nurgül ÖZPOYRAZ
Özden PALAOĞLU
Özkan PEKTAŞ
Jorge A. QUIROZ (USA)
Gary SACHS (USA)
Armağan SAMANCI
Bilgin SAYDAM
Seher SOFUOĞLU
Haldun SOYGÜR
Atilla SOYKAN
Ahmet Rıfat ŞAHİN
Rajiv TANDON (USA)
Işık TUĞLULAR
Zeliha TUNCA
Ömer TUNCER
Hamdi TUTKUN
Ümran TÜZÜN
Berna ULUĞ
Aylin ULUŞAHİN
Tayfun UZBAY
Alp ÜÇOK
Süheyla ÜNAL
Simavi VAHİP
Hans Peter VOLZ (Germany)
Axel WÜRZ (UK)
Olcay YAZICI
Nevzat YÜKSEL
Joseph ZOHAR (Israel)
SPEAKERS
JOINT SYMPOSIUMS WITH INTERNATIONAL PARTNER SOCIETIES
Canadian College of
Neuropsychopharmacology (CCNP)
The International Union of Basic and
Clinical Pharmacology (IUPHAR)
Czech NeuroPsychopharmacological
Society (CNPS)
Turkish Association for Cognitive
Behaviour Psychotherapy (TACBP)
Hellenic Society for the Advancement
of Psychiatry and Related Sciences
International Association for
Cognitive Psychotherapy (IACP)
Indian Psychiatric Society
Malaysian Psychiatric Association
INVITED INTERNATIONAL SPEAKERS
Ian ANDERSON
Kandasamy ARUN
Glen BAKER
Tanja BRUECKL
Ingolf CASCORBI
C. Robert CLONINGER
Alican DALKILIÇ
Rasim Somer DİLER
Serdar DURSUN
Serdar GÜNER
Mohamed Husain HABIL
Stefan HOFMANN
Jirí HORÁCEK
Cyril HOSCHL
Alan Leslie HUDSON
Nikolaos KAZANTZIS
Irving KIRSCH
Adrián LLERENA
Peter R. MARTIN
Pavel MOHR
Tomas PALENICEK
Thomas J. PAPARRIGOPOULOS
Antigone S. PAPAVASILIOU
Rusdi Abd. RASHID
Umi Adzlin SILIM
Constantin R. SOLDATOS
A. Shyam SUNDAR
Tahir TELLİOĞLU
Manickam THIRUNAVUKARASU
Axel WÜRZ
Hazli ZAKARIA
Joseph ZOHAR
CV’s of international guest speakers can be found at
AT A GLANCE
NOVEMBER 23, 2011 WEDNESDAY
TIME
HALL A
HALL B
HALL C
ARRIVING TO HOTEL - REGISTRATION
13.30
OPENING CONFERENCE
15.00-16.00
Evolution of human brain functions: Identifying
psychobiological targets for promoting well-being
Claude Robert Cloninger, USA
COFFEE BREAK
16.30-17.00
17.30-19.30
ABBREVIATIONS
PS-01
PS-02
PS-03
Epigenetics or genetics: Gene-environment
interactions over the life - span
Behavioral addictions and treatments:
Review of recent data
Painful syndromes in psychiatry and their
managements
OC Opening Conference KL Lecture PS Symposium MD Debate JS Joint Symposium KC Course WS Workshop
AT A GLANCE
NOVEMBER 24, 2011 THURSDAY
TIME
09.00-10.30
HALL A
KL-01
Treatment of opioid
dependence
during pregnancy
HALL B
HALL C
PS-04
Adult attention - deficit
hyperactivity disorder
(ADHD) and comorbidity
PS-05
Brain mapping, TMS, NVS,
biofeedback and deep brain
stimulation in treatment of
psychiatric disorders
Peter R. Martin, USA
HALL D
HALL E
THERAUPATIC ALLIENCE
EDUCATION PROGRAM
COFFEE BREAK
10.30-11.00
MD-01: DEBATE
Antidepressants are not
associated with suicide risk
11.00-12.30
Serdar Dursun, Canada
Nesrin Dilbaz, Türkiye
Hakan Türkçapar, Türkiye
PS-06
Neuroimaging in
psychopharmacology: An
update
POSTER SESSIONS
LUNCH
12.30-13.30
SATELLITE SYMPOSIUM
13.30-14.30
MD-02: DEBATE
Antidepressants are useful
in treatment of depression
14.30-16.00
ORAL SESSIONS
M. Zihni Sungur, Türkiye
Ian Anderson, UK
Irving Kirsch, UK / USA
COFFEE BREAK
16.00-16.30
15.00-19.00
16.30-18.00
KL-02
Benzylpiperazine; a major
contaminant of ecstasy,
induces marked changes
in rat brain neurochemistry
and behavior
JS-01
THERAUPATIC ALLIENCE
EDUCATION PROGRAM
International Association for
Cognitive Psychotherapy (IACP)
Advances and problems in
Cognitive Behavior Therapy
(CBT)
Hakan Türkçapar
Sponsored by
Alan Leslie Hudson, Canada
COFFEE BREAK
18.00-18.30
18.30-20.30
JS-02
Malaysian Psychiatric
Association
Malaysian perspective of
substance dependence
PS-07
The rationale of
antipsychotic combinations
in schizophrenia:
Epidemiological and clinical
evidences
PS-08
Advances in complementary
alternative psychotropic
drugs: Fish oil (omega-3
fatty acids), vitamine B12,
folate ve other add-on
therapies in psychiatric
disorders
COURSE
20.30-22.30
ABBREVIATIONS
KC-04
Mindfulness and acceptance
based therapies
KC-01
Biostatistics - Basic
part 1
KC-02
Biostatistics Intermediate part 1
Kültegin Ögel, Türkiye
Selim Kılıç, Türkiye
Cengiz Han Açıkel, Türkiye
AT A GLANCE
NOVEMBER 25, 2011 FRIDAY
TIME
09.00-10.30
HALL A
HALL B
HALL C
KL-03
Unipolar versus bipolar depression
in children: What do we know
about the etiology, diagnosis, and
treatment?
PS-09
From preclinical studies to clinical
practice in anxiety disorders
PS-10
Will glutamatergic modulators be
a target for the future therapy of
depression?
HALL D
HALL E
Rasim Somer Diler, USA
COFFEE BREAK
10.30-11.00
MD-03: DEBATE
Antidepressants are useful in the
treatment of bipolar disorders
11.00-12.30
Haluk Savaş, Türkiye
Selçuk Kırlı, Türkiye
Kaan Kora, Türkiye
PS-12
Vitamin and mineral
supplementation in treatment of
childhood psychiatric disorders
LUNCH
12.30-13.30
13.30-14.30
PS-11
Psychotropic drug treatments
during pregnancy and lactation
SATELLITE SYMPOSIUM
COURSE
14.30-16.00
PS-13
Hormones and psychiatric
disorders
PS-14
Clinical course of psychiatric
disorders associated with trauma
and treatment issues
KC-03
CBT in somatization disorders
Axel Würz, UK
COFFEE BREAK
16.00-16.30
JS-03
16.30-18.00
KL-04
Transcultural psychiatry (a
comparison of USA - Türkiye and
sample cases)
Hellenic Society for the Advancement
of Psychiatry and Related Sciences
Disorders of sleep and wakefulness
and their pharmacological
management
PS-15
Depression and pain
Alican Dalkılıç, USA
COFFEE BREAK
18.00-18.30
18.30-20.30
JS-04
The International Union of Basic
and Clinical Pharmacology
(IUPHAR)
Pharmacogenomics of
psychoactive drugs
PS-16
Marijuana; from mellow to
madness
PS-17
Overcoming treatment resistance:
An update
COURSE and WORKSHOP
20.30-22.30
“DÜŞÜNEN ŞARKILAR”
SOSYAL PROGRAM
21.30
WS-01
Management of panic disorder
KC-01
part 2
KC-02
Serdar Güner, The Netherlands
AT A GLANCE
NOVEMBER 26, 2011 SATURDAY
TIME
HALL A
09.00-10.30
Current concept of obsessive
compulsive disorder (OCD)
JS-05
HALL B
HALL C
KL-05
Medical marijuana use in
psychiatry
HALL D
HALL E
PS-18
Chronobiotics and
chronotherapeutics in psychiatry
Tahir Tellioğlu, USA
COFFEE BREAK
10.30-11.00
11.00-12.30
KL-06
Early intervention in anxiety and
depression: What we know, what
we don’t know and what we
should know?
Joseph Zohar, Israel
PS-19
Are the effects of
psychopharmacological and
other therapeutic approaches
neuroregenerative or
neurodegenerative? Review of
recent data
PS-20
Controversial topics in eating
disorders
LUNCH
12.30-13.30
JS-06
13.30-15.30
Czech NeuroPsychopharmacological
Society (CNPS)
From models of schizophrenia
to clinical outcome: A
psychopharmacological perspective
PS-21
Treatment approaches to
comorbidities of ADHD
COFFEE BREAK
15.30-16.00
JS-07
16.00-18.00
18.00-18.30
Canadian College of
Neuropsychopharmacology
Advances in psychotropic drug
development: Promising novel targets
and agents for psychiatric disorders
PS-22
How to fight with bipolar disorder?
From guidelines to clinical
practice: Myths and realities
PS-23
Individualized medicine:
Focus on pharmacogenetics
COFFEE BREAK
COURSE and WORKSHOP
18.30-20.30
WS-02
Residency and fellowship training
and short-term research / clinical
possibilities in psychiatry in USA
Tahir Tellioğlu, USA
KC-05
EMDR course
KC-01
part 3
KC-02
NOVEMBER 27, 2011 SUNDAY
TIME
09.00-10.30
HALL A
PS-24
Effects of psychotropics and other drugs on quality of life, employee security, flight and traffic safety
10.30-11.00
COFFEE BREAK
11.00-12.00
CLOSING and AWARDS CEREMONY
ABBREVIATIONS
SCIENTIFIC PROGRAM
NOVEMBER 23, 2011 WEDNESDAY
HALL A
13.30
Arriving to hotel - registration
15.00-16.00
OPENING CONFERENCE
Chairperson: M. Kemal Sayar, Türkiye
Evolution of human brain functions: Identifying
psychobiological targets for promoting well-being
Claude Robert Cloninger, USA
16.30 - 17.00 COFFEE BREAK
17.30-19.30
PS-01: Epigenetics or genetics: Gene-environment interactions over the life - span
Co-chairs: Neşe Kocabaşoğlu, Türkiye - Alan Leslie Hudson, Canada
From genes to epigenetics: Etiopathogenic mechanisms of diseases
Psychiatric disorders: Genes or childhood traumas?
ADHD: Genetics and /or acquired?
Psychosis: Genes and /or addictive subtances?
Alzheimer’s dementia: Genes and /or life-style?
Alzheimer’s disease, genes and biomarkers
Ahmet Korkmaz, Türkiye
Ümit Başar Semiz, Türkiye
Özgür Öner, Türkiye
Ali Doruk, Türkiye
Engin Eker, Türkiye
Işın Baral Kulaksızoğlu, Türkiye
HALL B
17.30-19.30
PS-02: Behavioral addictions and treatments: Review of recent data
Co-chairs: Bekir Aydın Levent - Lütfullah Beşiroğlu, Türkiye
Internet addiction
Shopping addiction
Pathological gambling
From Don Juanism and nymphomania to hypersexual disorders
Trichotillomania
Is binge eating a type of addiction?
Lut Tamam, Türkiye
Levent Sevinçok, Türkiye
Ömer Şenormancı, Türkiye
Sultan Doğan, Türkiye
Ramazan Konkan, Türkiye
Fulya Maner, Türkiye
HALL C
17.30-19.30
PS-03: Painful syndromes in psychiatry and their managements
Co-chairs: Abdülkadir Çevik - Erol Göka, Türkiye
Personality characteristics of pain in psychiatric disorders
At the pain junction fibromyalgia syndrome and depression
Alexithymia and painful syndromes
Differences of SSRI and SNRI antidepressants of painful
syndromes treatments in psychiatry
Hypnotherapy for painful syndromes in psychiatry
Mehmet Ak, Türkiye
M. Kemal Sayar, Türkiye
Hüseyin Güleç, Türkiye
Abdurrahman Altğndağ, Türkiye
M. Kerem Doksat, Türkiye
SCIENTIFIC PROGRAM
HALL A
09.00-10.30
KL-01: Treatment of opioid dependence during pregnancy
Peter R. Martin, USA
Chairperson: Nazan Aydın, Türkiye
11.00-12.30
MD-01: Antidepressants are not associated with suicide risk
Moderator: Serdar Dursun, Canada
Proponent : Nesrin Dilbaz, Türkiye
Opponent : Hakan Türkçapar, Türkiye
12.30 - 13.30 LUNCH
13.30-14.30
SATELLITE SYMPOSIUM
14.30-16.00
MD-02: Antidepressants are useful in treatment of depression
Moderator: M. Zihni Sungur, Türkiye Proponent : Ian Anderson, UK
Opponent : Irving Kirsch, UK / USA
16.30-18.00
KL-02: Benzylpiperazine; a major contaminant of ecstasy, induces
marked changes in rat brain neurochemistry and behavior
Chairperson: İlhan Yargıç, Türkiye
18.30-20.30
JS-02: Malaysian Psychiatric Association
Malaysian perspective of substance dependence
Co-chairs: Mohamed Husain Habil, Malaysia - Haluk Savaş, Türkiye
Drug problems and harm reduction approach in Malaysia
National methadone maintenance therapy program (MMTP):
An update of five pilot projects in Malaysia
Spiritually enhanced drug addiction rehabilitation (SEDAR) program:
The innovative ways to upscale MMTP in Malaysia
National MMTP: Paving the way towards liaison with the community
ABBREVIATIONS
Mohamed Husain Habil, Malaysia
Hazli Zakaria, Malaysia
Rusdi Abd Rashid, Malaysia
Umi Adzlin Silim, Malaysia
SCIENTIFIC PROGRAM
HALL B
09.00-10.30
PS-04: Adult attention - deficit hyperactivity disorder (ADHD) and comorbidity
Co-chairs: Alan Leslie Hudson, Canada - Nesrin Dilbaz, Türkiye
ADHD and prognosis
ADHD in adults: Impulsivity components and links with aggression
ADHD and substance use
ADHD and mood disorders in children
ADHD and psychotic disorders
Academic and occupational problems in ADHD
Yasemen Işık Taner, Türkiye
Yankı Yazgan, Türkiye
Cengiz Tuğlu, Türkiye
Cengiz Başoğlu, Türkiye
Mücahit Öztürk, Türkiye
11.00-12.30
PS-06: Neuroimaging in psychopharmacology: An update
Co-chairs: Peter Martin, USA - Ali Saffet Gönül, Türkiye
Neuroimaging studies in dementia, psychiatric disorders, drug discovery and more...
Imaging of the serotonergic system in depression and anxiety
Can psychiatric disorders be predicted by neuroimaging studies?
What is the real meaning of ventricular enlargement in schizophrenia? From two dimensions to the third dimension
Devrim Ünay, Türkiye
Murad Atmaca, Türkiye
Ali Saffet Gönül, Türkiye
Buğçe Vedin, Türkiye
12.30 - 13.30 LUNCH
16.30-18.00
JS-01: International Association for Cognitive Psychotherapy (IACP)
Advances and problems in Cognitive Behavior Therapy (CBT)
Co-chairs: M. Zihni Sungur, Türkiye - Stefan Hofmann, USA
Recent advances in the treatment of anxiety disorders
Recent advances in translating science into practice: Collaborative empiricism and engagement with homework assignments
As an evidence based approach CBT: Alarms in the treatment and
application mistakes
Stefan Hofmann, USA
Nikolaos Kazantzis, Australia
M. Zihni Sungur, Türkiye
18.30-20.30
PS-07: The rationale of antipsychotic combinations in schizophrenia: Epidemiological and clinical evidences
Co-chairs: Pavel Mohr, Czech Republic - İsmail Ak, Türkiye
Comorbidity vs co-occurrence in schizophrenia
Özcan Uzun, Türkiye
What are the scientific bases of the use of atypical antipsychotics?
Ender Taner, Türkiye
Pharmacogenetics and antipsychotic combinations
Filiz Karadağ, Türkiye
Is there any connection between depression and schizophrenia?
Abdullah Akpınar, Türkiye
Between extrapyramidal and metabolic side effects of antipsychotics: What can we do?
Erdal Işık, Türkiye
Other side effects of antipsychotics: What can we do?
H. Murat Emül, Türkiye
SCIENTIFIC PROGRAM
HALL C
09.00-10.30
PS-05: Brain mapping, TMS, NVS, biofeedback and deep brain stimulation in treatment of psychiatric disorders
Co-chairs: Ercan Abay, Türkiye
Brain mapping and computerized EEG treatment and biofeedback
of psychiatric disorders
Transcranial Magnetic Stimulation (TMS) as a treatment for depression
What is the best method of targeting TMS for depression? Novel rTMS depression treatment protocols
What does transcranial magnetic stimulation (TMS) promise in
psychiatric disorders other than depression? Future perspectives
Deep brain stimulation as an alternative treatment for
neuropsychiatric disorders
Nervus Vagus Stimulation (NVS) in depression treatment
Mert Savrun, Türkiye
Ayhan Algül, Türkiye
Nevzat Tarhan, Türkiye
Bahadır Bakım, Türkiye
Mehmet Aydın, Türkiye
Sadiye Visal Buturak, Türkiye
11.00-12.30
POSTER SESSIONS
Co-chairs: Haluk Savaş - Ayhan Algül, Türkiye
12.30 - 13.30 LUNCH
14.30-16.00
ORAL SESSIONS
Co-chairs: Ali Saffet Gönül - Yasin Bez, Türkiye
18.30-20.30
PS-08: Advances in complementary alternative psychotropic drugs: Fish oil (omega-3 fatty acids),
vitamine B12, folate ve other add-on therapies in psychiatric disorders
Co-chairs: Manickam Thirunavukarasu, India - Mesut Çetin, Türkiye
What are the mechanisms of omega-3 fatty acids, vitamine B12,
folate and other add-on therapies in psychiatric disorders?
Omega-3 fatty acids in ADHD treatment
Are omega-3 fatty acids useful in maintenance treatments?
Is fish oil promising in treating depression during pregnancy and lactation?
Can St. John’s Wort be an alternative treatment of depression?
Complementary medicine alternatives in other psychiatric disorders
(sleep, pain, etc.)
ABBREVIATIONS
Cemal Kaya, Türkiye
İbrahim Durukan, Türkiye
Armağan Samancı, Türkiye
Evrim Özkorumak, Türkiye
Çiçek Hocaoğlu, Türkiye
Bülent Bahçeci, Türkiye
COURSES
HALL D
20.30-22.30
KC-01: Biostatistics - Basic part 1
HALL E
20.30-22.30
KC-02: Biostatistics - Intermediate part 1
HALL C
20.30-22.30
KC-04: Mindfulness and acceptance based therapies
Kültegin Ögel, Türkiye
KC-01 & KC-02 Course participants should bring NOTEBOOK or NETBOOK with them.
KC-01 & KC-02 Course registration is limited to 15 people for each and early application is recommended to register.
There is no limit to the number of participants for courses other than KC-01 and KC-02 courses which are limited with 15
participants each. Registration is required for each course and workhop. Registration fee is 10.-Euro
THERAUPATIC ALLIENCE EDUCATION PROGRAM
15.00-19.00
THERAUPATIC ALLIENCE EDUCATION PROGRAM
Hakan Türkçapar
Sponsored by
Theraupatic Allience Education Program is limited to 40 people. Early application is recommended to register.
SCIENTIFIC PROGRAM
HALL A
09.00-10.30
KL-03: Unipolar versus bipolar depression in children: What do
we know about the etiology, diagnosis, and treatment?
Chairperson: Tümer Türkbay, Türkiye
11.00-12.30
MD-03: Antidepressants are useful in the treatment of bipolar disorders
Moderator: Haluk Savaş, Türkiye
Proponent : Selçuk Kırlı, Türkiye
Opponent : Kaan Kora, Türkiye
12.30 - 13.30 LUNCH
13.30-14.30
SATELLITE SYMPOSIUM
14.30-16.00
PS-13: Hormones and psychiatric disorders
Co-chairs: Constantin Soldatos, Greece - İbrahim Balcıoğlu, Türkiye
The hypothalamic - pituitary - adrenal axis
Thyroid axis
Effects of oxytocin on the social behavior
Insulin
Sex steroids
Melatonin
Ertuğrul Eşel, Türkiye
Tayfun Turan, Türkiye
Nuray Atasoy, Türkiye
Mesut Çetin, Türkiye
Erdem Deveci, Türkiye
Müfit Uğur, Türkiye
16.30-18.00
KL-04: Transcultural psychiatry (a comparison of USA - Türkiye
and sample cases)
Chairperson: Erol Göka, Türkiye
18.30-20.30
JS-04: The International Union of Basic and Clinical Pharmacology (IUPHAR)
Pharmacogenomics of psychoactive drugs
Co-chairs: Ingolf Cascorbi, Germany - Feyza Arıcıoğlu, Türkiye
Role of polymorphic drug transporters in treatment resistant depression
Relationship between pharmacogenetic traits and personality
Genetic causes of hypersensitivity to antipsychotics - the clozapine story
ABBREVIATIONS
Tanja Brueckl, Germany
Adrián Llerena, Spain
Ingolf Cascorbi, Germany
SCIENTIFIC PROGRAM
HALL B
09.00-10.30
PS-09: From preclinical studies to clinical practice in anxiety disorders
Co-chairs: Hayriye Elbi - Raşit Tükel, Türkiye
Behavioral models in anxiety disorders
Pharmacological models in anxiety disorders
Genetic models in anxiety disorders
New drug molecules in pre-clinical applications of anxiety disorders
The frequency of anxiety disorders in general hospitals
Pharmacotherapy vs psychotherapy in anxiety disorders?
Hüseyin Günay, Türkiye
M. Murat Demet, Türkiye
Nurper Erberk Özen, Türkiye
Raşit Tükel, Türkiye
Hayriye Elbi, Türkiye
Şebnem Pırıldar, Türkiye
11.00-12.30
PS-11: Psychotropic drug treatments during pregnancy and lactation
Co-chairs: Medaim Yanık - Nihat Alpay, Türkiye
Schizophrenia
Bipolar disorders
OCD
Depression
Substance dependency
Panic disorder
Bülent Kayahan, Türkiye
Fisun Akdeniz, Türkiye
Servet Ebrinç, Türkiye
Gökay Alpak, Türkiye
Zehra Arıkan, Türkiye
Faruk Uğuz, Türkiye
12.30 - 13.30 LUNCH
14.30-16.00
PS-14: Clinical course of psychiatric disorders associated with trauma and treatment issues
Co-chairs: Nahit Özmenler - Ümit Başar Semiz, Türkiye
Trauma and psychotic disorders
Trauma and mood disorders
Trauma and anxiety disorders
Trauma and personality disorders
Trauma and dependencies
Trauma and sexual dysfunctions
Selma Bozkurt Zincir, Türkiye
Medine Yazıcı Güleç, Türkiye
Esin Evren Kılıçaslan, Türkiye
Barbaros Özdemir, Türkiye
Taner Öznur, Türkiye
Murat Erdem, Türkiye
16.30-18.00
JS-03: Hellenic Society for the Advancement of Psychiatry and Related Sciences
Disorders of sleep and wakefulness and their pharmacological management
Co-chairs: Constantin Soldatos, Greece - Sunar Birsöz, Türkiye
Insomnia and the effects of hypnotics on sleep
Hypersomnias and the effects of vigilance - promoting compounds
Depression and the effect of antidepressants on sleep
Constantin Soldatos, Greece
Antigone Papavasiliou, Greece
Thomas Paparrigopoulos, Greece
SCIENTIFIC PROGRAM
HALL B
18.30-20.30
PS-16: Marijuana; from mellow to madness
Co-chairs: Mohamed Husain Habil, Malaysia - Zehra Arıkan, Türkiye
What is prevalence of cannabis dependence in Türkiye?
The effect of cannabis use on cognitive functions
The differences of marijuana psychosis from other substance induced psychoses
Pharmacological treatment of cannabis psychosis
Selective serotonin reuptake inhibitors (SSRIs) in the treatment of cannabis dependence
Pharmacological drug treatment of substance-induced psychosis,
drug interactions, and considerations
ABBREVIATIONS
Hakan Coşkunol, Türkiye
Cüneyt Evren, Türkiye
Mükerrem Güven, Türkiye
Ömer Geçici, Türkiye
Musa Tosun, Türkiye
Osman Vırıt, Türkiye
SCIENTIFIC PROGRAM
HALL C
09.00-10.30
PS-10: Will glutamatergic modulators be a target for the future therapy of depression?
Co-chairs: Cyril Höschl, Czech Republic - Glen Baker, Canada
Treatment with traditional antidepressants and related problems
Glutamatergic system and its importance in the neurobiology of depression
Glutamatergic system and genetic markers associated with
antidepressant treatment
Ketamine and other glutamatergic modulators as an antidepressant
Do atypical antipsychotics have any glutamatergic effect?
Ayşegül YIldız, Türkiye
Feyza Arıcıoğlu, Türkiye
Hasan Herken, Türkiye
Kemal Yazıcı, Türkiye
11.00-12.30
PS-12: Vitamin and mineral supplementation in treatment of childhood psychiatric disorders
Co-chairs: Tümer Türkbay - Özgür Öner, Türkiye
Iron supplementation
Zinc supplementation
Calcium and Vitamin D supplementation
Cholesterol and Omega 3 fatty acids supplementation
Vitamin B 12 and folate supplementation
Antioxidant vitamin supplementation
Ayhan Bilgiç, Türkiye
Ebru Kültür Çengel, Türkiye
Ömer Faruk Akça, Türkiye
Sabri Hergüner, Türkiye
Burak Doğangün, Türkiye
Betül Mazlum, Türkiye
12.30 - 13.30 LUNCH
16.30-18.00
PS-15: Depression and pain
Chairperson: Selçuk Kırlı, Türkiye
Epidemiology of pain in depression
Clinical characteristics and mechanism of pain in depression
Interaction of pain and depression in terms of clinical characteristics and mechanism
Impact of pain on treatment in depression
Saygın Eker, Türkiye
Selçuk Kırlı, Türkiye
Yusuf Sivrioğlu, Türkiye
Cengiz Akkaya, Türkiye
18.30-20.30
PS-17: Overcoming treatment resistance: An update
Co-chairs: Orhan Doğan- Sefa Saygılı, Türkiye
Treatment resistant psychiatric disorders and comorbidities
Treatment resistant psychiatric disorders and trauma history
Strategies in treatment resistant psychotic disorders
Strategies in treatment resistant depression
Strategies in treatment resistant panic disorders
Psychosocial interventions in resistance to treatment
Tunç Alkın, Türkiye
M. Akif Ersoy, Türkiye
M. Emin Ceylan, Türkiye
Selçuk Aslan, Türkiye
Erhan Bayraktar, Türkiye
Mustafa Yıldız, Türkiye
COURSES
HALL C
14.30-16.00
KC-03: CBT in somatization disorders
Axel Würz, UK
HALL C
20.30-22.30
WS-01: Management of panic disorder
HALL D
20.30-22.30
HALL E
20.30-22.30
ABBREVIATIONS
SCIENTIFIC PROGRAM
HALL A
09.00-10.30
JS-05: Indian Psychiatric Society
Current concept of obsessive compulsive disorder (OCD)
Co-chairs: Manickam Thirunavukarasu, India - Numan Konuk, Türkiye
Current understanding of the concept of obsessive compulsive disorder
Biological theories of obsessive compulsive disorder
Psychopharmacological and somatic interventions in OCD
Psycho-social interventions in OCD
Manickam Thirunavukarasu, India
A. Shyam Sundar, India
Kandasamy Arun, India
Manickam Thirunavukarasu, India
11.00-12.30
Joseph Zohar, Israel
KL-06: Early intervention in anxiety and depression: What we know,
what we don’t know and what we should know?
Chairperson: Oğuz Karamustafalıoğlu, Türkiye
12.30 - 13.30 LUNCH
13.30-15.30
JS-06: Czech NeuroPsychopharmacological Society (CNPS)
From models of schizophrenia to clinical outcome: A psychopharmacological perspective
Co-chairs: Cyril Höschl, Czech Republic - Özcan Uzun, Türkiye
Basic concepts of schizophrenia: Experimental approaches
Prediction validity in animal models of schizophrenia
The ins and outs of human model of schizophrenia
Safety first, efficacy second? Fear and needs of treatment in the
absence of controlled data
Cyril Höschl, Czech Republic
Tomas Palenicek, Czech Republic
Jiri Horacek, Czech Republic
Pavel Mohr, Czech Republic
16.00-18.00
JS-07: Canadian College of Neuropsychopharmacology
Advances in psychotropic drug development: Promising novel targets and
agents for psychiatric disorders
Co-chairs: Glen Baker, Canada - Mesut Çetin, Türkiye
Novel imidazoline compounds as potential new therapies for psychiatric disorders
Advances in antipsychotic targets and drug development
Advances in antidepressant targets and drug development
Glen Baker, Canada
SCIENTIFIC PROGRAM
HALL B
09.00-10.30
Tahir Tellioğu, USA
KL-05: Medical marijuana use in psychiatry
Chairperson: Ömer Geçici, Türkiye
11.00-12.30
PS-19: Are the effects of psychopharmacological and other therapeutic approaches
neuroregenerative or neurodegenerative? Review of recent data
Co-chairs: Rüstem Aşkın - A. Saffet Gönül, Türkiye
What is the hippocampal neurogenesis?
Effects of psychotropics
Effects of ECT, TMS, and others
Effects of psychotherapies
Effects of physical exercise
Çağdaş Eker, Türkiye
Ömer Aydemir, Türkiye
Alpay Ateş, Türkiye
Mine Özmen, Türkiye
Hakan Balıbey, Türkiye
12.30 - 13.30 LUNCH
13.30-15.30
PS-21: Treatment approaches to comorbidities of ADHD
Co-chairs: Meral Berkem, Türkiye - Rasim Somer Diler, USA
Treatment approaches to psychiatric comorbidities of ADHD in children
Treatment approaches to psychiatric comorbidities of ADHD in adolescents
Treatment approaches to psychiatric comorbidities of ADHD in adults
Treating children with ADHD and comorbid neurological disorders
Drug interactions in medications for comorbidities of ADHD
Tümer Türkbay, Türkiye
Bengi Semerci, Türkiye
İlhan Yargıç, Türkiye
Murat Yüce, Türkiye
Osman Abalı, Türkiye
16.00-18.00
PS-22: How to fight with bipolar disorder? From guidelines to clinical practice: Myths and realities
Co-chairs: Haluk Savaş - Erhan Kurt, Türkiye
How the guidelines are prepared? Are they necessary?
How to use them? Their benefits and limitations?
Manic episode: Treatment recommendations in guidelines and clinical challenges / realities?
Bipolar depression: Treatment recommendations in guidelines and
clinical challenges / realities?
Maintenance in bipolar disorder: Treatment recommendations in
guidelines and clinical challenges / realities?
Mixed episode in bipolar disorder: Treatment recommendations in
guidelines and clinical challenges / realities?
Type II bipolar disorder: Treatment recommendations in guidelines and
clinical challenges / realities?
Yasin Bez, Türkiye
Numan Konuk, Türkiye
Haluk Savaş, Türkiye
İbrahim Eren, Türkiye
Ahmet Ünal, Türkiye
Cengiz Başoğlu, Türkiye
ABBREVIATIONS
SCIENTIFIC PROGRAM
HALL C
09.00-10.30
PS-18: Chronobiotics and chronotherapeutics in psychiatry
Co-chairs: Tunay Karlıdere - Ahmet Korkmaz, Türkiye
Phylogenetic aspects of biological rhythms and behavior
Melatonin and mood
A general overview of chronotherapeutics
Psychotropic drugs affecting biological rhythms (chronobiotics)
Bright light therapy use in treatment of depressions other than
seasonal affective disorder
Sleep deprivation use in treatment of depressive disorders
Okan Çalıyurt, Türkiye
Ahmet Korkmaz, Türkiye
Yavuz Selvi, Türkiye
Elif Oral, Türkiye
Mustafa Güleç, Türkiye
Adem Aydın, Türkiye
11.00-12.30
PS-20: Controversial topics in eating disorders
Co-chairs: Atila Erol, Türkiye - Alican Dalkılıç, USA
Psychopharmacological treatments in eating disorders
Night eating syndrome
Efficacy of psychotherapy in bulimia nervosa
Body image issues in eating disorders
Obesity and impulsivity
Comorbidities in eating disorders
Özlem Orhan, Türkiye
Başak Yücel, Türkiye
Erdal Vardar, Türkiye
Bilge Burçak Annagür, Türkiye
Atila Erol, Türkiye
12.30 - 13.30 LUNCH
16.00-18.00
PS-23: Individualized medicine: Focus on pharmacogenetics
Co-chairs: Rüstem Aşkın - Feyza Arıcıoğlu, Türkiye
Genetics and drugs: From research to clinical studies Turkish perspective
Pharmacogenomic biomarkers and individualized medicine in psychiatry
What is the rationale of individualized medicine in psychiatry?
Pharmacogenetics: Management of side effects and drug interactions of antipsychotics
Pharmacogenetics and how individualized medicine can be
applied to the practice of psychiatry?
Pharmacogenetics: Side effects and drug interactions of
antidepressants and their management
Cem Şengül, Türkiye
Yeşim Aydın Son, Türkiye
Hasan Herken, Türkiye
Murat Kuloğlu, Türkiye
Çiğdem Aydemir, Türkiye
Oğuz Karamustafalıoğlu, Türkiye
COURSES
HALL D
18.30-20.30
HALL E
18.30-20.30
HALL C
18.30-20.30
KC-05: EMDR course
HALL B
18.30-20.30
WS-02: Residency and fellowship training and short-term research / clinical observership
possibilities in psychiatry in USA
Tahir Tellioğlu, USA - Alican Dalkılıç, USA
ABBREVIATIONS
SCIENTIFIC PROGRAM
NOVEMBER 27, 2011 SUNDAY
HALL A
09.00-10.30
PS-24: Effects of psychotropics and other drugs on quality of life, employee security, flight and traffic safety
Co-chairs: Ali Çayköylü - Mecit Çalışkan, Türkiye
Psychotropics and other drugs: Sleep and road traffic accidents
Effects of psychotropics and other drugs on flight and flight safety
Effects of psychotropics and other drugs on cognitive functions and employee security
Sexual side effects of psychotropic and other drugs
Their side effects of psychotropics and other drugs on quality of life
11.00 - 12.00 CLOSING and AWARDS CEREMONY
Mustafa Bilici, Türkiye
Muzaffer Çetingüç, Türkiye
Serhat Çıtak, Türkiye
Adnan Özçetin, Türkiye
Ömer Böke, Türkiye
Contents
Author(s)
Title
Abstracts of the Invited Speakers
1
C. R. Cloninger
The evolution of human brain functions: Implications for psychobiological targets for wellbeing
S34
2
P. R. Martin
Opioid dependence during pregnancy: Balancing risk versus benefit
S35
3
A. L. Hudson, N. Zepeda, A. Perreault
M. Lalies, G. Baker
l-Benzylpiperazine, a major contaminant of ecstasy, induces marked changes in rat brain
neurochemistry and behaviour
S35
4
R. S. Diler
Unipolar versus bipolar depression in children: What do we know about the etiology,
diagnosis, and treatment?
S36
5
A. Dalkilic
Transcultural psychiatry: Practice and sample cases in USA and status in Turkiye
S37
6
T. Tellioglu
Medical marijuana use in psychiatry
S37
7
I. Anderson
Antidepressants are useful in the treatment of depression: the case for the motion
S38
8
I. Kirsch
Have clinically significant benefits of antidepressants been demonstrated?
S38
9
S. Kırlı
Antidepressants are useful in the treatment of bipolar disorders
S39
10
S. Hofmann
S40
11
N. Kazantzis
Translating science into practice, collaborative empiricism and engagement in homework
assignments in cognitive behavior therapy
S41
12
M. Z. Sungur
CBT as an evidence based treatment approach: Warning signs in therapy and common
mistakes in daily practice
S41
13
R. A. Rashid, A. K. B. A. Bakar,
H. B. Zakaria, U. B. Adzlin, M. H. Habil
A harm minimization program against drug use and HIV problems in Malaysia
S42
14
T. Paparrigopoulos
S42
15
C. R. Soldatos, T. PaparrigopoulosI
S43
16
A. Papavasiliou
Hypersomnias and the effects of vigilance-promoting compounds
S44
17
T. Brueckl, M. Uhr
Role of polymorphic drug transporter in treatment-resistant depression
S44
18
A. Llerena
Relationship between pharmacogenetics and personality traits: Relevance for suicide
S45
19
I. Cascorbi
Genetic causes of hypersensitivity to antipsychotics – the clozapine story
S45
20
M. Thirunavukarasu
S46
21
A. S. Sundar
S46
22
K. Arun
Psychopharmacological and somatic interventions for OCD
S47
23
M. Thirunavukarasu
Psycho-social interventions for OCD
S47
24
P. Mohr, D. Hnidek, D. Seifertova
Safety first, efficacy second? Fear and the need for treatment in the absence of
controlled data
S48
25
C. Höschl
S48
26
J. Horacek, V. B. Valesova,
T. Palenicek, F. Spaniel, C. Höschl
The ins and outs of the human model of schizophrenia
S49
27
S. Dursun, G. B. Baker, M. Mackay
Recent advances in the neurochemistry of schizophrenia and potential targets for
antipsychotic drug development
S50
28
G. B Baker, N. D Mitchell,
J. M. Le Melledo, S. Dursun
S50
Contents
Author(s)
Title
29
E. Eker
Alzheimer’s disease: Genes and/or life style
S51
30
S. Doğan
S52
31
Ö. Şenormancı
Pathological gambling: review of recent data
S53
32
F. Maner
S53
33
M. Ak
Pain and personality
S54
34
A. Altındağ, G. Elboğa
The differences between SSRIs and SNRIs in the treatment of psychiatric pain syndromes
S55
35
H. Güleç
How does alexithymia lead to painful syndromes?
S55
36
K. M. Doksat
S56
37
R. S. Diler
S57
38
M. Öztürk
S57
39
N. Tarhan, G. Hızlı, S. Aydın
Concomitant use of qEEG and rTMS in treatment of depressive disorder, new approaches
S58
40
B. Bakım
What does transcranial magnetic stimulation (TMS) promise in psychiatric disorders other
than depression? Future perspectives
S59
41
Ayhan Algül
Transcranial magnetic stimulation (TMS) as a treatment for depression
S59
42
Ş. V. Buturak
Vagus Nerve Stimulation (VNS) in depression treatment
S60
43
M. D. Aydın
Neurophysical basis of neurostimulative psychosurgery: A historical review, new
perspectives, and future insights
S60
44
N. B. V. Özçelik
What is the real meaning of ventricular enlargement in schizophrenia?
S61
45
D. Ünay
Neuroimaging studies in dementia, psychiatric disorders, drug discovery, and more
S62
46
F. Karadağ
S62
47
E. Taner
Scientific bases of use of atypical antipsychotics
S63
48
E. Özkorumak
Is fish oil promising in the treatment of depression during pregnancy and lactation?
S64
49
Ç. Hocaoğlu
Can St. John’s Wort be an alternative treatment for depression?
S64
50
B. Bahçeci
Complementary medicine alternatives for other psychiatric abnormalities
(Like insomnia and pain)
S65
51
İ. Durukan
Essential fatty acids in ADHD treatment
S66
52
M. C. Kaya
Mechanisms of fish oil (Omega-3 fatty acids), vitamin B12, folate and other add-on
treatments in psychiatric disorders
S66
53
H. Elbi
Medical disease and anxiety disorders
S67
54
N. E. Özen
S68
55
H. Günay
Anxiety models in experimental animals
S68
56
S. Dursun, G. Baker, N. Mitchell
Ketamine and other glutamate modulators as potential antidepressants
S69
57
F. Arıcıoğlu
The glutamatergic system and its importance in the neurobiology of depression
S70
58
F. Uğuz
Pharmacotherapy of panic disorder during pregnancy and lactation
S70
59
S. Ebrinç
Psychotropic drug treatment during pregnancy and lactation in obsessive compulsive disorder
S71
Contents
Author(s)
Title
60
Ö. F. Akça
Vitamin and mineral supplementation in treatment of childhood psychiatric disorders –
Calcium and vitamin D supplementation
S72
61
S. E. Ç. Kültür
Zinc supplementation in psychiatric disorders of children
S73
62
A. Bilgiç
The impacts of iron deficiency on mental health in childhood
S73
63
B. Mazlum
Antioxidant vitamin supplementation therapies in child psychiatry
S74
64
S. Hergüner
Effectiveness of omega fatty acid supplementation for childhood psychiatric disorders
S74
65
M. Uğur
Melatonin and human behaviour
S75
66
N. Atasoy
Effects of oxytocin on social behaviour
S76
67
T. Turan
Thyroid hormones and psychiatric disorders
S76
68
E. Deveci
Sex steroids and psychiatric disorders
S77
69
M. Cetin
Insulin and psychiatric disorders
S78
70
M. Y. Güleç
S78
71
S. B. Zincir
S79
72
M. Erdem
Relationship of sexual dysfunction with trauma
S80
73
C. Akkaya
S81
74
S. Kırlı
S81
75
C. Evren
Effect of cannabis use on cognitive functions
S82
76
M. Güven
The differences between marijuana psychosis and other substance induced psychoses
S83
77
M. Tosun
Selective serotonin reuptake inhibitors in the treatement of cannabis dependence
S84
78
S. Aslan
Treatment strategies for treatment resistant depression
S85
79
M. A. Ersoy
S85
80
M. Yıldız
Pyshosocial approaches for treatment resistant symptoms in patients with schizophrenia
S86
81
A. Aydın
The use of sleep deprivation in the treatment of depressive disorders
S87
82
E. Oral
Psychotropic drugs effecting biological rhythm (Chronobiotics)
S88
83
Y. Selvi
S88
84
M. Güleç
Bright light therapy in treatment of depressive disorders other than seasonal affective disorder
S89
85
Ö. Aydemir
Is the effect of psychotropic drugs neurodegenerative or neuroprotective?
S90
86
M. Özmen
Effect of psychotherapy on neurogenesis
S90
87
H. Balıbey
Are the effects of psychopharmacological and other therapeutic approaches neuroregenerative
or neurodegenerative? Review of recent data and effects of physical exercise
S91
88
A. Erol
S92
89
A. Dalkilic
S93
90
B. B. Annagür
S94
91
B. Yücel
S94
Contents
Author(s)
Title
92
T. Türkbay
S95
93
B. Semerci
S96
94
M. Yüce
Treatment of neurological co-morbid disorders in children with ADHD
S96
95
O. Abalı
Drug interactions of medications for comorbidities of ADHD
S97
96
A. Ünal
Treatment of mixed episodes of bipolar disorders in manuals. What are the recommendations?
S97
97
Y. Bez
How are the guidelines prepared? Are they necessary? How to use them? Their benefits and
limitations?
S98
98
I. Eren
Maintenance treatment in bipolar disorder: What do guidelines recommend?
S99
99
C. Şengül
S100
100
Ç. Aydemir
Pharmacogenetics and how individualized medicine can be applied to the practice of psychiatry
S101
101
Y. Aydın Son
Pharmacogenomics biomarkers and personalized medicine in psychiatry
S101
102
M. Çetingüç
The effects of psychotropic and other drugs on flight and flight safety
S102
103
A. Özçetin
S103
104
S. Kılıç
Basic Biostatistics
S104
105
A. Würz
S104
106
K. Ögel
Mindfulness and acceptance based therapies
S105
107
S. Güner
Eye movement desensitization and reprocessing method [EMDR] Specifically designed for
Turkish patient population in the Netherlands
S106
108
S. Güner
Alternative CBT method of panic disorder treatment for Turkish patients
S106
Abstracts of Oral Presentations
1
C. Neale, A. Scholey, M. Hughes,
P. Johnston
Bacopa monniera: Current trends and future directions
S108
2
C. B. Şengül, M. E. Erdal, C. Şengül,
Ö. İ. Ay, M. Efe, M. E. Ay, H. Herken
Association of the DRD2 TaqIA, 5-HT1B A-161T, and CNR1 1359 G/A polymorphisms
with alcohol dependence: A single center study in the Denizli Province of Turkey
S108
3
M. C. Pieri
Treating psychotic substance abuse patients with opioid agonist therapy and the atypical
antipsychotic olanzapine
S109
4
O. Erbas, S. Bora
A comparison of the effects of typical and atypical antipsychotics on the basolateral
amygdala of rats using deep brain EEG recordings
S109
5
S. Abolghasemi, G. Mahmodi, M. Zafari
The effect of cognitive-behavioral therapy in reducing the feeling of emotional
pressure and blood sugar control in patients with type 2 diabetes
S111
6
M. M. Abtahi, H. Molavi, J. Moshtaghian,
K. Askari
Acute effects of nicotine on working and reference memory in rats using
a 12-arm radial maze
S111
7
J. Shafaie, S. Farjad
The relationship between personality characteristics and internet addiction in adolescents
S112
8
M. Allahtavakoli, B. Jarrott
The sigma-1 receptor ligand, PRE-084, reduced infarct volume, neurological deficits,
pro-inflammatory cytokines, and enhanced anti-inflammatory cytokines after embolic
stroke in rats
S112
9
F. Hashemian, M. S. Tabatabayi,
A. Sharifi, M. Majd
Comparison of the effects of bupropion and fluoxetine on reaction time in adults
with major depressive disorder in a 4-week, single-blind study
S113
Contents
Author(s)
Title
10
O. Bigdeli, F. Hashemian, M. Shohrati,
A. Mokri, M. Majd
A placebo-controlled double-blind add-on study of Ginseng in opioid withdrawal syndrome
S113
11
M. Altın, L. Alev, K. Özbek, D. Hobbs,
J. Karagianis, T. Treuer, J. Raskin
An in vitro analysis of disintegration times of different formulations of orally disintegrating
olanzapine
S114
12
L. Alev, M. Altın, K. Özbek, D. Sheehan,
A. Meyers, J. Ahl, A. Prakash,
T. M. M. Oakes
Effect of duloxetine on functional outcomes in patients with major depressive disorder
S115
13
Z. Kechrid, M. Hamdikene
Effect of vitamin D on zinc status, carbohydrate metabolism, and activities of some
enzymes in alloxan-diabetic rats fed on a zinc deficient diet
S115
14
G. R. Kheirabadi, M. Salehi,
M. R. Maracy, M. Ranjkesh
Gabapentin in the treatment of opioid withdrawal
S116
15
Serwa Mohamadzadeh Ashna
The role of transcranial magnetic stimulation in cognitive processes and treatment of
psychiatric disorders
S117
16
O. Erbas, V. Evren, S. Bora,
G. O. Peker
Oxytocin inhibition of pentylenetetrazole-induced convulsions and its identification by
behavioral measurement and thalamic EEG in the rats
S117
17
O. Erbas
The effects of metoprolol and diltiazem in the prolonged QTc interval caused by
ziprasidone injection in rats
S118
Poster Presentation
1
S. Korkmaz, M. Kuloglu, S. Saglam,
M. Atmaca
Visual hallucinations induced by bupropion: A case report
S121
2
R. Konkan, E. Aydın, O. Güçlü,
Ö. Şenormancı, M. Z. Sungur
Clinical features of patients with panic disorder in outpatient clinics of a psychiatric training
and research hospital
S121
3
M. Zafari, A. Aghamohammadi
Effect of calcium in treatment of premenstrual syndrome
S122
4
H. Balibey, A. Balikci
Eye movement desensitization and reprocessing (EMDR) treatment in a patient with
post-traumatic stress disorder: A case report
S123
5
R. N. Yuksel, Z. E. Kaya, N. Dilbaz
Cabergoline induced manic episode: A case report
S124
6
J. S. Ahn, J. Shin, K. C. Park, S. Min,
M. H. Kim
Substance use and eating patterns of female adolescent students
S124
7
H. Yaci, E. K. Koca, Y. Uz, A. Demir,
A. A. Ozşahin, F. M. Domac
Neuroleptic malignant syndrome: A case report
S125
8
F. Canan, U. Aydınoglu, G. Sinani
Treatment of clozapine induced obsessive compulsive behavior in a schizophrenic patient
with valproic acid augmentation: A case report
S125
9
Ç. H. Yeloglu, H. Guveli, K. Sarp,
B. Bahceci, C. Hocaoglu
Treatment of bipolar disorder in adolescents: A case report
S126
10
E. O. Sonmez, N. Kaya
Leukopenia and neutropenia due to venlafaxine use: A case report
S127
11
M. Ak, E. Sinici, O. Maden, A. Bozkurt,
A. Ozsahin
EMDR treatment for a sexual rape victim: A case report
S127
12
E. Valzdorf
Influence of family and education factors on the inclination to commit crimes in
Soviet times and today
S128
13
M. Nachnani, S. Beatson
Survey of referral pathways to a crisis team
S128
14
E. Valzdorf
Fluanxol and haloperidol efficacy evaluation in treatment of schizophrenic patients
S129
15
S. Karayılan, A. Erol
Anorexia nervosa and cannabis abuse: A case report
S129
Contents
Author(s)
Title
Poster Presentation
16
A. Yucel, M. Gulec, A. Aydin
Fluoxetine-induced thrombocytopenia: A case report
S130
17
M. López, P. Dorado, A. Ortega,
E. P. Lledó, N. Monroy, E. Machín,
M. E. Alonso, A. Llerena
Interethnic differences in UGT1A4 genetic polymorphisms in Mexican and Spanish
populations
S131
18
P. Dorado, E. P. Lledó, E. Machín,
A. Llerena, E. Terán, L. Beltrán
Influence of CYP2C9 genetic polymorphism on losartan oxidation in an Ecuadorian
population
S131
19
S. E. Herizchi, I. T. Piri, I. T. Asvadi,
Z. T. Sanaat, M. T. Golchin,
R. T. Shabanloui
Efficacy of progressive muscle relaxation training on anxiety, depression and quality of life
in cancer patients under chemotherapy
S132
20
O. Erbas, S. Bora, S. Demirgoren,
G. Peker
Anxiety reducing effects of oxytocin on the basolateral amygdala by using an
electrophysiological method
S133
21
F. Maner, O. Hisim, O. Sahmelikoglu,
O. C. Girit, A. Ermis, M. E. Ceylan
Genital mutilation in a patient with schizophrenia: A case report
S133
22
Ö. Ç. Girit, F. Maner, E. Kılınç,
D. İpekçioğlu, M. E. Ceylan
Hoarding and mood disorder: A case report
S134
23
M. Zafari, A. Aghamohammady
Effect of fish oil on treatment of premenstrual syndrome
S134
24
M. G. Ayhan, F. Uguz, N. Kaya
Improvement of risperidone-induced hyperprolactinemia with the addition of aripiprazole:
Case report
S135
25
M. Altın, L. Alev, T. M. Durell,
L. A. Adler, D. W. Williams, A. Deldar,
J. J. Mcgough, P. E. Glaser, R. L. Rubin,
E. S. Sarkis, T. A. Pigott, B. K. Boardman
Atomoxetine for the treatment of ADHD in young adults with an assessment of associated
functional outcomes
S135
26
R. M. Alowesie
Role of psychopharmacological intervention in cognitive and psychological recovery in
hemorrhagic brain injury
S136
27
R. Konkan, E. Aydın, O. Güçlü,
Obsessive beliefs in patients with panic disorder
S136
28
N. R. N. Jaafar, N. Mislan, A. Baharudin,
N. Ibrahim, S. A. Aziz, H. Sidi
Erectile dysfunction in patients on methadone maintenance therapy in Malaysia
S137
29
B. Tıkır, E. Göka, M. Ç. Aydemir,
S. Duran
Cerebellar contusion presenting with pure psychiatric symptoms and cerebellar cognitive
affective syndrome: A case report
S138
30
E. A. Sünbül, M. Sünbül, F. F. Cengiz
Self-perception and anger with chest pain without cardiac etiology
S138
31
S. Hergüner, A. Hergüner
Mirtazapine treatment for weight loss and insomnia associated with methylphenidate:
A chart review depression and somatic symptoms
S139
32
J. S. Choi, H. W. Lee, J. Y. Lee,
H. Y. Jung
Rapid-onset hyponatremia induced by duloxetine in a middle-aged male with
depression and somatic symptoms
S139
33
S. Kesebir, B. Baykaran, B. Toprak,
A. E. Tezcan
Gender specific metabolic adverse effects in bipolar patients: A comparison between lithium,
quetiapine and olanzapine
S140
34
K. Chichinadze, T. Domianidze,
T. Matitaishvili, I. Labadze,
A. Lazarashvili, M. Khananashvili
New model of psychogenic stress-induced depression and antioxidant system of rat brain
S140
35
R. R. Hegazy, H. F. Zaki, O. A. Sharaf,
I. E. Ismail, S. A. Kenawy
Effects of strawberry leaf and celery seed extracts in terlipressin-induced chronic
hyponatremia in rats
S141
36
M. İ. Atagün, Ü. Altınok, Ö. D. Balaban,
Z. Atagün, L. R. Alpkan, K. Öneş
Post traumatic stress disorder in patients with spinal cord injury and relevant factors
S141
Contents
Author(s)
Title
Poster Presentation
37
S. Kesebir, F. Akdeniz, A. Demir,
M. Bilici
A comparison before and after using lamotrigine in long term continued treatment: the effect
of blood levels
S142
38
S. Ö. Kavzoğlu, A. G. Hariri
ICAM, VCAM and E-selectin levels in first episode schizophrenic patients
S142
39
F. Canan, G. Sinani, Ü. Aydınoğlu
Body dysmorphic disorder incidentally treated with bupropion
S143
40
Ö. Şenormancı, O. G. Güçlü, R. Konkan,
Y. Altunkaynak, G. Şenormancı
Tardive akathisia with aripiprazole: A case report
S144
41
M. Kazemi, S. Karimi, H. Hasankhani,
S. Kazemi
Comparing mental disorders between divorced couples and normal couples in a city of Iran
S144
42
S. S. A. Hashmi, A. A. A. Sabri,
N. M. A. Felati
Suicide rate in Oman in the period between January 2000 and December 2010
S145
43
A. Ansari, T. Negahban, A. R. Sayyadi
The effect of the recitation of the Quran on depressed patients in the psychiatry department
of Moradi hospital in Rafsanjan (IRAN)
S145
44
A. Aydın, P. G. Özdemir, Y. Selvi, F. Uğuz
Dissociative symptoms associated with piracetam use: a case report
S146
45
F. Canan, Ü. Aydınoğlu, G. Sinani
Reversible normoprolactinemic galactorrhea induced by fluoxetine
S147
46
Y. Yang, J. Kim, B. Kim, M. Shin, S. Cho
Influence of polymorphism of the norepinephrine transporter gene (SLC6A2) and alpha-2
adrenergic receptor gene (ADRA2A) on regional cerebral blood flow in a Korean ADHD
sample: a preliminary study
S148
47
F. Jan, V. Kennedy
Do we need specialist clinics to monitor metabolic side effects on chronic bipolar patients
in Treatment? – Audit of management of bipolar disorder against NICE guidelines in South
Staffordshire NHS Trust, UK
S148
48
K. Ögel, G. Karadayı, Z. Karaman,
H. A. Arıcan, N. Kaya, U. Karaman,
A. M. Altuğ
Assessment of risk of absenteeism in elemantary school students
S149
49
K. Ögel, C. Koç, B. Karalar, A. Başabak,
A. Aksoy, M. İşmen, R. Yeroham
Effectiveness of an addiction treatment program called SAMBA: A pilot study
S150
50
K. Ögel, A. Başabak, C. Koç, A. Aksoy,
G. Karadayı
Psychometric properties of different forms of the Addiction Profile Index (BAPI)
S151
51
S. Ulusoy, İ. Alnıak, K. F. Yavuz, T. Kara
Aripiprazole treatment for the choreoathetoid movements and psychotic symptoms of
Huntington’s disease: A case report
S152
52
C. Neale, S. Benson, C. Stough, A. Scholey
Acute effects of Bacopa monnieri on mood in healthy young adults
S152
53
N. Sarp, A. A. Çoban, K. Ögel
Anxiety and depressive symptom levels among adolescents with risk taking behaviour
S153
54
F. Yousefi, S. Mohamadzadeh
The relationship between mental health and academic achievement among Kordestan high
school students
S154
55
K. Ögel, F. Karadağ, C. Evren,
D. T. Gürol
Does the profile of addiction change according to the type of the substance used?
S154
56
M. A. Abnavi, A. Javadpour,
S. Mohamadzadeh
Death anxiety among terminally ill inpatients
S155
57
A. A. Nasiripour1, G. Mahmodi,
M. Zafari
The effective features of access to medical care in Iran
S155
58
N. A. Kumsar, A. Erol
Smoking behaviour during the course of paroxetine treatment: A case report
S156
59
H. A. Döm, M. A. Döke, Y. Y. Tuncel,
G. Üstünkar, Y. A. Son
Development of a SNP genotyping panel and a medical decision support algorithm to predict
drug response in schizophrenia
S156
Contents
Author(s)
Title
Poster Presentation
60
Barış Yılbaş, Murat Gönen
Basal ganglial hemorrhage induced mania
S157
61
B. E. Cumurcu, R. Karlıdağ, Ş. Kartalcı,
I. G. Gül, S. Demir, B. Yeşil
Evaluation of cognitive functions in euthymic bipolar patients using mono- and multi- drug
treatments
S158
62
U. M. Aksoy, Ş. G. Aksoy, F. Maner
Adult ADHD symptoms in cannabis dependence and the importance of comorbidity
in Adult ADHD
S158
63
B. Soyer, J. Kenar, K. S. Karataş
Ganser syndrome as a dissociative disorder: A case report
S159
64
A. A. Bilgin, B. Çam
Escitalopram induced galacthorrea: Phenomenon presentation
S160
65
Y. Taner, H. A. Taner
Amisulpride use in treatment of Tourette’s disorder
S160
66
H. Toğul
Lithium associated glossodynia syndrome: A case report
S160
67
H. Ünübol, B. Ünübol, J. Güler, A. Ünal
Two cases of affective disorder due to immunosuppresive treatment that followed renal
transplantation
S161
68
İ. İnanlı, İ. Eren, T. Etli
Varenicline induced psychotic disorders: A case report
S162
69
F. Büyükşahin, J. Güler, B. Ünübol,
H. Ünübol, A. Ünal
Affective disorders and catatonia: Report of two cases
S162
70
H. Balıbey, T. Türker, Z. Perdeci1,
N. Bayar, M. B. Evren
The relationship of incarceration, past suicide attempts, depression, anxiety and attention
deficit hyperactivity disorder in cases of anti-social personality disorder
S162
71
A. Aghamohammadi, M. Zafari
Relation between unintended pregnancy and post-partum blues
S163
72
T. Kuru, M. E. Karadere, S. Çelenk,
B. Demirel, K. F. Yavuz
Comparison of antipsychotic prescribing in the treatment of schizophrenia between the years
of 2004-2009
S163
73
Y. Yılmaz, Ö. Yanartaş, İ. Saygılı,
Ü. B. Semiz
Valproate-induced hyperammonemic encephalopathy: A case report
S164
74
Ö. Yanartaş, Y. Yılmaz, İ. Saygılı,
S. B. Zincir, Ü. B. Semiz
Two cases of tardive dyskinesia associated with the use of paliperidone ER and their
management
S165
75
F. Arıcıoğlu, T. Utkan
Effects of agmatine in rats with chronic unpredictable mild stress
S166
76
F. F. Cengiz, E. A. Sünbül
A case of obsessive compulsive disorder with psychotic features that suffered from sexual
trauma
S166
77
A. A. Budaklı, M. A. Ateş, A. Algül
Priapism associated with zuclopenthixol treatment: A case report
S167
78
F. Amani, A. Shaker
Prescribing patterns and inappropriate use of medications in patients referred to doctors in
Ardabil City of Iran
S168
79
K. S. Karataş, J. Güler, Ö. B. Topçuoğlu,
E. D. Bostancı, B. Soyer
Bipolar affective disorder and normal pressure hydrocephaly: A case report
S168
80
S. Gümrü, E. Yarcı, Ö. Şehirli, Y. Yazır,
T. Utkan, F. Arıcıoğlu
Agmatine attenuats cognitive impairment and oxidative damage following chronic
unpredictable mild stress: A behavioral, biochemical, and histological study
S169
81
M. C. Kaya, Y. Bez, S. Selek,
H. A. Savaş, H. Çelik, H. Herken
Ceruloplasmin levels before and after treatment in patients with depression:
A case-control study
S170
82
E. Mutlu, M. E. Ceylan, A. Aydın
Foetality in schizophrenia
S171
83
M. Ak, A. Bolu, S. Akarsu, D. Sezlev,
T. Yanık, Ö. Uzun, F. Özgen, A. Özşahin
Metabolic changes in the acute phase with olanzapine treatment
S171
84
R. Konkan, Ö. Şenormancı, O. Güçlü,
E. Aydın, Mehmet Z. Sungur
Do cultural factors effect clinical manifestations of OCD? Clinical features of
a Turkish sample
S172
Contents
Author(s)
Title
Poster Presentation
85
C. Evren, S. Çelik, R. Aksoy, T. Çetin,
M. Ülkü, S. Yiğiter, E. Mutlu
Reliability and validity of Turkish version the Brief Fear of Negative Evaluation Scale II
(BFNE-II) among male patients with alcohol dependency
S173
86
C. Evren, S. Çelik, R. Aksoy, T. Çetin,
S. Yiğiter, M. Ülkü, E. Mutlu
Reliability and validity of Turkish versions of the Social Phobia Scale and Social Interaction
Anxiety Scale among male patients with alcohol dependency
S173
87
M. Ak, C. Yükselir, A. Bozkurt,
M. Erdem, A. Özşahin
ECT in treatment of pathological gambling: A case report
S174
88
A. Bolu, S. Akarsu, C. Çelik,
B. Özdemir, K. N. Özmenler
Venlafaxine-mirtazapine combination in the treatment of post traumatic stress disorder
S175
89
O. Durmaz, M. A. Ateş, M. Çetin,
S. Ebrinç, C. Başoğlu, A. Algül
Efficacy and 3-month follow-up of repetitive transcranial magnetic stimulation (rTMS) in
treatment resistant depression: Three cases
S175
90
R. Tükel, H. Gürvit, B. Özata,
B. A. Ertekin, E. Ertekin, B. Baran,
Ş. A. Kalem, N. Öztürk, G. S. Direskeneli
The effects of brain-derived neurotrophic factor Val66Met polymorphism on executive
functioning in patients with obsessive-compulsive disorder
S176
91
S. G. Kabak, M. B. Baykaran, S. B. Zincir
Diagnostic confusion about OCD and schizophrenia: A case report
S177
92
R. Konkan, M. Bayrak, O. Güçlü,
Is vaginismus a specific phobia?
S177
93
A. Aydın, M. E. Ceylan, E. M.,
A. F. Maner
Are personality traits helpful to predict psychosis?
S178
94
P. G. Özdemir, A. Aydın, M. Güleç,
E. Füsün A. Çim
Switching to fluoxetine due to sertraline-induced urinary incontinence: A case report
S179
95
F. Karadağ, H. Herken, B. Kaptanoğlu,
Y. Enli, Ö. Kalkancı, C. B. Şengül,
H. A. Alaçam
The relationship between the serum bilirubin levels and metabolic syndrome
in schizophrenia patients
S179
96
Olanzapine abuse: A case report
S180
97
E. Valzdorf
Various reasons for self-destructive acts and objects used to commit them in 1991
S181
98
S. Barlak, A. Ateş, C. Başoğlu, S. Ebrinç
Topiramate induced acute psychotic disorder
S181
99
Glass-aating behaviour with radiological findings: A pica case
S182
100
Ö. Ö. Sarıkaya, D. G. Öyekçin
The use of bupropion in treatment Kleptomania’s: Two cases
S182
101
F. Hashemian, M. Majd, S. M. Hosseini,
A. Sharifi, M. V. S. Panahi, O. Bigdeli
A randomized, double-blind, placebo-controlled trial of celecoxib augmentation of sertraline
in the treatment of a drug-naïve women with major depression
S183
102
S. Karimi, M. Kazemi, H. Hasankhani,
S. Kazemi
To compare marital conflicts, between divorced and normal couples in Sirjan of Iran
S184
103
Y. Yılmaz, Ö.Yanartaş, İ. Saygılı,
A. G. Hariri
Adult primary enuresis nocturna: A case report
S185
104
P. Dorado, H. Trejo, E. Alonso,
E. P. Lledó, A. Llerena, M. López
Major depressive disorder and the 5-HTTLPR in Spanish and Mexican populations
S185
105
P. Dorado, E. L. Torres, E. M. P. Lledó,
J. M. Antón, A. Llerena
Phenytoin toxicity in a pediatric epileptic patient and CYP2C9, CYP2C19, and ABCB1
genetic polymorphisms
S186
106
M. López, E. P. Lledó, H. Trejo,
P. Dorado, J. Guerrero, M. E. Alonso,
A. Llerena
Influence of CYP2D6 genetic polymorphism on fluoxetine and amitriptyline
clinical response
S187
107
A. Karahan, A. Tiryaki, B. İskender,
E. Özkorumak
Evaluation of insight and functional recovery in patients with schizophrenia
S187
Contents
Author(s)
Title
Poster Presentation
108
O. Özdemir, Y. Selvi, H. Özkol,
Y. Tülüce, L. Beşiroğlu
Comparison of superoxide dismutase, glutathione peroxidase, and adenosine deaminase
activities between respiratory and nocturnal subtypes of patients with panic disorder
S188
109
C. Neale, A. Scholey, M. Hughes,
P. Johnston
The neural and cognitive effects of Bacopa Monniera: An fMRI study
S189
110
S. Özdemir, F. A. Özdemir
Methlyphenidate induced thrombocytopenia in a pediatric patient with ADHD and stuttering
S190
111
M. Güleç, Y. Selvi, Ü. Aydınoğlu
Use of mirtazapine and olanzapine in treatment of major depressive disorder with psychotic
features developed during pregnancy: A case report
S190
112
S. B. Zincir, Ü. B. Semiz, A. Yenel,
E. Başoğlu, M. Bilici, C. Tulay
Effects of group musical therapy on inpatients with schizophrenia: A preliminary study
S191
113
S. B. Zincir, Ü. B. Semiz, A. Demir,
Y. Yılmaz, S. G. Kabak
Clinical correlations of childhood trauma and dissociation in a sample of female inpatients
diagnosed with schizophrenia spectrum disorders and severe nonpsychotic disorders: the
preliminary data
S192
114
S. B. Zincir, A. Yenel, S. Ç. Parlak,
G. Şimşek, A. Bayrak, D. Bilge,
Ü. B. Semiz, M. Bilici
Comparison of neurocognitive skills between generalized anxiety disorder and premenstrual
dysphoric disorder patients: A controlled study
S192
115
M. Akbıyık, O. Karamustafalıoğlu
Evaluation of olfactory function and olfactory bulb volume in major depressive disorder
S193
116
M. Özten, A. Erol
Fluoxetine induced hypomanic shift in a bulimic patient: A case report
S194
117
S. Karayılan, A. Erol
Schizophrenia and Mega Cisterna Magna: A case report
S194
118
M. Özten, A. Erol
Congenital hypogonadism and comorbid anorexia nervosa in a male patient:A case report
S195
119
K. S. Karataş, J. Güler, A. Hariri
Review of diagnosis and treatment of pregnant psychiatric patients in a state hospital
S195
120
B. Çam, H. Kurt
Peripheral edema associated with mirtazapine: Presentation of a case
S196
121
H. Özer, A. Erol
Abuse of tianeptine: A case report
S197
122
O. Kadıoğlu, G. Üstünkar, Y. A. Son
GWAS with AHP based SNP prioritization approach to identify SNP biomarkers for
Alzheimer’s disease
S197
123
A. Büyükkınacı, D. Ö. Can, G. Silsüpür
A case report of a relapse in a major depression patient with valsartan/hydrochlorothiazide
S198
124
Y. Şimşek, G. E. Sarıdoğan, E. Şahan,
M. Nebioğlu, C. Cerit, M. Çalışkan
Monosymptomatic hypochondriacal psychosis: A case report
S198
125
O. Yılmaz, M. A. Ateş, G. Meral,
C. Başoğlu, A. Algül, S. Ebrinç, M. Çetin
Amisulpride in the treatment of treatment resistant tic disorder: A case report
S199
126
E. Özkorumak, H. Hıdıroğlu, A. Tiryaki,
İ. Ak
Evaluation of patients with obstructive sleep apnea syndrome referred to the sleep disorders
unit of a university hospital
S200
127
M. Güleç, E. Oral, E. F. Aydın
Clozapine use in idiopathic tardive dystonia and paranoid schizophrenia comorbidity:
A case report
S201
128
T. Kara, A. Çiftçi
The clinical use of Buprenorphine-Naloxone in the opioid-dependent patient with Hepatitis C
S201
129
H. A. Altaiar
The use of z hypnotics in the management of insomnia in forensic psychiatric
units in Oxford, England
S202
4th International
Antalya, Turkey
ABSTRACTS OF THE INVITED SPEAKERS
OPENING CONFERENCE
The evolution of human brain functions: Implications for psychobiological targets for well-being
Claude Robert Cloninger
Washington University, St. Louis, MO, USA
E-mail: [email protected]
The natural building blocks of human personality are described based on the evolution of human brain functions (Cloninger, 2009;
Cloninger, 2011). The phylogeny of human beings is traced from early vertebrates through mammals. The functional capacities that
emerge along this lineage of ancestors are described. Comparative neuroanatomy is reviewed to identify the brain structures and
networks that emerged coincident with the emergent brain functions.
Neocortical development in mammals proceeded in 5 major transitions from early mammals to early primates, monkeys and apes, early
humans, and modern Homo sapiens. These transitions provide the foundation for human self-awareness related to sexuality, materiality,
emotionality, intellectual communication, and spirituality respectively.
The evolution of functions in humans is compared to the psychobiological model of temperament and character previously described on
the basis of individual differences in learning and genetic variation in human beings. The psychobiological model of personality provides
a natural and thorough description of both the evolution and the development of personality in human beings.
These evolutionary findings are related to clinical approaches to assessment and treatment of children and adults. Identification of the
causal processes underlying well-being and ill-being is helpful in improving assessment and treatment in comparison to the frequent
drop-out relapse rates obtained when diagnosis and treatment are based on symptoms, rather than their causes. Monitoring symptoms
of illness and past lifestyle behavior has failed to promote change in well-being in a strong and consistent way in either individual care
or public health. A clinician’s effectiveness in treatment depends substantially on his or her attitude toward, and understanding of, the
patient as a person endowed with self-awareness and the will to direct his or her own future (Cloninger and Cloninger, 2011a).
The causes of well-being operate as components of a virtuous circle of reciprocally interactive processes (Cloninger and Cloninger, 2011a)
which evolved and develop in a stepwise manner. For example, emotions, cognitions, and actions have reciprocal interactions with one
another. The induction of a positive mood by humor or kindness leads to a broadening of attention to be more inclusive and less defensive
in thinking, which I have described as an outlook of unity (Cloninger, 2004; Cohn et al., 2009; Fredrickson, 2004; Fredrickson and Losada,
2005). In turn, an outlook of unity allows a person to cultivate greater self-acceptance, environmental mastery, and creativity, which in
turn lead to greater health and happiness, thereby completing the self-reinforcing cycle.
Positive emotional states can be induced by a variety of self-transcendent activities, such as acts of virtues, including cheerful humor,
generosity, and humility (Cloninger and Cloninger, 2011b). Virtues interact with functional practices of well-being, including working in
the service of others, letting go of fighting and worrying, and growing in awareness. In turn, virtues and self-regulatory functions interact
with the body to promote human plasticity. Human beings probably show greater plasticity, and hence variability, than other animal
species, which has allowed us to adapt to highly variable environmental conditions successfully.
Key words: Cognition, emotionality, human characteristics, thinking, personality, character, health, happiness, wellness, well-being
References:
1.
Cloninger, C.R., 2004. Feeling Good: The Science of Well-Being. Oxford University Press, New York.
2.
Cloninger, C.R., 2009. The evolution of human brain functions: the functional structure of human consciousness. Australian and New Zealand Journal of Psychiatry
43, 994-1006.
3.
Cloninger, C.R., 2011. The Phylogenesis of Human Personality: Identifying the Precursors of Cooperation, Altruism, and Well-Being. In: Sussman, R.W. and Cloninger,
C.R. (Eds.), The Origins of Cooperation and Altruism. Springer, New York, pp. 63-110.
4. Cloninger, C.R., Cloninger, K.M., 2011a. Development of instruments and evaluative procedures on contributors to Illness and health. International Journal of
Person-centered Medicine 1, in press.
5.
Cloninger, C.R., Cloninger, K.M., 2011b. Person-centered Therapeutics. International Journal of Person-centered Medicine 1, in press.
6.
Cloninger, C.R., Zohar, A.H., 2011. Personality and the perception of health and happiness. J Affect Disord 128, 24-32.
7.
Cloninger, C.R., Zohar, A.H., Cloninger, K.M., 2010. Promotion of well-being in person-centered mental health care. Focus 8, 165-179.
8.
Cohn, M.A., Fredrickson, B.L., Brown, S.L., Mikels, J.A., Conway, A.M., 2009. Happiness unpacked: positive emotions increase life satisfaction by building resilience. Emotion 9, 361-368.
9.
Fredrickson, B.L., 2004. The broaden-and-build theory of positive emotions. Philos Trans R Soc Lond B Biol Sci 359, 1367-1378.
10. Fredrickson, B.L., Losada, M.F., 2005. Positive affect and the complex dynamics of human flourishing. Am Psychol 60, 678-686.
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S34
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Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
LECTURES
[KL-01]
Opioid dependence during pregnancy: Balancing risk versus benefit
Peter Robert Martin
Departments of Psychiatry and Pharmacology, Vanderbilt University, Nashville, Tennessee, USA
Public health consequences of opioid dependence during pregnancy can only be inferred as increasing proportions of opioid-dependent
women are addicted to non-medically prescribed analgesics and receive obstetrical care without being identified as addicted or treated.
Because treatment recommendations for management of opioid dependence in pregnancy have primarily derived from studies in heroindependent pregnant women, there is a need to characterize and compare the clinical courses and complications of injection drug use
(IDU) and non-medically prescribed opioids. Intrauterine overdose or withdrawal and the neonatal abstinence syndrome (NAS) may occur
regardless of the route of opioid administration; whereas other obstetrical complications are likely consequences of poor prenatal care/selfneglect typical for IDU. Methadone maintenance compared to active IDU is associated with improved prenatal care, increased fetal growth,
reduced fetal mortality, decreased risk of HIV infection, decreased risk of pre-eclampsia, decreased NAS and reduced foster care placement;
however, significant NAS is still observed in >50% of these births. Benefits of methadone maintenance during pregnancy for addiction to nonmedically prescribed opioid analgesics may be attributed to support, structure, and prenatal obstetrical oversight compared to the stressful
and chaotic lifestyle of active addiction. While methadone has been the standard of care for >40 years, the Schedule III (methadone is Schedule
II) partial opioid agonist buprenorphine merits examination in pregnancy because it has been found highly effective for treatment of opioid
dependence, is associated with less severe withdrawal and is available in the U.S. under less severe restrictions than methadone. In the MOTHER
study, maternal and neonatal outcomes of treatment with buprenorphine or methadone throughout pregnancy were compared in pregnant
opioid-dependent women, in an international multi-center randomized, controlled, double-blind/double-dummy clinical trial (Jones et al.,
N Engl J Med 2010;363:2320-31). Although comparable numbers of methadone-exposed (57%) and buprenorphine-exposed (47%) babies
required treatment for NAS, buprenorphine-exposed neonates required 89% less morphine to treat NAS; spent 43% less time in the hospital;
and spent 58% less time in the hospital being medicated for NAS. The safety of opioid maintenance treatment during pregnancy must be
judged in the context of comprehensive services (other than the administered medication per se) provided to addicted women by treatment
programs. Buprenorphine is not inferior to methadone but may be preferable in terms of certain fetal outcome measures. Further research is
needed to implement safe buprenorphine induction procedures in pregnant women, to balance reported teratogenic effects of opioids and
benefits of opioid maintenance, and to determine the comparative safety and efficacy of methadone and buprenorphine for mother/fetus
with co-occurring alcohol/benzodiazepine dependence or other psychiatric disorders and the psychoactive medications used to treat them.
Key words: Opioid dependence, pregnancy, buprenorphine, methadone
[KL-02]
l-Benzylpiperazine, a major contaminant of ecstasy, induces marked changes in rat brain
neurochemistry and behaviour
Alan Leslie Hudson1, Nubia Zepeda1, Amanda Perreault1, Maggie Lalies1, Glen Baker2
Department of Pharmacology, University of Alberta, Edmonton, Canada
1
Department of Psychiatry, University of Alberta, Edmonton, Canada
2
Ecstasy [(±) -3-4-methylenedioxymethamphetamine, MDMA] is a widely abused drug which in overdose can lead to serotonin syndrome.
The patient presents with agitation, tremors, and muscle spasms, followed by hyperthermia which can lead to fatal organ failure. Recently
ecstasy tablets have been found to contain piperazines, particularly 1-benzylpiperazine (BZP). The purpose of cutting ecstasy with BZP is
to enhance the psychostimulant effects of MDMA. BZP is also marketed as a “legal high” in some countries; therefore some ecstasy tablets
contain solely BZP. BZP is the active metabolite of an antidepressant drug, trelibet, which failed in clinical trials. There has been little study
on the pharmacological effects of combining BZP with MDMA so we have investigated the bioavailability, neurochemistry and behavioral
S35
profile of these drugs administered alone or in combination in rats. We have used the technique of brain microdialysis in rat frontal cortex,
to monitor extracellular levels of noradrenaline, dopamine and serotonin in response to peripheral administration of BZP and MDMA. We
were also able to monitor the animals for evidence of rodent serotonin syndrome. BZP (10mg/kg, i.p.) was able to elevate extracellular
levels of dopamine, noradrenaline and to a lesser extent, extracellular serotonin in rat frontal cortex. MDMA (3mg/kg, i.p.) potently
elevated extracellular serotonin and noradrenaline and to a lesser extent extracellular dopamine in frontal cortex. These neurochemical
effects lasted for at least 2 to 3 hours relative to saline treated control animals. Combined BZP and MDMA administration led to markedly
elevated extracellular levels of all three monoamines indicating the effects of the drugs were additive. BZP (10mg/kg, i.p.) caused marked
behavioral activation, for example, increased locomotor activity and rearing behavior, whereas MDMA (3mg/kg, i.p.) resulted in flat body
posture and less rearing. Similar to MDMA (3mg/kg, i.p.), BZP increased grooming, forepaw treading, sniffing and head weaving relative
to saline injected animals. We also investigated a 5-HT2A receptor antagonist, ketanserin (3mg/kg i.p.), to see if it could attenuate BZPinduced behaviors. Ketanserin alone had little effect on rat behavior but when co-administered with BZP, was able to decrease locomotion
and rearing behavior. Interestingly, ketanserin had little effect on the increased sniffing and head weaving induced by BZP. At the doses
of drugs used in this study hyperthermia was not apparent in any of the animals but we were able to measure blood and brain levels
of BZP and MDMA hence we know bioavailability was not a problem. Overall, these results suggest that BZP and MDMA share certain
psychopharmacological and neurochemical properties in the rat. Furthermore, combined administration of BZP with MDMA leads to a
marked elevation of extracellular levels of all three monoamines in the frontal cortex rather than just serotonin which, if translated into
the clinical setting, may explain the agitation and sympathomimetic toxic syndrome reported in some patients. All animal studies were
conducted in accordance with the Canadian Council on Animal Care Guidelines and Policies with approval from the Animal Care and Use
Committee in Health Sciences for the University of Alberta. This work is supported with a grant from Canadian Institute of Health Sciences.
Key words: Ecstasy, (±) -3-4-methylenedioxymethamphetamine, 1-benzylpiperazine, serotonin syndrome, rat behaviour, brain microdialysis
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S35-6
[KL-03]
Unipolar versus bipolar depression in children: What do we know about the etiology,
diagnosis, and treatment?
Rasim Somer Diler
Department of Psychiatry, University of Pittsburgh, PA, US
Bipolar disorder (BP) is a familial and recurrent illness that significantly affects the child’s normal development. BP is often manifested by periods of
depression during which the child has significant psychosocial problems and increased risk for suicide. However, most clinical studies have focused
on the manic phase of the illness. The depressed phase of the illness in youth is less recognized and less often treated than mania. Moreover,
depressed youth with BP are more likely to have more severe depression, greater suicidality, and higher rates of comorbidities and functional
impairment relative to depressed youth with major depressive disorder (MDD or “unipolar depression”). However, it is difficult to clinically
differentiate the symptoms of BP depression from those of MDD. This issue is very important because youth with BP depression may be treated
with antidepressants that can precipitate an episode of mania or mixed BP symptoms. Also, it may take up to 10 years from the initial symptoms
of depression until BP is diagnosed and appropriate treatment is prescribed. Thus, early identification of BP youth, especially during depression, is
critical not only to improve the long-term prognosis of BP, but also to prevent inappropriate treatments for BP youth. As demonstrated recently in
BP adults, improving the accuracy of early diagnosis of BP in youth may be achieved by identifying objective neural biomarkers at an early age that
are specific to BP and not common to MDD. Treatment guidelines for BD in children and adolescents were recently developed, but the panel left out
depression and agreed that there was insufficient evidence to develop a treatment algorithm for it. Several studies suggest that there are effective
and well-tolerated treatment options (e.g., lithium, mood stabilizers, second-generation antipsychotics [SGA]) for manic or mixed episodes of BD
in youth; however, there are no maintenance studies in depressed children and adolescents with BP and available data for depressive episodes
in BP is limited to one small randomized and two open-label acute treatment studies in adolescents. Management of depression is very different
in BP depression than in MDD; antidepressants are widely used in MDD, but may exacerbate or induce mania and suicide in depressed BP youth.
Antidepressant monotherapy is therefore contraindicated for the treatment of BP depression, and studies in depressed BP adults show that
combining antidepressants with mood stabilizers may also not be effective. In conclusion, early differential diagnosis and treatment of depression
in youth is a key factor to enable youth to follow a normal developmental path and prevent an unrecoverable loss in their development.
Key words: Child, bipolar, depression, neuroimaging
S36
[KL-04]
Transcultural psychiatry: Practice and sample cases in USA and status in Turkiye
Alican Dalkilic
Virginia Commonwealth University, Richmond, VA & SEH, Washington, DC, USA
E-mail: E-mail: [email protected]
Culture refers to unique behavior patterns and lifestyle shared by a group of people that distinguish it from other groups. The views, beliefs, values, and
attitudes of a group characterize their culture. Culture and people influence and interact with each other reciprocally (1). In clinical practice patient’s
culture, physician’s culture, and medical culture play a significant role. Adequate and appropriate understanding of cultural dimensions is essential for
culturally competent practice (1). Also the impact of culture in evaluation and treatment of children and adolescents is significant in psychiatric patients (2).
Cultural competency is a requirement for medical licensure in most states the US. To prove clinical competency clinicians are required
demonstrate cultural competency. Clinicians typically work in multicultural and multiethnic societies (1). Ongoing globalization and
interconnection of economies and rapidly spreading new social media platforms will increase diversity in all communities, but especially
in developing countries including Turkiye. Therefore cultural competency training should be incorporated into residency training and
continuous medical education systems especially for mental health clinicians.
Clinicians should be familiar with culturally relevant relations and interactions of their patients (1), in order to establish therapeutic alliance and
provide competent care and therapy besides demonstrating cultural sensitivity, knowledge, and empathy. Also most psychotherapies are based
on Euro-American values of individualistic and egocentric concept, which can be contrasted with more sociocentric, ecocentric, and cosmocentric
views (3). This issue should be taken into consideration when treating patients from other cultures or subcultures in the US and Europe.
In this presentation I will review transcultural psychiatry practice in the US, provide and discuss some cases and summarize the status in Turkiye.
Key words: Transcultural psychiatry, Turkish American cases, transcultural psychiatry in USA
References:
1.
Focus, winter 2006 Vol. IV. No. 1, 81-89. Introduction: Culture and Psychiatry. Tseng W-S, Streltzer J.
2.
Child Adolesc Psychiatr Clin N Am. 2010 Oct;19(4):661-80. Culture and development in children and youth. Pumariega AJ, Joshi SV.
3.
Transcult Psychiatry. 2007 Jun;44(2):232-57. Psychotherapy and the cultural concept of the person. Kirmayer LJ
[KL-05]
Medical marijuana use in psychiatry
Tahir Tellioglu
Brown University, Rhode Island Hospital Dept Psychiatry, Providence USA
Medical marijuana refers to the use of parts of the cannabis plant or synthetic forms of specific cannabinoids as a physician-recommended
form of medicine. The cannabis plant has been known to have medicinal use as an analgesic, appetite stimulant, antiemetic, muscle
relaxant and anticonvulsant agent. A number of clinical studies, some disputed, claim that cannabinoids present an interesting
therapeutic potential as antiemetics, appetite stimulants in debilitating diseases (cancer and AIDS) and analgesics, and in the treatment
of multiple sclerosis, spinal cord injuries, Tourette’s syndrome, epilepsy and glaucoma.
Despite its illegality, patients have continued to obtain cannabis on the black market for self-medication for its self reported anti-anxiety
or antidepressant effects. A survey of 3,000 patients in California from 1993-2000 revealed about 27% of individuals used it primarily for
psychiatric conditions such as as an antidepressant or anxiolytic.
Understanding the mechanisms of action of cannabinoids has revived therapeutic interest in these substances. However, clinical studies
about the use of cannabis for psychiatric conditions are very limited. Further clinical trials, well-designed, carefully executed, and powered
for efficacy, are essential to clearly define the role of cannabinoids in the treatment of psychiatric conditions.
Key words: Medical marijuana, cannabis, psychiatric disorders
S37
DEBATES
[MD-02]
Antidepressants are useful in the treatment of depression: the case for the motion
Ian Anderson
Neuroscience and Psychiatry Unit, University of Manchester, UK
The group of drugs we call antidepressants have been available for nearly 60 years and are the first available physical treatment for
depression that became accepted by the public and clinicians alike. However in the last decade, associated with the rise of evidencebased medicine and a concern about the medicalisation of distress, there has been a questioning and re-evaluation of their efficacy
and place in the treatment of depression. This has occurred against the backdrop of increasing distrust of ‘Big Pharma’ and emphasis
on psychological treatment approaches. I will be addressing some of the main challenges that have been put forward questioning the
usefulness of antidepressants, ranging from the denial that depression is a disorder that can be treated by physical means, to the argument
that there is no pharmacological or empirical evidence for a clinically useful benefit over psychologically-mediated placebo effects. To
do this I will touch on recent developments in the understanding of how antidepressants might directly influence the processing by the
brain of emotional material, consider the evidence that direct pharmacological effects are necessary to maintain the therapeutic effects of
antidepressants and review the empirical evidence for clinically important efficacy from treatment trials in depression. I will conclude that
while antidepressants are certainly not a panacea, denying their place in treating depression is based on prejudice rather than objective
appraisal of the evidence.
Key words: Depression, antidepressants, placebo, efficacy
[MD-02]
Have clinically significant benefits of antidepressants been demonstrated?
Irving Kirsch
Associate Director, Program in Placebo Studies (PiPS) and Lecturer in Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Professor Emeritus of
Psychology, University of Hull & University of Connecticut
Despite their widespread use, clinically significant benefits of antidepressants have not been demonstrated for most of the patients to
whom they are prescribed. Meta-analyses of complete data sets consistently show a drug-placebo difference in improvement on the
Hamilton Rating Scale for Depression (HAMD) of approximately two points, which is well below the 3-point difference set by the National
Institute for Health and Clinical Excellence (NICE) as a criterion of clinical significance (1).
Drug placebo differences increase with increasing severity of depression, but reach clinical significance only for 10% of the patients to
whom they are prescribed (2). Defenders of antidepressants claim that depression scores are inflated by researchers who are anxious to
qualify patients for clinical trials. To the extent that this is true, it compromises the clinical trial data leading to drug approval, but even if
these trials are discarded, the absence of negative evidence does not constitute positive evidence of effectiveness.
Discontinuation studies show a relapse rate of approximately 50% when patients are switched to placebo. However, approximately
half of the relapses may be due to prior administration of the active agent. In extension trials, in which responders are kept on
placebo, the relapse rate is only 25% (3). These data suggest that antidepressants might induce a biological vulnerability to relapse.
Consistent with this hypothesis, a meta-analysis of tryptophan depletion studies indicates that the risk of becoming depressed after
acute lowering of serotonin levels is greatest between three and six months after discontinuation of an antidepressant (4). It is also
consistent with the results of the STAR-D trial, which was designed to be more representative than typical clinical trials of what
happens in clinical practice. Following successful treatment in the STAR-D trial, 93% of patients either relapsed or dropped out of the
trial within a year (5). Taken together, these data suggest that in the long run, rather than helping depressed people, antidepressants
may make them worse.
S38
References:
1. Kirsch I, Deacon BJ, Huedo-Medina TB, Scoboria A, Moore TJ, Johnson BT. Initial severity and antidepressant benefits: A meta-analysis of data submitted to
the Food and Drug Administration. PLoS Medicine [serial on the Internet]. 2008; 5(2): Available from: http://medicine.plosjournals.org/perlserv/?request=getdocument&doi=10.1371/journal.pmed.0050045.
2.
Fournier JC, DeRubeis RJ, Hollon SD, Dimidjian S, Amsterdam JD, Shelton RC, Fawcett J. Antidepressant Drug Effects and Depression Severity: A Patient-Level Metaanalysis. Journal of the American Medical Association2010;303(1):47-53.
3.
Andrews P, Kornstein S, Halberstadt L, Gardner C, Neale MC. Blue again: Perturbational effects of antidepressants suggest monoaminergic homeostasis in major
depression. Frontiers in Psychology. [Original Research]. 2011;2.
4.
Ruhé HG, Mason NS, Schene AH. Mood is indirectly related to serotonin, norepinephrine and dopamine levels in humans: a meta-analysis of monoamine depletion
studies. Molecular Psychiatry2007;12:331-59.
5.
Pigott HE, Leventhal AM, Alter GS, Boren JJ. Efficacy and Effectiveness of Antidepressants: Current Status of Research Psychotherapy and Psychosomatics2010;70:267-79.
[MD-03]
Antidepressants are useful in the treatment of bipolar disorders
Selçuk Kırlı
Department of Psychiatry, Uludag University, Bursa, Turkey
Using antidepressant drugs in Bipolar Depression (BD) has not been adequately considered or explored. This matter is indeed an area of
ambiguity which should to be clarified as soon as possible due to the following facts concerning bipolar disorder:
• It is repetitive and progresses relatively slowly
• It tends to become chronic
• It involves a high risk of suicide
• It causes more disability than the other variations of the disease (1).
Treatment manuals, expert views and practices do not fully agree with each other on the issue of whether or not it is appropriate to
use antidepressant (AD) drugs to treat BD. There are also differences in the manuals of various countries although they have similar
approaches. Americans and Canadians, in particular, strictly oppose the use of ADs in BD. They generally recommend using mood
stabilizers (MSs) in treating less severe depressions, using ADs alongside these drugs only in severe depressions and discontinuing ADs as
soon as possible. In Germany and some other countries, there is a long and firm tradition of using ADs as a first line treatment (2). Despite
different approaches, it is a fact that the decision to use antidepressant drugs in BD is not easy.
The difficulty might stem from a number of reasons including:
• Studies supporting the effectiveness of ADs in BD are few in number and they are not sufficient to approve the use of ADs in this area.
• Although the issue has not been supported by placebo-controlled studies, there is a common belief that ADs cause manic transitions and rapid cycles (3).
The matters of debate that may clarify this issue can be summarized as follows (2):
• Transition to mania and rapid cycling are significant phenomena in Bipolar Disorder (BD).
• The issue of suicide is, in fact, of minimal importance in BD.
• The efficacy of antidepressants in BD has not been supported by satisfactory evidence.
• MSs having an AD effect in BD has been supported by satisfactory evidence.
Here are some brief answers to the matters of debate:
• Like ADs, MSs have also not been officially approved in the treatment of BD. It is worthwhile to discuss the new generation antipsychotics
(NGAPs) which have been approved in this context.
• The data on manic transition and rapid cycling are problematic for the use of tricyclics to a certain extent; the data obtained from modern
antidepressants have largely removed this issue from being a special problem area. There are also other alternatives to diminish the risk (4).
• The antidepressant effect is directed towards the syndrome, thus these drugs are also effective in BD, but there are no noteworthy
positive data on this issue for MSs other than a slight benefit obtained from Lithium.
• The issues of suicide and chronicity cause a greater risk than all other issues in terms of contribution to a bad result for BD.
In view of these and similar benefit/risk comparisons, we can conclude that it is reasonable and necessary to use ADs as a single agent or
in combination with MSs or NGAPs in the treatment of BD. This approach is already commonly applied in practice.
Key words: Bipolar disorder, antidepressants, depression
S39
References:
1.
Gijsman HJ, Geddes JR, Rendell JM, Nolen WA, Goodwinn GM: Antidepressant for bipolar depression: A systematic review of randomized, controlled trials. Am J
Psychiatry 2004;161:1537-1547.
2.
Möller HJ, Grunze H: Have some guidelines fort he treatment of acute bipolar depression gone too far in the restriction of antidepressants? Eur Arch Psychiatry
Clin Neurosci 2000;250:57-68.
3. Sachs SG, Nierenberg AA, Calabrese JR, Ketter TA, Marangeli LB, Milowitz DJ, Miyahara MS, Bauer MS: Effectiveness of adjunctive antidepressant treatment for
bipolar depression. N Eng J Med 2007;356:1711-1722.
4. Ghaemi SN, Rosenquist KJ, Ko YJ, Baldassano CF, Kontos NJ, Baldessarini RJ: Antidepressant treatment in bipolar versus unipolar depression. Am J
Psychiatry2004;161:163-165.
JOINT SYMPOSIA
[JS-01]
International Association for Cognitive Psychotherapy (IACP)
Symposium title: Advances and problems in cognitive behavior therapy (CBT)
Stefan Hofmann
Department of Psychology, Boston University, Boston, USA
Cognitive behavioral therapy (CBT) is the first-line psychological treatment for anxiety disorders. Although effective, partial or nonresponse to treatment remains an all-too-common occurrence, with over half of patients failing to respond fully to first-line cognitive
behavioral therapy. The same is true for pharmacological interventions for anxiety disorders. Combining CBT with conventional anxiolytic
medication is typically not more effective than unimodal therapy for treating anxiety disorders. This presentation will examine strategies
to augment and modify CBT to enhance its efficacy. Recently, the search for new strategies to augment CBT has turned to a unique model
of combination therapy. Rather than using pharmacotherapy as an anxiolytic in its own right, it is used to augment the core learning
processes of cognitive-behavior therapy and exposure procedures. Moreover, recent work in emotion research points to new intervention
strategies for anxiety disorders, such as mindfulness-based therapies and meditation practices.
The first half of this presentation will review the current literature on conventional and novel combination strategies. A particularly
successful prototype of a novel augmentation strategy of CBT is the use of d-cycloserine (DCS), a partial agonist at the glycine recognition
site of the glutametergic N-methyl-D-aspartate receptor, to facilitate extinction learning. The second half the presentation will review
novel and adaptive emotion regulation strategies, including mindfulness and loving-kindness mediation.
The efficacy of CBT for anxiety disorders can be enhanced by (1) augmenting the treatment with the cognitive enhancers such as DCS,
and (2) modifying the intervention using novel emotion regulation strategies. The augmentation strategies are based on the fact that
exposure-based treatments in humans partly rely on extinction to reduce the fear response in anxiety disorders. In fact, animal studies
have consistently shown that DCS facilitates extinction learning. Similarly, recent human trials have shown that DCS enhances fear
reduction during exposure therapy of some anxiety disorders. Positive findings so far have been reported in placebo-controlled trials for
specific phobia, social anxiety disorder, panic disorder, and obsessive compulsive disorder. The strongest effects were observed in studies
in which patients receive a small dose of DCS (50 mg) acutely 1 hour before the exposure trials with no more than 5 administrations
weekly. The modification strategies of CBT have primarily focused on enhancing adaptive emotion regulation strategies, beyond
traditional reappraisal strategies. Whereas cognitive reappraisal strategies are antecedent focused, these novel strategies are primarily
emotion response focused. Although these strategies have only recently been studied as treatments for anxiety disorders, they are rooted
in ancient Eastern and Buddhist practices. CBT is an evolving science that integrates traditional and modern approaches and is in line with
modern emotion and neuroscience theories.
Key words: Cognitive behavior therapy, anxiety disorders, combination drug therapy, NMDA, glutamate, mindfulness, meditation, emotion
regulation
S40
Translating science into practice, collaborative empiricism and engagement
in homework assignments in cognitive behavior therapy
Nikolaos Kazantzis
La Trobe University, Australia
Cognitive-behavioral therapy is more efficacious when between-session ‘homework’ tasks are included. Although the evidence for the
effectiveness of homework appears compelling, only limited research is available to guide day-to-day practice. Recently, the search for
strategies to enhance homework compliance (or engagement) has centered on practitioner competence in developing collaborative and
empirical therapeutic relationships. Rather than viewing practitioner competence as a “trait”, newer measures are better equipped to
capture the fluctuations in competence from session-to-session, as well as the relationship between therapist competence and patient
compliance, and their combined effects on positive treatment outcomes.
This presentation will use meta-analytic methods to review the empirical data demonstrating the causal and correlational effects of
CBT homework assignments in enhancing positive treatment outcomes. Positive results have been obtained in the treatment of major
depressive disorder, social anxiety disorder, panic disorder, and generalized anxiety disorder. Data supporting the development of
therapeutic relationships characterized by strong patient and therapist involvement in the therapeutic work (collaboration) of identifying
and evaluating the patients’ belief system (empiricism) will also be covered. A recent study in the treatment of major depressive disorder
suggests that therapist competence in following a compliance enhancement protocol, which focused on collaborative empiricism,
enhanced treatment outcomes. In conclusion, the results of these studies suggest that patient engagement with homework assignments
is an important determinant of positive CBT outcomes, but practitioner competence may enhance the effect when the patient-therapist
relationship is characterized by collaborative empiricism.
Key words: Cognitive behavior therapy; homework assignments; therapeutic relationship; treatment outcome
CBT as an evidence based treatment approach: Warning signs in therapy and common
mistakes in daily practice
Mehmet Zihni Sungur
Medical School of Marmara University, Dept. of Psychiatry, Istanbul, Tukey
The remarkable results obtained from integration of cognitive and behavioral therapies and the simplicity and straightforward
approaches of the treatment modality have attracted many therapists to practice cognitive-behavioral psychotherapy today.
Unfortunately a considerable number of these therapists adhere to guidelines of a textbook-kind of therapy without formal training and
adequate supervision, and therefore suggest standard package-type treatments with little or no attempt to develop individually tailored
programmes. There are some crucial points that clinicians need to consider during the practice of CBT to increase positive treatment
outcomes. This presentation will focus on significant points that should be taken into account during the daily practice of CBT, discuss
common mistakes made in daily practice and the reasons why psychotherapy is devalued during delivery of psychological services, and
suggest alternative ways to improve the efficiency of CBT for public care.
Key words: Cognitive behavioral therapy, evidence based treatment, treatment principles and pitfalls
S41
[JS-02]
Malaysian Psychiatric Association
Symposium title: Malaysian perspective of substance dependence
A harm minimization program against drug use and HIV problems in Malaysia
Rusdi Abd. Rashid1, Abdul Kadir Bin Abu Bakar2, Hazli Bin Zakaria3, Umi Binti Adzlin4, Mohammad Hussain Habil5
University of Malaya Centre for Addiction Sciences(UMCAS), Kuala Lumpur, Malaysia
1
Hospital Permai, Johor Bharu, Malaysia
2
Dept. of Psychiatry, Hospital Universiti Kebangsaan Malaysia,Kuala Lumpur, Malaysia
3
Dept. of Psychiatry, Kajang Hospital, Selangor, Malaysia
4
Dept of Psychological Medicine,Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia
5
This symposium highlights the drug use and HIV situations in Malaysia from the perspective of the development of a harm minimization
program, methadone assisted therapy for opiate dependents, and the world’s first integrated Islamic psychospiritual intervention with
methadone treatment in a mosque setting.
The speakers will present four topics that related to the drug problems in Malaysia. The first speaker will talk about harm minimization
and the current drugs and HIV situations in Malaysia. The second speaker will highlight the harm reduction services available emphasizing
pharmacotherapy options available in Malaysia, the challenges and future directions. The third speaker will focus on psychosocial
intervention in particular an innovative psychospiritual intervention called the Spiritual Enhancement of Drug Addiction Rehabilitation
(SEDAR) program in the Malaysian Ar-Rahman mosque. The fourth speaker will discuss Assisted Medication Therapy (AST) from an Islamic
perspective.
Harm minimization approaches in Malaysia are promising. However, the program needs large scale implementation and new strategies
in order to make an impact on HIV/AIDS prevalence.
New and larger platforms and more aggressive promotions are required to implement more harm minimization programs in the
community.
Key words: Addiction, harm minimization, HIV/AIDS, psychospiritual interventions
[JS-03]
Hellenic Society for the Advancement of Psychiatry and Related Sciences
Symposium title: Disorders of sleep and wakefulness and their pharmacological management
Thomas Paparrigopoulos
Athens University Medical School, 1st Department of Psychiatry, Athens, Greece
Sleep mechanisms and the pathophysiology of depression are closely interrelated. Monoaminergic and cholinergic neurotransmission
are heavily involved in both. Therefore, it is not surprising that depression is almost invariably associated with sleep abnormalities.
Several hypotheses have been advanced to explain their occurrence. One suggests that an increased pressure of REM sleep might be
responsible. Another proposes that a deficiency in the mechanism responsible for non-REM sleep, as explained by the two-process
model of sleep regulation, may be implicated. Finally, a third hypothesis suggests that an imbalance between the monoaminergic and
cholinergic systems in the central nervous system (CNS) could be responsible for the pathophysiology of depression and the observed
sleep aberrations.
In principle, most antidepressants increase synaptic levels of norepinephrine, serotonin, and dopamine; yet they may also act on
muscarinic and histamine (H1) receptors. These effects purportedly underlie their principal therapeutic mode of action, as well as their
potential mechanism of altering sleep architecture. In this line of thought it has been proposed that central to the therapeutic effect
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of the majority of antidepressants is the observed strong and sustained suppression of REM sleep, without overlooking other factors
involved in the mechanisms underlying treatment response. Moreover, tryptophan depletion and studies of selective serotonin reutake
inhibitors (SSRIs) in sleep have shown that increases in serotonin levels could mediate the effect on REM sleep, which is often observed
during antidepressant treatment. However, changes in non-REM sleep and sleep maintenance may be mediated through the action of
other neurotransmitter systems.
Although each antidepressant drug affects sleep architecture differently, there are some common features that characterize the various
types of antidepressants. Thus, the majority of antidepressant drugs suppress REM sleep. Some, however, with little or no noradrenergic
or serotoninergic reuptake inhibition, such as amineptine, tianeptine, nefazodone, trazodone, bupropion, and trimipramine, do not
have clear-cut REM suppressant effects. Sleep continuity and total sleep time are improved with sedative medications, such as most
tricyclic antidepressants (TCAs) and several antidepressants with 5-HT2c receptor antagonist properties, such as mianserin, mirtazapine,
nefazodone, and trazodone. On the other hand, most (SSRIs) and clomipramine, show evidence early in treatment of stimulating effects,
thereby reducing total sleep time and sleep efficiency, and promote wakefulness. However, these effects are fairly short-lived and there
are few significant differences among drugs after a few weeks of treatment.
In conclusion, the majority of antidepressant drugs suppress REM sleep and increase REM latency, although this is not always the case. As
far as sleep efficiency and total sleep time are concerned, antidepressants can be distinguished as either sedative or energizing agents.
This individualized profiling of antidepressants provides a diversity of therapeutic options in terms of the management of concomitant
sleep disturbances in depression.
Key words: Depression, antidepressants, medication, sleep
Constantin R. Soldatos, Thomas Paparrigopoulos
Athens University Medical School
Insomnia is conceived as the subjective complaint of reduced sleep quantity and/or quality and affects a significant proportion of
the general population. Approximately 10% of the population worldwide meet the full ICD-10 criteria for chronic insomnia. Insomnia
is the outcome of the interplay of many environmental, biological, and psychological factors; consequently, its treatment should not
only focus on ameliorating sleeplessness but should also address all those predisposing, precipitating and perpetuating factors that
cause and maintain insomnia. Insomniacs need an integrative individualized management, which includes sleep hygiene measures,
psychotherapeutic techniques, and the utilization of sleep-promoting drugs. The focus of treatment should be nighttime symptoms, the
feeling of non-restorative sleep, and impaired daytime functioning as well.
Benzodiazepine or benzodiazepine-like hypnotics (z-drugs) are still considered as the drugs of choice for the treatment of insomnia.
However, due to their abuse potential, their pharmacological properties, and their widespread use (there are estimates that one of
every four adults in developed countries takes sleeping aids at some time point during the year), it is highly recommended that the
use of hypnotic drugs is restricted to the initial period of treatment mostly as adjuncts to other psychotherapeutic measures. Both
types of hypnotics focus primarily on the inhibitory neurotransmitter GABA through binding to GABAA receptors; however, other
neurotransmitter systems, such as the serotoninergic and histaminergic, are also involved in the regulation of sleep-wakefulness and
may be targeted by other compounds. The non-benzodiazepine drugs are generally preferred as a result of their improved binding
selectivity and pharmacokinetic profile. However, their potential adverse effects, such as amnestic symptoms, next day residual
sedation, and abuse potential, indicate the need for novel pharmacotherapies. In this line, agents acting on the melatonergic system
and circadian mechanisms have been developed and approved for the treatment of insomnia (melatonin and the melatonin receptor
agonist, ramelteon). Furthermore, a variety of other compounds targeting several neuroreceptors (i.e., GABAA agonism, melatonergic
MT1/MT2 agonism, 5-HT2A antagonism, orexin receptor OX1/OX2 antagonism) are under investigation and may be added in the
psychopharmacological armamentarium in the near future.
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Hypersomnias and the effects of vigilance-promoting compounds
Antigone Papavasiliou
Department of Neurology, Pendeli Children’s Hospital
Hypersomnia is characterized by a propensity to fall asleep in situations when one is expected to be awake and alert. It may present with
prolonged sleep episodes coupled with excessive daytime sleepiness (EDS) and frequent napping. It is described in narcolepsy, a neurological
disorder characterized by EDS occurring with or without cataplexy; in idiopathic hypersomnia, also of central origin, characterized by EDS
and episodes of prolonged nocturnal sleep; in recurrent hypersomnias, rare disorders manifesting with recurrent episodes of more or
less continuous sleep (average duration of 1 week), recurring at highly variable intervals (one to several months), such as, Kleine–Levin
syndrome and menstrual-related hypersomnia. Chronic sleep loss and/or poor sleep quality may be underlying reasons for EDS; these occur
in numerous sleep disorders, such as obstructive sleep apnea (OSA) and in psychiatric disorders, particularly depression. Approximately
80% of depressive states are associated with insomnia; patients do not necessarily have a higher propensity to fall asleep in daytime but
report subjective sleepiness that differs from the EDS encountered in narcolepsy and OSA. There are also hypersomnias attributable to other
medical conditions, drugs, or substances, as well as behaviorally induced hypersomnia caused by insufficient time to sleep.
Transition between sleep and wakefulness is simply described as oscillations between two opponent processes, one promoting sleep,
another promoting wakefulness. The complex neurobiological mechanisms and the neurotransmitters and neuromodulators underlying
these processes, including noradrenergic, serotonergic, cholinergic, adenosinergic, and histaminergic systems and more recently, the
hypocretin/orexin and dopamine systems, have been established. The mechanisms of action of some vigilance-promoting agents are as
follows: psychostimulants act through enhanced dopamine action (amphetamines, methylphenidate) or acetylcholine action (caffeine);
modafinil may act through enhanced central histamine, hypocretin, and possibly dopamine action; γ -hydroxybutyrate (GHB), acts on GABA
and GHB receptors. EDS in narcolepsy is traditionally treated with psychostimulants; these are rarely effective in idiopathic hypersomnia,
although this was not examined through randomized controlled trials. Modafinil, a first-line wakefulness-promoting medication, is a
useful alternative to psychostimulants for EDS in narcolepsy (Level I evidence). It may be effective for EDS due to idiopathic hypersomnia
(one Level IV study and expert consensus). It is not associated with rebound hypersomnolence, cardiovascular problems, or abuse
potential, as may be seen with amphetamines. Modafinil alleviates sleepiness and fatigue in shift work disorders, residual sleepiness in
treated sleep apnea syndrome, multiple sclerosis, Parkinson’s disease and depression. It is promising as an alternative to psychostimulants
for excessive fatigue associated with medical and psychiatric disorders and as an augmentation medication for treatment-resistant
depression. Due to rare serious complications (allergic and psychiatric), the EMA concluded that its benefit/risk balance was positive for
narcolepsy but negative for other sleep disorders and neurological diseases, including idiopathic hypersomnia. The FDA has approved it
for EDS in narcolepsy, shift work sleep disorder, and OSA. In narcolepsy, GHB at bedtime reduces nocturnal awakenings, increases stage
3 and 4 sleep, and consolidates REM sleep periods; these effects coincide with improvement in daytime symptoms, including cataplexy.
Key words: Vigilance-promoting agents, hypersomnia, psychostimulants, modafinil, γ -hydroxybutyrate
[JS-04]
The International Union of Basic and Clinical Pharmacology (IUPHAR)
Symposium title: Pharmacogenomics of psychoactive drugs
Role of polymorphic drug transporter in treatment-resistant depression
Tanja Brueckl, M. Uhr
Max Planck Institute of Psychiatry, Germany
To be effective antidepressants and other centrally acting drugs have to penetrate the blood-brain barrier. Transport proteins such as
p-glycoprotein that are located at the BBB do not only transport toxic substances but also many drugs back into the blood. In preclinical
animal models and a study examining more than 400 patients, the relationship between polymorphisms in the ABCB1 gene coding
for p-glycoprotein and the clinical efficacy of antidepressants could be demonstrated. With respect to those antidepressants that are
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substrates of p-glycoprotein there is a significant statistical relationship between polymorphism and remission rate after 4 to 6 weeks.
Clinically, genetic analysis of ABCB1 polymorphisms may be used to predict how likely it is that a patient will respond to therapy with
antidepressants or other centrally acting drugs. This in turn will help to select the right drug and/or dosage (Neuron 2008, 57:203-209).
Further data from a preliminary pilot study suggest that the treatment of depression could be optimized by a routine application of
an ABCB1 gene test. Patients carrying the less favourable ABCB1 genotype with respect to the clinical efficacy of antidepressants may
especially benefit from a dosage increase.
P-glycoprotein in the membrane of vascular cells causes centrally acting drugs such as citalopram, paroxetine, venlafaxine and others to be
transported from the brain back to the vascular lumen. If the protein is missing or if its function is impaired, more drugs pass from the blood into
the brain. Depending on changes (polymorphisms) in the ABCB1 gene, p-glycoprotein allows varying amounts of a drug to pass into the CNS.
Relationship between pharmacogenetics and personality traits: Relevance for suicide
Adrián Llerena
International Union of Basic and Clinical Pharmacology (IUPHAR), Extremadura University Hospital
CYP2D6 genetic polymorphism is related to variability of the enzyme’s hydroxylation capacity. Subjects carrying zero CYP2D6 active
genes are classified as Poor Metabolizers (PMs). The rest are Extensive Metabolizers (EMs) with one or two active genes, including a group
of Ultra-rapid Metabolizers (UMs) with more than two active alleles. UMs have a hydroxylation capacity more than 100 times higher than
PMs. The frequency of PMs and UMs in Spain is 7-10% and 4.9%, respectively (Llerena et al., 2009).
A higher frequency of UMs has been found among individuals who committed suicide vs. those who died from natural causes (Zackrisson
et al, 2010). One explanation for this relationship could be treatment failure with antidepressant drugs metabolized by CYP2D6
(fluoxetine, paroxetine, fluvoxamine, venlafaxine, citalopram, etc.) (Llerena et al., 2004; Llerena et al., 2009) widely used to prevent suicide
or to treat mood disorders. A complementary explanation could be via the implication of the polymorphic CYP2D6 in the endogenous
metabolism. Since we found an association between this drug metabolizing enzyme and psychological functioning, CYP2D6 has been
associated with behavioral and clinical risk factors such as personality and vulnerability to psychopathology (Llerena et al., 1993; Llerena
et al., 2007; Gonzalez et al., 2008; Peñas-Lledó et al., 2009, Peñas-LLedó et al., 2010). These two hypotheses could explain the relationship
found between CYP2D6 and suicide (Peñas-LLedón et al 2011, in press)
The biotransformation of several antidepressants and antipsychotic drugs is mainly determined by genetic factors mediating the
CYP2D6 gene polymorphism. Additionally, the potential interaction between CYP2D6 and endogenous metabolism must be taken into
consideration due to its potential implication for personality traits (LLerena et al 1993; Gonzalez et al 2008) and functioning, such as:
neurocognition (Peñas-Lledó et al 2009) and psychopathology, eating disorders (Peñas-LLedó et al., 2010) and suicide (Peñas-Lledó et al.,
2011). In summary, the pharmacogenetics of CYP2D6 may be a useful tool to predict unexpected side-effects, interactions, or therapeutic
failures of many relevant drugs and may explain the interethnic differences oberserved in the response to psychotropic drugs, but also
vulnerability to psychopathology including suicide.
Genetic causes of hypersensitivity to antipsychotics – the clozapine story
Ingolf Cascorbi
Institute of Experimental and Clinical Pharmacology, University of Kiel, Germany
Clozapine is considered to be the most efficacious drug to treat schizophrenia, but despite these benefits, clozapine prescriptions
comprise only 2-10% of the total antipsychotic market for schizophrenia in the United States. It was introduced on the market in 1971 but
was withdrawn in 1975 after reports of clozapine-induced agranulocytosis (CIA) in Finland. Due to its high efficacy in treatment-resistant
schizophrenia, it was reapproved in 1990 by the FDA and health authorities in most other countries; however, regular hematological
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monitoring was required. The implementation of this monitoring system has successfully reduced the incidence of CIA from 1.3% to 0.4%.
Currently 239 cases of agranulocytosis are registered at the FDA adverse drug reaction data bank.
There have been certain attempts to predict agranulocytosis by genetic association studies in particular in the NADPH myeloperoxidase
complex (1) and FC-gamma receptors (2). We could identify an association to the polymorphic myeloperoxidase, responsible for oxidative
reaction in neutrophils. More recently, confirmatory studies in two independent cohorts of 33 and 49 CIA cases and 54 and 78 controls
indicated that markers in the HLA system are highly significantly associated with the risk of CIA. HLA-DQB1 6672G>C was associated with
CIA conferring an odds ratio of 16.9 (3). Currently a large consortium led by Duke University has aimed to collect a large sample of well
defined cases of CIA in order to allow genome-wide association studies.
Key words: Clozapine, agranulocytosis, NADPH-oxidase, myeloperoxidase, HLA-system, genetic association
References:
1. Mosyagin I, Cascorbi I, Schaub R, Krüger T, Dettling M. Drug-induced agranulocytosis: impact of different fcgamma receptor polymorphisms? J Clin
Psychopharmacol. 2005;25:435-40.
2. Mosyagin I, Dettling M, Roots I, Mueller-Oerlinghausen B, Cascorbi I.. Impact of myeloperoxidase and NADPH-oxidase polymorphisms in drug-induced
agranulocytosis. J Clin Psychopharmacol. 2004;24:613-7.
3.
Athanasiou MC, Dettling M, Cascorbi I, Mosyagin I, Salisbury BA, Pierz KA, Zou W, Whalen H, Malhotra AK, Lencz T, Gerson SL, Kane JM, Reed CR. Candidate gene
analysis identifies a polymorphism in HLA-DQB1 associated with clozapine-induced agranulocytosis. J Clin Psychiatry. 2011;72:458-63.
[JS-05]
Symposium title: Current concept of obsessive compulsive disorder (OCD)
Manickam Thirunavukarasu
Professor & Head, Department of Psychiatry, SRM MC & RC, Kattankulathur, 603203, India
Obsessive-compulsive disorder (OCD) is a relatively common disorder, occurring in around 2-3% of general population. In the past
century, the understanding of the disorder has improved and has been clearly delineated as a valid nosological entity. The heterogeneity
of the disorder has been explained based on various phenotypic subtypes. Factor analytic studies have provided consistent evidence that
distinct obsessive-compulsive symptom dimensions exist, including obsessions/checking, contamination/washing, symmetry/ordering,
and hoarding. It has been hypothesized that each symptom dimension may be underpinned by a distinctive set of bio-behavioral
mechanisms. There has been a good deal of interest recently in the disorders characterised by similar phenomenology and psychobiology
called obsessive compulsive spectrum disorder (OCSD). These include tic disorder, body dysmorphic disorder, impulse control and eating
disorders. In view of all these changes in understanding and newer conceptualisation, OC(S)D might find a separate place for itself in the
DSM V and ICD 11, rather than being classified under anxiety / neurotic spectrum disorders.
A. Shyam Sundar
Assistant Professor, Department of Psychiatry, SRM Medical College Hospital and Research Centre, Kattankulathur, 603203, India
Although the pathophysiology of OCD is still far from resolved, the existence of a biological basis for OCD has been clearly established.
Twin, family, segregation and linkage studies have demonstrated that genetic factors contribute to the pathogenesis of OCD. There
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is a general consensus that fronto-striato-thalamo-cortical dysfunction is the neuronal basis of obsessive-compulsive disorder. The
differential response of OCD to clomipramine and SSRIs, compared to other antidepressants, has led to the primacy of the serotonin (5HT)
hypothesis of OCD. Currently serotonin has also been implicated in the pathophysiology of other OC spectrum disorders. However, several
lines of research suggest that the dopamine system, with which 5HT interacts, may play a major role in the expression of OC symptoms.
Recent genetic and neurochemical studies also implicate glutamate in the pathophysiology of OCD. The recognition of PANDAS (Pediatric
autoimmune neuropsychiatric disorders associated with streptococcal infection) has increased the interest in the possibility of an
immune-mediated pathophysiology of obsessive-compulsive disorder. In this presentation, these recent advances in biological models
of OCD will be discussed.
Psychopharmacological and somatic interventions for OCD
Kandasamy Arun
Assistant professor, Department of Psychiatry, SRM Medical College & Research Center, Kattankulathur, 603203, India
OCD was initially thought to be unresponsive to treatment but subsequently, a range of effective treatments has been developed on the
basis of two approaches, pharmacological and psychosocial. Pharmacological agents such as Selective Serotonin Reuptake Inhibitors
(SSRIs) and clomipramine have changed the face of OCD management. Around 50–60 % of patients showed remission after treatment. In
treatment resistant cases, augmenting agents like clonazepam, risperidone and buspirone are used. Intravenous clomipramine is another
option. Other strategies which are currently under study include riluzole and other drugs which act on the glutaminergic system, opioid
agonists and inositol augmentation. Immunomodulatory therapies have also been studied especially in PANDAS. Development of newer
somatic methods of treatment like repetitive trans-cranial stimulation (rTMS) and Deep Brain Stimulation (DBS) are promising in targeting
the fronto-striato-pallido-thalamo-cortical circuits for treatment resistant OCD. Although controversial, stereotactic and gamma knife
assisted neurosurgical procedures such as cingulotomy and anterior capsulotomy are also possible treatments for resistant cases.
Psycho-social interventions for OCD
Manickam Thirunavukarasu
Professor & Head, Department of Psychiatry, SRM MC & RC, Kattankulathur, 603203, India
We will review recent advances in the psychological treatments for obsessive compulsive disorder. In the early 20th century, psychological
treatment for OCD consisted largely of psychodynamic psychotherapy. The general consensus of that era was that OCD was an
unmanageable condition with a poor prognosis. Starting from the 1950s, laboratory studies on extinction of conditioned responses
followed by clinical research led to the formulation of Exposure and Response Prevention (ERP) for OCD.We have developed a model
combining ERP and CBT. This behavioral approach currently is the first-line intervention for adult obsessive-compulsive disorder. Recently
predominantly cognitive approaches have been evaluated to overcome the shortcomings of ERP. Methodologically rigorous controlled
trials have suggested that the benefits from CBT exceed those from placebo and attention-control conditions and have similar or greater
efficacy than serotonergic monotherapy. The clinical predictors for response to CBT include symptom severity, symptom subtype, severe
depression, the presence of comorbid personality disorders, family dysfunction and the therapeutic alliance. Combination treatment with
pharmacotherapy has generally revealed promising results. Nevertheless, more studies are still needed in certain areas. We will explain in
detail how we practice in our patients and the results.
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[JS-06]
Czech NeuroPsychopharmacological Society (CNPS)
Symposium title: From models of schizophrenia to clinical outcome: A psychopharmacological perspective
Safety first, efficacy second? Fear and the need for treatment in the absence of controlled data
Pavel Mohr, David Hnidek, Dagmar Seifertova
Prague Psychiatric Center, Czech Republic
In clinical practice, physicians are routinely asked to make decisions about whether to initiate or continue antidepressant treatment in
a situation where no safety data are available. Pregnancy and breast-feeding can serve as an example, where controlled clinical trials
provide little guidance. Females of fertile age are rarely included in the early phases of clinical testing, indeed, Phase IIb and III trials have
a standard provision to use a reliable method of contraception. Pregnancy during a drug trial is considered as a ‘serious adverse event’
with subsequent study discontinuation. The reasons are not just ethical and legal but also marketing, including the drug manufacturers’
fear of having their products associated with potentially grave side effects, such as malformations. Drug treatment in pregnancy and
lactation thus pose a highly relevant clinical problem that cannot be addressed in controlled trials. Excessive concerns of negative
consequences could erroneously result in a generalized recommendation to not get pregnant or to abort an existing pregnancy. However,
the fetus may already have been exposed to drugs early in the first trimester during frequently unplanned pregnancies; in addition, recent
epidemiological data indicate increasing consumption of psychotropics, including antidepressants, by pregnant women. Psychiatrists
have to weigh the known risks of treatment discontinuation versus the potential risks for the fetus and infant. They should also consider
whether alternative non-pharmacological interventions (psychotherapy, ECT, rTMS) are accessible or effective. The only available safety
data on antidepressants come from animal studies, epidemiological trials, drug registries, case series, anecdotal case vignettes and clinical
observations.
Moreover, published findings have to be viewed with caution and interpreted correctly. For example, recent data suggested an increased
teratogenic risk for the antidepressant paroxetine. While it is true that a meta-analysis confirmed an increased relative incidence of
malformations, the absolute risk was raised from 3% to 4% for all congenital malformations and from 1% to 2% for cardiac malformations.
In 2005 the Prague Psychiatric Center established a specialized consultation outpatient center for pharmacotherapy in pregnancy and
breastfeeding. The center provides services and information on safety and treatment recommendations directly to patients, their treating
psychiatrists and other physicians as well. The database consists of patients records, data on their illness, treatment and pregnancy
outcome. Currently, a prospective study for the longitudinal follow-up of offspring exposed in utero to psychotropics has been designed.
The focus is on their developmental milestones, physical health, neuropsychological performance and general well-being.
Key words: Psychotropic drugs, pregnancy, lactation, drug safety, psychiatric disorders
Cyril Höschl1
Prague psychiatric centre, Centre of neuropsychiatric studies,
1
3rd Medical faculty, Charles University, Prague, Czech Rep.
One of the crucial questions in the study of schizophrenia is, whether the diagnosis of the disease represents one entity or a group of
disorders (“Gruppe der Schizophrenien”). Nancy Andreasen suggests the term “lathomenology” for a bottleneck on the pathogenetic way
from various possible etiological factors to diverse phenomenological expressions (symptoms) (Arch Gen Psych 1999;56:781-787). In the
background of this common denominator, there is an anatomical and functional disruption in neuronal connectivity and communication,
which can be a consequence of incomplete or erroneous neuron formation, migration, synaptogenesis or pruning during ontogenesis.
Also apoptosis and activity dependent changes might play a role in this development. This all can happen from conception to early
adulthood and can lead to the impairment in fundamental cognitive functions. This leads to the development of clinical symptoms,
either positive or negative. Schizophrenia can be regarded as a “disconnection” or “information processing disorder”. There are many
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neural circuits, where the clinical impact of the disconnection or misconnection is worthy of study. One of them is the fronto-thalamocerebellar circuit with the special role of the cerebellum not only in the synchronization of motor processes, but also in the coordination
of motor-cognitive sequences. The disconnection of these circuits leads to “cognitive dysmetria”. Mezo-cortical pathways also represent
a crucial pathogenetic point. Dopaminergic fibers from the ventral tegmental area to the pre-frontal cortex are under serotonergic
inhibition via 5-HT2 receptors. This configuration can help in the understanding of the dual mode of action of novel antipsychotic agents,
which are effective in both positive (hyperdopaminergic state in mezo-limbic areas) and negative (hypodopaminergic state in prefrontal
cortex) symptoms. Disconnection can play a role also in circuits involved in executive functions (fronto-parieto-temporo-cingulate).
On the neurochemical level, many imbalances in information processing can be explained by the framework of Carlsson’s scheme of
psychotogenic pathways. The crucial mechanism involves striato-thalamic GABA-ergic control of gating, which is under glutamatergic
control from cortex. The scheme can also explain the amphetamine model of psychosis, the dopamine hypothesis of schizophrenia, the
glutamatergic model of schizophrenia and the psychotogenic effects of hallucinogens (LSD), atropine, phencyclidine etc. Our own study
on the role of serotonin regulation of psychotogenic pathways will be reported (Bubeníková et al., The effect of tryptophan depletion on
the action of haloperidol in MK-801 treated rats. Eur J Pharmacol, 2004; 502, 1-2:109-116).
The background of disconnection may involve gene-environment interaction including early neuroinfection (inflammatory process).
The classical antipsychotic drugs exert primarily antidopaminergic properties, which are responsible also for their side-effects such
as hyperprolactinemia and extrapyramidal syndrome. Nevertheless, psychotogenic pathways in the brain involve several different
mechanisms, which could serve as targets of antipsychotic modalities, e.g., facilitation of glutamatergic neurotransmission, blockade of
serotonin 5-HT2A receptors, expression of BDNF and bcl2, inhibition of GSK-3β phosphorylation and thus apoptosis etc.
Key words: Schizophrenia, glutamate, dopamine, serotonin, information processing disorder, gating
The ins and outs of the human model of schizophrenia
Jiri Horacek1, Vera Bubenikova Valesova1, Tomas Palenicek1, Filip Spaniel2, Cyril Höschl1
Prague Psychiatric Center, Prague, Czech Rep.
1
3 Medical Faculty of Charles University, Prague, Czech Rep.
2 rd
The experimental models of schizophrenia are based on morphological, biochemical and genetic findings in the clinical population. These
models serve as an important tool for the research of etiology and pathophysiology, and for testing novel potential treatment methods.
The experimental models of schizophrenia are divided into neurodevelopmental, pharmacological and genetic. Only the pharmacological
model is useful in humans.
An important role of the glutamatergic neurotransmitter system in the pathogenesis of schizophrenia has been supported by findings
on various levels from molecular interactions up to the structural layout of the neuronal network in the human brain. The research of
the glutamatergic system in schizophrenia has advanced with the use of non-competitive antagonists of glutamate NMDA receptors
(phencyclidine, ketamine, and dizocilpine). These compounds change both human and animal behavior and induce schizophrenia-like
manifestations in the field of different neurobiological modalities and markers.
The models based on both acute and chronic administration of non-competitive antagonists of glutamate NMDA receptors in humans
and rats show phenomenological validity and are suitable for searching for new substances with antipsychotic effects. In particular, the
human model of schizophrenia based on infusion of ketamine exerts high face validity in term of induction both positive and negative
symptoms, and characteristic cognitive, electrophysiological (qEEG) and metabolic (PET) changes.
Nevertheless, the pathophysiology of schizophrenia remains unexplained. In the light of the neurodevelopmental model of schizophrenia
based on the early administration of NMDA receptor antagonists, it seems that increased cellular destruction by apoptosis or changes
in function of glutamatergic NMDA receptors in the early development of the central nervous system are decisive for subsequent
development of psychosis, which often does not manifest itself until adulthood. Chronic administration of NMDA (not applicable
in humans) antagonists initializes a number of adaptation mechanisms, which correlate with findings obtained in patients with
schizophrenia; therefore, this animal model is necessary for research into the pathophysiology of this disease.
This work was supported by project 1M0517 from the MEYS Czech Republic
Key words: Schizophrenia, models, NMDA receptors, ketamine, glutamate, neurodevelopment
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[JS-07]
Canadian College of Neuropsychopharmacology
Symposium title: Advances in psychotropic drug development: Promising novel targets and agents for psychiatric disorders
Recent advances in the neurochemistry of schizophrenia and potential targets for
antipsychotic drug development
Serdar Dursun, Glen Baker, Marnie Mackay
Neurochemical Research Unit, University of Alberta, Edmonton, Canada
The dopamine hypothesis of schizophrenia has been a major influence for many years in stimulating research in schizophrenia
and in assisting in the development of antipsychotic drugs. However, it has become obvious that other neurotransmitters and/or
neuromodulators must also be involved. The antipsychotic drugs currently available are far from ideal and there is an urgent need to
continue to search for new targets for potential antipsychotics.
Much of the recent research on non-dopaminergic systems has focused on the amino acids glutamate and GABA, with the bulk of
the results suggesting hypofunction of both in schizophrenia. Glutamate does not pass the blood-brain barrier readily and studies
conducted to develop drugs that act at one or more of its multiple receptors have not, to our knowledge, yet produced potential new
effective antipsychotics. Two other amino acids, glycine and D-serine, co-agonists at the NMDA glutamate receptor, have received
considerable attention, and administration of these amino acids, usually in conjunction with currently available antipsychotics, have
been reported in some studies to result in improvement of some symptoms of schizophrenia. However, these amino acids have to
be administered in relatively high doses which may result in side effects such as peripheral neuropathies. There is now a great deal of
interest in testing drugs that inhibit their uptake by neurons and/or glial cells (astrocytes and activated microglia), thus making increased
levels of these amino acids available to interact with the NMDA receptor or, particularly in the case of D-serine, altering metabolism
of the amino acid. This research also emphasizes the importance of glial cells. Microglia are also involved in immune responses and
when activated release a number of proinflammatory cytokines that can result in some behavioural, cognitive, and neuroendocrine
changes characteristic of schizophrenia. It is also of interest that there is now research indicating that there may be a dysfunction of
oligodendrocytes and myelination problems in schizophrenia. Another exciting area of research with regard to schizophrenia is in
the study of neuroactive steroids, rapid acting steroids which can act as positive or negative allosteric modulators at several types of
neurotransmitter receptors, most notably GABA-A receptors and NMDA receptors. Plasma levels of several of these steroids are altered
in a number of psychiatric disorders, including schizophrenia and some clinical studies suggest that pregnenolone may be a useful
adjunctive agent in schizophrenia. Brain levels of some of these steroids have also been reported to be altered in laboratory animals
following administration of currently available antipsychotics.
In addition to the compounds mentioned above, potential interventions which may be added to the usual antipsychotic treatments
include lamotrigine and minocycline. Furthermore, modulation of the nitric oxide pathway continues to gain considerable interest as a
possible therapeutic target in the treatment of schizophrenia. We will report the results of an RCT double-blind crossover study on the
addition of L-arginine, the precursor amino acid for nitric oxide, to usual treatment with antipsychotics in schizophrenic patients.
Key words: Schizophrenia, antipsychotic development, glutamate, nitric oxide, D-serine, glycine, glia, neuroactive steroids
Glen B. Baker, Nicholas D. Mitchell, Jean Michel Le Melledo, Serdar Dursun
Department of Psychiatry, University of Alberta, Edmonton, AB, Canada
The biogenic amine hypothesis of depression, which suggests that depression is the result of a functional deficiency of noradrenaline
(NA) and/or serotonin (5-hydroxytryptamine, 5-HT) at certain synapses in the brain, has had a major influence on research into the
neurochemistry of depression for over fifty years, and most of the antidepressants currently available have an effect on one or both of
these biogenic amines. However, it was obvious early on that other neurotransmitters or neuromodulators must also be involved, and the
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search continues for other targets that may give clues for the development of future antidepressant drugs that are effective in a greater
number of depressed patients, are faster acting and have an improved side effect profile over those currently available. Some of those
targets will be discussed in this overview.
The amino acids γ-aminobutyric acid (GABA) and glutamate are major inhibitory and excitatory neurotransmitters, respectively in the
brain, and a delicate balance between them must be maintained for normal brain function. Research on GABA at the animal model and
clinical levels implies a GABAergic deficit in depression, and animal studies and the rapid antidepressant action of intravenous ketamine
in human subjects suggest hyperglutamatergia in depression, although the results of some neuroimaging studies to date do not seem
to support these ideas. In recent years, there has been a great deal of interest in the possible roles of neuroactive steroids (rapid acting
neurosteroids which can act as positive or negative modulators of a number of neurotransmitter receptors, most notably GABA-A and
NMDA glutamate receptors) in the etiology and pharmacotherapy of depression. Allopregnanolone has received particular attention
in this regard. Several researchers have proposed that the hypothalamic-pituitary-adrenal (HPA) axis plays a central role in the etiology
of depression and there has been considerable interest in corticotropin-releasing hormone (CRH) receptor antagonists as potential
antidepressants. The peptide substance P acts on neurokinin 1 (NK1) receptors, and there is ongoing interest in NK1 receptor antagonists
as potential antidepressants. The role of the immune system in depression has been the focus of considerable research and it has been
proposed that excessive proinflammatory cytokines (which are released by activated microglia) may result in depressive symptoms; it
is of interest that such cytokines can activate CRH release and reduce levels of 5-HT in the brain. Although there are some contradictory
results, several studies suggest that antidepressants increase expression of cyclic AMP-regulated element-binding protein (CREB) and
brain-derived neurotrophic factor (BDNF). Dysfunction of melatonin secretion in depression has been suggested and this may account,
at least in part, for sleep disorders experienced by many depressed subjects. Agomelatine, a melatonin receptor agonist and 5-HT2C
receptor antagonist, is now marketed as an antidepressant. The potential interactions of several of the targets mentioned above will be
discussed.
Acknowledgements: The authors are grateful to the Canadian Institutes of Health Research (CIHR), the Canada Research Chairs program
and the University of Alberta for Funding.
Key words: Antidepressants, biogenic amines, GABA, glutamate, HPA axis, CRH, substance P, neuroactive steroids, glia
SYMPOSIA
[PS-01]
Symposium Title: Epigenetics or genetics: Gene-environment interactions over the life - span
Alzheimer’s disease: Genes and/or life style
Engin Eker
Istanbul University, Cerrahpaşa School of Medicine, Department of Psychiatry
A number of genetic risk factors have been identified, but only a small proportion of Alzheimer’s disease (AD) cases can be explained by
specific gene mutations. Several genetic risk factors have been linked to AD. Mutations in APP, PS1, and PS2 genes have consistently been
associated with early-onset familial Alzheimer’s disease (FAD). A majority of AD cases manifest as sporadic late onset form (LOAD) typically
with onset above the age of 65 years. Most people who develop Alzheimer’s are diagnosed after age 80. More recently a large number
of genes have been implicated as a risk to LOAD, but only a few of these associations have been replicated such as the gene encoding
for the APOE4 allele or loci in the clusterin (CLU), phosphatidylinositol binding clathrin assembly protein (PICALM), and complement
receptor1 (CR1).
Most diseases of aging are influenced by gene-environment interactions. AD has both genetic and environmental risk factors. The genetic
susceptibility influenced by genes like ApoE4 are factors to be aware of, but perhaps more important are the environmental risk factors.
Environmental risk factors can act as triggers in the expression of gene potential. Numerous studies indicate that ApoE4 carriers may be
more vulnerable to environmental factors.
Recent studies have shown that dietary factors, such as exposure to a Mediterranean diet, fish and high omega-3 diets, cigarette
smoking, head trauma, infections, systemic inflammation, and metal exposure can significantly alter an individual’s risk of developing
AD. On the other hand psychosocial factors such as education, social network, leisure activities and physical activity, chronic stress, and
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depression also seem to be connected to the risk of developing AD. There are some somatic factors that are under the direct influence of
environmental exposures, such as blood pressure, obesity, diabetes mellitus, cardio- and cerebrovascular diseases, and hyperlipidemia,
have additionally been implicated in AD etiology.
Key words: Alzheimer’s disease, genes, environmental risk
[PS-02]
Symposium Title: Behavioral addictions and treatments: Review of recent data
Sultan Doğan
Namik Kemal University, School of Medicine, Department of Psychiatry
Hypersexual Disorder is proposed as a new psychiatric disorder for consideration in the sexual disorders section of the DSM-V. Historically,
excessive sexual behaviors were clinically documented by diverse clinicians such as the 19th century Western European pioneer sexologists
Richard von Krafft-Ebing (1840–1902), Havelock Ellis (1859–1939), and Magnus Hirshfeld (1868–1935). Benjamin Rush(1745–1813), a
physician and founding father of the United States (Rush, 1746-1813) also studied the same subject. These clinicians and investigators
described a frame of persistent socially deviant sexual behaviors as well as clinical examples of males and females whose nonparaphilic
(i.e., normophilic) sexual appetite was excessive and maladaptive. The clinical examples of such appetitive behaviors described by these
investigators were precursors to the 20th century characterization of protracted promiscuity as Don Juanism (Stoller, 1975) or satyriasis
(Allen, 1969) in males and nymphomania (Ellis & Sagarin, 1965) in females. The DSM-II (American Psychiatric Association, 1968) recognized
sexual deviations as personality disorders but there was no mention of excessive or maladaptive nonparaphilic sexual behavior disorders.
By 1980, the DSM-III (American Psychiatric Association, 1980) classified paraphilic disorders as distinct pathologies (Psychosexual
Disorders) and a residual diagnostic category, Psychosexual Disorder Not Otherwise Specified included ‘‘distress about a pattern of
repeated sexual conquests with a succession of individuals who exist only as things to be used (Don Juanism and nymphomania)’’. In the
DSM-IV (American Psychiatric Association, 1994) and its text revision, DSM-IV-TR (American Psychiatric Association, 2000), the original
DSM-III characterization of these behaviors was reestablished. Sexual Disorders Not Otherwise Specified (302.9) included a condition
characterized by: ‘‘distress about a pattern of repeated sexual relationships involving a succession of lovers who are experienced by
the individual only as things to be used’’. Until recently, authors have used different terms for hypersexual disorders, such as “sexual
addiction” (Carnes), “paraphilia-related disorders and non-paraphilic hypersexuality” (Kafka), “excessive sexual desire disorders” (Marshal),
“problematic hypersexuality” (Finlayson) and “compulsive sexual bahavior” (Cooper and Coleman). These disorders were described as
markedly increased expressions of culturally normative sexual desire (fantasies, urges, and behaviors) persisting for a minimum duration
of 6 months and associated with clinically significant personal distress, impairment in reciprocal romantic relationships or other adverse
psychosocial consequences. Thera are several form of hypersexual disorders such as compulsive masturbation, pornography dependence,
telephone sex dependence, cybersex, severe sexual desire incompatibility, anonymous sex and multiple sexual partners (Coleman 1995,
Carnes 2007, Kafka 2000, Kafka 2007, Cooper 2002, Cooper 2003).
There are significant gaps in the current scientific knowledge base regarding the clinical course, developmental risk factors, family history,
neurobiology, and neuropsychology of hypersexual disorder. As is true of so many psychiatric disorders, the comment that ‘‘more research
is needed’’ is certainly applicable to these conditions. Although there are significant shortcomings in the state of our current empirical
knowledge, there is little doubt that patients with such conditions commonly present to clinicians as well as to specialized treatment
programs.
Key words: Don Juanism, nymphomania, hypersexual disorders
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Pathological gambling: review of recent data
Ömer Şenormancı
Bakirkoy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, İstanbul, Turkey
Gambling, which could also be defined as risking one’s chances for a possible outcome, is a cultural phenomenon as old as humanity. While
gambling is a form of entertainment without any drawbacks for the great majority, pathological gambling develops in a small minority.
The prevalence (0.2%- 5.3%) in the adult population is gradually increasing due to the ease of accessibility such as Internet gambling. This
increase and the accessibility of gambling becoming easier, have led to some sociodemographic changes in the population who have
trouble with gambling. Recent studies have shown pathological gambling to be higher in the psychiatric patient population compared
to the normal population (with no assigned psychiatric diagnosis) and that it is necessary to be included as part of the questioning in a
psychiatric evaluation.
Some drugs once thought to be a new hope in the pharmacological treatment of pathological gambling, have been proven ineffective
in recent randomized, double-blind, and placebo-controlled studies. Current studies are testing GABAergic and antiglutamatergic drugs,
that are thought to be effective in chemical and behavioral addictions, in the treatment of pathological gambling.
Two large meta-analysis studies have reported that non-pharmacological therapy approaches are more effective in the treatment
of pathological gambling. Behavioral therapy, cognitive behavioral therapy and short, motivational, individualized approaches are
demonstrated to be effective. Although it is suggested that behaviorial therapy + cognitive behavioral therapy and short, motivational,
and individualized approaches are equally effective, combining the two may improve the efficacy of the treatment. This presentation aims
to describe pathological gambling accompanied by contemporary information with respect to treatment.
Key words: Pathological gambling, impulse control disorder, pharmacotherapy, psychotherapy
Fulya Maner
Binge eating is characterized by recurrent episodes of eating, in a discrete period of time, an amount of food that is much larger than most
people would eat in a similar time period under similar circumstances. There is a sense of lack of control over eating during the episode.
Eating is much more rapid than normal and one eats until feeling uncomfortably full. After overeating one feels disgusted, depressed or
guilty. Binge eating disorder is included in eating disorders not elsewhere specified in the DSM-IV and is a symptom of bulimia nervosa
and anorexia nervosa.
Research has shown that patients with eating disorders have high rates of co-occuring substance use disorders. The substance of abuse
and food appear to compete for sites in the brain and abstinence from substance use causes craving for the substance and also for food.
Addictions involving food and substances share similar etiologies and behavioral symptoms. Individuals suffering from binge eating
disorder are more likely to have first degree relatives with a substance abuse disorder. According to retrospective reports of patients,
the initiation of disordered eating usually began before substance abuse. The general reward pathway includes the ventral tegmental
area and basal forebrain. Substance abuse has been shown to change the neural processes around these connections. The mesolimbic
dopamine system connects the ventral tegmental area to the basal forebrain and is critical for the self-administration of psychomotor
stimulants. Dopamine deficiency has been suggested to be a common characteristic of individuals who are prone to substance or food
addiction. Striatal dopamine receptor (DRD2) availability is significantly lower in obese individuals than in controls. Body mass index is
shown to correlate inversely with measures of D2 receptors.
Functional neuroimaging studies have revealed that pleasant smelling, looking, and tasting food has reinforcing characteristics similar
to drugs of abuse. Many of the brain changes reported for hedonistic eating are also seen in various types of addiction. Overeating may
have an acquired drive similar to drug addiction with respect to motivation and incentive craving. In both cases, the desire and continued
satisfaction occur after early and repeated exposure to stimuli.
Addictive behavior manifests itself in permanent preoccupation with food and eating, withdrawal symptoms, continuation of disturbed
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eating behavior in spite of negative consequences, loss of control, and frequent relapse.
Human and animal studies have demonstrated that in some brains the consumption of sugar-rich foods or drinks primes the release of
euphoric endorphins and dopamine within the nucleus accumbens, in a manner similar to some drugs of abuse. The neurobiological
pathways of drug and “sugar addiction” involve similar neural receptors, neurotransmitters, and hedonistic regions in the brain. Craving,
tolerance, withdrawal, and sensitization have been documented in both human and animal studies. In addition, there appears to be cross
sensitization between sugar addiction and narcotic dependence in some individuals There also appears to be some common genetic
markers between alcohol dependence, bulimia, and obesity, such as the A1 allele gene and the dopamine 2 receptor gene.
Key words: Binge eating, eating disorder, addiction
[PS-03]
Symposium Title: Painful syndromes in psychiatry and their managements
Pain and personality
Mehmet Ak
Department of Psychiatry, Gulhane School of Medicine, Ankara, Turkey
There is a dynamic two-way interaction between pain and personality and the psychophysiology and anatomy of this relationship are
not elucidated fully. Is there a specific personality type of pain or do some people perceive and express pain more than others? Probably
there is no clear answer to this question. So far chronic pain has been shown to affect personality, as indicated by studies using Cloninger’s
Temperament and Character Inventory. A relationship has been demonstrated between some personality traits and pain. In studies that
reported the prevalence of personality disorders, associations with chronic pain vary between 31% to 81%. The most frequently identified
personality trait is one with paranoid features.
Today I will talk mainly about studies using Cloninger’s model, because Cloninger’s integrative psychobiological approach provides a
flexible framework for both clinical assessment and treatment planning. The most significant and consistent result of these studies was
elevated harm avoidance scores. Harm avoidance scores still remain high even after controlling for the effect of depression and anxiety.
Thus this temperament dimension is possibly an important state and trait feature for development of psychosomatic illnesses. These
findings also confirmed that serotonergic systems are involved in the process of psychosomatic organization. Cloninger described that
people with chronic anxiety, avoid harm that is characterized by more pain, are difficult to calm, tire easily, and display specific signs
based on specific anticipatory anxiety. Harm avoidance refers to an inherited tendency to block the behavior in the answers given to the
blocking, non-rewarding, and punishment signals. High harm avoidance behavior is observed in the form of social withdrawal, becoming
tired easily, staying away from strangers, fear of uncertainty, and being pessimistic that there would be some problems in a situation even
when others do not worry.. These people are timid, passive, insecure, and pessimistic individuals.
Looking at the size of the character, it is seen that low self-directedness scores are the most common finding. The original meaning of
self-directedness is in accordance with choosing goals and values of the individual, optimization of the behavior to maintain a situation,
editing capabilities, and being strong-willed.
Individuals with low self-directedness do not expect to be able to control and positively influence an aversive situation and overcome
obstacles. Self-directedness is closely related to the concept of self-efficacy. Self-efficacy is defined as the personal conviction that one
can successfully show problem-solving behavior in a given situation. There is much evidence which suggests that low self-efficacy plays
an important role in pain control, coping with disability, and treatment outcome. Our clinical experiences show that pain can sometimes
be the symbol of help, sometimes the quest for attention, and other times problems that can not be expressed. Emotions that are not
expressed can mean pain and unexpressed emotions can be the cause of pain for some people that do not heal. In order to understand
and to treat these people, employing a holistic assessment and approach are very important.
Key words: Character, pain, temperament
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The differences between SSRIs and SNRIs in the treatment of psychiatric pain syndromes
Abdurrahman Altındağ, Gülçin Elboğa
Gaziantep University, Medical School, Department of Psychiatry, Gaziantep, Turkey
E-mail: [email protected], [email protected]
The occurrence of depression with physical symptoms and pain is common. On the other hand, comorbid depression is also common
in chronic pain syndromes. Antidepressants are effective in the treatment of psychological and physical symptoms of depression and
chronic pain symptoms of non-depressed patients.
It is not well described how antidepressants relieve the pain. However, it is suggested that this effect is related to serotonin and
noradrenaline. Analgesic effects of antidepressants are independent from their effects on the mood. Antidepressants which have effects
on both serotonin and noradrenaline are more effective than those with effects on one of these neurotransmitters in the treatment of
depression and comorbid pain syndromes. Tricylic antidepressants (TCAs) have serotoninergic and noradrenergic effects. Therefore, they
are superior to monoaminergic antidepressants, such as SSRIs, with regard to analgesic and antidepressant effects. The usage of TCAs is
limited because of their safety profile and side effects. SNRIs have similar analgesic effects to TCAs. On the other hand they have lower
side effects and a better safety profile. Additionally, SNRIs are more effective than SSRIs in the treatment of physical pain syndromes. SNRIs
have a similar safety profile to SSRIs and almost similar costs to the older agents.
Better diagnosis and treatment of pain symptoms, which are strong indicator of depressive relapses, will provide better quality of life and
productivity in patients with depressive disorders.
Key words: SSRI, SNRI, pain
How does alexithymia lead to painful syndromes?
Hüseyin Güleç
Erenkoy Psychiatry Hospital, Istanbul, Turkey
Several studies have focussed on defining the network of brain structures involved in pain. Pain perception (sensory discriminative,
affective/emotional, cognitive/evaluative) has been shown to depend on different areas of the brain. Modern neuroimaging methods
have been used to determine whether different pain symptoms involve similar brain structures. These studies indicated that acute
physiological pain and neuropathic pain have distinct although overlapping brain activation patterns, but that there is no unique pain
matrix/allodynia network.
Several contemporary neuroscientists and cognitive scientists make a similar distinction between emotions as bodily events and feelings
as mental events and regard symbolization as an important element in the cognitive processing of emotions. Awareness of feelings,
together with the thoughts, fantasies, and memories that they elicit, facilitates modulation of the emotional arousal induced by stressful
events. Feelings are attributed to the symbolic representation in working memory of the activity of unconsciously operating subsymbolic
systems that generate the brain states and bodily responses which comprise emotions. These representations become integrated with
representations of past experiences and representations of the self. Attributing the feeling of specific basic emotions to ‘viscerosomatic
self-representations’ in the lower levels of the brain, attributing reflective awareness and the capacity for experiencing higher-order
feelings to linguistic symbolizations and an ability to think in perceptual images is important for the parsing and regulation of emotional
states.
According to Lumley alexithymia is associated with tonic physiological hyperarousal, certain types of unhealthy behavior, and a biased
perception and reporting of somatic sensations and symptoms. Alexithymia probably influences illness behavior, but there is little
support for the hypothesis that alexithymia leads to chronic organic disease. Alexithymia links with physical illness due to four possible
pathways: a) alexithymia leads to organic disease through physiological or behavioral mechanisms, b) alexithymia leads to illness behavior
through cognitive or social mechanisms, c) physical illness leads to alexithymia, and d) both alexithymia and physical illness result from
sociocultural or biological factors. Research on the effects of emotional trauma resulted in the hypothesis that traumatic experiences in
childhood or adult life may have adverse consequences for physical health. It has been shown that there is evidence of a correlational
association between childhood trauma and somatization in adulthood, and several retrospective studies with very large samples have
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demonstrated an association between childhood trauma and the development of somatic disease in adult life. An unanswered question
is: what are the psychological/biological mechanisms that might render trauma in earlier years a risk factor for the development of disease
later in life? The associations between alexithymia, somatization, dissociation and trauma, have led to the suggestion that dissociation
acts as a defense against emotionally distressing memories that are associated with the traumatic avents. Attachment insecurity and
associated deficits in affect development and affect regulation are linked not only to the experience of being raised by parents with
impaired capacities for mentalization, but sometimes also to more severe developmental traumas. Dissociation within emotion schemas
is initially an adaptive response to external danger arousal and is especially severe when the child experiences the parent as a threat, for
then there is no safe place to be.
Key words: Alexithymia, cognitive processing of emotions, trauma, attachment, mentalizing, somatization
Kerem M. Doksat
MD, Professor of Psychiatry, POLIMED Psychiatric Center
E-mail: [email protected], [email protected], [email protected]
Hypnosis is a misnomer first used by Scottish Surgeon James Braid for a phenomenon probably as ancient as mammalian history. After the
Austrian Neuropsychiatrist Sigmund Freud has fouled hypnosis in order to glorify his own theory, especially American Psychiatrist Milton
Hyland Erickson rebuilt the reputation of hypnosis (1).
In 1846, James Esdaile successfully performed 345 major operations by using mesmeric method in India. English surgeon John Ellitson
mentioned similar success in many operations in 1843. With the introduction of ether in 1846 and chloroform in 1847, the mesmeric
method, which has already serious oppositions, was forgotten. Hypnosis may be used alone or in combination with other methods. Its
use in cancer pain, especially during the terminal phase, may reduce the requirement for opioids, or even totally eliminate them. Hypnosis
may help the patients to experience with their consciousness fully open and free from side-effects like grogginess of the opioids during
last phase before their terminal coma. It can be used in burns and for pain free labor. In dentistry it can be used for analgesia, dentists’
chair phobia, and getting rid of gag reflex. It is effective in 30 to 50 percent of phantom limb pain cases.
Hypnosis is reported to be effective for the treatment of migraine and other headaches and in many other pain syndromes; I also have a lot
of anecdotal evidence. The approach should be adjusted for the patient; the skill and experience of the hypnotist, his or her relationship
with the patient and the patient’s personal characteristics and preferences must be adjusted according to all of these. Indeed, hypnotic
procedures may help people who are not much hypnotizable. For example, in cases experiencing both pain and tension intensively, even
induction of relaxation reduces pain and in many of the hypnotic procedures, relaxation is utilized. If the patients cooperate well and
accepts the procedure seriously, even if they are not hypnotizable, they may practice the hypnotist’s relaxation suggestions with success
while sitting or lying comfortably (2).
The principal techniques are (2,3): 1) Direct suggestion, 2) Utterance of neurophysiological metaphors, 3) Glove anesthesia replacement
technique, 4) Replacement pain symptom’s site or differentiating the pain symptom, 5) Dissociation by using the imagination, 6)
Technique of different interpretation of pain, 7) Auto-hypnosis (self-hypnosis).
As a summary, the effect of hypnosis on pain is mediated by two mechanisms:
1) Muscle relaxation,
2) Change in perception and cognitive distraction.
Hypnotherapy can be effective in many painful syndromes if suitable patients are chosen. Group psychotherapy and hypnosis can be
effective in the treatment of cancer patients’ pain (4).
References:
1.
Doksat R. Tatbikatı ve Nazariyatı ile Hipnotizma. İstanbul: Kader Basımevi, 1962. 253-281.
2.
Doksat MK. Ağrı ve Psikiyatri. Bursa: Psikiyatri ve Sanat Yayın Evi, 2003. 165-172.
3.
Arred Barabasz, Johnn G Watkins Hypnotherapeutic Techniques 2E. New York: Brunner-Routledge. 2005. 219-239.
4.
Porter LS, Keefe FJ. Psychosocial issues in cancer pain. Curr Pain Headache Rep. 2011 Aug;15(4):263-70.
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[PS-04]
Symposium Title: Adult attention - deficit hyperactivity disorder (ADHD) and comorbidity
Rasim Somer Diler
Department of Psychiatry, University of Pittsburgh, PA, US
Five to 40% of children and adolescents with attention deficit hyperactive disorder (ADHD) also have comorbid major depressive disorders
(MDD). Moreover, youths with ADHD have up to a 4 times higher risk of developing depressive disorders than the general adolescent population.
Comorbidity with MDD has been associated with elevated impairment and higher rates of hospitalization versus ADHD alone. However,
depression in youths with ADHD may be more difficult to diagnose, given that some symptoms overlap between the two disorders. Moreover,
many of the medications used to treat ADHD cause side effects resembling symptoms of MDD. Available studies suggest the particular
importance of anhedonia, social withdrawal, psychomotor retardation, negative views of self and future, and suicidal thoughts as symptoms that
distinguish MDD in youths who have ADHD. Despite ongoing controversy, the view that pediatric bipolar disorder (PBD) is rare or non-existent
has been increasingly challenged not only by case reports but also by systematic research; however, a significant portion of bipolar youth,
especially children, have high comorbidity with ADHD. Significant debate exists on whether early onset bipolar disorder is mistakenly attributed
to attention deficit hyperactivity disorder (ADHD), or whether ADHD is frequently misdiagnosed as mania. Among pediatric-onset cases of
bipolar disorder, comorbid ADHD is frequently seen, and there is strong evidence to suggest that this pattern has a familial and genetic basis.
Differentiating bipolarity in children with ADHD is not an academic discussion but also a great concern because of the associated complication of
the treatment of these disorders. It is suggested that manic symptoms should represent a distinct change from a child’s usual level of functioning
(e.g., change or worsening of distractibility during a mood episode in children with ADHD). There are some symptoms that mainly occur in BD
youth as compared to other disorders (e.g., ADHD) and may help to differentiate between BD and these disorders, such as clinically relevant
euphoria, grandiosity, decreased need for sleep, hypersexuality (without history of sexual abuse or exposure to sex), and hallucinations. We need
larger longitudinal studies to better understand the risks and resilience factors of developing BP in ADHD youth.
Key words: ADHD, depression, bipolar, child
Mücahit Öztürk
PEDAM Psikiyatri Merkezi, İstanbul, Turkey
Attention Deficit Hyperactivity Disorder (ADHD) is a syndrome of inattention, hyperactivity, impulsiveness and other deficits of
executive functions. It’s now well known that ADHD often continues into adulthood (1, 2). ADHD is a chronic disorder which leads to a
negative impact on functioning throughout the life cycle (3). Children with ADHD are at significant risk of multiple forms of adolescent
maladjustment. Approximately up to 60% of childhood cases continue symptomatic into adulthood. In the remaining 40 percent
symptoms may remit in early adulthood (4). The manifestation of ADHD changes over the course of life. In some cases the hyperactivity
may disappear but decreased attention span and impulse control problems persist (5).
Approximately 1 in 25 adults have ADHD, 90% of whom may be currently untreated, with a potentially negative impact on the lives of
patients and their families (6). Significant legal, academic, social, and occupational problems have been observed in adults with ADHD (7).
Follow up studies suggest that up to 33% of ADHD teens versus 1% to 9% of controls drop out high school. Children with ADHD are at
risk of negative academic outcomes. ADHD and similar problems entail a risk of underachievement at school. The results indicate that
students with ADHD underachieve in the school situation in relation to their optimal cognitive capacity (3).
Adolescents with ADHD complete less education by 2-3 years and demonstrate lower occupational performance at the age of 25 years. Adults
with ADHD may struggle with frequent job changes, frequent partner changes, higher rates of divorce, increased motor vehicle accidents,
poor money management and higher rates of unwed pregnancy (8). Although their educational performance is lower than people without
ADHD, their early employment histories don’t differ from those people with similar education (5). Adolescents with ADHD were more likely
to smoke cigarettes and use illicit drugs. Their academic attainment was below age norms with more than one fourth repeating grades (9).
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Studies show that effective treatment significantly improves quality of life (3). Severity of childhood ADHD and treatment significantly
predict the persistence of ADHD into adulthood (5). As previously shown by some research for children and adolescents, stimulant
medications alone did not eliminate the academic achievement deficit of ADHD undergraduates. ADHD patients who were treated with
stimulants were significantly less likely to subsequently develop depressive and anxiety disorders and disruptive behavior and less likely to
repeat a grade compared with participants with ADHD who were not treated. Adolescents with ADHD were also significantly more likely
to be absent during the academic year, and they were over eight times more likely than adolescents without ADHD to drop out of high
school. These findings demonstrate that children with ADHD continue to experience severe academic impairment into high school (10).
Key words: Attention deficit hyperactivity, academic performance, occupation
References:
1.
Barkley RA. Major life activity and health outcomes associated with attention-deficit / hyperactivity disorder. J. Clin Psychiatry 2002;63 12:10-15.
2.
Weiss G, Hechtman L. Hyperactive Children Grown Up: ADHD in Children, Adolescents, and Adults. New York, NY: Guilford Press; 1993
3.
Cheng K, Myers KM, Stubble DE. Attention deficit hyperactivity disorder Child and Adolescent Psychiatry The Essentials Lippincott Williams &Wilkins
4.
Biederman J, Mick E, Faraone SV. Age dependent decline of symptoms of attention deficit hyperactivity disorder: Impact of remission definition and symptoms
type. Am J Psychiatry 2000 157:816-818
5.
Sadock BJ, Sadock VA. Textbook of Child and Adolescent Psychiatry. 2009 Lippincott Williams &Wilkins
6.
Culpaper L, Mattingly G. Challenges in Identifying and Managing Attention-Deficit/Hyperactivity Disorder in Adults in the Primary Care Setting: A Review of the
Literature Prim Care Companion J Clin Psychiatry 2010 v. 12(6);
7.
McCann BS, Roy-Byrne P Attention-deficit/hyperactivity disorder and learning disabilities in adults. Semin Clin Neuropsychiatry. 2000 Jul;5(3):191-7.
8.
Spetie L, Arnold EL. Attention deficit hyperactivity disorder in Lewis Child and Adolescent Psychiatry A Comprehensive Textbook 2007 Lippincott Williams &Wilkins
9.
Lam AK, Ho TP Early adolescent outcome of attention-deficit hyperactivity disorder in a Chinese population: 5-year follow-up study. J Fam Pract. 2011 Jun;60(6):364-7.
10. Kent KM, Pelham WE Jr, Molina BS, Sibley MH, Waschbusch DA, Yu J, Gnagy EM, Biswas A, Babinski DE, Karch KM.The academic experience of male high school
students with ADHD.Pediatrics. 2009 Jul;124(1):71-8.
[PS-05]
Symposium Title: Brain mapping, TMS, NVS, biofeedback and deep brain stimulation in treatment of psychiatric disorders
Concomitant use of qEEG and rTMS in treatment of depressive disorder, new approaches
Nevzat Tarhan, Gökben Hızlı, Serap Aydın
Üsküdar University, Neuropsychiatry Istanbul Hospital, Istanbul, Turkey
Repetitive transcranial magnetic stimulation (rTMS) therapy has been approved for treatment of depression by the FDA in 2008, and was
included in APA Guidelines as published in October, 2010 issue of American Journal of Psychiatry. Although its efficacy is not as high as
the efficacy of ECT, rTMS is safer in the treatment of depression in older patients. Especially the absence of common treatment side effects
of ECT, such as confusion and memory problems, makes rTMS treatment more valuable in patients with high side effect risk.
This study was performed by the quantitative EEG (qEEG) monitoring before and after rTMS treatment. The aim was to examine the
predictive value of qEEG as a biological indicator of response to rTMS treatment.
In Neuropsychiatry Istanbul Hospital, between dates of 2006-2010, rTMS had been applied to 1283 patients with a diagnosis of treatmentresistant depressive disorder. The patients discontinued the psychotropic medications 12 hours before the qEEG monitoring. qEEG records were
taken just before the first and the last rTMS sessions. HAM-D 17 was performed before and after 15-20 (mean was 18) sessions of rTMS treatment.
The patients with a medical history of epilepsy were excluded. The cases with no history of seizures, but with suspicious epileptical
abnormality in pre-treatment EEG were included with special medical caution. rTMS treatment was performed at left DLPFC, as 25 hz. and
1000 pulse, one session on each day, a total of 15-20 sessions, with Magstim Rapid.
From 1283 cases, one patient had epileptic seizure as an adverse effect. Due to contraction of facial muscles, one patient had a broken
tooth. In 3 patients suffering from tinnitus occurred, but later tinnitus decreased significantly.
The statistical analyses of the cases are ongoing. The initial results with remission and response rates will be presented. qEEG power
spectrum changes and changes in the activation compared to normative data base in LORETA will be evaluated.
Key words: Repetitive transcranial magnetic stimulation (rTMS) therapy, quantitative EEG, depression treatment
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What does transcranial magnetic stimulation (TMS) promise in psychiatric disorders other than
depression? Future perspectives
Bahadır Bakım
Sisli Etfal Research and Teaching Hospital, Psychiatry Clinic, Istanbul, Turkey
Up to 40% of OCD patients fail to respond satisfactorily to generally adequate treatment options, and 10% cannot be helped at all. Because OCD
may be related to increased neural activity in prefrontal subcortical circuits, the inhibitory effect of rTMS was hypothesized to be beneficial in OCD
treatment. rTMS has recently demonstrated remote effects, with left prefrontal stimulation inducing changes in cerebral perfusion in the bilateral
anterior cingulate and orbitofrontal cortex. In conclusion, in open-label studies, high-frequency rTMS of the right and/or left DLPFC appears to
be effective in reducing obsessive-compulsive symptoms. However, this could not be replicated in double-blind, sham-controlled studies. As the
efficacy of rTMS is often time limited, the necessity of a second rTMS after several weeks should be investigated and functional MRI studies of rTMS
in OCD are needed to clarify the specific stimulation region of rTMS. Otherwise, as the improvement of symptoms is often noted in sham settings,
it would be interesting to investigate the neural underpinnings of the placebo effect caused by sham rTMS.
Several initial studies on negative symptoms of schizophrenia have suggested that the condition seems to respond to high frequency (20 Hz, 10 Hz)
repetitive transcranial magnetic stimulation (rTMS). Low frequency rTMS ( <= 1 Hz) inhibits cortical excitability and leads to a weakening of the transfer
at the synapses. Some authors documented the superiority of 10 Hz rTMS using a sham-controlled parallel design (110% of motor threshold, over
left dorsolateral prefrontal cortex), and found a statistically significant improvement in negative symptoms of schizophrenia patients. Interestingly, in
this study, positive symptoms deteriorated from baseline. However, in another recent study with a similar controlled design, some authors failed to
find significant improvement. Positive symptoms, as globally assessed by PANSS-P, do not show a statistically significant improvement after rTMS but
a marked and significant improvement in severity of auditory hallucinations is obtained. More studies need to be conducted for further investigation
of the effects of short term and prolonged application of TMS on negative and positive symptoms in schizophrenia.
TMS has also been applied to study motor cortex changes in patients with cognitive disorders such as AD, frontotemporal dementia, and dementia
with Lewy bodies. Further investigations with larger sample sizes are needed to identify MCI and AD subjects and separate them from the healthy
population, and to identify connectivity changes occurring during the development of AD. Active rTMS with exposure may have symptomatic
and physiological effects. Larger studies are needed to confirm and verify whether rTMS plus exposure therapy has a role in the treatment of PTSD.
Some authors reported antimanic effects from rapid transcranial magnetic stimulation of the right prefrontal cortex. Further systematic studies are needed.
The prefrontal cortex may be a promising TMS target for reducing pain in neuropathic, rheumatologic and post-surgical populations
although the mechanisms by which it might work remain unclear. Future studies are needed to determine TMS treatment parameters and
cortical targets that can optimize its effects and duration.
Key words: TMS, OCD, bipolar disorder, PTSD, schizophrenia, neuropathic pain
Transcranial magnetic stimulation (TMS) as a treatment for depression
Ayhan Algül
Department of Psychiatry, GATA Haydarpasa Training Hospital, Istanbul, Turkey
Transcranial magnetic stimulation (TMS) is a noninvasive method of brain stimulation in which magnetic fields are used to induce electric currents in
the cerebral cortex, thereby depolarizing neurons. TMS based on focal electromagnetic induction, was introduced in 1985 by Anthony Barker (1). Both
repetitive TMS (rTMS) and electroconvulsive therapy (ECT) use electrical energy to induce neuropsychiatric change; however, the magnetic fields in TMS
are unaffected by the high impedance of the skull and thus, TMS can be applied relatively with no pain to conscious patients without the need for sedation.
TMS/rTMS is found to be a promising noninvasive treatment for various neuropsychiatric conditions. Therapeutic utility of TMS has been reported
in the literature for psychiatric disorders, such as depression, acute mania, bipolar disorders, panic, hallucinations, obsessions/compulsions,
schizophrenia, catatonia, post-traumatic stress disorder, or drug craving. Single-pulse TMS was first used as a possible therapeutic tool for
depression in 1993. Since then, depression continues to be the most commonly studied psychiatric condition in the application of rTMS (2).
Most studies have suggested that the active rTMS treatment has greater antidepressant efficacy than sham stimulation (3). A number of clinics
have been set up offering TMS for treatment of various diseases worldwide and rTMS is already approved by some countries for treatment of
depression (i.e., Canada and Israel). In 2008, rTMS was approved by the Food and Drug Administration in the United States for the treatment
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of patients with medication-refractory unipolar depression who have failed one good (but not more than one) pharmacological trial.
Key words: Transcranial magnetic stimulation, depression, rTMS
References:
1.
Barker AT, Jalinous R, Freeston IL. Non-invasive magnetic stimulation of human motor cortex. Lancet1985;1(8437):1106-7.
2.
Nivoli AM, Colom F, Murru A, Pacchiarotti I, Castro-Loli P, González-Pinto A, et al. New treatment guidelines for acute bipolar depression: A systematic review. J
Affect Disord 2011; 129(1-3):14-26.
3. Fitzgerald PB, Hoy K, McQueen S, Maller JJ, Herring S, Segrave R, et al. A Randomized Trial of rTMS Targeted with MRI Based Neuro-Navigation in TreatmentResistant Depression. Neuropsychopharmacology 2009; 34(5):1255-62.
Vagus Nerve Stimulation (VNS) in depression treatment
Şadiye Visal Buturak
Department of Psychiatry, Kırıkkale University, Faculty of Medicine, Kırıkkale, Turkey
Major Depressive Disorder (MDD) is a prevalent, chronic, recurrent and disabling disorder and it is predicted that MDD will be the second most common
cause of incapacitating disease in 2020 (1). Although a broad range of effective treatments is available, a considerable proportion of patients do not
respond adequately (2). Patients who have already experienced recurrent depressive episodes often relapse and do not achieve full remission despite
treatment with conventional therapies (3). A need for the development of alternative treatments for treatment resistant depression (TRD) that are
effective, have fewer side-effects or have longer-lasting antidepressant effects has been identified. Vagus nerve stimulation (VNS) therapy is a type of
treatment where a small electrical pulse is administered through an implanted neurostimulator to a bipolar lead attached to the left vagus nerve (4).
VNS was approved by the US Food and Drug Administration in 2005 for the adjunctive long-term treatment of chronic or recurrent depression for
patients 18 years or older who are experiencing a major depressive episode (MDE) and have not had an adequate response to 4 or more adequate
antidepressant treatments. The mechanism of action of VNS is not fully understood although emerging data suggest that VNS therapy modulates the
function of neural structures implicated in depression and also influences monoaminergic neurotransmission (5). In a randomized sham-controlled
trial, VNS only showed a response rate of 15.2% compared to 10% with sham treatment (p=0.251) during a 10 week trial (6). But most of the open-label
studies about the short and long-term efficacy of the VNS in patients with TRD showed significant reductions in response and remission rates. Rush et
al. examined the effect of VNS in adult outpatients with nonpsychotic, treatment-resistant major depressive or bipolar I or II (depressed phase) disorders.
Response rates were 40% for the Hamilton Depression Rating Scale (HDRS) (7). In an open pilot study of VNS in outpatients with treatment-resistant
MDEs the response rate was 30.5% for the primary HDRS (28) measure, after 10 weeks of VNS (p =.0057) (8). George et al. compared data from the 205
patients who completed the 12-month naturalistic study that was done by Rush et al. (9) with a matched control group of 124 patients with TRD who
received only treatment as usual (TAU). Response rates according to the HDRS (24) at 12 months were 27% for VNS+TAU and 13% for TAU (p <.011)
(10). In an open, uncontrolled multi-centre study of VNS therapy as an addition to stable pharmacotherapy, the response and remission rates were
found to be 37% and 17% after 3 months of VNS and 53% and 33% after 1 year of VNS, respectively (11). The most common side effects due to the VNS
were incision pain, voice alteration, neck pain, headache, cough, dysphagia and dyspnoea. Although it has a good safety profile, the present evidence
supporting its use is still limited. VNS seems to be an interesting new approach to treating TRD. However, despite the promising results reported mainly
in open studies, further clinical trials are needed to confirm its efficacy in major depression and to understand its mechanism of action.
Key words: Depression, vagus nerve stimulation
Neurophysical basis of neurostimulative psychosurgery: A historical review, new perspectives, and
future insights
Mehmet Dumlu Aydın
Department of Neurosurgery, Medical Faculty of Ataturk University, Erzurum, Turkey
Psychosurgery most likely began with burr holes in skulls for mystical causes over a millennium ago. Modern psychosurgery is concerned
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with the determination of disordered brain structures at the levels of neurons and neuronal populations in brain mapping by creating
mathematical formulations and treatment. Psychosurgery aims to regain systematic and comprehensive brain functions via minimally
invasive nondestructive neurosurgical applications. Psychosurgery is indicated for treatment-refractory major mental illnesses such as
depression, obsessive compulsive disorder, schizophrenia and others. Neurostimulative methods are preferred to neuroablative methods.
Neurons have highly complex morphological, electrophysiological, and biochemical properties as reflected in many psychomotor
functions, continuation of mental homeostasis, repertoire of activity patterns and multiple signaling pathways. Morphologically,
neurochemically and electrophysiologically heterogeneous neuron groups project to the cerebral cortex, deep brain structures, brain
stem, spinal cord and autonomous ganglia. These highly complex ascending and descending pathways participate in different functions,
including cognition, motivation, emotion, speech, calculation, memory and autonomic regulation.
Disorders of neuronal populations can cause neuropsychiatric illnesses. Neurostimulative applications are the most useful treatment
methods for intractable cases. However, in experimental studies, stem cells and teacher neurons specifically educated by computerised
mediums have begun to be implantated into the brain for education and stimulation of dysfunctional neuron groups.
Psychosurgery has been directed to neurocomputer interfacing technologies. Hybride neuroelectric devices, neuromimetic protheses,
sonic and photonic multichip modules, biotic-abiotic neuromodulators, bio-robotics and reconfigurable neural nanodevices have shown
promise for future excellent treatment strategies for mental illnesses.
Key words: Psychosurgery, deep brain stimulation
[PS-06]
Symposium Title: Neuroimaging in psychopharmacology: An update
What is the real meaning of ventricular enlargement in schizophrenia?
Nazlı Buğçe Vedin Özçelik
Department of Psychiatry, Ege University, Izmir, Turkey
Schizophrenia usually starts during adolescence or young adulthood but tends to persist throughout life. Even at the time that the
concept of schizophrenia was first defined, it was thought to be a brain disease. Before the development of brain imaging techniques,
post-mortem brain examinations were performed. It was reported that patients had frontal atrophy and less brain weight than the normal
population. After the development of computed tomography and magnetic resonance imaging techniques, the number of the studies
in this field increased.
Structural MRI imaging studies indicated that brain abnormalities were present at the onset of the disease. One strong piece of evidence
indicating that schizophrenia is a neurodevelopmental disorder derives from the fact that many types of brain abnormalities are present
at the time of the first episode off illness. These include decreased cerebral size, decreased frontal and temporal lobe sizes, decreased
thalamic size, decreases in gray matter and white matter volumes and enlargement of the ventricles. These findings support the likelihood
that this illness arises because of aberrations in the complex neurodevelopmantal processes that modulate brain maturation during the
adolescent and young adult period.
Lateral ventricular enlargement is one of the most consistent findings in patients with schizophrenia. However whether progressive
ventricular dilatation occurs during the course of the illness has been controversial. Some findings suggest that there is progressive
ventricular enlargement with no significant effect of age of onset, duration of illness or age at the baseline scan. In some longitudinal
studies there was evidence that negative symptoms have an association with increases in total CSF volume and in the ventricles as
indicated by the ventricular–brain ratio. Patients who achieve longer periods of remission have less expansion of the CSF, although, some
findings support the premise that there is a subgroup of patients with neuroprogression.
Key words: Schizophrenia, magnetic resonance imaging, lateral ventricle
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Neuroimaging studies in dementia, psychiatric disorders, drug discovery, and more
Devrim Ünay
Department of Electrical-Electronics Engineering, Bahcesehir University, Istanbul, Turkey
The continuous progress achieved in medical imaging technology in the past decades has led to considerable improvement in patient
care. In consequence of this progress, neuroimaging (imaging the structure or function of the brain) has gained an increasingly important
role in research and clinical practice.
Dementia, a psychiatric/mental disorder defined as progressive loss in cognitive skills such as learning, memory, orientation and
language, is a devastating and irreversible brain syndrome. Due to its increasing prevalence (especially in aging populations), long
duration, caregiver burden and high financial cost of care, dementia has emerged as one of our major public health problems affecting
20% of those over 80 years of age. As a result there is an increasing demand for a more accurate and earlier diagnosis and the value of
neuroimaging in improving the diagnostic process is becoming widely accepted.
Neuroimaging assessments may aid in the diagnosis of neurodegeneration as opposed to healthy aging, improve differential diagnosis,
assist in the prediction of conversion to dementia in individuals at a higher risk of developing the disorder, improve the tracking of disease
progression and finally may serve as an outcome measure for assessing drug efficacy. Hence, in clinical settings the diagnosis of dementia
is increasingly taken based on combined analysis of data such as the patient’s cognitive skills, demographic status, family history of
dementia and neuroimaging findings (such as the degree and distribution of atrophy).
In addition to the improvement in patient care, recent advances in neuroimaging technology also have increased the need for tools to
analyze and interpret the growing amount of neuroimaging data acquired. Accordingly, various semi-/fully automatic tools for analysis
and interpretation of such data are made available by research centers as well as medical imaging companies.
In view of the above, this work aims to provide a non-exhaustive summary of neuroimaging studies in psychiatric disorders with special
emphasis on dementia and drug discovery. State of the art studies employing both structural (CT, MRI, etc.) and functional (fMRI, PET,
SPECT, etc.) neuroimaging techniques and their potential contribution to diagnostic research as well as to drug discovery will be discussed.
The work will also include a brief introduction on the related advances and open questions from an image processing standpoint, and
finally present our recent research effort on computer-based measurement of dementia-related neuroimaging findings as compared with
experts’ visual assessments for improved disease understanding, diagnosis, prognosis, and therapy planning.
Key words: Dementia, drug discovery, fMRI, MRI, neuroimaging, PET, psychiatric disorders, SPECT
[PS-07]
Symposium Title: The rationale of antipsychotic combinations in schizophrenia: Epidemiological and clinical evidences
Filiz Karadağ
Pamukkale University Medical Faculty, Psychiatry Department, Denizli, Turkey
Pharmacogenetic studies in schizophrenia aim to use genetic information as a guide to establish individualized treatment options and to
optimize the effectiveness of treatment. The heterogeneity of response to antipsychotics results in polypharmacy along and combination
therapy into clinical practice, which lead to an increase in drug-related side effects and non-adherence to treatment.
Dopamine and serotonin systems may provide some of the genetic polymorphisms and have been proposed to predict the efficacity
of antipsychotic drugs. Affecting the intensity of the D2 receptors in the striatum, the DRD2- 141C Ins/Del polymorphism has been
associated with unresponsiveness to clozapine in treatment-resistant patients and a longer response time to olanzapine and risperidone
in first-episode patients. The D3 receptor DRD3 Ser9Gly polymorphism has been associated with unresponsiveness to clozapine and good
response to first generation antipsychotics.
The 5-HT2A receptor gene HTR2A-A-1438G and T102C polymorphisms may cause lower promoter activities and decreased 2A receptor
density in some brain regions. A-1438G G/G carriers have been found to be less likely to respond to clozapine, olanzapine, and aripiprazole.
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The T102C SNP C/C genotype has been associated with no response to clozapine and good response to risperidone and aripiprazole.
The long allele of the serotonin transporter gene has been reported to be associated with better response to antidepressants, but
there are only a few studieson schizophrenic patients. The effectiveness of pharmacogenetics-based combination therapies in patients
unresponsive to treatment has not been studied yet; the DRD2 and DRD3 genes may be candidates for study.
Antipsychotic metabolism: The Met/Met genotype of the COMT gene causes a 3- to 4-fold lower enzyme activity. The met allele carriers
were more likely to respond to clozapine, especially showing improvement in cognitive functions. This polymorphism, seems to deserve
assessment of the effectiveness of combination therapies in dealing with cognitive symptoms.
The CYP2D6 enzyme plays an important role in the metabolism of antipsychotic drugs. Individuals carrying duplicate or multiple
copies of the CYP2D6 gene are known as ultrarapid metabolizers. In ultrarapid metabolizers, due to the decrease in therapeutic efficacy
of antipsychotic drugs, a combination of drugs that are metabolized by the same cytochrome enzyme would not provide further
improvement in drug response.
Antipsychotic-induced side effects: The DRD2 A2 allele of SNP Taq1A, the DRD3 Ser9 Gly Gly allele genetic polymorphisms related to
D2 and D3 receptors, the COMT Val allele and the CYP2D6 gene variants have been reported to be associated with an increased risk of
tardive dyskinesia.
CYP2D6 poor and intermediate metabolizers may be more sensitive to the extrapyramidal side effects of antipsychotics. The 5HT2C gene
(759T SNP) and the leptin gene are the most studied polymorphisms for antipsychotic-induced weight gain. All of the aforementioned
polymorphisms may have implications for choice of rational antipsychotic combinations.
Pharmaco-genetics-based rational antipsychotic combinations may yield promising results for cytochrome enzyme and COMT genes
and the genes associated with side effects in schizophrenia. However, this issue should be supported and confirmed by clinical
pharmacogenetics studies.
Key words: Pharmacogenetics, schizophrenia, antipsychotics, side effects, dopamine, serotonin, polymorphism
Scientific bases of use of atypical antipsychotics
Ender Taner
Department of Psychiatry, Gazi University Faculty of Medicine, Ankara, Turkey
The predominant hypothesis regarding the pathophysiology of schizophrenia is that it is associated with impaired dopamine
neurotransmission. The mesolimbic pathway originates from the midbrain ventral tegmental area and innervates the ventral striatum
(nucleus accumbens), olfactory tubercle, and parts of the limbic system. The mesocortical pathway, also originating from the midbrain
ventral tegmental area, innervates areas of the frontal cortex and has been implicated in learning and memory. Overactivity of the
mesolimbic pathway has been implicated in the development of the positive symptoms of schizophrenia. The negative and some cognitive
symptoms have been associated with a reduction of dopamine activity in the mesocortical pathways together with a hypostimulation
of dopamine receptors in the prefrontal cortex. There are 2 overall goals of treatment: (1) to reduce the activity of hyperactive pathways
mediating psychosis and (2) to increase the activity of hypoactive pathways that seem to mediate negative and cognitive symptoms,
while simultaneously preserving the activity of the pathways that regulate motor movement and prolactin secretion. There is also a
putative interrelationship between N-methyl-D-aspartate (NMDA) hypofunction and dopamine (DA) dysregulation and these processes
may be linked to the pathogenesis of schizophrenia. It has been postulated that NMDA hypofunction in the prefrontal cortex and its
connections may result in a pattern of dopamine dysregulation. In the prefrontal area, this pattern consists of a dopamine deficit and
a hypostimulation of D1 receptors that are linked to the appearance of negative symptoms and cognitive impairment. However, at the
subcortical level, NMDA hypofunction results in dopamine excess, hyperstimulation of D2 receptors, and the appearance of positive
symptoms. It has also been suggested that the prefrontal dopamine deficit and the subcortical dopamine excess feed back, in turn, to the
NMDA circuitry. In addition there is evidence that the deficit in cortical dopamine may also be linked to the generation of a subcortical
dopamine excess. There is a complex modulation of dopamine by different serotonergic receptor systems as well as by nicotinic receptors.
These may be additional sites for effects of antipsychotics. This conference tries to underline the current possible scientific basis for the
use of atypical antipsychotics.
Key words: Atypical antipsychotics, schizophrenia, mechanism of action, scientific basis
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Is fish oil promising in the treatment of depression during pregnancy and lactation?
Evrim Özkorumak
Karadeniz Technical University, Psychiatry Department, Trabzon, Turkey
Increasing concerns about neonatal syndromes following antidepressant use in the late phase of pregnancy(1) have caused more
hesitation about their use. Although inadequate data about in utero exposure of antidepressants may present risks, the risks of untreated
maternal depression must be considered as well. One candidate as an antidepressant is fish oil, in light of its omega-3 constituent.
Omega-3 fatty acids are long-chain, polyunsaturated fatty acids found in plant and marine sources and helpful in treating various medical
conditions (2). Omega-3 fatty acids may prove to be efficacious in a number of psychiatric disorders. Evidence suggests that omega-3
fatty acids may have beneficial effects in mood disorders, including bothmajor depression and bipolar disorder, schizophrenia and
dementia. Furthermore, omega-3 fatty acids may prove to be a safe and efficacious treatment for psychiatric disorders during pregnancy
and breastfeeding (2).
Major depressive disorder (MDD) is prevalent among women of childbearing age. Approximately 15% of women experience an episode
of perinatal depression (PND), antenatally and/or postnatally (3). Because there are increasing concerns about possible adverse effects
of antidepressant medication use during pregnancy and in breastfeeding mothers (4), it is important to investigate possible alternative
treatments. Main dietary risk factors of postnatal depression are low riboflavin, low folate, low docosahexaenoic acid, low eicosapantaenoic
acid, low calcium, low magnesium and low zinc. Oil-rich fish are a rich source of n-3 fatty acids, in particular eicosapentaenoic acid (EPA)
and docosahexaenoic acid (DHA) (5). Evidence indicates that these fatty acids may be involved in the synthesis and regulation of brain
neurotransmitters (dopamine, monoamine and serotonin), which are thought to be reduced in cases with depressive symptoms (6). More
specifically, it is thought that high concentrations of DHA located in non-myelin cell membranes of the central nervous system may help
support synaptic transmissions (7). Different human studies were identified investigating dietary and/or supplemental sources of n-3
in relation to the development of postnatal depression. Only two of these trials were randomised controlled trials (8,9). Among others,
three studies support the theory that dietary and supplemental sources of n-3 are associated with fewer postnatal depression symptoms
(8,10,11) and five studies contest this theory (12,13,14).
Key words: Omega-3 fatty acids, depression, perinatal depression
[PS-08]
Symposium Title: Advances in complementary alternative psychotropic drugs: Fish oil (omega-3 fatty acids), vitamine B12, folate
ve other add-on therapies in psychiatric disorders
Can St. John’s Wort be an alternative treatment for depression?
Çiçek Hocaoğlu
Rize University, Medical School, Department of Psychiatry, Rize, Turkey
The herb St. John’s Wort (Hypericum perforatum) has been used for centuries to treat a variety of medical illnesses. In certain areas of
Europe, St. John’s Wort has been a commonly prescribed treatment for depression. In some countries extracts of the plant Hypericum
perforatum L. (popularly called St. John’s Wort) are widely used for treating patients with depressive symptoms. Extracts of the plant
Hypericum perforatum have been used in folk medicine for a long time for a range of indications including depressive disorders. Some
researchers believe that specific chemical constituents of St. John’s Wort produce changes in depression in a manner similar to that of
antidepressant medications, yet this hypothesis is problematic. In addition, studies that support the efficacy of St. John’s Wwort in patients
with mild-to-moderate depression have limitations that may affect the accuracy of their conclusions. Studies measuring the effect of St.
John’s Wort in major depression have reported conflicting results and need to be reexamined. In patients who meet the criteria for major
depression, several recent placebo-controlled trials suggest that the tested hypericum extracts have minimal beneficial effects while
other trials suggest that hypericum and standard antidepressants have similar beneficial effects. Preliminary data suggest that hypericum
extract is effective in atypical depression based on the reported outcome of an 8-week double-blind, placebo-controlled, randomized
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trial (positive results in patients with vegetative features of atypical depression, i.e. hyperphagia or hypersomnia). The study supports the
beneficial effect of St. John’s Wort in depression with atypical features and the validity of the definition of atypical depression on the basis
of reversed vegetative signs.
Consequently, St. John’s Wort is considered by some to be an alternative to conventional therapies but, clinicians need to know whether
it is an effective and safe treatment for different levels of severity of depression. Current evidence does not support its use and because
of potential drug interactions, St. John’s Wort is not a benign treatment.
Key words: St. John’s Wort, depression
References:
1.
Shelton RC. St John’s wort (Hypericum perforatum) in major depression. J Clin Psychiatry. 2009;70 Suppl 5:23-7.
2.
Mannel M, Kuhn U, Schmidt U, Ploch M, Murck H.St. John’s wort extract LI160 for the treatment of depression with atypical features - a double-blind, randomized,
and placebo-controlled trial. J Psychiatr Res. 2010 Sep;44(12):760-7. Epub 2010 Feb 23.
3.
Kasper S, Gastpar M, Müller WE, Volz HP, Dienel A, Kieser M, Möller HJ. Efficacy of St. John’s wort extract WS 5570 in acute treatment of mild depression: a reanalysis
of data from controlled clinical trials. Eur Arch Psychiatry Clin Neurosci. 2008 Feb;258(1):59-63. Epub 2007 Dec 14.
4.
Trautmann-Sponsel RD, Dienel A. Safety of Hypericum extract in mildly to moderately depressed outpatients: a review based on data from three randomized,
placebo-controlled trials. Affect Disord. 2004 Oct 15;82(2):303-7.
5.
Linde K, Mulrow CD, Berner M, Egger M. St John’s wort for depression. Cochrane Database Syst Rev. 2005 Apr 18;(2):CD000448.
Complementary medicine alternatives for other psychiatric abnormalities
(Like insomnia and pain)
Bülent Bahçeci
Department of Psychiatry, Rize Üniversity, Rize,Turkey
Complementary and alternative medicine have been used for the treatment of a variety of diseases for a long time. Since the applications
of these two branches of medicine have been increasingly spreading globally and have been accompanied by inadequate scientific
studies in the literature, the NIH has established the National Centre for Complementary and Alternative Medicine (NCCAM). The aims of
the centre are to investigate the safety/reliability and efficacy of complementary and alternative medicine applications, and to integrate
those that are scientifically proven to be effective into conventional therapies. All health protection and medical applications/practices
outside of conventional medicine are referred to as complementary and alternative medicine (CAM).
CAM applications are becoming widespread in Turkey, as well, and are sought by 34-77% of sufferers as the first choice for therapy.
Recently CAM, which has found applications in a wide range of areas, has also been used for psychiatric diseases. The use of CAM in the
treatment of chronic pain, eating and sleeping abnormalities, alcohol and substance addiction, Alzheimer’s disease and delirium has
yielded contradictory results in the national and international literature. Therefore, it has been reported that CAM methods require further
evidence-based studies.
Taking into consideration the widespread use and popularity of CAM, it is evident that these methods must be investigated further for
their side effects, dosages, indications, interactions with other drugs, and standardisations. In addition, the regulations concerning their
use must be redrawn and physicians must follow the relevant literature in order to prevent possible harm to their patients before initiating
CAM treatments.
Key words: Complementary and alternative medicine, psychiatry, education
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Essential fatty acids in ADHD treatment
İbrahim Durukan
Deparment of Child and Adolescent Psychiatry, Gülhane Military Medical School, Ankara, Turkey
Attention deficit hyperactivity disorder (ADHD) is characterized by problems with attention, hyperactivity and impulsivity. These problems
often severely affect families, relationships and school performance. Although stimulants and atomoxetine are efficacious in many
children, these medications can have side effects such as insomnia, decreased appetite, irritability and impaired growth. The etiology
of ADHD is generally accepted to be complex and multifactorial. Little progress has been made in elucidating predisposing biological
factors. Related contributory factors for ADHD etiology are diet, nutrition and particular abnormalities in the metabolism of the longchain polyunsaturated fatty acids (LCPUFAs).
Essential fatty acids (EFAs) as a complementary or alternative treatment for ADHD have been used as both a primary and an adjunctive
treatment in many countries. Humans are unable to synthesize linoleic acid (an omega-6 fatty acid), and a-linolenic acid (ALA), an omega3 fatty acid. The main dietary sources of linoleic acid and ALA are vegetable oils and their seeds.
Both omega-3 and omega-6 LCPUFAs have critical importance for normal brain development and function. Large amounts of both omega6 and omega-3 LCPUFAs are deposited in the central nervous system during fetal life. During infancy, dietary intake of both omega-3 and
omega-6 LCPUFAs continues to be essential for neuronal development. LCPUFAs and their derivates work as facilitators of dopamine,
serotonin and norepinephrine release, as regulators of gene transcription, as modulators of Na+ -K+ ATPase channel function and as the
precursors of pro-inflammatory and anti-inflammatory molecular families. The most abundant LCPUFA in the brain is DHA from the omega3 series, which is concentrated at nerve cell synapses and is important for neural cell signalling and neurotransmitter processes.
There is increasing evidence that omega-3 LCPUFAs play a part in many neurodevelopmental and psychiatric disorders. ADHD, dyslexia,
developmental coordination disorder and autistic spectrum disorder are suggested to be related to the omega-6/omega-3 spectrum of
disturbances. Several studies of LCPUFA supplementation in children with ADHD symptoms have been conducted. Open-label EFA trials
in ADHD demonstrate that ADHD symptoms are responsive to EFA supplementation. Despite successful open-label trials, randomized
controlled trials of EFA in ADHD have generally been unsuccessful in demonstrating treatment effects and some of them even displayed
better results for the placebo group. There are three studies with partial positive results but these studies represent a small minority and
two of them have several methodological limitations.
The side effects of EFA are generally related to the gastrointestinal system and usually include diarrhea, nausea, fishy aftertaste, belching
and indigestion. These side effects seem to be mild, transient and infrequent, and also appear in the placebo groups.
Current findings from randomized clinical trials of EFA in children with ADHD are not promising. Most randomized trials have clearly
demonstrated lack of superiority compared to placebo. Moreover, the studies that showed positive findings did not use children properly
diagnosed with ADHD and none of them demonstrated clinical improvement in more than one setting. This delineation does not support
the use of EFA supplements as a treatment for children with ADHD. Future studies should be planned to consider methodological issues
such as proper ADHD diagnosis, blinded controls, adequate sample size and behavioral assessment in more than one setting.
Key words: ADHD, essential fatty acids
Mechanisms of fish oil (Omega-3 fatty acids), vitamin B12, folate and other add-on treatments
in psychiatric disorders
Mehmet Cemal Kaya
Dicle University School of Medicine, Department of Psychiatry, Diyarbakir, Turkey
The need for new treatments has led several investigators to examine the potential role of omega-3 fatty acids, found in marine and plant
sources, in the treatment of psychiatric disorders. Omega-3 fatty acids are associated with normal brain development, neuronal plasticity,
and function (1). Cell biology and molecular studies suggest that omega-3 fatty acids modulate membrane fluidity and dopaminergic
and serotonergic neurotransmission (2). It has been observed that omega-3 fatty acids have effects on the phospholipid cell membrane
and the secondary messenger system similar to mood stabilizing drugs like lithium (3). It has been also demonstrated by recent studies
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that add-on treatments with omega-3 fatty acids in mood disorders significantly improved the symptoms. Another way to investigate the
effects of omega-3 fatty acids is by estimating the regional brain concentrations of various metabolites with proton magnetic resonance
spectroscopy (PMRS). In a study that used this method in a population with first-episode psychosis, improvement of the negative
symptoms of the patients were observed parallel to the increase in glutathione availability and modulation of the glutamine/glutamate
cycle with ethyl-eicosapenthaenoic acid augmentation treatment (4). Post-mortem polyunsaturated fatty acid concentrations in the
prefrontal areas of antipsychotic-naive schizophrenia patients were found to be lower than those of schizophrenia patients treated with
atypical antipsychotics. Additionally, in an animal study, increases in the omega-3 fatty acid concentration in erythrocytes and prefrontal
cortex were observed after long-term treatment with risperidone.
One of the earliest reports about the possible psychiatric effects of vitamin B12 deficiency belongs to Langdon in 1905. Vitamin B12
together with folate are essential for conversion of homocysteine to methionine and synthesis of adenosyl-methionine. S-adenosylmethionine is responsible for methylation in the metabolism of neurotransmitters (5). There are various studies that showed associations
of depression, dementia and schizophrenia with deficiencies of folate and vitamin B12. Some studies have focussed on folate rather
than vitamin B12 and have suggested a stronger role for folate in depression. Independent from serum levels of folate and vitamin
B12, augmention with these vitamins may be beneficial to patients who have predominantly cognitive symptoms, who are resistant to
treatment, pregnantor use lithium (6).
Consequently, augmentation with omega-3 fatty acids, folate and vitamin B12 may have some clinical benefits in the treatment of some
psychiatric disorders. However, mechanisms of their actions still need to be further elucidated.
Key words: Omega-3 fatty acids, vitamin B12, folate, psychiatric disorders
References:
1.
Bazan NG. Lipid signaling in neural plasticity, brain repair, and neuroprotection. Mol Neurobiol 2005; 32: 89–103
2.
Yao JK, Leonard S, Reddy R. Altered glutathione redox state in schizophrenia. Dis Markers 2006; 22: 83–93
3.
Frangou S, Lewis M, Wollard J, Simmons A. Preliminary in vivo evidence of increased N-acetyl-aspartate following eicosapentanoic acid treatment in patients with
bipolar disorder. J Psychopharmacol 2007; 21: 435-439
4.
Berger GE, Wood SJ, Wellard RM, Proffitt TM, McConchie M, Amminger GP, Jackson GD, Velakoulis D, Pantelis C, McGorry PD. Ethyl-eicosapentaenoic acid in firstepisode psychosis. A 1H-MRS study. Neuropsychopharmacology 2008; 33: 2467-2473
5.
Bottiglieri T. Folate, vitamin B12, and neuropsychiatric disorders. Nutr Rev 1996; 54:382-390
6.
Lindeman RD, Romero LJ, Koehler KM, Liang HC, LaRue A, Baumgartner RN, Garry PJ. Serum vitamin B12, C and folate concentrations in the New Mexico elder
health survey: Correlations with cognitive and affective functions. J Am Coll Nutr 2000; 19: 68-76
[PS-09]
Symposium Title: From preclinical studies to clinical practice in anxiety disorders
Medical disease and anxiety disorders
Hayriye Elbi
Ege University, School of Medicine, Dept. of Psychiatry, İzmir, Turkey
E-mail: [email protected];[email protected];[email protected]
Chronic medical illness causes us to face our vulnerabilities and is a significant risk factor for the development of an anxiety disorder.
The vulnerability could be associated with the stress of illness and coping with the limitations of illness. Anxiety disorders may also
develop secondary to predisposing biological mechanisms (as in diabetes or thyroid disorders) or may be related to a patient’s specific
medications.
We need to explore the causes of an anxiety disorder and plan our treatment so that it will not interfere with the medical disease and its
treatments. Drug interactions are very important in medical comorbidity cases. Every disorder comes with a new life style and necessity
for new adaptations. The uncertainty and barriers to daily life worsen the situation. I will review the anxiety associated with medical
diseases and the current treatments for it.
Key words: Medical diseases, anxiety disorders
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Nurper Erberk Özen
Department of Psychiatry, Ufuk University, Ankara, Turkey
Animal models are key to our understanding of many human diseases and psychiatric disorders are no exception. Animal models have
provided insight into the neurotransmitter systems and brain circuitry underlying psychiatric illnesses that have enabled the screening
of potential psychiatric medications for efficacy and guided the search for new pharmacotherapies. However, modeling complex
psychiatric disorders in animals presents distinct challenges. Modeling psychiatric disorders in animals is difficult due to the complexity
of human thoughts, emotions, and behavior; the heterogeneity of many psychiatric disorders; and the requirement of self-reporting of
internal state for diagnosis. According to the DSM-IV, most psychiatric diagnoses are made when a patient displays a certain number of
diagnostic criteria. However, patients with the same diagnosis can differ significantly in specific symptoms, perhaps implying differences
in the underlying etiology of their disorders and explaining the heterogeneity of response to pharmacotherapy. Many symptoms are
identified by the patient’s report of internal state (e.g., obsessive obtrusive thoughts or ruminations). This leads to questions of how we
can best model disorders in animals that are, by definition, both heterogeneous and dependent on report of internal state. Rather than
attempting to model a psychiatric disorder in its entirety, most neuroscientists focus on individual aspects or dimensions of a disorder
and use physical manifestations and measurable behaviors when modeling a particular aspect.
Inferences from experiments with animal models have the potential to impact clinical practice; therefore, stringently validating such
models is of utmost importance. The strengths and weaknesses of a model can be conceptualized with different types of validity.
Three important types of validity are suggested as predictive, face, and construct validity. In the first one, the animal should display
reduced anxiety when treated with anxiolytics (predictive validity). In the second type, the behavioral response of an animal model to
a threatening stimulus should be comparable to the response known for humans (face validity). Finally, in the third type of validity, the
mechanisms underlying anxiety as well as the psychological causes should be identical (construct validity). In the meantime there is no
consensus about which type of validity is superior. Some authors argue that predictive validity is most essential but the others suggest
that constructive validity is the most crucial. On the other hand, these three requirements are difficult to achieve in any animal model for
each anxiety disorder. Moreover, in the related literature, the term“animal model of anxiety” is used for animals that are altered in their
anxiety-related behavior, as well as for test assays conceptualized to assess anxiety-related behavior in animals.
Key words: Anxiety disorders, genetic, rat, transgenic
Anxiety models in experimental animals
Hüseyin Günay
Etimesgut Military Hospital, Psychiatry Clinic, Ankara, Turkey
The basic measure in testing validity of an animal model is its prediction validity, which means making true assumptions for a disorder
in humans. The necessary features of an animal model are analogy to a disorder in humans, objective testing, effective interventions in
humans and the capability of retesting. Structural validity is the capability to retest of the target condition and first sight validity is the
measurement of phenomenological similarity. First sight validity points to the surface similarity between the model and the disease and
structural validity points to the underlying mechanisms. Anxiety models are mainly used in understanding causes and mechanisms and
also determining drug effects. Anxiety in animals, which is similar to humans, can be developed with different environmental conditions.
These situations can help to understand and intervene to treat anxiety. Three ways are used in the development of anxiety models: using
a new environment, reward and punishment applications, and punishment procedures.
Anxiety models using new environment:
These are the methods for establishing and evaluating anxiety models in a new environment, such as elevated plus maze and derivers,
elevated T-maze, open field, staircase test, social isolation, novelty suppressed feeding, social interaction, holeboard, predatory odor,
operant conflict tests for reward-punishment applications and experiments with punishment procedures such as defensive burying,
passive avoidance, foot shock, hot plate and four plate tests.
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The purpose of this study is to show the usefulness of the tests in the literature and to compare the advantages and disadvantages in
terms of structural validity and first sight validity.
Key words: Anxiety, anxiety models
[PS-10]
Symposium Title: Will glutamatergic modulators be a target for the future therapy of depression?
Ketamine and other glutamate modulators as potential antidepressants
Serdar Dursun, Glen Baker, Nick Mitchell
Neurochemical Research Unit, University of Alberta, Edmonton, Canada
Depression is seen as a complex neuropsychiatric disorder affecting integrated pathways connecting discrete cortical, subcortical, and
limbic regions and their associated neurotransmitter and molecular mediators. One episode of major depression is a strong predictor of
future episodes, and more than 50% of individuals who have an episode of major depression experience a recurrence.
Unfortunately, currently approved pharmacological treatments for depression require several weeks for onset of efficacy. Despite
advances in the understanding of the psychopharmacology of depression and the introduction of several novel classes of antidepressants
in the last 3-4 decades, patient response to any given pharmacological approach continues to be unsatisfactory.
Although almost all of the prescription drugs currently available as antidepressants have effects on noradrenaline (NA) and/or
5-hydroxytryptamine (5-HT), it is obvious that other factors are also important in the etiology and pharmacotherapy of depression and
that the monoamines cannot be considered in isolation. Perhaps the most exciting system and that for which there is now substantial
translational evidence for a role in depression is that involving glutamate. Ample evidence indicates that glutamate homeostasis and
neurotransmission are disrupted in major depressive disorder but the nature of these disruptions and the mechanisms by which they
contribute to the syndrome are unclear. Likewise, the specific effects of existing antidepressants on glutamate are unclear, as is the
potential of drugs directly targeting glutamatergic neurotransmission to act as novel antidepressant medications. However, these are
areas of active research and some exciting results have been obtained.
This presentation will review the current knowledge of the contribution of the N-methyl-D-aspartate (NMDA) receptor, one of the several
types of glutamate receptors, to depression and its treatment. Several lines of evidence, in humans and in animal models, support
the contention that neurotransmission via the NMDA receptor is dysregulated in depression. Drugs targeting the NMDA receptor as
antagonists have shown antidepressant properties in both clinical and preclinical studies. Nevertheless, other effects of such medications,
including both cognitive side effects and their psychotomimetic properties, complicate such an application and represent a challenge to
the development of clinically useful agents.
There is a recent hypothesis that the therapeutic effects of monoaminergic antidepressants and the NMDA receptor antagonist ketamine
may be mediated by increased alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-to-NMDA glutamate receptor activity
in critical neuronal circuits. It has been hypothesized that ketamine directly mediates this receptor activity, whereas monoaminergic
antidepressants work indirectly and gradually; this may explain, in part, the lag of onset of clinical improvement of several weeks that
is observed with traditional antidepressants. Ketamine (intravenous) is the first medication reported to produce rapid, relatively longlasting antidepressant efficacy. Although the precise antidepressant mechanisms of action of ketamine remain unclear, there is preclinical
evidence to suggest that both AMPA and NMDA receptor subtypes are involved. In terms of neuroanatomical sites of action, it has been
shown that the subgenual cingulate cortex (Sg CG) is overactive in depression while the dorsal frontal regions and posterior cingulate are
underactive and that successful treatment normalizes the pattern. There is also evidence from functional magnetic resonance imaging
(fMRI), which has demonstrated that the effect of ketamine resembles the pattern of normalisation after successful antidepressant
treatment, i.e., in healthy volunteers there is decreased orbitofrontal cortex (OFC)–Sg CG blood oxygen level-dependent (BOLD) signal
response and increased BOLD signal response in the dorsolateral prefrontal cortex (PFC) (Brodmann area 8) and the posterior cingulate
region. These findings suggest that an overactive Sg CG may be the dysfunctional organising region in depression.
Key words: Ketamine, rapid antidepressant efficacy, glutamate, NMDA receptor
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The glutamatergic system and its importance in the neurobiology of depression
Feyza Arıcıoğlu
Department of Pharmacology, Marmara University, Istanbul, Turkey
Recent advances in research on depression have confirmed that it is common, recurrent and disabling mental disorder affecting millions
of individuals worldwide. Current medications for the treatment of depression have limited efficacy and delayed onset of therapeutic
action. Existing antidepressants used to treat these disorders are insufficient for many. Patients continue to have low remission rates,
delayed onset of action, residual subsyndromal symptoms, and relapses. New therapeutic agents able to exert faster and more sustained
antidepressant effects are urgently needed to treat these disorders. Multiple lines of evidence suggest that inflammation and glutamate
dysfunction contribute to the pathophysiology of depression. Excess levels of inflammatory mediators occur in a subgroup of depressed
patients. Patients with depression have been found to exhibit increased blood inflammatory biomarkers, including inflammatory cytokines,
which have been shown to be involved in depression. Activation of inflammatory pathways is believed to contribute to a confluence of
decreased neurotrophic support and altered glutamate release/reuptake, as well as oxidative stress, leading to excitotoxicity and loss of
glial elements, consistent with findings that characterize depressive disorders. Neurotrophic factors such as brain-derived neurotrophic
factor (BDNF) are involved in the pathogenesis of mood disorders and in the action of at least some drugs. It has been shown that serum
BDNF levels are decreased in patients with depressive disorder and antidepressant treatment induces BDNF expression. In this context,
the glutamatergic system has been implicated in the pathophysiology of depression in unique clinical and neurobiological ways. The data
from depressed patients, suggest that inhibiting proinflammatory cytokines or their signaling pathways may improve depressed mood
and increase treatment response to conventional antidepressant medication. The past decade of efforts to find improved treatment for
depression has been dominated by genome-driven programs of rational drug discovery directed toward highly selective ligands for
nonmonoaminergic agents. To date, the monoaminergic systems (serotonin, norepinephrine, and dopamine) have received the most
attention in the neurobiology of depression, and all classes of antidepressants target these monoaminergic systems. Accumulating
evidence suggests that the glutamatergic system plays an important role in the neurobiology and treatment of depression. Many
reports have highlighted alterations in glutamate signaling as well as changes in the expression of AMPA or NMDA receptor subunits
in depression. In parallel, there is growing interest in the non-competitive NMDA receptor antagonist, ketamine, which produces a
rapid and sustained antidepressant response in patients with treatment-resistant depression. Importantly, such effects of ketamine are
seen at subpsychomimetic doses of the drug. Moreover, ketamine produces a profound reduction in suicidality. Based on findings with
ketamine, there is interest in developing subtype-selective NMDA antagonists, particularly those that act through allosteric mechanisms.
A final glutamatergic strategy for treating depression may be through modulating metabotropic (G protein-coupled) glutamate (mGlu)
receptors. During the last 10 years, several selective mGlu receptor competitive antagonists and potentiators have been discovered.
Selective mGlu receptor antagonists are among the most promising agents under development for the treatment of depression. Overall,
this system holds considerable promise for developing the next generation of therapeutics for the treatment of depression.
Key words: Glutamate, depression, cytokines, neurotrophic factors, NMDA, mGLU receptors
[PS-11]
Symposium Title: Psychotropic drug treatments during pregnancy and lactation
Pharmacotherapy of panic disorder during pregnancy and lactation
Faruk Uğuz
Selcuk University, Meram Faculty of Medicine, Department of Psychiatry
E-mail: [email protected];[email protected]
Panic disorder is one of important psychiatric problems during pregnancy and lactation. The prevalence rate of this disorder has been
reported to be 0.4%-4.0% in the perinatal period. In addition, the perinatal period may affect the onset or course of panic disorder.
Although pharmacotherapy of panic disorder is well known, data on treatment of this disorder during pregnancy and lactation are very
limited. It is difficult to decide about pharmacotherapy of panic disorder during the perinatal period, particularly during pregnancy,
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because both effective pharmacological agents and untreated maternal anxiety seem to be associated with several negative outcomes
on the course of pregnancy and the fetus. Despite the absence of practical guidelines for pharmacological management of panic disorder
during pregnancy and lactation, some general points about pharmacological treatment include the following: (1) Pharmacotherapy
should be preferred when the potential impact of untreated maternal panic disorder is higher than the impact of the pharmacological
agent on the fetus or new mother. (2) The patient and relatives should be informed about the benefits and risks of pharmacological
treatment or nontreatment of the current maternal psychiatric picture and written informed consent forms should be obtained. (3)
Selective serotonin reuptake inhibitors except paroxetine and low dose imipramine may be preferred during pregnancy. (4) Sertraline,
paroxetine, orlow doses of imipramine or clomipramine appear to be appropriate pharmacological agents during the lactation period.
Key words: Panic disorder, pregnancy, lactation
Psychotropic drug treatment during pregnancy and lactation in obsessive compulsive disorder
Servet Ebrinç
GATA Haydarpasa Training Hospital, Clinic of Psychiatry, Istanbul, Turkey
According to recent studies, obsessive compulsive disorder(OCD) is one of the leading cause of disability and the prevalence of OCD is
found to be 0.2-3.5% in pregnancy and 2.7-9% in the postpartum period.
The efficacy and tolerability of SSRIs and SNRIs in the treatment of OCD are well-determined in many double-blind randomized controlled
trials. Despite the fact that it is well known that OCD patients may benefit from antiobsessional therapy during pregnancy and the
postpartum period, very little data are available about the efficacy of the treatment and no evidence suggests that patients would react
differently to these drugs. Hence, OCD women who are pregnant and in the postpartum period might be treated using standardized
treatment approaches.
During pregnancy and the postpartum period, the treatment of OCD should clinically take the risks and benefits of several treatment
modalities and the expectations of the patient into account. While cognitive-behavioral therapy (CBT) is the leading choice in nonpharmacological treatment of OCD, pharmacoterapy might be used if necessary.
If CBT is inadequate and pharmacotherapy is needed, during pregnancy, fluoxetine, and during the lactation period, paroxetine, are
proposed to be the first line treatments. Although evidence is limited, other SSRIs are acceptable as alternative treatment options.
All of the antidepressant drugs are transferred to the nursing infant during breastfeeding. The American Academy of Pediatrics classifies
psychotropic drugs as “drugs whose effects are unknown, but may be of concern.” The best way of determining the exposure to the drug is
measuring the drug concentration in the plasma of the baby. Clinical evaluation is important to identify any side effects while monitoring the baby.
There is no evidence indicating an increase in the rates of intrauterine death or malformation in the case of exposure to tricyclics or
SSRIs. Whether exposure to SSRIs causes a decrease in birth weight or an increase in premature births is not certain and the evidence is
controversial. Nonetheless, The Food and Drug Administration (FDA) has determined that first trimester exposure to paroxetine might
cause an increase in the risk for congenital malformations particularly cardiac defects. Therefore, the FDA has changed paroxetine’s
pregnancy category from C (risk can not be ruled out) to D (positive evidence of human fetal risk).
A “withdrawal syndrome,” consisting of symptoms in the locomotor, central nervous, respiratory and gastrointestinal systems may occur
in newborns exposed to SSRIs in the third trimester. Although monitoring is required in an exposed newborn, this syndrome is relatively
mild, can be managed with supportive therapy and diminishes within 2 weeks. Some evidence points out an increase in the rates of
persistent pulmonary hypertension in infants exposed to SSRIs during the third trimester. Before delivery, lowering the dosage of the
mother’s drugs that might have been augmented due to the symptom severity of OCD, is recommended.
Key words: lactation, obsessive-compulsive disorder (OCD), psychopharmacotherapy, pregnancy
References:
1. Clinical Management Guidelines for Obstetrician-Gynecologists Use of Psychiatric Medications During Pregnancy and Lactation. ACOG Practice Bulletin,
(Reprinted with permission from Obstetrics & Gynecology 2008; 111:1001–1020)
2.
Brandes M, Soares CN, Cohen LS. Postpartum onset obsessive-compulsive disorder: diagnosis and management. Arch Womens Ment Health 2004; 7:99–110
3.
Use of Psychoactive Medication During Pregnancy and Possible Effects on the Fetus and Newborn Amerikan Academy of Pediatrics Committee on Drugs Pediatrics
2000; 105; 880-887
4.
Koran LM, Hanna GL, Hollander E et al. Practice Guidline for theTreatment of Patients with Obsessive-Compulsive Disorder. Copyright 2010, American Psychiatric
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Association.
5.
McGuinness M. OCD in the Perinatal Period: Is Postpartum OCD (ppOCD) a Distinct Subtype? A Review of the Literature. Behavioural and Cognitive Psychotherapy
2011, 39, 285–310
[PS-12]
Symposium Title: Vitamin and mineral supplementation in treatment of childhood psychiatric disorders
Vitamin and mineral supplementation in treatment of childhood psychiatric disorders – Calcium and
vitamin D supplementation
Ömer Faruk Akça
Samsun Psychiatry Hospital, Child and Adolescent Psychiatry Clinic, Samsun, Turkey
Vitamin D has significant roles in cell proliferation, the immune system and the nervous system as well as in bone development. Adult
studies indicate that vitamin D deficiency may be related to some neurological and psychiatric disorders like Parkinson’s disease,
Alzheimer’s disease and depression (1). Childhood studies on this subject are mainly related to the impact of vitamin D deficiency on the
development of autism. Because vitamin D has an essential role in the development of the nervous system, some investigators suggest
that vitamin D deficiency during pregnancy may contribute to the development of autism. Autism is stated to be more frequent in people
with dark skin and people who live in countries at higher latitudes. Additionally, children of mothers who consume more vitamin D in
pregnancy have better mental development and present with fewer autistic signs. This knowledge indicates that vitamin D may be a
mediator in the emergence of autism for genetically vulnerable people (2). Autism frequency has increased in recent years and this increase
has occurred at the same time as the suggestions on the avoidance of sunlight have arisen. This coincidence is claimed to be supportive
of the autism-vitamin D hypothesis (2,3). This hypothesis suggests two possible mechanisms: 1) vitamin D deficiency during pregnancy
may cause inappropriate development of the fetal brain and then autistic signs may emerge, 2) in light of the hypotheses that autism
is an autoimmune disorder and vitamin D is important for immune system functions, it may be assumed that vitamin D deficiency may
cause autistic signs in vulnerable individuals (4). Some studies have stated that autism is more frequent in children of winter pregnancies
and people of higher latitude countries (4). Additionally, it is stated that autistic patients have the lowest vitamin D levels among all kinds
of psychiatric disorders in a psychiatry inpatient clinic (5). In another recent study, autistic children have lower 25-hydroxy vitamin D,
1,25-hydroxy vitamin D and calcium levels in comparison with healthy children (6). These findings are supportive of this hypothesis.
According to this hypothesis, it can be estimated that children with rickets would have more autistic symptoms. There is no recent study
on this assumption. However, in past studies it has been stated that these children had more mental disorders, which disappeared after
treatment (7).
On the other hand, because children with autism may have food selectivity, vitamin D and calcium deficiency may occur in these children
more frequently. Some investigations were made on this subject and many of them found supportive findings (8,9).
We may conclude that autism-vitamin D relationship needs to be investigated more with larger sample studies.
Key words: Autism, vitamin D, calcium
References:
1.
Kesby JP, Eyles DW, Burne TH, McGrath JJ. The effects of vitamin D on brain development and adult brain function. Mol Cell Endocrinol 2011; Article in press.
2.
Cannell JJ. Autism and Vitamin D. Med Hypotheses 2008; 70: 750-759
3.
Cannell JJ, Hollis BW. Use of Vitamin D in Clinical Practice. Altern Med Rev 2008; 13:6-20.
4. Grant WB, Connie MS. Epidemiologic evidence supporting the role of maternal vitamin D deficiency as a risk factor for the development of infantile autism.
Dermatoendocrinol 2009; 1:223-228.
5.
Humble MB, Gustafsson S, Bejerot S. Low serum levels of 25-hydroxyvitamin D (25-OHD) among psychiatric out-patients in Sweden: relations with season, age,
ethnic origin and psychiatric diagnosis. J Steroid Biochem Mol Biol 2010;121:467-470.
6. Meguid NA, Hashish AF, Anwar M, Sidhom G. Reduced Serum Levels of 25-Hydroxy and 1,25-Dihydroxy Vitamin D in Egyptian Children with Autis J Altern
Complement Med 2010; 16:641-645.
7.
Cannell JJ. On the aetiology of autism. Acta Paediatr 2010; 99:1128–1130.
8.
Zimmer MH, Hart LC, Manning-Courtney P, Murray DS, Bing NM, Summer S. Food Variety as a Predictor of Nutritional Status Among Children with Autism. J Autism
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Dev Disord. 2011 Article in press.
9.
Emond A, Emmett P, Steer C, Golding J. Feeding Symptoms, Dietary Patterns, and Growth in Young Children With Autism Spectrum Disorders Pediatrics 2010;
126:337-342.
Zinc supplementation in psychiatric disorders of children
Sadriye Ebru Çengel Kültür
Department of Child and Adolescent Psychiatry, Hacettepe University, Ankara, Turkey
Micronutrient supplementation is considered as a useful intervention in many cases. Zinc is one of these micronutrients and an essential cofactor
for over 100 enzymes, both metalloenzymes and metal-enzyme complexes that are required in the metabolism of carbohydrates, fatty acids,
proteins and nucleic acids. Zinc is considered as an essential element in neuronal development, synaptogenesis and synaptic transmission.
In experimental animal studies, zinc deficiency during early brain development is mainly related with malformations. In humans,
neuropsychological and neurobehavioral effects of zinc deficiency are largely studied in severely zinc deficient groups or cases exposed to
deficiency during early developmental stages. In addition zinc supplementation studies mainly occur in the gestational period or infancy
and use zinc doses higher than the protective dosage. Limited numbers of interventional trials have been performed to demonstrate
the effects of zinc supplementation on behavioral, cognitive and neuropsychological functioning in school-aged children. Some of these
studies showed no significant effects on average attention span and short-term memory. On the other hand some found improvement
in neuropsychological performance and decrease in the number of children with clinically significant parents’ scores for attention deficit
and hyperactivity. When searched for internalizing symptoms, no significant effect was revealed in parent-teacher rated scales.
In clinical cases with attention deficit hyperactivity disorder (ADHD) and autism low serum zinc levels were reported. Zinc supplementation
studies in ADHD cases showed significant improvement reported in parents’ and teachers’ ratings of hyperactivity, impulsivity and
socialization scores. Furthermore, one study found that improvement was mainly in parent-teacher-rated inattentive symptoms in ADHD
cases. In a placebo controlled study, zinc supplementation in addition to ADHD treatment revealed a 37% reduction in d-amphetamine
dose compared to placebo, though no significant superiority of zinc supplementation for ADHD symptoms was observed.
In conclusion, zinc supplementation studies suggest a special relationship to ADHD diagnosis. However it is not possible to establish
either an etiological relation or an alternative treatment approach in ADHD.
Key words: Zinc supplementation, ADHD
The impacts of iron deficiency on mental health in childhood
Ayhan Bilgiç
Department of Child and Adolescent Psychiatry, Meram Faculty of Medicine, Selcuk University, Konya, Turkey
Numerous studies have found associations between iron deficiency (ID) and iron deficiency anemia (IDA) and poor cognitive and motor
development in infancy and early childhood. In addition, it has been reported that there are associations between ID/IDA and some
childhood neuropsychiatric disorders including attention deficit hyperactivity disorder, conduct disorders, autism spectrum disorders,
restless leg syndrome, sleep disturbance and Tourette’s syndrome. Iron is required for proper function of some enzymes that are engaged
in the myelinization process and in monoamine neurotransmitter synthesis. Therefore, it has been considered that these negative effects
of ID and IDA are related to the vital roles of iron in the brain. Thus, authors have suggested that the presence of ID without anemia is
sufficient for occurrence of functional disturbances, although exceptions exist. There are studies which considered that, especially early
in life, the negative impacts of ID on psychomotor and neurological development do not seem to be reversible by iron supplementation
and ID may cause permanent hazards in the brain. However, some studies have reported that iron supplementation resolved the effects
of ID including cognitive and motor development problems in children and the development of psychiatric disorders. Despite there being
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large amounts of data, the possible confounding effects of poor socioeconomic backgrounds prevent causal inferences. Even nowadays,
it is still not clear whether poor development of iron-deficient children is related to poor social backgrounds or irreversible damage due
to ID and if it is remediable with iron treatment.
Key words: Iron deficiency, children, development, psychiatric disorders
Antioxidant vitamin supplementation therapies in child psychiatry
Betül Mazlum
İstanbul University, Institute of Experimental Medicine, Department of Neuroscience, İstanbul, Turkey
Oxidative stress can be defined as an imbalance between pro-oxidant molecules produced by the body during metabolism and members
of the antioxidant system, in favor of the former. Antioxidant defense mechanisms include antioxidant enzyme systems and molecules
(vitamins, minerals, etc.) which have the ability to detoxify free oxygen radicals.
The brain is highly vulnerable to oxidative stress since it has limited antioxidant capacity, high energy demand and high lipid content.
Moreover, each brain region may have a genetically determined different vulnerability levels to oxidative stress.
Oxidative stress, which is included in the pathogenesis of cancer, aging, cardiovascular and neurodegenerative disorders, is also
considered for pathogenetic mechanisms underlying psychiatric disorders including schizophrenia, bipolar disorder, depression, autism
and attention deficit hyperactivity disorder. There are accumulating data about increased oxidative stress particularly in childhood autism
and therefore antioxidant therapies are considered as an alternative treatment option. In addition, vitamin and mineral supplementation
are recommended to compensate low intake when children with autism have feeding problems. The data about the effects of antioxidant
therapies in autism are restricted but promising. Since oxidative stress is a common finding in the pathogenesis of different disorders, it can
be suggested that individual differences, including single nucleotide polymorphisms of the genes coding for members of the antioxidant
defense system, might determine the vulnerability level to oxidative stress. Individual genetic differences might also be the determinant
of the level of benefit from antioxidant vitamin therapies. Not only the factors related to the biochemistry of leading antioxidant vitamins
(vitamin A, C and E) but also the disease and patient related differences might be acting on the response to supplementation with these
vitamins. These two groups of factors might determine the details of supplementation therapies with antioxidant vitamins in the future:
1) Factors related to the patient and the nature of the disease, i.e. the affected brain areas for a specific disorder, the vulnerability of these
brain areas to oxidative stress, accompanying diseases and possible effects of antioxidant vitamin supplementation on the pathogenesis
of these comorbid diseases; 2) Factors related to the biochemistry of the antioxidant vitamins in the body, i.e., polymorphisms of
molecules mediating intestinal absorption and blood-brain transfer of vitamins, important effects of these vitamins on specific gene
regulation and effects of vitamins on brain mechanisms.
Antioxidant vitamin supplementation is a promising alternative therapy in psychiatry, but it should be kept in mind that these vitamins
might also have undesirable results through their effects on other biological processes. This part of the panel will focus on the study
results of antioxidant vitamin supplementation therapies in child psychiatry and molecular data about the genetic and biochemical
processes of antioxidant vitamins in the body.
Key words: Antioxidant vitamins, psychiatry
Effectiveness of omega fatty acid supplementation for childhood psychiatric disorders
Sabri Hergüner
Selcuk University, Meram Faculty of Medicine, Department of Child and Adolescent Psychiatry, Konya, Turkey
Neuronal membranes are composed of phospholipids containing large amounts of polyunsaturated fatty acids (PUFA), especially the
omega-3 and omega-6 acids. Because humans cannot manufacture these de novo, they are “essential” in the diet. Membrane stability is
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essential for neuronal maturation as well as for advanced integrated central system activities including attention, alertness and motor
coordination. PUFA are critically important for normal brain development and functioning. During fetal life, large amounts of PUFA are
deposited in the central nervous system. During infancy, dietary intake of PUFA, both omega-3 and omega-6 acids, continues to be
essential for neural development.
PUFA are metabolized to prostaglandins and other eicosanoids, which modify many metabolic processes and immune functions. They
moderate dopamine, serotonin and norepinephrine release, regulate gene transcription and Na-K-ATPase channel function. There is
increasing evidence that omega acids play a part in many neurodevelopmental and psychiatric disorders including attention deficit
hyperactivity, dyslexia, developmental coordination disorder and autism spectrum disorders.
The focus of this speech will be on the effects of PUFA supplementation on pediatric neurodevelopmental disorders.
Key words: Children, neurodevelopmental disorders, omega fatty acids
[PS-13]
Symposium Title: Hormones and psychiatric disorders
Melatonin and human behaviour
Müfit Uğur
İstanbul Üniversitesi, Cerrahpaşa Tıp Fakültesi, Psikiyatri AD, Cerrahpaşa, İstanbul, Turkey
Melatonin is secreted from the pineal gland and regulates the sleep wake cycle, core body temperature, ovulation, and sexual behavior
in females, as well as immune and cardiovascular functions. It also has antioxidant, antiinflammatory, and glucose regulatory properties.
Melatonin also changes behavior especially in depressed patients or patients who are prone to a psychiatric illness.
External noradrenergic stimuli act on the suprachiasmatıc nuclei and control melatonin secretion, which in turn regulates autonomic
functions and daily behaviors by acting as an endogenous synchronizer.
Melatonin, which manages body core temperature, the sleep wake cycle, and gonadal sex steroids, also causes some behavioral problems
in case of depression. In bipolar manic patients nocturnal melatonin is found to be higher than in depressed patients because of
noradrenergic stimulation.
Melatonin secretion and body core temperature are also closely related. Core body temperature is the lowest when the nocturnal melatonin
secretion is high. By controlling core body temperature, melatonin also helps to regulate the body metabolism and glucose utilization.
Ovulation in females is under the control of melatonin. When melatonin is the lowest nocturnally, which causes high core body
temperature, it is time for ovulation in females. High core body temperature and low nocturnal melatonin secretion return to normal
after the ovulation occurs. It also controls the secretion of sex steroids by its suppressive effect on the gonads. Nowadays some research
is working on using it as an oral contraceptive agent.
It also regulates immune functions by acting on T lymphocytes and help organisms to have a high defense against infections, supplying
an anti-inflammatory effect and serving as an antitumor agent.
Today it is used specifically for the treatment of sleep disorders such as:
-Advanced sleep phase syndrome
-Delayed sleep phase syndrome
-Circadian rhythm disorders
-Insomnia
-Irregular sleep wake cycle
-Jet-Lag
-Seasonal affective disorders
-REM related behavior disorders
Key words: Melatonin
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Effects of oxytocin on social behaviour
Nuray Atasoy
Zonguldak Karaelmas University, Faculty of Medicine, Psychiatry Department, Zonguldak, Turkey
Oxytocin (OXT) is traditionally viewed as a female hormone that is primarily associated with labor and it has a very special affect on
mothering. In mothers it increases their attachment to their infant, promoting the feeling of love, and makes her infant more valuable
to her. Oxytocin has been called the love and bonding hormone. Furthermore, oxytocin mediates attachment behavior over the course
of development, with lower urinary concentrations of oxytocin found in maltreated children and in adult males with a history of early
separation. Psychologically, oxytocin promotes a feeling of well being and tranquility. It also suppresses the fear that would normally
cause a mother to back off from a threat. In humans, based on the animal literature, it has been postulated that beyond these peripheral
actions, central OXT modulates cognition in the context of social interactions, thus promoting positive sociality.
In particular, recent experiments have shown that OXT promotes trusting behavior, enhances facial emotion recognition and memory
for positive social information, reduces social stress, improves social cognition in socially impaired individuals with autism, and alters
dysfunctional cognition in social phobia.
Functional imaging studies have just begun to elucidate the underlying neural correlates of these pro-social effects. A number of studies
have provided evidence that the amygdala might be a key structure for the mediation of the social cognitive effects of OXT. Several studies
have shown that a single dose of OXT reduced amygdala reactivity to pictures of aversive scenes and faces with negative valence.
While studies of oxytocin and monogamous behavior in humans have not been conducted to date, one study found that in co-habiting
couples, greater partner support is associated with higher plasma oxytocin in both men and women before and after a period of warm
partner contact.
The OXT system is a sexual dimorphic system. For example, OXT plasma levels tend to be higher in females and synthesis, as well as OXT
receptor affinity, appears to be modulated by gonadal steroids such as estradiol and progesterone. It has been shown, in a study on
prairie voles, that female parenting behavior is more dependent on OXT, whereas male parenting behavior is associated with vasopressin.
Another study demonstrated that aggression is associated with OXT in females, but not in males. However, the hypothesis of homology
between paternal and maternal behavior has not yet been adequately tested and it is possible that different neuroendocrine circuits could
lead to the same behavior in males and females. Future studies should include both sexes to determine a possible sexual dimorphism in
the neural effects of OXT, considering gonadal steroids and OXT receptor affinity.
Key words: Oxytocin, social behaviour
Thyroid hormones and psychiatric disorders
Tayfun Turan
Department of Psychiatry, Erciyes University, Kayseri, Turkey
The role of the hypothalamic-pituitary-thyroid (HPT) axis in psychiatric symptoms and disorders has been stressed in many studies.
Secretion of thyroid hormones is controlled by this axis. Hypothalamic thyrotropin releasing hormone (TRH) stimulates pituitary
thytrotropin-stimulating hormone (TSH) and the latter controls the secretion of thyroid hormones. Serum thyroid hormones regulate the
HPT axis by a negative feedback system. The main secretion of the thyroid gland is thyroxine (T4). T4 is converted into triiodothyronine (T3)
in various tissues, especially in brain, by enzymes called “deiodinases”. Transthyretin, a hormone transporter, transports T4 into the brain (1).
Thyroid hormones play a critical role in the developing and functioning of the brain (2). In this regard, it is suggested that interactions
between thyroid hormones and neurotransmitter systems, especially serotonin (5-HT), norepinephrine (NE) and acetyl choline (Ach),
probably contribute to the regulation of mood and behaviour (1). T3 enhances the effects of NE, 5-HT and γ-aminobutyric acid, which are
thought to be involved in the etiology of some psychiatric conditions (3).
In the literature there are many case reports and studies indicating probable relationships between clinical or subclinical thyroid diseases
and psychiatric disorders. So far, many cases have been reported of hypothyrodism or hyperthyroidism associated with psychiatric
disorders, including mania, depression, schizophreniform psychosis, paranoid psychosis, cognitive disturbances, delirium and anxiety
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(4-9). One percent of thyrotoxic patients are suggested to have been first diagnosed with a psychiatric disease (5). Interestingly, it
seems that both hyperthyroism and hypothyroidism could lead to mania, anxiety or schizophrenic symptoms. The underlying reason
for the co-occurrence of thyroid diseases and psychiatric disorders is not yet known. However, in these cases, combined hormonal and
psychotropic interventions may improve symptoms.
Several studies have assessed HPT axis activity in various psychiatric disorders, especially mood disorders and anxiety disorders. Up
to 45% of the euthyroid patients with major depression showed blunted TSH response to TRH stimulation (10). Moreover, thyroid
hormones accelerate the antidepressant effect of tricyclic antidepressants (11). HPT axis alterations may play an important role in the
pathophysiology of bipolar disorder, but this area has received much less attention than major depressive disorder. However, it seems
that abnormalities of this axis are not uncommon among bipolar patients, especially among the rapid cycling subgroup. So far, thyroid
dysfunctions such as hypothyroidism and exaggerated TSH response to TRH have been found in rapid cycling patients (12,13). In some
bipolar patients, latent thyroid dysfunction becomes overt by lithium treatment. Moreover, it has been suggested in a recent study that
bipolar disorder itself may cause increased thyroid volumes and decreased thyroid hormones as well as lithium treatment in patients (14).
Few studies have investigated possible thyroid dysfunctions in psychotic patients. In a study, schizophrenic patients showed increased
serum T4 levels, which normalized after antipsychotic treatment. Elevated serum T4 levels in schizophrenic patients may suggest an
impairment of T4 metabolism in the brain (4).
A few studies of panic disorder have demonstrated evidence of a blunted TSH response to TRH. A previous study showed higher TSH
levels in non-medicated patients with severe panic attacks (7). Increased TSH levels seen in patients with panic disorder might be due to
reduced intracerebral 5-HT concentrations (15).
Eletroconvulsive therapy (ECT) itself may affect the HPT axis as do psychotropic drugs. In a previous study, elevated TSH levels were found
following ECT in depressed patients. This response might contribute to the therapeutic effect of ECT (16).
In conclusion, the HPT axis and thyroid hormones play an important role in the pathophysiology of many psychiatric disorders. However,
further well-designed studies are needed to clarify the confusion in this field.
Key words: Hypothalamic-pituitary-thyroid axis, thyroid hormones, psychiatric disorders
Sex steroids and psychiatric disorders
Erdem Deveci
Regional Training and Research Hospital, Department of Psychiatry, Erzurum, Turkey
Sex steroids play very important roles in the development and function of the central nervous system and have long been known to
exert powerful effects on brain differentiation, neural plasticity, central neurotransmission and behavior. Estrogens, progestins, and
androgens are able to induce several effects in brain areas of the central nervous system, through binding with specific receptors (1).
Sex steroid hormones act through genomic mechanisms, modulating synthesis, release and metabolism of many neuropeptides and
neurotransmitters, and through non-genomic mechanisms, influencing electrical excitability, synaptic function, morphological features
and neuron-glia interactions (2).
Animal research has shown that estrogens, progesterone and testosterone are critically involved in myelination, forming the basis of white
matter connectivity in the central nervous system. Animal studies have also provided evidence that estrogen modulates dopaminergic
activity and affects dopamine related behaviors in animals in a variety of ways.
Clinical observations suggest that sex steroids have potent effects on mood, mental state and cognitive functions. Data also suggest
that estrogen has a pivotal role in modulating other neurotransmitter systems such as serotonergic and glutamatergic systems that
have implications for schizophrenia and mood disorders (3,4). Sex steroid deficiency causes many neuroendocrine changes. At the
hypothalamic level, estrogen withdrawal gives rise to vasomotor symptoms, eating behavior disorders, and altered blood pressure
control. On the other hand, at the limbic level, the changes in serotoninergic, noradrenergic and opioidergic tones contribute to
modifications in mood, behavior and nociception.
Studies of testosterone concentrations in depression have yielded inconsistent results reporting low as well as high testosterone levels
associated with depression (5). On the other hand anabolic steroid use has increased in prevalence in many countries over the past
decade, and it can lead to aggression, depression, mania and psychosis, in addition to a range of physical complications which seem to
be important in clinical practice (6).
Key words: Depression, estrogen, mood disorders, progesterone, schizophrenia, testosterone
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References:
1.
McEwen BS Steroid hormones are multifunctional messengers to the brain. Horm Res. 1992; 37(Suppl 3):1-10.
2.
Genazzani A.R. et al. Endocrinology of Menopausal Transition and Its Brain Implications CNS Spectr. 2005 Jun;10(6):449-57.
3.
Janice R, Stevens MD Schizophrenia: reproductive hormones and the brain. Am J Psychiatry 2002; 159:713-719.
4.
Seeman MV. The role of estrogen in schizophrenia. J Psychiatry Neurosci 1996; 21:123-125.
5.
Zarrouf FA, Artz S, Griffith J, Sirbu C, Kommor M. Testosterone and depression: systematic review and meta-analysis. J Psychiatr Pract 2009;15:289-305.
6.
Hall, R. C. W., Hall, R. C. W. & Chapman, M. J. Psychiatric complications of anabolic steroid use. Psychosomatics, 2005; 46- 285.
Insulin and psychiatric disorders
Mesut Cetin
Department of Psychiatry, GATA Haydarpasa Training Hospital, Uskudar, Istanbul, Turkey
Insulin is a hormone central to regulating carbohydrate and fat metabolism in the body. Insulin also influences other body functions, such
as enhancing acute thermoregulatory and glucoregulatory responses to food intake. It is also a neuropeptide transmitter and enhances
learning and memory.
Hypoglycemia is a lack of sufficient glucose and a scarcity of the sources of glucose, which can dramatically manifest itself with impaired
functioning of the central nervous system and can cause dizziness, speech problems, and even loss of consciousness. While producing
those symptoms, hypoglycemia also provokes a rapid increase in epinephrine secretion, which leads to tremulousness, lightheadedness,
perspiration, anxiety, hunger, nausea, and tachycardia. These symptoms present like a panic attack, suggesting that if hypoglycemia does
provoke anxiety attacks it may be through its action as a nonspecific stressor, perhaps by interacting with an underlying CNS disorder
that predisposes to panic. The fear of hypoglycemia-induced bodily symptoms of arousal has been implicated in the pathogenesis of
both spontaneously occurring and experimentally provoked panic attacks. The fear of bodily symptoms may be a characteristic of panic
disorder and is hypothesized to predict state anxiety and panic frequency during experimentally induced peripheral arousal.
Insulin resistance and metabolic syndrome (MS) have become worldwide problems. MS is a cluster of risk factors associated with
increased risk of cardiovascular diseases and type 2 diabetes. Based on research data from 2004, 40% of adults in Turkey meet the criteria
for diagnosis of metabolic syndrome. The use of certain medications, such as atypical antipsychotics, may increase insulin resistance and
the risk of the metabolic syndrome.
Key words: Insulin, panic disorder, insulin resistance, hypoglycemia, depression
[PS-14]
Symposium Title: Clinical course of psychiatric disorders associated with trauma and treatment issues
Medine Yazıcı Güleç
Erenkoy Mental Research and Training Hospital, Istanbul, Turkey
There is increasing evidence for the role of adverse childhood experiences in the occurence of mood disorders (MD). A great number of
studies have shown that there is a correlation between MD and parental indifference, neglect and sexual and physical abuse. Angst et
al., in a 20-year longitudinal study, suggested that childhood family issues have a robust correlation with the chronicity of bipolar and
unipolar MD, and adverse childhood experiences give rise to low self-esteem and anxious personality. The presence of childhood trauma
(CT) has found to be associated with increases in rates of substance abuse, early age of onset, rapid cycling, and suicide. There is severe
CT in half (49%) of bipolar MD patients.
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Individuals with CT have both an overall increased risk for depression and a substantially increased sensitivity to the depressogenic
effects of stressful life events. The relation between CT and stressful life events is dose dependent and correlated with the intensity of the
neuroticism. It has been shown that the severity of CT predicts an early age of onset and the number of life time depressive episodes,
and that it is associated with more comorbidity. Increased rates of emotional CT, depressive symptoms and anxiety have been reported
in treatment resistant group of patients.
Childhood adverse life events are associated with various neuroendocrine and neuroanotomical changes. There is a 6 times larger ACTH
response to stress in depressive female patients who reported CT. These patients also have an increased cortisol response and heart
rate response to psychosocial stress. Women, who have reported CT but were not depressed, have exhibited normal cortisol responses,
despite having increased an ACTH response. This can be interpreted as resilience against depression, an adrenal adaptation to central
sensitization. It has been reported that decreased hippocampal volume (18%) in depression is related to CT and that the hippocampal
volumes of depresssive patiens who did not report CT were equal to those of the control group. Repeated bursts of CRF in response to
stress during development and increased cortisol reactivity over the course of time may contribute to smaller hippocampi after childhood
trauma exposure, leading to further sensitization of the stress responses. These results would suggest that there are biologically distinct
subtypes of depression as a function of childhood trauma.
The effect of CT on predisposition to illness is associated with genotype. The s/s allele of the serotonin transporter gene, the gene
polymorphism of BDNF and the CRF-1 gene have been shown to be related to vulnerability to trauma effects.
CT is associated to decreased response to pharmacological treatment. Among chronically depressed patients with no history of early
trauma, combination treatment was most effective in attaining remission compared to pharmacotherapy and psychotherapy. In contrast,
in chronically depressed patients with early-life trauma, remission rates were significantly higher for psychotherapy alone versus
pharmacotherapy. Combination treatment did not have any further advantage over psychotherapy alone. Improved effects of cognitive
and behavioral therapies, group therapies and EMDR have been reported in various studies. Questioning about CT in MD patients seems
to be important for treatment planning, assessment of risks and prophylactic interventions.
Key words: Childhood trauma, mood disorders
Selma Bozkurt Zincir
Erenkoy Mental Health and Diseases Training and Research Hospital, Istanbul, Turkey
In recent years, there has been a growing awareness of the importance of abuse or trauma in shaping the course of people’s lives. There
is growing literature to indicate that trauma is also linked with more severe psychiatric disturbances, including symptoms indicative of
psychosis in general and schizophrenia in particular. Several lines of evidence suggest an association between trauma and psychosis with
a dose-response effect. First, studies have demonstrated a high incidence of trauma in the lifetimes of patients with psychosis. Abused
patients are particularly likely to experience positive symptoms, such as paranoid ideation, thought insertion, visual hallucinations, ideas
of reading someone else’s mind, ideas of reference, and hearing voices making comments. Secondly, it has been suggested that of all
diagnostic categories, psychosis displays the strongest association with child abuse. Thirdly, according to some researchers childhood
sexual abuse is the most powerful predictor of later psychiatric symptoms and disorders after controlling for significant demographic
variables.
It has been suggested that the experience of abuse may create a biological or psychological vulnerability for the development of
psychotic symptoms, including sub-clinical psychotic experiences such as low-grade delusional ideation, suicidal thinking and isolated
auditory hallucinations. Exposure to psychological trauma worsens the prognosis of expression of psychosis, in terms of greater likelihood
of transition to a more severe psychotic state. According to recent cognitive models of psychosis early adverse experiences such as
social marginalization, childhood loss or severe childhood trauma may create an enduring cognitive vulnerability characterized by less
subjective control over these experiences, negative schematic models of the self and a world that facilitates external attributions. This
tendency to externally attribute events may lie beneath paranoid ideation.
Current ideas about biological consequences of early adversities lend even more credibility to the notion of an enduring psychological
vulnerability. It has been suggested that adverse life events or significant losses might be able to mould the neurodevelopmental
abnormalities that underlie sensitivity to stressors, if they occur early enough or are sufficiently severe. Thus abnormal neurodevelopmental
processes may originate from traumatic events in childhood. Specifically, when exposure to stressors persists and heightened stress-
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induced glucocorticoid release is chronic, permanent changes in the hypothalamic-pituitary-adrenal (HPA) axis may ensue. This may
account for the dopaminergic abnormalities considered central to biological accounts of psychosis. Other researchers are also examining
the role of dissociative processes, attachment styles, and trauma related cognitive biases to try to better understand precisely how
childhood trauma can lead to psychosis later in life.
Clinically it is imperative to routinely enquire about traumatic experiences to respond appropriately and to offer psychosocial treatments
to those who report traumatic life events in the context of psychotic experiences.
Key words: Trauma, psychotic disorders, schizophrenia
Relationship of sexual dysfunction with trauma
Murat Erdem
Gulhane Military Medical Faculty, Psychiatry Department, Ankara, Turkey
Exposure to sexual trauma in adulthood is perceived as helplessness and loss of control even if sexuality has been defined as a pleasant
event before trauma. Feelings of guilt and shame occurring after trauma as well as secondary clinical pictures such as depression,
post traumatic stress disorder, and alcoholism are major causes of sexual dysfunction. Also sexual abuse in childhood raises a sense of
weakness and perception of inadequacy. These individuals are at risk of developing inappropriate sexual behaviors over time. Indulging
in sexual behaviors and thoughts that are evaluate sexuality as a gift or privilege are precursors for these inappropriate behaviors. In
addition, the stigmatization caused by feelings of shame and guilt in these children is another cause of sexual problems in the future.
Childhood sexual trauma is associated with negative attitudes about sexuality, lack of sexual satisfaction, orgasmic failure, need for sexual
therapy and low self-esteem about sexual attractiveness. Chronic pelvic pain is a significant clinical entity which causes sexual dysfunction
in many ways. In studies, the rate of traumatic childhood sexual experiences was found to be over 60% in these patients (N. Leithner,
2006). The difference between patients with chronic pelvic pain and a healthy control group was found to be even greater in terms of the
increasing violence of sexual trauma. In a study of 63 patients with chronic pelvic pain, a history of sexual trauma was identified in 64.5%
of cases and deficiencies in sexual function were found to be associated with the level of depression in these patients (ME Randolph,
2006).
There are several studies that show that physical and sexual trauma plays a role in the etiology of vaginismus. In a study comparing the
childhood and adolescent sexual traumas of patients with vaginismus and dyspareunia and control groups -(each group consisting of
29 patients) childhood sexual trauma was found to be twice as high as the control group in the vaginismus group (Reissing ED, 2003).
In the literature there are case reports suggesting that EMDR is effective in cases of vaginismus resulting from childhood sexual trauma.
In studies evaluating the relationship between childhood sexual traumas and a specific sexual dysfunction, aand in studies examining
sexual functioning in general, a strong relationship has been found between these two situations. Structural vulnerability and the severity
of sexual trauma were also reported to affect this relationship. While childhood sexual trauma is associated with sexual stimulation
disorder, orgasmic disorder, vaginismus, dyspareunia and emotional problems about sexuality (sexual guilt, sexual anxiety etc.) in most
individuals, high-risk sexual behaviors, characterized by extreme preoccupation with sexuality and uncontrolled sexual relationships, are
seen in fewer individuals.
Sexual childhood trauma in men is being reported, recognized and treated less frequently than the actual prevalence. Sexual dysfunction
in these individuals was reported to be seen at least five times more than people who have not been exposed to a trauma. In a study of
1793 individuals, exposure to sexual trauma before age 16 has been reported at more than 1/3 of women and about 1/6 of men. In both
sexes, especially in women, an association between the presence of childhood sexual trauma and sexual dysfunction has been identified
(Najma JM, 2005). Leonard et al. found that problems associated with orgasm are the most frequent sexual problems seen in individuals
who were exposed to a childhood sexual trauma (2008).
Key words: Trauma, sexual dysfunction
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[PS-15]
Symposium Title: Depression and pain
Cengiz Akkaya
Departments of Psychiatry, Uludag University, Bursa, Turkey
Major depressive disorder (MDD) is a chronic, disabling condition with a wide range of symptoms, including core mood symptoms of
depression and anxiety, cognitive and behavioral deficits, and somatic/physical disturbances. Approximately two-thirds of patients with
depression experience physical pain symptoms (e.g. headache, neck and back pain, abdominal pain, diffuse musculoskeletal pain). Pain
as a symptom of depression, often has a negative impact upon other depressive symptoms (for example, it may induce or exacerbate
low energy, sleep disturbance, and anxiety), adherence to medication, and obtaining adequate therapy. Therefore, pain influences both
the course of depressive illness and the treatment outcome. Also the severity of pain is found to be a strong predictor of poor response
and health-related quality of life. Impairments in social and occupational functioning may increase when depression and pain coexist.
Patients who fail to achieve remission after antidepressant therapy are more likely to suffer residual pain and other physical symptoms
compared with remitted patients.
The close relationship between pain and depression, and the growing evidence of a connection between treatment outcomes in these
conditions, suggests that maximal patient benefit may result from treatments which effectively address both emotional and physical
symptom domains. Therefore, treatments that address both depression and pain are highly desirable. Neurobiological evidence suggests
that mood and chronic pain are connected via serotonin and noradrenaline neurotransmitter pathways. Serotonin and norepinephrine
play a key modulating role in pain mechanisms in the central nervous system. Serotonin modulates both descending inhibitory and
facilitatory pathways and thus exerts both an antinociceptive and a pronociceptive effect. Noradrenaline, however, typically acts centrally
in an antinociceptive manner, exerting its effects via a-2-adrenoreceptors in the descending antinociceptive pathways.
Efficacy for treating pain is best established for tricyclic antidepressants. But through the last decade, antidepressant medications,
particularly selective serotonin reuptake inhibitors (SSRIs) and selective serotonin and norepinephrine reuptake inhibitors (SNRIs), are
widely used in the management of MDD. SSRIs are often favored in practice because of their tolerability and safety. However, their efficacy
in pain is thought to be relatively weak. On the other hand the mechanism of SNRIs has been hypothesized to confer analgesic effects
independent of antidepressant action. Evidence suggests that potentiation of both serotonin and norepinephrine is required for effective
analgesia; drugs that inhibit only one of these systems (particularly serotonin) appear to have a limited effect. Whether antidepressants
relieve pain through direct analgesic effects or indirectly through antidepressant action is still under discussion. There may be a close
association between analgesic and antidepressant effects and pain relief may be secondary to mood improvement.
Key words: Pain, depression, antidepressant
Selçuk Kırlı
Department of Psychiatry, Uludag University, Bursa, Turkey
Although there is a large amount of data indicating that depression and pain symptoms are closely interrelated, they are not included in
depression symptoms in the classification systems. Even so, new developments in neuroscience have carried the data on this interrelation
and co-occurrence beyond the epidemiological dimension to the awareness of a common underlying mechanism (1,2).
Although such a co-occurrence and the mechanisms that influence it are being discussed more and more, pain symptoms still cannot
be well assessed or monitored and they are usually described by terms such as ‘medically unexplainable’, ‘functional’ or ‘psychosomatic’.
The following statements may be made about the clinical characteristics of the symptoms (1):
• They do not conform to the anatomic localizations which would help explain their causes.
• They may vary in severity and location.
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• Pain symptoms occur in 1/5 – 1/3 of patients with depression. These ratios are approximately 4 times higher than the ratios of those
with no depression. The ratios in the literature about pain symptoms in patients with depression are approximately 65% on average (3).
• Chronic pain is a significant individual risk factor for suicide and self-injury.
• Chronic pain results in increases in treatment costs and a poorer outcome.
• The presence of pain as a residual symptom is the strongest predictor of recurrence.
It should be kept in mind that chronic pain, which is considered as being ‘functional’ in terms of the mechanisms involved in having pain
during depression, is medically unexpected, self-generated and associated with vulnerability to pain. Therefore, central factors should
play a leading role in experiencing it (4). Living with pain causes negative emotions, but beyond that, continuous pain is a physical
symptom of depression. A neurobiological explanation of experiencing these two situations concurrently is not all that difficult when the
broadness and diversity of the mechanisms involved in experiencing depression are taken into consideration (5).
The mechanisms involved in this co-occurrence may be summarized as follows:
• The connection between the emotional and somatic (e.g. pain) symptoms of depression is probably set up through the HPA axis. This
system plays an important function in vulnerability to stress.
• The changes that emerge in the transfer of NA and 5HT in the CNS are of critical significance in terms of both depression and chronic
pain pathophysiology (6). Monoamines regulate both mood symptoms and sensations of pain.
• Pain stimuli are carried from the periphery to the CNS by primary afferent fibers and are regulated by stimulating glutamate and
suppressor GABA.
• The sub-cortical areas involved are the hypothalamus, periaqueductal gray matter, raphe dorsalis and locus coeruleus. These areas are
also regulated by 5HT and NA.
• Cortical processing of a pain sensation is carried out in the relevant areas of the cortex.
In conclusion, it is obvious that common pathophysiological processes underlie the co-occurrence of depression and somatic pain
symptoms seen in this picture and it is important to take such pain symptoms into consideration in a comprehensive treatment approach.
Key words: Pain, depression, clinical characteristics
References:
1.
Peveler R, Katona C, Wessley S, Dowrick C: Painfull symptoms in depression: under-recognized and under treatment. British J Psychiatry 2006;188:202-203.
2.
Von Knorring L, Ekselius L: Idiopatic pain and depression. Quality of Life Research 1994;3:557-568.
3.
Bair MJ, Robinson RL, Katon W, Kroenke K: Depression and pain comorbidity. A literatüre rewiev. Arch Gen Psychiatry 2003;163:2433-2445.
4. Mohr P, Bitter I, Svestka J, Seifritz E, Karamustafalıoğlu O, Koponen H, Sartorius N: Management of depression in the presence of pain symptoms. Psychiatria
Danubina 2010;22:4-13.
5.
Nemeroff CB, Vale WW: The neurobiology of depression: inroads to treatment and new drug discovery. J Clin Psychiatry 2005;66 (suppl. 7):5-13.
6.
Wise TN, Fishbain DA, Holder-Perkins V: Painfull physical symptoms in depression: a clinical challenge. Pain Med 2007;8 (suppl. 2):75-82.
[PS-16]
Symposium Title: Marijuana; from mellow to madness
Effect of cannabis use on cognitive functions
Cüneyt Evren
Bakirköy Training and Research Hospital for Psychiatry, Neurology, and Neurosurgery AMATEM, İstanbul, Turkey
If we look at the data of recent years, probation admissions to AMATEM Istanbul, which are mostly related to cannabis use, have increased
significantly; the number of first admissions/number of control admissions for 2008, 2009 and 2010 are 2318/24261, 3759/31862 and
5639/30959, respectively. As for other psychoactive substances, the negative effects of cannabis use on cognitive functions are well
known. Some cannabis-related cognitive function deficits improve after cessation of cannabis use, but growing evidence also suggests
that other deficits persist after cannabis is discontinued and may hinder an individual’s ability to make the best use of behavioral
therapies, putting him or her at greater risk for relapse of cannabis use (1).
Cannabis seems to continue to exert impairing effects in executive functions even after 3 weeks of abstinence and beyond. Although
basic attentional and working memory abilities are largely restored, most enduring and detectable deficits are seen in decision-making,
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concept formation, and planning. Those subjects reporting chronic, heavy cannabis use show the most enduring deficits (2). One can
suggest that some of these impairments are not completely reversible upon cessation of cannabis use and moreover may interfere with
the treatment of cannabis addiction. Therefore, targeting cognitive impairment associated with chronic cannabis use may be a promising
novel strategy for the treatment of cannabis addiction (3).
While acute administration of cannabis to patients with schizophrenia exacerbates symptoms and cognitive impairments and may have
enduring effects, cannabis has also been found to have some beneficial effects on cognition, at least in certain subgroups of patients (4).
Cannabis using patients had better attention and executive functions than non-cannabis using patients at baseline and after one year of
treatment in a representative sample of first-episode schizophrenia patients. Cannabis using patients appear to comprise a subgroup of
patients with better premorbid adjustment and premorbid frontal cognitive functions (5).
Thus, while cannabis use is traditionally associated with cognitive impairment, the relationship is more complex in the case of schizophrenia.
Key words: Cannabis, cognitive functions
References:
1.
Blume AW, Marlatt GA. The role of executive cognitive functions in changing substance use: what we know and what we need to know. Ann Behav Med 2009;
37:117-25.
2.
Crean RD, Tapert SF, Minassian A, Macdonald K, Crane NA, Mason BJ. Effects of chronic, heavy cannabis use on executive functions. J Addict Med 2011; 5:9-15.
3.
Sofuoglu M, Sugarman DE, Carroll KM. Cognitive function as an emerging treatment target for marijuana addiction. Exp Clin Psychopharmacol 2010; 18:109-19.
4.
Yücel M, Bora E, Lubman DI, Solowij N, Brewer WJ, Cotton SM, Conus P, Takagi MJ, Fornito A, Wood SJ, McGorry PD, Pantelis C. The impact of cannabis use on
cognitive functioning in patients with schizophrenia: a meta-analysis of existing findings and new data in a first-episode sample. Schizophr Bull 2010 (In press)
5.
Rodríguez-Sánchez JM, Ayesa-Arriola R, Mata I, Moreno-Calle T, Perez-Iglesias R, González-Blanch C, Periañez JA, Vazquez-Barquero JL, Crespo-Facorro B. Cannabis
use and cognitive functioning in first-episode schizophrenia patients. Schizophr Res 2010;124:142-51.
The differences between marijuana psychosis and other substance induced psychoses
Mükerrem Güven
Akdeniz University Research and Practice Center for Alcohol and Substance Addiction, Antalya,Turkey
Psychosis may be observed in intoxication from cannabis, alcohol, opiates, inhalants, stimulants, amphetamines, hallucinogens,
phencyclidine, anxiolytics, sedatives and hypnotics. The condition of psychosis may also occur due to abstinence from alcohol, anxiolytics,
sedatives, and hypnotics (1). Although mostly alcohol-dependent psychotic disorders are reported, the cannabis-psychosis relationship
arouses more interest among researchers. Hypomania and agitation are more frequently noted in cannabis users compared with users
receiving other substances. The symptoms of cannabis-psychosis usually disappear with a decrease in cannabis use, but the true nature
of perception (flashbacks) hallucinations may be re-lived. As distinct from psychosis depending on other substances, evidence regarding
the relationship between cannabis usage and the first attack of schizophrenia is increasing (2). There are long-term clinical follow-up
studies to distinguish the acute toxic psychosis revealed in cannabis users from psychoses similar to schizophrenia, and also some
studies conducted on the assumption that “cannabis psychosis” is distinct from other psychoses caused by other substances. Auditory
hallucinations and emotional blunting are reported less commonly in cannabis psychosis compared to non-substance dependent
psychoses. In a study investigating cannabis-induced psychoses, no significant relationship was determined between usage and the onset
age of receiving cannabis; however, it has been put forth that a relation exists between cannabis use, the length of addiction and the quality
and amount of cannabis received (3). Capsi et al. have reported that the risk for cannabis-induced psychosis is high in people carrying
the valine-158 allele of the catechol-O-methyltransferase (COMT) gene (2005). Abuse substances affect different neurotransmitters in the
central nervous system (4). Positive psychotic symptoms such as paranoid delusions and hallucinations are observed in half of cocaine
addicts. As the period of cocaine use increases, negative symptoms and paranoid psychosis can be recorded. Stimulants such as cocaine
and amphetamine can reveal psychosis by increasing dopaminergic activity in the central nervous system (CNS). Cannabinoid-1 (CB-1)
receptors are responsible for the effects of cannabis in the CNS. In the lateral putamen, pallidum and substantia nigra, CB-1 receptors
are determined to be present in a high degree. Many neurotransmitter systems taking part in the etiology of schizophrenia, especially
glutamatergic and dopaminergic systems, are affected by activation of the CB-1 receptor (5). Effects of substances on neurotransmission
should be better investigated to understand how substance-induced psychotic disorder develops.
Key words: Addiction, cannabis, psychosis, substance abuse
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References:
1.
American Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental Disorders (4th edn) (DSM-IV). Washington, DC: APA.
2.
Van Os J, Bak M, Hanssen M, Bijl RV, de Graaf R, Verdoux H. Cannabis use and psychosis: a longitudinal population-based study. Am J Epidemiol 2002;15:319-327.
3. Makkos Z, Fejes L, Inczedy-Farkas G, Kassai-Farkas A, Faludi G, Lazary J. Clinical characteristics of cannabis-induced schizophrenia spectrum disorder.
Neuropsychopharmacol Hung. 2011 Sep;13(3):127-38.
4.
Caspi A, Moffitt TE, Cannon M, McClay J, Murray R, Harrington H, Taylor A, Arseneault L, Williams B, Braithwaite A, Poulton R, Craig IW. Moderation of the effect of
adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O methyltransferase gene: longitudinal evidence of a gene X
environment interaction. Biol Psychiatry 2005; 15;57(10):1117-7.
5.
Müller-Vahl KR, Emrich HM. Cannabis and schizophrenia: towards a cannabinoid hypothesis of schizophrenia. Expert Rev Neurother. 2008 Jul;8(7):1037-48. Review.
Selective serotonin reuptake inhibitors in the treatement of cannabis dependence
Musa Tosun
Istanbul Universit Cerrahpasa Medical Faculty, Department of Psychiatry, İstanbul, Turkey
Treatment of cannabis dependence should aim cannabis abstinence and psychosocial support as in general dependency treatment
approach.
The cannabis detoxification of the patient might be achieved by treatment interventions in hospital setting or following up the patient
closely in outpatient setting. In outpatient setting, the regular urinalyses and close monitoring of the patient must be carried out. The
metabolites of the cannabinoids could be detected in urinalysis from 3 days up to 4 weeks following the last use.
Individual, family, and group psychotherapies might be beneficial while supporting the patient. Education is the most important element
for both “abstinence” and “support programs,” as the motivation to quit and not to restart is primarily due to education on the effects and
harmful consequences of cannabis abuse. Tranquilizer drugs might be efficient in short term withdrawal symptoms that might be seen
in cannabis abusers or addicts.
Selective serotonin reuptake inhibitors (SSRIs) as other antidepressant agents may be used in the treatment of depressive patients, who
use cannabis as a self treatment for depression, and in co-morbid depression of cannabis use disorders or in depressive symptoms caused
by cannabis abuse. In addition, SSRIs might also be used in the treatment of cannabis-induced anxiety disorders.
There is growing interest in the use of antidepressants in cannabis abuse because of highly reported depression rates during the
treatment of cannabis abuse or after the cessation. Nevertheless, there is a dearth of knowledge about the treatment of cannabis abuse
with SSRIs. In a double blind placebo controlled study, fluoxetine has been reported to decrease the frequency of cannabis use in alcoholic
patients with depression.
References:
1.
Cornelius JR Salloum IM, Haskett RF, Ehler JG, Jarrett PJ, Thase ME, Perel JM. Fluoxetine versus placebo for the marijuana use of depressed alcoholics. Addict Behav.
1999 Jan-Feb;24(1):111-4.
2. Hall W. & Degenhardt L. : Cannabis-Related Disorders. in Kaplan & Sadock’s Comprehensive Textbook of Psychiatry 8th ed. Lippincott Williams & Wilkins,
Philadelphia, 2005. Vol. I: 1211-1220
3.
Tosun M. : Alkol ve Diğer Maddeler ile İlişkili Bozukluklar. İ.Ü.Cer.Paş.Tıp Fak. Yayınları, Rektörlük Yay.No: 4215, Fak.Yay.No. 229, İstanbul, 2000 : 96-100.
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[PS-17]
Symposium Title: Overcoming treatment resistance: An update
Treatment strategies for treatment resistant depression
Selçuk Aslan
Gazi University, Medical School, Psychiatry Department, Ankara, Turkey
Depression is a disorder with heterogenic etiology and variable clinical features. Response to the treatment is defined as a 50% reduction
in admission symptoms. Recent studies with large numbers of patients have revealed that acute phase treatment should last for 6 weeks,
including at least 4 weeks with effective dosages. Approximately 60% of patients have a response to the first antidepressant treatment.
The remainder, 40% of patients, either has a partial response or they are non-responders (Fava 1996).
At the end of 6 weeks with optimum treatment dosing, if symptoms have not reduced by 20-25%, patients are described as nonresponders and drug treatment should be switched to another type of antidepressant medication. Patients, who do not respond to
trials of adequate dosages and periods of two or more different classes of antidepressant treatments, are considered as treatmentresistant depression (TRD). If there is a partial response to antidepressant treatment, waiting for couple of weeks is the rational approach.
The patients who have high depression scores at the initial evaluation have relatively higher degrees of partial or non-response to
antidepressant medications. These cases are more likely to have comorbid axis 1 and axis 3 physical disorders. An 8-12 week period of
effective antidepressant treatment should be applied in these cases. Thase and Rush, proposed 5-stage-model for the description of TRD
(1997). Later in the STAR D study, Rush et al. developed sequences of treatment alternatives for relieving depression (Rush et al. 2003).
On the other hand, increasing drug dosages results in more side effects and adverse reactions. Some patients may be low metabolizers
and higher doses may result in significant side effects. Also fast metabolizer patients may respond to higher doses of medications. Efficacy
of atypical antipsychotics, stimulants, pindolol, lithium, and lamotrigine have been tested for augmentation in ongoing treatment for TRD
in clinical trials (Caravalho et al 2009). In severe cases with no response or partial response to treatment, inpatient treatment should be
considered.
Non-responders or partial responders can be treated with electro convulsive therapy with anesthesia or non-responders can be treated
with rTMS (Paul et al 2006). Selected non-responsive cases may be treated with more invasive techniques such as deep brain stimulation
or vagus nerve stimulation. Biological predictors should be identified to irecognize patients who will not respond to two adequate trials
of different antidepressant.
In addition, psychotherapeutic interventions during the treatment period, such as observing and revealing automatic thoughts,
assumptions, and basic beliefs and depressive schemas, should be evaluated and behavioral and cognitive interventions can be applied.
Activity scheduling and participating in regular exercise might also be helpful to some degree.
Key words: Depression, treatment resistant depression
Mehmet Akif Ersoy
Ege University School of Medicine, Department of Psychiatry, Izmir, Turkey
Although many clinicians depending on their experience will agree that childhood trauma history will cause treatment resistance
regardless of the diagnosis, studies investigating this issue directly are scarce. During our search of literature we have found publications
on the relationship between childhood trauma and treatment resistance in a few disorders such as obsessive compulsive disorder (OCD),
major depression, and bipolar affective disorder. One study reported that 82% of OCD cases had a history of childhood trauma. In this
study 39% of the cases met the criteria for post traumatic stress disorder (PTSD) and half of those who had a history of trauma met the
PTSD criteria. It is noticeable that those who had major depression or borderline personality disorder, in addition to OCD, had a higher
risk of having comorbid PTSD. Treatment resistant OCD cases should be screened for PTSD and having comorbid major depression and/
or borderline personality disorder helps to predict PTSD and may help to determine the severity of the illness.
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An indirect approach is looking for comorbidity of trauma related disorders in treatment resistant cases. One study has pointed out that
OCD cases with comorbid PTSD have worse treatment outcomes. A meta-analysis study has revealed that childhood trauma not only
effects lifetime risk of major depression, it also negatively effects severity of clinical parameters and results of treatment. This particular
study, which included 16 epidemiological studies (23544 cases), showed that childhood abuse is related to recurrent and persistent
depressive episodes. Another meta-analysis of 10 clinical studies with a total of 3098 cases, found that childhood abuse is related to
absence of remission and absence of treatment response in depression.
In bipolar disorder, those who have had childhood trauma, had earlier onset of illness, more severe current symptoms of mania or
depression and more frequent episodes of depression. Half of adult bipolar disorder patients were found to have severe childhood trauma.
In patients with early childhood trauma such as early loss of parents and physical or sexual abuse or neglect, psychotherapy alone had
favorable results compared to monotherapy of antidepressants, while interestingly combination of psychotherapy and pharmacotherapy
was slightly more effective than psychotherapy alone. Researchers have stressed that psychotherapy must be included in the treatment
of chronic depression patients with childhood trauma.
Studies which directly investigate the relationship of treatment resistance and childhood trauma are scarce. Some comorbid conditions,
such as personality disorders, that complicate treatment of depression are known to be related to childhood trauma.
As a result, we can with great confidence state that childhood trauma is related to treatment resistance in most psychiatric conditions.
Especially in cases of treatment resistance, childhood trauma should be investigated and appropriate treatment modalities should be
added to the treatment regime.
Key words: Treatment resistance, childhood trauma
Pyshosocial approaches for treatment resistant symptoms in patients with schizophrenia
Mustafa Yıldız
Kocaeli University School of Medicine, Department of Psychiatry, Kocaeli, Turkey
One of the main goals in the treatment of schizophrenia is to increase psychosocial functioning and to provide a satisfying life for patients
with schizophrenia who have persistent symptoms although all treatment efforts, including ECT, had been performed. Whatever the
clinical conditions of the patients are, they have a right to live in dignity in their community like other people. The emphasis in psychiatric
rehabilitation approaches is on enhancing psychosocial functioning and quality of life of patients. Increasing the functioning of patients
depends on controlling symptoms as much as possible and preventing exacerbations. Patients should learn and practice coping skills
(humming or singing, reading aloud, thinking “stop”, listening to the radio, watching TV, doing favorite hobbies, telling the voices to go
away, doing physical exercise, going to movies etc.) for their persistent symptoms. Sometimes it may be necessary to use behavioral
techniques; for example, a patient showing 20 aggressive behaviors due to command hallucinations a week, showed on aggressive
behavior a month after applying a behavior modification program. Patients should be placed in a program, in which their healthy
aspects can be developed and keep them in continuing daily activities, so that they become empowered. All these results can take place
by collaboration and coordination of different services. Being provided a safe environment, getting positive feedback, participating in
occupational activities and working in a less stimulating milieu are also important for patients.
It could be possible for patients to live a more satisfying and more normal life by integrating treatment and rehabilitation services. The
elements of integrated approaches are: patients’ participation in treatment and the maintenance of treatment, development of treatment
alliances, teaching illness management, using cognitive behavioral treatment methods, modifying new resources to attain personal
goals, accommodating community resources, establishing relationships with psychosocial clubs, involving families in the treatment, and
providing personal support services (case management), supported employment, supported residence, and peer supports.
Key words: Schizophrenia, persistent symptoms, functioning, rehabilitation
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[PS-18]
Symposium Title: Chronobiotics and chronotherapeutics in psychiatry
The use of sleep deprivation in the treatment of depressive disorders
Adem Aydın
Department of Psychiatry, Yuzuncu Yıl University, Van, Turkey
Sleep deprivation has been used for exploring functions of sleep among healthy individuals and for treating patients suffering from
depressive symptoms. Sleep deprivation is a rapid, effective and brief therapeutic alternative. Two types of sleep deprivation applications
have been implemented; one is deprivation of sleep for whole night and the other is partial deprivation of sleep in the second part of
the night. Although various hypotheses have been developed pertaining to the treatment potential of sleep deprivation in depression,
the mechanisms underlying the process are still obscure (1). Early systematic research conducted by Pflug and Tolle proposed that
patients characterized by endogenous depressive symptoms receptive to sleep deprivation have deficits in their circadian systems and
sleep deprivation aids at ameliorating the dysregulation in the biological rhythm (2). Sleep deprivation and REM sleep deprivation act
like antidepressants and some antidepressants have suppressing effects on REM sleep. Hence the role of REM sleep on the development
of depression has received more attention. The reduction of REM latency and REM intensity are prominent features in patients with
depression. Sleep deprivation reverses these two effects (3).
The psychological response to sleep deprivation seems to occur regardless of diagnostic category such as endogenous-reactive,
psychotic, nonpsychotic, unipolar, bipolar, schizoaffective, or seasonal (4). Merely diurnal variation (soothing of affect is typical in patients
with depression in the later hours of daytime) and chronobiological differences are substantial in the psychological response to sleep
deprivation (5).
About 50-60 percent of patients with depression are prone to reflect antidepressant influences after one-night of sleep deprivation
therapy. Deceleration in symptom severity as well as amelioration in suicidal thoughts occurs. The temporary antidepressant influence of
the initial application does not predict inadequacy of further applications. If applications of sleep deprivation are continued one or two
times per week, it has been claimed that it is likely to provide effective prophylaxis (6).
Although sleep deprivation provides a rapid psychological response and a potent influence, its application is not prominent in major
depression. Sleep deprivation can be qualified as an awkward method, because the application requires constant monitoring and to
ensure wakefulness of patients as well as carrying a relapse risk in fiesta. The most prominent advantage of sleep deprivation compared
to other medications and ECT is that it causes rapid and apparent improvement in affect. Therefore the pros and cons of sleep deprivation
should be taken into account in treatment planning.
Key words: Depression, sleep deprivation, treatment
References:
1.
Rechtschaffen A. Current perspectives on the function of sleep. Perspect Biol Med 1998;41:359-390.
2. Pflug B, Tolle R. Disturbance of the 24 hour rhythm in endogenous depression and treatment of endogenous depression by sleep deprivation. Int
Pharmacopsychiatry 1971;6:187-196.
3.
Giedke H, Schwarzler F. Therapeutic use of sleep deprivation in depression. Sleep Med Rev 2002;6:361–377.
4.
Wirz-Justice A. Biological rhythm disturbances in mood disorders. Int Clin Psychopharmacol 2006;21:11-5.
5.
Selvi Y, Gulec M, Agargun MY, Besiroglu L. Mood changes after sleep deprivation in morningness–eveningness chronotypes in healthy individuals. J Sleep Res
2007;16:241–4.
6.
Hemmeter UM, Hemmeter-Spernal J, Krieg JC. Sleep deprivation in depression. Expert Rev Neurother 2010;10(7):1101-15.
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Psychotropic drugs effecting biological rhythm (Chronobiotics)
Elif Oral
Department of Psychiatry, Faculty of Medicine, Atatürk University, Erzurum, Turkey
Biological clocks such as circadian, ultradian, and infradian rhythms have their own organizations, independently from environmental
conditions. Although there is biological sustainability, psychiatric disorders and also psychotropic medications have important effects
on the synchronization of biological clocks. Various biological mediators such as glutamate, γ aminobutyric acid, histamine, dopamine,
acetylcholine, serotonin and their receptor systems take on the mediation of inner clocks via psychotropic drugs.
Histaminergic activity is highly increased during wakefulness. H1 antagonists, generally increase Slow-Wave Sleep and stage 2 sleep
and reduce rapid eye movement sleep. Diphenhydramine can cause subjective sedation and decreased sleep latency with no effect
on memory or learning processes. The long elimination half-lives of these drugs can result in next-day sedation and impairment of
psychomotor and cognitive function the next morning.
Benzodiazepines shorten sleep-onset latency, increase total sleep time and stage 2 sleep, and suppress rapid eye movement sleep and
slow-wave sleep. The risk of rebound insomnia is greatest with rapid elimination of benzodiazepines.
About 65% of major depressive disorder patients report sleep complaints. Based on polysomnography studies, sleep architecture is
estimated to be disturbed in up to 90% of depressed patients. Except desipramine, all TCAs block H1 and α1 receptors to varying degrees.
As a general rule, the noradrenergic TCAs (e.g. desipramine, protriptyline) are considered ‘activating’. These agents have a tendency to
increase sleep-onset latency as well as to decrease total sleep time, associated with an increase in wake time after sleep onset. Paroxetine
and fluoxetine clearly suppress REM sleep, both among healthy volunteers and depressed patients. Compared to other SSRIs, citalopram
may be less activating and therefore less likely to disrupt sleep continuity.
Lithium and valproate have many acute, subacute, and chronic effects on systems, at the cellular and molecular levels. Lithium treatment
modifies circadian rhythms in humans and in most animals, primarily by lengthening the period of the cycle.
Most of the sleep-promoting effects of antipsychotic drugs have been related to their potency to antagonize α adrenergic, histaminergic,
or cholinergic neurotransmission. Among classical antipsychotics, drugs having these properties, such as phenothiazines and
thioxanthenes, are clearly sedative and promote sleep. Among atypical antipsychotics, drugs having this pharmacodynamics profile are
olanzapine, clozapine, and quetiapine. Clozapine and olanzapine increase total sleep time and sleep efficiency and have no clear-cut
effect on REM sleep.
Key words: Psychotropic drugs, biological rhythm
Yavuz Selvi
Department of Psychiatry, Yuzuncu Yil University, Van, Turkey
The sleep-wake cycle occurs because of the two independent but additive processes, homeostatic sleep and circadian processes. Circadian
rhythms play a significant role in regulating daily behavioral rhythms, cortisol and melatonin secretions, body temperature, sleep/wake
cycle, alertness and performance levels. Disrupted synchronization of circadian rhythms impairs cognition, behavior and mood with
deterioration of sleep-wake cycle and social rhythms. Some clinical and neurobiological findings suggest circadian dysregulation in
depressive patients. Diurnal variation of mood, early morning awakening, phase advance for body temperature, cortisol, latency of the
first phase of REM sleep for several other hormones and monoamines or their metabolites and sleep disturbances are core features of
depression that have linked depression with circadian rhythm function (1,2).
Clinical and neurobiological findings have promoted the idea that the restoration of circadian rhythm could have an antidepressant effect.
The term, chronotherapeutics, refers to biologically-based, non-pharmaceutical and clinical interventions that act on disrupted biological
rhythms in order to achieve therapeutic effects in the treatment of psychiatric conditions (3). Delayed therapeutic effects, tolerability,
side effects, and drug–drug interactions of pharmacotherapeutic agents, as well as pregnancy and the postpartum period, prevent
antidepressant use and promote chronotherapeutic interventions.
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Chronotherapeutics are applied effectively in endogenous, reactive, unipolar, bipolar, schizoaffective depression, depression in the
elderly, secondary depression, depression in pregnancy and postpartum depression. The target of chronotherapeutic interventions, as
in antidepressant drug treatments, is to modulate the same neurotransmitter systems (5-HT, NA, DA), the same brain structures, and the
same clinical symptoms and findings more rapidly and with fewer side effects. These interventions include wake therapy (the use of
prolonged periods of wakefulness; partial or total sleep deprivation), shifting of sleep time (sleep phase advance therapy; stepwise shift
forward of the sleep-wake cycle to the early evening); bright light therapy in correct time and sufficient dose, and dark or rest therapy for
bipolar mania and rapid cycling patients. When the therapeutic effects are transient, different chronotherapeutic interventions can be
combined to maximize antidepressant response and prevent relapse. Psychiatrists should consider chronotherapeutic interventions as
strong and safe treatment approaches (3,4).
Key words: Biological rhythm, chronotherapeutics, mood, sleep, sleep deprivation
References:
1.
Lack LC, Wright HR. Chronobiology of sleep in humans. Cell Mol Life Sci. 2007; 64(10):1205-15.
2.
Selvi Y, Besiroglu L, Aydin A. Chronobiology and Mood Disorders. Current Approaches in Psychiatry 2011; 3(3):368-386.
3.
Benedetti F, Barbini B, Colombo C. Smeraldi E. Chronotherapeutics in a psychiatric ward. Sleep Med Rev. 2007;11(6):509-22.
4.
Hajak G, Landgrebe M. Time and depression: when the internal clock does not work. Medicographia. 2010;32:146-151.
Bright light therapy in treatment of depressive disorders other than seasonal affective disorder
Mustafa Güleç
Department of Psychiatry, Ataturk University, Erzurum, Turkey
Studies of light therapy for non-seasonal depression have a history at least as long as studies of seasonal affective disorder (SAD), but
on the whole the results have been less clear-cut (Tuunainen et al., 2005). The APA work group found, within its selection, positive
evidence for efficacy except when light therapy and medication were combined (Golden et al., 2005). Studies completed by the time
of the present congress clearly would have reversed that conclusion (Benedetti et al., 2003; Martiny, 2004; Terman, 2006). The strategy
has been recommended by the Committee on Chronotherapeutics of the International Society for Affective Disorders (Wirz-Justice et
al., 2005) and in an international response (Wirz-Justice et al., 2004) to a review of new antidepressants that overlooked light therapy,
published in Science (Wirz-Justice et al., 2004). A difficulty with most non-seasonal studies has been their inability to confront the early
hypothesis that light therapy is specifically tuned to patients with SAD as a countermeasure to long winter nights. Seasonality lies on a
continuous dimension from noticeable (but not disturbing) to mildly, moderately and severely disturbing (Terman, 1988). SAD falls into
the latter category, with major depressive episodes restricted to winter. In a far larger number of cases, recurrent or chronic depressions
are exacerbated in winter but can occur at any time of year. Such patients provide moderate global seasonality scores (Rosenthal et al.,
1987) in comparison to higher scores for SAD. Thus, patients with non-seasonal depressions can still show seasonality, which might be
the key to their response to light therapy. Subsequent to the aforementioned inconclusive meta-analysis of light therapy for non-seasonal
depression (Tuunainen et al., 2005), some researchers conducted an investigation to clarify this issue with a patient sample in which
depression was chronic and without any seasonal modulation (Goel et al., 2005). Under morning light therapy, the proportion of subjects
with depression rating scale improvement of 50% or more was 0.60 vs. 0.10 for the low-output negative air ionizer placebo. Moreover,
there are also very recent reports claiming that bright light therapy alone is effective in some patient groups with non-seasonal major
depression (Kripke, 2011a; Kripke, 2011b; Martiny, 2011). Now, we can begin to surmise that light therapy for seasonal and non-seasonal
depression is equally effective. Perhaps the patients with non-seasonal depression are light deprived at any time of year, and this situation
results in exacerbation of circadian rhythm phase delay, given the absence of the critical early morning light signal that synchronizes the
internal clock to local time. Such delay may be depressogenic regardless of the season. However, the growing concern about medication
side effects would seem to fit well for our old-new alternative (Terman, 2007).
Key words: Seasonal affective disorder, non-seasonal affective disorder, depression, treatment, bright light
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[PS-19]
Symposium Title: Are the effects of psychopharmacological and other therapeutic approaches neuroregenerative or
neurodegenerative? Review of recent data
Is the effect of psychotropic drugs neurodegenerative or neuroprotective?
Ömer Aydemir
Department of Psychiatry, Celal Bayar University, Manisa, Turkey
Various stress experiences affect gene expression of neurotrophic/growth factors in the hippocampus. Among the neurotrophic factors,
brain-derived neurotrophic factor (BDNF) has the most prominent role. With the stress producing effects of early life traumas, the level
of BDNF decreases and susceptibility to depression develops. Recurrent and insufficiently treated depressive episodes have further
impact on decreased BDNF and increase neuronal atrophy. Decreased level of BDNF in patients with major depressive disorder has been
demonstrated in many studies and BDNF levels increase after antidepressant treatment, along with symptom recovery, in comparison
to those seen in healthy control subjects. This increase cannot be achieved in patients that do not respond to antidepressant treatment.
The neuroprotective effect of antidepressants are mediated by mitogen activated protein kinases/extracellular regulated kinases (MAPK/
ERK) and wingless/glycogen synthase kinases (Wnt/GSK). In a meta-analysis, 23 studies were evaluated and data for 1504 patients were
subjected to statistical analysis. The effect size was calculated as 0.62 (95% confidence interval: 0.36-0.88). As a result of meta-regression,
the change in the level of serum BDNF after antidepressant treatment was independent of the change in depressive symptomatology,
duration of treatment, and history of antidepressant use. As clinical improvement obtained with antidepressant treatment persists, the
level of serum BDNF remains unchanged.
Beside antidepressants, mood stabilizers, especially lithium have been studied with respect to neuroplasticity. Neuroprotective effects of
mood stabilizers are mediated by increasing transcriptional activity of (cAMP response element binding protein) CREB, inhibiting GSK-3B
and increasing the expression of BDNF. In studies both with lithium and valproate, increased cerebral grey matter volume was reported.
In lithium studies increases in left anterior cingulate volume, right anterior cingulate volume, hippocampal volume and amygdala volume,
and in valproate studies an increase in left anterior cingulate volume were found. Both mood stabilizers are associated with increased
hippocampal N-acetyl aspartate level.
Antipsychotic drugs do not have a group effect. While haloperidol does not have any effect on phosphorilated ERK (pERK), olanzapine
increases it. Haloperidol also decreases the level of BDNF and is suggested to have neurotoxic effects. Among the other antipsychotics,
clozapine, quetiapine and risperidone prevent cell death. It has been demonstrated that clozapine and quetiapine increase the level of
BDNF. Quetiapine is suggested to increase proliferation of mature neurons, although there is no evidence that clozapine and olanzapine
have the same effect.
Key words: Psychotropic drugs, neuroplasticity, neurodegeneration, neuroprotective effect
Effect of psychotherapy on neurogenesis
Mine Özmen
Istanbul Universit Cerrahpasa Medical Faculty, Department of Psychiatry, İstanbul, Turkey
Adverse life experiences in childhood are considered to be associated with emotional and cognitive development as well as brain
structure and functions. It is suggested that they might reduce neurogenesis, which in turn may cause memory, learning, functional
stress response disturbances. It is known that hippocampal neurogenesis is affected by stress, hormones, aging, environment and activity.
Exposure to acute or chronic stress may result in suppression of one or more phases of neurogenesis. In animal studies, reduction of
neurogenesis in the caudal part of the hippocampus was shown after maternal separation of 3-weeks old rats. Although it was reported
that the suppression was reversible after appropriate time and treatment in some studies, some other writers suggest that early life stress
in the first 2 weeks can cause irreversible reduction in neurogenesis. Besides, there is an argument that neurogenesis can not increase by
learning in the animals which were exposed to prenatal stress. One suggested reason for this lifetime persistency of reduced neurogenesis
is that stress occurring in early childhood coincides with the development of dentate gyrus. It has been shown that corticosteroids
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inhibit neurogenesis in the hippocampus, subventricular zone and olfactory epithelium and this inhibition can remit by pharmacological
treatments. There are case reports and studies with limited cases, which suggest that effective psychotherapy can reduce symptoms and
this reduction can change the in the hypothalamic-pituitary axis. It may be hypothesized that in an effective psychotherapy process,
coping with stress, new relationship experiences and learning can increase neurogenesis and this may be one of the mechanisms of
effectiveness of psychotherapy. This hypothesis should be tested with animal and human studies in which neurobiology; psychiatry and
neuroscience disciplines can interact and work together.
References:
1.
Korosi A et al. Early-life stress mediated modulation of adult neurogenesis and behavior. Behav Brain Res. (2011) doi:10.1016/j.bbr.2011.07.037
2.
McEven BS. Stress, sex, and neural adaptation to a changing environment: mechanisms of neuronal remodeling. Ann NY Acad Sci 2010 Sep;1204 Suppl:E38-59.
3.
Miranda Olffa, Giel-Jan de Vriesa, Yener Guzelcana, Johanna Assiesc, Berthold P.R. Gersons. Changes in cortisol and DHEA plasma levels after psychotherapy for
PTSD. Psychoneuroendocrinology (2007) 32, 619–626
Are the effects of psychopharmacological and other therapeutic approaches neuroregenerative or
neurodegenerative? Review of recent data and effects of physical exercise
Hakan Balıbey
Ankara Military Hospital, Psychiatry Clinic, Ankara, Turkey
Research in humans and animals has shown that exercise improves mood and cognition. Physical activity has been consistently shown
to be associated with improved physical health, life satisfaction, cognitive functioning, and psychological well-being. Conversely, physical
inactivity appears to be associated with the development of psychological disorders.
Physical activity also causes a robust increase in neurogenesis in the dentate gyrus of the hippocampus, an important brain area
for learning and memory. The results of epidemiological studies (cross-sectional, prospective and retrospective) support a positive
relationship between cognition and physical activities. They include supramolecular mechanisms (e.g. neurogenesis, synaptogenesis,
and angiogenesis) which, are in turn controlled by molecular mechanisms, such as brain-derived neurotrophic factor (BDNF), insulin-like
growth factor (IGF-1), hormones and second messengers.
An active lifestyle might prevent or delay loss of cognitive function with aging or neurodegenerative disease. Exercise could involve
common cellular pathways important for neurogenesis, cell survival, synaptic plasticity and vascular function. Optimal maintenance of
brain health might depend on exercise. The beneficial effects of exercise are likely to be mediated in part by hippocampal neurogenesis.
Further investigation into the functional significance of neurogenesis, by designing behavioral tasks that are specific for the dentate gyrus,
will help to determine the relative contribution of the new cells.
Exercise influences brain vasculature. In particular, physical activity increases the proliferation of brain endothelial cells and angiogenesis
throughout the brain. Growth factors such as insulin-like growth factor (IGF) and vascular endothelial growth factor (VEGF) play an
important role in the angiogenic and neurogenic effects of exercise on the brain. The neurotrophin BDNF is considered to be the most
important factor upregulated by physical activity because it has an important role in synaptic plasticity and cell genesis, growth and
survival. Interestingly, there is a positive interaction between BDNF expression and serotonin. Serotonin receptor activation enhances
BDNF expression in hippocampal cells, BDNF is recognized to be a key protein modulating brain plasticity and it is distributed widely
throughout the brain. In humans, serum BDNF concentrations rise after exercise.
The involvement of such pathways, particularly in the hippocampus, may in turn lead to an improvement in cognitive function,
enhancement of psychological well-being, and a decrease in the risks of Alzheimer’s disease (AD) and dementia as well as decreases in
symptoms of depression and anxiety. While intense exercise (as observed in conditions such as “excessive exercise” and “overtraining
syndrome”) leads to a lessening of anxiety, these mood variations are more related to the construct of depression than to the construct
of anxiety.
Physiological effects of exercise and the benefits of exercise on psychiatric disorders will be discussed in the light of current literature in
this presentation.
Key words: Physical activity, exercise, BDNF, hippocampal neurogenesis, neuroregeneration, neurodegeneration, synaptic plasticity, cognition,
mood
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References:
1.
Lista I, Sorrentino G. Biological mechanisms of physical activity in preventing cognitive decline. Cell Mol Neurobiol. 2010;30(4):493-503.
2.
van Praag H. Exercise and the brain: something to chew on. Trends Neurosci 2009;32(5 ):283–90.
3.
Little Exercise, Big Effects: Reversing Aging and Infection-Induced Memory Deficits, and Underlying Processes. Barrientos R. M., Frank M.G, Crysdale N.Y, Chapman
T.R, Ahrendsen J.T at all. The Journal of Neuroscience, 2011; 31(32):11578 –86.
4.
Christofoletti G, Oliani M.M, Bucken L.T, Gobbi S, Beinotti F, Stella F. Physical activity attenuates neuropsychiatric disturbances and caregiver burden in patients
with dementia. Clinics (Sao Paulo). 2011; 66(4): 613–8.
5.
Ma Q. Beneficial effects of moderate voluntary physical exercise and its biological mechanisms on brain health. Neurosci Bull. 2008;24(4):265-70.
6.
van Praag H. Neurogenesis and exercise: past and future directions. Neuromolecular Med. 2008;10(2):128-40.
7.
Ang. ET, Tai YK, Lo SQ, Seet R, Soong TW.Neurodegenerative Diseases: Exercising Toward Neurogenesis and Neuroregeneration. Front Aging Neurosci. 2010; 2: 25.
8.
Tomporowski P. D., Lambourne K., Okumura M. S. Physical activity interventions and children’s mental function: an introduction and overview. Prev Med. 2011;
52(Suppl 1): S3–S9.
9. Fadillioglu E., Kaya B., Uz E., Emre M.H., Ünal S. Effects of Moderate Exercise on Mild Depressive Mood, Antioxidants and Lipid Peroxidation. Bull Clin
Psychopharmacol 2000; 10(4):194-200.
[PS-20]
Symposium Title: Controversial topics in eating disorders
Atila Erol
Sakarya University, School of Medicine, Department of Psychiatry, Sakarya, Turkey
Patients with eating disorders exhibit high rates of psychiatric comorbidity and the number of comorbid psychiatric disorders is high.
The treatment of co-occurring psychiatric problems in eating disordered patients is essential for good clinical management and the
outcome of treatments. Higher rates of comorbidity often mean greater severity, treatment resistance and poor outcomes in eating
disorders. The most prevalent Axis I disorders seem to be mood and anxiety disorders, alcohol and substance abuse, and bipolar disorder.
Axis II disorders are also common. At least 80% of anorexia nervosa (AN) or bulimia nervosa (BN) patients have at least one additional
psychiatric disorder over their lifetime. Mood disorders are very common among patients with AN. Major depressive disorder occurs in
50-70% of AN patients. Bulimic patients have 52-75% affective disorder, with 63% having major depression. Lifetime prevalence rates of
major depression in BN are 50-65%.
Among study samples with restricting and binging /purging anorexia nervosa, prevalence rates of any anxiety disorder are found to be
between 24% and 71%, respectively. Among patients with BN prevalence rates for any anxiety disorder, social phobia, generalised anxiety
disoder (GAD) or panic disorder are reported to be 36%, 17%, 12% and 10% respectively. The approximate rates of any anxiety disorder in
BN are reported to be between 57 and 75 %.
Thirty-five percent of restricting AN patients have obsessive compulsive disorder (OCD) and binging/purging AN patients have 44% OCD.
BN patients have comorbid OCD 40% of the time. Lifetime prevalence rates of substance abuse in AN ranged from 12% to 18% and in
BN the rates ranged from 30% to 70%. The results of clinical studies indicate that patients with BPD have higher rates of eating disorders
compared with the general population. Rates of lifetime BPD in eating disorders patients are variable but higher than rates of BPD in the
general population. Among eating disorder patients post-traumatic stress disorder rates were found between 8% to 11%.
Key words: Eating disorders, anorexia, bulimia, comorbidity
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Alican Dalkilic
St. Elizabeths Hospital, Washington, DC 20032, USA
Pharmacological treatment options have limited evidence of benefit in treatment of eating disorders, yet a comprehensive psychiatric
evaluation besides a physical exam and basic screening tests (complete blood count (CBC), basic metabolic panel, Mg, P, thyroid
stimulating hormone (TSH), lipid panel, pregnancy test, urine analysis (UA), urine drug screen (UDS), ECG, and Dexa scan) should be
conducted. Establishing a therapeutic alliance with empathy, positive regard, reassurance, and support (1) sets up the foundation for a
successful treatment process. The patient’s safety should be evaluated with particular attention paid to suicidal ideation, plans, intentions,
history of attempts and impulsive or compulsive self-harm behaviors. After assessing eating disorder symptoms, signs, and behaviors and
the general medical condition of the patient a decision about treatment site (specialized inpatient unit, residential treatment or partial
hospital program, intensive outpatient, or outpatient care) can be made. In eating disorders in general, but especially in adolescences with
eating disorders, inclusion of the family and primary support group in the treatment process is essential.
The treatment options and goals in eating disorders include nutritional rehabilitation, psychosocial interventions, medications, and other
somatic treatments. Nutritional rehabilitation aims to restore weight, normalize eating patterns, achieve normal perception of hunger
and satiety cues, and correct biological and psychological problems caused by malnutrition (1). Psychosocial interventions include
individual and group based cognitive behavioral and interpersonal therapies, acceptance and mindfulness therapies, and psychodynamic
approaches, as well as nutritional counseling, dialectical behavioral therapy (DBT), and family therapies. There are more therapies with
specific names such as mealtime support and multifamily group therapy, but they use similar approaches to the previously mentioned
ones.
Although there is clinical evidence about use of antidepressants in treatment of eating disorders (especially SSRIs, calcium, vitamin D,
and zinc and limited data about benzodiazepines, mood stabilizers, and atypical antipsychotics), so far only fluoxetine is approved for the
treatment of bulimia nervosa by the Federal Drug Administration (FDA) 1,2). Sertraline has been found to be effective in a randomized
and controlled trial, as well. Medications have not been proven to be more effective than psychosocial interventions in treatment of eating
disorders so far. Some studies have found the combination of CBT with medication to be more effective. Topiramate has been found to
be effective in some small controlled trials especially in reducing binging behavior, but due to potential side effects is should be reserved
as a secondary medication (1,3). Topiramate or zonisamide are prescribed to target binging behavior and also for weight reducing effects
in patients who may benefit from weight loss. Bright light therapy is another intervention demonstrated to decrease binge frequency in
several controlled trials (1).
Although clinicians are advised to use caution when prescribing medications to eating disorder patients due to potentially dangerous
medical co-morbidities, some medications should be avoided or used only as last resorts. Bupropion is contraindicated in bulimia due to
a heightened seizure risk (1,3). Medications that increase the risk of arrhythmia or prolong the QTc interval should be avoided or if they are
used, adverse events should be monitored closely. Sibutramine was taken off the market in USA in 2010 due to cardiac adverse events. In
addition, medications with a narrow therapeutic range such as lithium should be avoided. Benzodiazepines, especially the ones with high
addiction potential, should not be used in patients with addiction risk. In clinical practice many eating disorder patients end up being on
multiple medications due to high rates of co-morbidity with anxiety and mood disorders, substance abuse and dependence conditions,
trauma related disorders, and personality disorders. Beside reviewing pharmacological treatment options in eating disorders we will also
discuss the management of cases with co-morbid conditions.
Key words: Eating disorders, pharmacology, pharmacotherapy, treatment, pharmacological treatment
References:
1. American Psychiatric Association Practice Guidelines for the Treatment of Psychiatric Disorders Compendium. American Psychiatric Association 2006 1,612
pages ISBN 978-0-89042-385-1.
2.
Pharmacotherapy of eating disorders. Jackson CW, Cates M, Lorenz R. Nutr Clin Pract. 2010 Apr;25(2):143-59. Review.
3.
Psychopharmacology of eating disorders in children and adolescents. Golden NH, Attia E. Pediatr Clin North Am. 2011 Feb;58(1):121-38, xi. Review.
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Bilge Burçak Annagür
Department of Psychiatry, Selcuk University, Selcuklu Medical School, Konya, Turkey
Obesity is not inlcuded in eating disorders characterized by the DSM-IV classification of the American Psychiatry Association. Current
clinical diagnosis depends on body mass index (BMI). Although it was not evaluated among eating disorders, it presents psychological
characteristics seen commonly in eating disorders. Characteristics related with eating disorders such as low self-esteem, body
dissatisfaction, perfectionistic attitudes, impulsivity and disinhibition have also been observed in obese patients (1,2). Obese patients are
divided into two subgroups, with or without binge eating disorder (BED). Body weights of subjects with binge eating disorder are related
to their overeating and psychopathologies, especially depression, are more frequent compared to the other group.
Aggressiveness and anger are involved in significant psychopathological characteristics common in patients with eating disorders (3).
Some researchers suggested that impaired eating behavior is related to low self-esteem and high self-directed hostility. Problems about
revealing their anger were detected among these individuals. Besides, problems in controlling the expression of anger, accompanying
impulsive explosive behaviors are also present (4).
The current status of obesity treatment is not satisfactory. Some treated individuals regain the lost weight in a short time (5). Many
researchers are investigating approaches to keep off the lost weight with treatment strategies to lose weight. In previous reports, it has
been demonstrated that most obese individuals returned back to their basal BMIs or to higher values within 1-5 years (6). Nowadays, the
question is ‘What is the difference between the ones who keeps off the weight they lose and those who do not?’. Impulsivity is the possible
predictor of relapse in obesity treatment (5). Obese subjects are suggested to be more impulsive than lean ones. Impulsive characteristics
are higher in obese patients with BED (7). Impulsive people appear to have no control over their behaviors on eating and they have more
interest in food with higher calories. Impulsivity is also considered as a predicting factor among patients who quit treatment. In a survey
among the children between the ages of 8-12 years in the Netherlands, impulsivity was measured by behavior and the results of treatment
were evaluated. As a result, it was demonstrated that impulsive children lose less weight compared to the others. It was also concluded
that impulsive children are more prone to eating delicious foods; therefore more attention should be given to their dietary control (5).
Another issue supporting the relationship between obesity and impulsivity is the occurrence of obesity in children with attention deficiency
and hyperactivity disorder (ADHD) (8). ADHD was detected in most of the children (58%) who were receiving obesity treatment. Also, the
BMI of children with ADHD was higher than the control group (9). In addition, there is evidence for decreased levels of D2 receptors in
the striatum of obese subjects (10-13). With regard to the therapeutic implications, recent studies indicate that methylphenidate (MPH),
a drug widely used for ADHD, reduced overall energy intake with a selective reduction in dietary fat (14,15). Dopamine (DA) exerts
neuromodulatory influences over behavior and cognition via the fronto-striato-cerebellar circuitry and pharmacotherapy is thought to
target these systems to ameliorate problems with impulsivity, inattention and hyperactivity. To explain the comorbidity of ADHD and
obesity, it has been hypothesized that a predisposition to glucose starving and obesity is due to inadequate dopaminergic activity in the
reward center of the brain. Consumption of large quantities of carbohydrates (carbohydrate binging) stimulates production and usage of
dopamine within the brain and it results in a kind of therapeutic effect (16,17).
All this information should guide the planning of treatment. Specific cognitive behavioral approaches developed for the treatment of
impulsive behavior could contribute much to the treatment of obesity(18).
Key words: Eating disorders, impulsivity, obesity
Başak Yücel
Department of Psychiatry, Istanbul University, Istanbul, Turkey
The efficacy and importance of psychotherapy in bulimia nervosa have been examined in many studies recently. Most of the eating
disorder experts acknowledge the notion that psychological interventions are the best available treatment for BN. Although different
psychotherapeutic recommendations have been offered by NICE (National Institute for Health and Clinical Excellence) and APA (American
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Psychiatric Association), several treatment approaches received strong endorsement for BN. Cognitive behavioral therapy (CBT) is
recommended as an effective treatment for bulimic patients and considered the ‘treatment choice’ for BN and binge eating disorder (BED),
it is also supported by strong evidence-based literature.
With regard to the efficacy of CBT specifically in BN, in various studies CBT was associated with more improvements in bulimic and
depressive symptoms of patients than symtoms of control patients in waiting-list and any other psychotherapy cases. In terms of general
psychiatric symptoms, studies have not shown any difference between CBT and any other psychotherapy.
Other psychotherapy choices have included interpersonal psychotherapy (IPT), dialectical behavior therapy, supportive and psychodynamic
psychotherapy, and certain self-help approaches. Thus, in clinical practice there have been a number of evidence-supported treatments
for BN patients.
IPT is a psychological treatment for BN that has demonstrated long-term outcomes that are comparable to those for CBT. Currently,
all controlled studies of IPT for BN have been comparison studies with CBT. Although there have been only few controlled trials of
psychodynamic treatment of eating disorders, these reports yielded important findings in this field. Standard dialectical behavior therapy
(DBT) has been adapted to address a variety of problematic behaviors associated with emotion dysregulation in bulimia nervosa and
also DBT may be used in BN patients with comorbid borderline personality disorder. Beside these, the knowledge in the field of self-help
treatments continues to develope.
Key words: Bulimia nervosa, psychotherapy
[PS-21]
Symposium Title: Treatment approaches to comorbidities of ADHD
Tümer Türkbay
GATA, Department of Child and Adolescent Psychiatry, Ankara, Turkey
Attention-deficit hyperactivity disorder (ADHD) is highly comorbid with other psychiatric disorders. Each of the comorbid disorders
modifies the overall clinical presentation and treatment response. Sometimes there can be more complex situations. For example,
depressed children demonstrate diminished concentration and irritability and it may be difficult to differentiate from the cardinal
symptoms of ADHD. Children with ADHD and comorbid disorders have poorer prognoses than those with ADHD alone.
Both stimulant medications and atomoxetine markedly reduce symptoms of comorbid oppositional defiant disorder, which often requires
adjunctive parent training and behavior management. Severely explosive anger may require the use of atypical antipsychotics. In conduct
disorder, stimulant medications and atomoxetine also reduce aggressive behavior and antisocial acts. Atypical psychotics or mood
stabilizers may be used for highly aggressive-explosive cases.
The majority of children with comorbid ADHD/depression can be managed with a psycho stimulant. However, initial treatment with
antidepressant drugs should be saved for treating children with more severe depression. Stimulants can exacerbate symptoms of anxiety
disorders. Atomoxetine, SSRIs and behavioral therapies reduce anxiety symptoms.
If tic disorders are mild or episodic, they usually require no treatment. Most ADHD/tic disorder patients will not demonstrate an
exacerbation of their tics with stimulants. Nevertheless, if tics worsen with stimulant use, an antipsychotic or alpha agonist should be
added to the psychostimulant.
Key words: Attention deficit hyperactivity disorder, comorbidity, management
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Bengi Semerci
Institute, Istanbul, Turkey
Adolescences with ADHD, who suffer from social problems, are under risk of depression, anxiety, destructive conduct disorder, and drug
addiction. If there are co-morbid disorders associated with ADHD, it makes the treatment difficult and causes some other complications.
The fundamental treatment principles of the psychiatric co-morbidities of ADHD are also effective for adolescence period. However,
especially, we should be careful about the conditions that have high prevalence during adolescence period and the conditions which
affect prognosis in a negative way. These situations need to be assessed in diagnosis and treatment plan.
Anxiety Disorders: Some researches indicate that a stimulant treatment has small effects on anxiety disorder. The treatment of ADHD
without anxiety disorder gets more successful results. However, according to recent research, treatment is also effective on anxiety
disorder.
In general, considering the effect of CBT on the anxiety disorder treatment, it is suggested that CBT beside medication treatment is
effective on ADHD having co morbidity with anxiety disorder. If there is co morbidity, it is suggested that the priority needs to be given
to ADHD and that if the anxiety symptoms continue, another medication treatment should be considered.
Mood Disorders: Depression is an important problem in adolescence period. The important point in treatment is to identify that if ADHD
causes to depressive findings or major depression.
If ADHD cooccurs with major depression, both of them need to be treated. The treatment may be done either by stimulants or atomoxetine
or only by SSRIs or tricyclic anti depressants. The last option is to use the two methods both.
When there is co-morbid depression and ADHD, the efficacy of antidepressants is lower than when it is depression alone. In clinical
observation, depression findings in adolescence period should be assessed attentively. If there is major depression, the treatment should
be carried out together with ADHD. Selective serotonin reuptake inhibitors (SSRI) may be used with stimulants.
Conduct Disorders: If ADHD is not treated, it may possibly turn to conduct disorder. In many studies, the use of stimulants for the
treatment of co-morbid ADHD and conduct disorder is investigated. The results of these studies show that stimulants are effective when
the morbidities are both separate or together.
However, if there are co-morbid ADHD and conduct disorder, the effectiveness of stimulants on aggression is lower. If there are co-morbid
ADHD and aggression and if the typical ADHD treatment does not work, it may be useful to add atypical antipsychotics to the treatment. If
ADHD is co-morbid with conduct disorder, working with adolescents, using behavioural approaches, supporting families and to providing
them education about the problem may be helpful.
If ADHD co occurs with drug addiction, both disorders should be treated. Stimulants can be used in a controlled way. However, due
to addiction, prescribing stimulants may be cause legal problems. Atomoxetine and bupropion could be other options. Eventhough,
antidepressants are effective in ADHD, their effectiveness in addiction is limited.
Key words: ADHD, adolescence, co-morbidity, treatment
Treatment of neurological co-morbid disorders in children with ADHD
Murat Yüce
Department of Child and Adolescent Psychiatry, Ondokuz Mayıs University, Samsun, Turkey
Attention Deficit Hyperactivity Disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, hyperactivity, and
impulsive behaviors. ADHD is one of the most common childhood psychiatric disorders.
Children with ADHD also have many comorbid disorders and psychiatric symptoms. ADHD may be accompanied with neurological
disorders such as epilepsy, headache, and cerebral palsy. Neurological co-morbid conditions can lead to reduction in the level of function,
adherence to treatment difficulty, increasing the price of healthcare and medical complications. Therefore, diagnosis and treatment of
these neurological co-morbid problems with ADHD are important.
ADHD is seen more commonly in children with epilepsy according to the normal population. Approximately 20% of children diagnosed
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with epilepsy have ADHD as well. Some antiepileptic drugs are known to cause lethargy and impairment of attention. Barbiturates and
benzodiazepines may worsen the symptoms of ADHD. It has been reported that some drugs such as tiagabin, zonisamide, and topiramate
can cause cognitive slowing and concentration problems. Psychostimulants are frequently used in the treatment of ADHD. It has been
reported that these medications do not severely effect epileptic seizures and may improve cognitive functions.
In this presentation treatment approaches for children and adolescents with ADHD and co-morbid neurological disorders will be
discussed.
Key words: ADHD, children, neurological co-morbidity, treatment
Drug interactions of medications for comorbidities of ADHD
Osman Abalı
İstanbul Medical Faculty, Child and Adolescent Psychiatry, İstanbul, Turkey
ADHD is a very common psychiatric disorder in childhood. Children with ADHD have frequently another psychiatric disorder. Conduct
disorder, learning disorder, addiction, and mood disorders are frequently seen in children with ADHD. It has been estimated that 23%42% of youth receiving psychiatric drugs are receiving multiple drugs (1). Recently drug interactions have been emphasized in these
patients. Stimulant drugs and atomoxetine, which is a non stimulant drug, are used in patients with ADHD. Interactions between these
drugs and other psychotropic drugs are important for treatment quality. Drug interactions should be considered to prevent adverse
effects and increase treatment quality. Possible drug interactions could impact on liver, intestine, or plasma. There are a lot of important
risks due to drug interactions in patients with ADHD. Drug plasma levels can change due to CYP-P450 system interactions. It is estimated
that approximately 7% of the population may be poor metabolizers, causing slow metabolism(2). Also inhibitors of the cytochrome P450
can increase drug levels by several folds. Some drugs inhibit these systems very potently so that concentration of drug can reach very
high levels. Important complications such as neuroleptic malignnant syndrome, serotonergic syndrome, and hallucinations can be seen
during these interactions. Treatment strategies should be reviewed from this perspective. Possible drug interactions couldn’t be exactly
predicted by the clinicians for every patient. But potential drug interactions should be considered for every patient. Drug interactions will
be discussed at this presentation. The treatment strategies will be updated for long term good quality treatment based on the literature.
Key words: ADHD, drug interactions, co-morbidity
References:
1. McIntyre RS, Jerrell JM. Polypharmacy in children and adolescents treated for major depressive disoerder: a claims database study. Journal of clinical
psychiatry.2009;70(2):24-46.
2.
Barton J: Atomoxetin: a new pharmacotherapeutic approach in the managment of ADHD, Archives of disease in childhood 2005;1(90):26-29.
[PS-22]
Symposium Title: How to fight with bipolar disorder? From guidelines to clinical practice: Myths and realities
Treatment of mixed episodes of bipolar disorders in manuals. What are the recommendations?
Ahmet Ünal
Gaziantep University, Faculty of Medicine, Department of Psychiatry, Gaziantep, Turkey
There are still clinical states with uncertainties in psychiatry in terms of diagnosis and treatment. Mixed states in bipolar disorders is one
of these states. The Diagnostic and Statistical Manual of Mental Disorders – IV (DSM – IV) defines mixed states as a period in which manic
and depressive diagnosis criteria prevail together. However, observing all depressive and manic symptoms together during the mixed
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episode is not a common occurrence. The Cincinnati criterion has a more flexible approach in terms of diagnosis; a complete manic states
together with at least three depression symptoms is enough to diagnose the case as mixed mania. There are studies that identify mixed
mania as “a severe form related to mania,” “a transition period between manic and depressive episodes,” or “a separate emotional state.”
15-20% of all manic episodes have characteristics that belong to the mixed mania. In comparison to a classic manic episode, the mixed
mania has a more severe psychopathology. Episodes of dysphoria are observed more frequently, and it is frequently reported that
dysphoria is an important part of mixed states. In comparison to a classic manic episode, the duration of hospitalization is longer, the
number of attacks is higher, and the good periods are shorter during mixed episode. In addition, the psychotic characteristics and
catatonic symptoms are more, and the rate of suicide is higher.
The most important element of treating the mixed episode is making the right diagnosis. The basis used to determine the treatment
method is the same as those recommended for treating manic episodes. Unfortunately, there are no comprehensive studies that address
treating mixed mania. There are limited data related to the efficacy of medications on mixed mania or which medication is better than
the other. In general, combining drugs and clinical experiments are required for the short-term and long-term treatment of mixed mania
patients. According to the Turkish Psychiatric Association (TPA), the treatment for mixed episodes of bipolar disorder is as follows: The
treatment starts with valproate, lithium is added if the decrease in symptoms is not >25% within 4-5 days; in the event that the degree of
symptoms do not get better by 50% at the end of three weeks, an alternative is using an atypical antipsychotic and stopping the lithiumvalproate combination by gradually reducing the amount given to the patient, or moving on to a lithium – carbamazepine combination,
and if >50% progress is not reached at the end of Week 6, it is recommended that patients receive ECT.
In comparison to classic manic episodes, the rate of response to mood stabilizers for mixed episodes is lower. Antidepressants should also
not be used to treat symptoms of depression during this period. This situation proves the need for other treatment options. Olanzapine
can be used effectively in acute and preventative treatment of mixed mania; however, its disadvantages are weight gain, diabetes, and
metabolic syndrome risk. Ziprasidone has a high level of effectiveness that incorporated psychotic and mixed mania. There is evidence
that risperidone is effective in treating manic episodes; however, the amount of information related to its efficacy in mixed episodes is
limited. The number of studies about the efficacy of quetiapine on mixed episodes is also limited. The efficacy of aripiprazole on manic
and mixed episodes is addressed by some studies.
In conclusion, mixed states in bipolar disorder are common clinical reflections. Mood stabilizer treatment strategies are the form of
treatment that gives the best results. Mood stabilizer and antipsychotics can be used in the form of monotherapy or combination. Among
these mood stabilizers, valproate is the one that has been studied most and is the most recommended. Aripiprazole, ziprasidone, and
olanzapine are the antipsychotics that should be utilized first and foremost.
Key words: Bipolar disorder, mixed mania
How are the guidelines prepared? Are they necessary? How to use them?
Their benefits and limitations?
Yasin Bez
Some important points when preparing guidelines are search strategies and methods to assess evidence and the criteria for rating the
strenght of evidence and making a clinical recommendation. The development of treatment guidelines mostly aims to standardize
treatment and to provide clinicians with algorithms, which would be able to carry research findings to everyday clinical practice, by
organizing information from diverse sources into an easily accessible format (1). From this point of view, treatment guidelines may be useful
to avoid non-evidence-based treatment decisions. Thus, their common use should be supported. On the other hand, they get quickly outof-date and may interfere with following the most recent treatment approaches. Besides, they may not fully apply to the everyday clinical
setting. Besides the benefits and limitations of guidelines another important point is the adherence of the clinicians to these guidelines (1).
Despite considerable efforts to develop them, adherence to the treatment guidelines for bipolar disorders are not enough yet. For
example a study from United States demostrated adherence of 64.1% of the psychiatrists to the treatment guidelines (2). Another study
conducted in France reported a 40% non-adherence rate to treatment guidelines of bipolar disorder among psychiatrists (3).
Current and more detailed data about preparation, use, benefits, and limitations of treatment guidelines will be further discussed in this
presentation.
Key words: Bipolar disorders, guidelines
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References:
1.
Fountoulakis KN, Vieta E, Sanchez-Moreno J, Kaprinis SG, Goikolea JM, Kaprinis GS. Tretament guidelines for bipolar disorder: A critical review. J Affective Dis 2005;
86: 1-10.
2.
Perlis RH. Use of treatment guidelines in clinical decision making in bipolar diorder: a pilot survey of clinicians. Curr Med Res Opin 2007; 23; 467-475.
3.
Samalin L, Guillaume S, Auclair C, Llorca PM. J Nerv Ment Dis 2011; 199: 239-243.
Maintenance treatment in bipolar disorder: What do guidelines recommend?
Ibrahim Eren
Konya Research and Training Hospital, Psychiatry Department, Konya, Turkey
Bipolar disorder is a serious mental illness presenting with exacerbations and remissions. Relapses should be minimized and that is
achieved by preventive treatments. Developing easily applicable and reachable algorithms by incorporating data coming from various
sources, implementing research findings in daily practice, and providing standardized treatment choices are all important. Many
guidelines have been published for bipolar disorders so far.
American Psychiatric Association (APA) Guidelines: This guidelines recommend preventive treatment after one manic episode. The
main goals of treatment are to prevent relapse, resolve subclinical residual symptoms, and to decrease suicide risk. Lithium and valproate
are primary agents, as they have the most evidence of efficacy. Their alternatives lamotrigine, carbamezapine, and oxscarbamezapine are
secondary agents. In general continuation of preventive medications used during acute management is first choice during maintenance
treatment. ECT can be used as a maintenance treatment. Antipsychotics should be discontinued if there is no persistent psychotic symptoms.
Cognitive behavioral, interpersonal, and psychodynamic therapies can be used in addition to medications. Psychoeducation is reported
to be beneficial. Keeping lithium levels between 0.8-1.0 mEg/L during maintenance phase were mentioned to be more effective. In this
guideline generally accepted treatments were mentioned as non-definite recommendations.
Texas Medication Algorithm: Acute phase doses should be continued at least 3 months. All patients are recommended to receive
antimanic medications during maintenance phase, if necessary some can receive low dose antidepressants. Lifelong maintenance
treatment is recomended if patients had 2 manic episodes or one manic episode with positive family history, or the acute episode was
very severe. This group of authors think antimanic medications are the core of the treatment and they emphasize depression less. In
addition they recommend ECT and tricyclics, which were demonsterated to be effective, in final stages due to side effects and patient
preferences.
Expert Opinion Series on Medication Treatment in Bipolar Disorder: They recommend continuation of treatment, which was effective
in acute phase except in divalproex monotherapy and predominantly depressive cases. They suggest adding lithium in those cases.
They recommend that antipsychotics should be stopped during maintenance phase, but some patients may need to continue taking
antipsychotics. In that case, one of olanzapine, risperidone, or quetiapine can be chosen. Against manic episode risk they suggest to
increase the dose of mood stabilizer, add another mood stabilizer, and try additional treatments afterwards. This algorithm has many
structural features and is very detailed.
British Psychopharmacology Association Guidelines: According to this guideline lithium is the first choice and second choice
medications include valproate, olanzapine, carbamazepine, oxcarbazepine, and lamotrigine. Treatment resistant cases can be treated with
medication combinations, clozapine, or ECT.
World Federation of Biological Psychiatry Associations Biological Treatments in Bipolar Disorders: It is recommended to use
combination of antidepressant and mood stabilizers after depressive episodes. After manic episodes lithium, anticonvulsants, or
antipsyhotics are suggested. When first line treatments fail, trying combinations of first line agents is recommended. It seems to be
the most balanced guideline published so far. While they avoid newly discovered treatments , they support use of antipsychotics and
antidepressants with caution.
Canmat: Once the patient becomes asymptomatic, it is suggested to discontinue all medications other than mood stabilizers and to
continue maintenance treatment for 6-12 months after a single episode of illness. This guideline has similarities with APA guideline and
recommends lifelong maintenance treatment in patients with recurrent episodes or positive family history.
Australia and New Zealand Bipolar Disorder Treatment Algorithm: It suggests to avoid antidepressant use during maintenance phase
after depressive episodes due to precipitating mania and rapid cycling, but recommends mood stabilizer and antidepressant use in cases
with recurrent depressive episodes. The duration of treatment after first manic episode is 6 months and lithium, valproate, carbamazepine,
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or lamotrigine are listed as recommended medications to prevent recurrent episodes.
NICE Treatment Guidelines: They recommend at least 2 year of maintenance treatment after 1 episode. Long term preventive treatment
should be considered in the following cases: One manic episode with prominent risk factors and negative results and bipolar II cases
with significant functional loss, suicide risk, and frequent recurrent episodes. Lithium, olanzapine, or valproate can be used in long term
maintenance treatment, but valproate should not be used in women with pregnancy potential.
When monotherapy with one of those is not adequate, one of three can be added as a second agent or monotherapy can be tried with a
different agent. Possible combinations are lithium-valproate, lithium-olanzapine, or valproate-olanzapine.
Turkish Psychiatry Association Guidelines: Maintenance treatment is suggested in general after second episode, but it can be started in cases
with risk factors. If a mood stabilizer was initiated during acute phase, it should be continued in maintenance phase, if not, then one should be
started. When a mood stabilizer will be chosen for maintenance phase, it should be lithium. After second episode, whatever the type of episode
was, the same mood stabilizer should be continued if there was one. When there is not adequate response and recurrence occurs a second
mood stabilizer should be added. In cases using lithium as first mood stabilizer, valproate should be given priority as the second mood stabilizer.
In conclusion, even there are similarities in many areas among guidelines, there are also different recommendations regarding treatment options.
Those differences stem from complex clinical presentations of bipolar disorder and different cultural and traditional treatment approaches.
Key words: Bipolar disorder, maintenance phase, guidelines
References:
1.
Fountoulakis KN, Vieta E, Sanchez-Moreno J, Kaprinis SG, Goikolea JM, Kaprinis GS. Tretament guidelines for bipolar disorder: A critical review. J Affective Dis 2005;
86: 1-10.
2.
Perlis RH. Use of treatment guidelines in clinical decision making in bipolar diorder: a pilot survey of clinicians. Curr Med Res Opin 2007; 23; 467-475.
3.
Samalin L, Guillaume S, Auclair C, Llorca PM. J Nerv Ment Dis 2011; 199: 239-243.
[PS-23]
Symposium Title: Individualized medicine: Focus on pharmacogenetics
Cem Şengül
Pamukkale University, School of Medicine, Department of Psychiatry, Denizli, Turkey
Genetic studies in psychiatry are on the rise and they form an important portion of all psychiatric research in last years. The genetic studies
in psychiatry vary from classical association and linkage studies to genome wide association, and copy number variant studies. Genetic
studies were focusing on different dimensions of psychiatric conditions. First of all, associations of target genes with psychiatric disorders
were investigated in majority of studies. Association of drugs and genetics were also studied in many research projects. Genetic drug
association studies consist of studies with efficacy and frequency of side effects of drug on different genetic polymorphisms. Recently,
μ-opiate receptor gene (OPRM1) Asn40Asp single-nucleotide polymorphism was found to be associated with naltrexone drug response in
alcoholic patients. This finding was very important for revealing effect of genetics on drug response. Naltrexone was effective in aspartate
(Asp) 40 allele carriers but drug was ineffective in homozygote asparagine (Asn) carriers. Different genetic polymorphisms of genes
encoding enzymes and receptors that were related to dopaminergic, serotonergic and glutamatergic systems were also associated with
antipsychotic and antidepressant drug response and side effects. For example 5-HT2C receptor 759C/T gene polymorphism was associated
with antipsychotic induced weight gain and T102C polymorphism of 5HT2A receptor gene was associated with response to risperidone.
Genome wide association and copy number variations are new genetic techniques revealing more detailed and reliable results. Studies
using these techniques might be more useful for exploring interactions between drugs and genetics. Studies on association of genetics
with psychiatric disorders were limited and there were only a few studies available on association of genetics with psychiatric drugs in
Turkey. Financial problems and approval speed and requirements of ethics committees are important barriers for conducting studies on
genetic drug interaction. Resolving these issues might increase interest of psychiatrists on this topic.
Key words: Genetics, polymorphism, drug
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Pharmacogenetics and how individualized medicine can be applied to the practice of psychiatry
Çiğdem Aydemir
Ankara Numune Research and Education Hospital, First Psychiatry Clinic, Ankara, Turkey
Choice of psychotropic agents is a critical problem during the follow up of mentally ill patients. Some of the patients experience remission,
however significant proportions of the patients continue to suffer from psychiatric symptoms and side or adverse effects.
Psychotropic drug efficiency may not occur until a considerable time after the initiation of the therapy after which the clinician can
determine, whether the regimen is effective or not. During this period treated patients may experience continuous psychiatric symptoms,
employment loss, social dysfunction, and medical morbidity.
Efforts to identify the best possible drug regimen for the patients focused on many points, such as clinical variables, predictors of possible
side effects, plasma and CSF neurotransmitter levels, metabolite levels, and brain imaging, but they have only limited success. Up to date
in practice, drug selection is made based on clinical symptom profile and possible side effects of treatments.
The pharmacogenetics of the psychotropic drugs is a possible way to decide the suitable drug for the patient. Pharmacogenetics is the
study of genetically determined interindividual differences in response to pharmalogical agents. In this field there are genetically coded
pharmacokinetics (genetically based differences that influence the bioavailability of a drug), pharmacodynamics (genetically based
differences in the proteins at which a drug acts) of the drugs, and dynamics of their side effects.
The renal clearance of drugs appears to be similar in age- and weight-matched healthy subjects with no defined genetic polymorphisms.
Studies regarding the inheritance mostly account for the ability to eliminate drugs. The genetic differences in pharmacokinetics have
proved that they may be applied to the most of the drugs metabolism. Genetic polymorphisms have been identified and defined for
some drug transporters, primarily P-gp, and several hepatic enzymes important for the cellular transport and metabolism of many drugs
used in psychopharmacology. Genetic polymorphism in a drug-metabolizing enzyme can result in subpopulations of people who may
deviate from the population mean in their ability to metabolize substrates of the affected enzyme. People who are poor metabolizers
constitute at least 1% of the population, but the majority of people are normal or rapid metabolizers, and some are identified as ultra rapid
metabolizers. The practical implications of metabolic phenotyping are most meaningful when the metabolic pathways of therapeutically
administered drugs are known and when drug concentration has been correlated to either therapeutic or toxic effects.
Genetic differences in the receptors, on which the drugs act, are another important factor in predicting the effects and side effects. Findings
in this field are scarce in comparison to pharmacokinetics studies however some research projects are in progress. After the results of these
studies are obtained; different variables other than plasma concentration of the drug would be available in pharmacotherapy practice.
There is a dramatic increase in the amount of availability of the genetic information in public since samples can be easily collected by
peripheral blood collection or mucosal smearing. Progress in genetic-molecular technology made possible to conduct genetic research
on individual genes or entire genomes. In the future by the help of pharmacogenetic approach clinicians will be able to understand the
predictors of drug efficacy and side effects, as a result individualized medicine will be applied in the practice of psychiatry.
Key words: Pharmacogenetics, psychiatry, treatment, individualized medicine
Pharmacogenomics biomarkers and personalized medicine in psychiatry
Yeşim Aydın Son
Middle East Technical University, Informatics Institute Department of Health Informatics, 06800, Ankara, Turkey
Transformation of clinical medicine was one of the long term goals of the Human Genome Project, expected to impact the practice
within 10-20 years after the announcement of first draft of human genome. As of 2011 we are just entering into this era and emerging
applications of technologies based on genomic research is indicating that Human Genome Project will be able keep its promise.
Translational and clinical research to develop new personalized medicine approaches are going strongly; identification of predictive and
diagnostic biomarkers is accelerating with the help of high-throughput technologies, and molecular diagnostics and pharmacogenomics
is one of the growing markets worldwide with the goal of early detection, prevention, and intervention of diseases and to predict drug
efficacy to guide dosing and avoid adverse reactions.
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Single Nucleotide Polymorphisms (SNPs) are the most common form of genomic variations and the main genetic reason behind
individual phenotypic differences. Also SNP variations are suggested to be the underlying reason of many complex diseases, they are
considered as a good candidate for personalized medicine and pharmacogenomics applications. Genome-Wide Association Studies
(GWAS) of SNPs are among the promising approaches for the identification of disease causing variants. The high-dimension of the SNP
genotyping data presents a challenge for the understanding of the genotype and its possible implications for the etiology of the diseases
and also for the identification of the representative SNPs to design the follow up studies for the validation of the associations. One of
the bioinformatics tools developed to overcome this challenge is METU-SNP (http://metu.edu.tr/~yesim/metu-snp.htm), which aims to
fasten the identification of associations described through GWAS. Today through genomic research and meta-analysis of genotyping
experiments we are able to reveal SNP biomarkers associated with disease and drug reactions. Next, translational research has to be
conducted in order to develop genomic diagnostics to apply this information into practice in medical clinics. Design of diagnostic assays
for the diagnosis and prediction of drug response in psychiatric disorders can especially guide the initial selection of antipsychotics or
antidepressants based on the individual genomic information of the patients.
Development of personalized medicine approaches and utilizing genomic diagnostic assays like the examples will be presented in this
talk will eliminate or decrease the number of trial-and-errors in selection of right therapy and dosage for the right patient and will also
minimize emergency visits due to side effects of the drugs. Also prescription of right medicine and therapy plan at the initial diagnosis
will increase trust between the healthcare professionals and the patients, which in return expected to provide higher cooperation and
adherance rates of patients to their therapy. Application of pharmacogenomics and personalized medicine approaches in clinical decision
making is expected to decrease the cost of healthcare in psychiatry as in other disciplines, while offering higher quality healthcare..
Key words: Personalized medicine, biomarkers, molecular diagnostics, pharmacogenomics, Single Nucleotide Polymorphisms (SNPs), METU-SNP,
rational drug use
[PS-24]
Symposium Title: Effects of psychotropics and other drugs on quality of life, employee security, flight and traffic safety
The effects of psychotropic and other drugs on flight and flight safety
Muzaffer Çetingüç
Aviation and Space Medicine Center, Anadolu University, Eskisehir, Turkey
There are data that the side effects of many prescription drugs impair the psychomotor and cognitive performance of patients; with
psychotropic drugs having even more of these negative side effects. Particularly drugs like benzodiazepines, antipsychotics, barbiturates,
trycyclic antidepressants, stimulants, narcotic analgesics, and antihistamines that affect the central nervous system top the list for risks of
accidents, injuries, and cognitive impairments. Along with these, anticoagulants, chemotherapeutic agents, antidiarrheals, antiemetics,
and steroids should not be allowed for pilots. It is debatable that SSRIs have a mild side effect profile. SSRIs and bupropion are given
to military pilots up to 6 months after resolution of anxiety and depressive symptoms in Canada and Australia. But the civil aviation
authorities did not grant any privileges to these drugs.
The gold standard in aviation for a pilot to fly efficiently and safely is to be in good mental and physical health and not to be affected by
any medication during flights. The regulations both international and national have clear rules that permanently or temporarily restrain
pilots from flying activities in the case of any sickness or medication treatment. The rules stating that a sick person cannot function as
a pilot in a plane or an air traffic controller in a tower are rational. However since the notion of being sick and the tasks during a flight
spread over a wide range, local health authorities can issue “waivers” for special situations. For example pilots with conditions like type-2
diabetes, asthma, rheumatoid arthritis, sarcoidosis, or melanoma cannot fly; but in certain forms of these conditions that are stabilized
with treatment, that have not caused serious limitations, and that do not affect performance, the pilot may be allowed to fly. Atopic
dermatitis that recover with application of pomades, allergic rhinitis that is treated with nasal sprays, asthma that is treated with steroid
inhalers, type-2 diabetes that is controlled with metformin are examples of allowed conditions. The drugs that are assumed not to have
any side effects that might affect flight safety are: Aspirin, paracetamol, most antibiotics, depot penicillins, gout and thyroid medication,
antiacids, nasal decongestants, oral contraceptives, topical analgesics and steroids, nonsteroidal anti-inflammatory drugs, vitamins,
metformin, modafinil, caffeine, etc. Clearly, the patients need to be monitored for the first few days of use considering these drugs may
have idiosyncrasies.
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It is a problem when pilots take drugs without consulting authorized doctors for fear of flight suspensions. Adding to that reasons like
the cost of doctor’s visits, losing compensation for the duration of suspension, upsetting supervisors due to disrupted flight schedules
may lead pilots to taking OTC drugs. What’s worse is that they can order DTC drugs over the internet based on unscientific news, articles,
and ads. There are several herbal supplements available in the market today that contain suspicious ingredients that claim to treat pain,
help flu like symptoms, reduce stress, aid sleep, improve sexual performance, reduce blood fat levels, help lose weight, prevent aging, or
provide vitamins and minerals. Therefore the attempts of the pilots to treat themselves create risks and the unknown side effects of those
preparations pose serious problems to flight safety.
Key words: Psychotropic drugs, SSRI, flight safety, pilots
Adnan Özçetin
Department of Psychiatry, Duzce University, Duzce, Turkey
Sexual dysfunctions are revealed by different organic and/or psychogenic factors and proceed with the addition of psychogenic reasons
to almost all organic reasons. The organic/psychogenic discrimination of etiologies is crucial in sexual dysfunctions. The most important
and practical way of discrimination is systematic and detailed history. The diffuse type sexual dysfunction established in elderly people
should be considered primarily based on organic reasons. Furthermore alcohol/narcotics, drug abuse, the existence of somatic or systemic
diseases also strengthen the possibility of organic based sexual dysfunction. The drugs and ingredients causing significant sexual side
effects include: Alcohol and narcotics, antihistaminics, decongestants, diuretics, chemotherapeutics, antiulcer drugs, antihypertensives,
anticonvulsants, asthmatic drugs, cardiac drugs, psychotropic drugs (antipsychotics, antidepressants, mood stabilizers, anxiolytics,
sedative hypnotics), and others.
It is mostly difficult even impossible to learn about the sexual side effects of drugs by physicians. Previous studies have revealed that
patients usually didn’t mention the sexual side effects of drugs to their physicians. Therefore the physicians should specifically ask
about the sexual side effects of drugs beside the dosage, preferred effects, and other side effects. Besides, relationship between sexual
dysfunction and other diagnosis and drugs used by the patient should be considered.
There are major unfavorable results of sexual side effects including: Loss of adaptation to drug use, abandonment of drug therapy,
deterioration of psychiatric or other diseases, continuation of sexual dysfunctions, and disruption of quality of life. Significant side effects
exist during the medical treatment of psychiatric disorders. The mechanism of emergence of sexual dysfunction due to medication use
is complicated. Sexual dysfunctions due to medications occur by the effects of medications on peripheral and central neurotransmission.
Serotonin mostly reveals negative effects on sexual behavior. However, its effects can also be positive according to receptor subtype
and localization. Higher prolactin levels cause sexual dysfunction. The increase in dopaminergic activity has positive effects on sexual
desire. Antipsychotics, antidepressants, anxiolytics, and other psychotropic drugs mostly have negative effects on sexual desire and
behavior. Psychotropic drugs like bupropion, mirtazapine, moclobemid, reboxetine, and tianeptin have little or no sexual side effects.
Even dopaminergic drugs like bupropion have positive effects on sexual desire.
Key words: Drug, sexual dysfunction, side effect
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COURSES
[KC-01]
Basic Biostatistics
Selim Kılıç
Gulhane Military Medical School, Department of Epidemiology, Ankara, Turkey
E-mail: [email protected], [email protected], [email protected]
The aims of this course are to teach the basic statistical approach and terminology, to teach the use of the SPSS for Windows package
program and its basic characteristics and principals, to perform the basic descriptive and analytical statistics by using SPSS for Windows
package program and to interpret the results.
At the end of the course, the participants will be able to perform descriptive statistics, select the appropriate statistical tests to compare
differences between or within groups and be able to draw some graphics by using the SPSS for Windows package program in a datasheet
which is composed by the course director.
The participants, upon completion of this course, will be able to generate and test hypotheses, compose a datasheet iusing the SPSS for Windows
program, enter data in the datasheet, transform the data to other forms, select the appropriate statistical test for comparison of groups and computation
of basic statistics, interpret and write the results, interpret the p value and confidence interval, and draw some graphs by using the SPSS program.
The participants will learn to calculate mean, median, mode, standard deviation, quartiles, frequency and percents as descriptive statistics.
They will learn and differentiate categorical, ordinal, and continuous variables by studying examples. To compare categorical variables, the
use of the chi-square test and interpretation of the results will be discussed. For continuous variables, the appropriate test will be determined
with respect to group numbers, whether groups are dependent or independent and whether the variables are parametric or nonparametric.
According to the existing conditions, the participants will decide when they should use the independent samples t test, ANOVA, paired samples
t test, or repeated measures of ANOVA as parametric tests and Mann Whitney U, Kruskal Wallis, Wilcoxon ranked signs test, or Friedman test
as a nonparametric tests. They will also use correlation analysis to determine the linear association between continuous and ordinal variables.
By using the SPSS program, participants will compose bar and pie graphs for nominal and box plot graphs for continuous variables to
demonstrate the results.
Key words: descriptive statistics, p value, confidence interval
[KC-03]
Axel Würz
Department of Psychiatry, Marmara University, Istanbul, Turkey
Despite a high prevalence of somatic symptoms without demonstrable organic cause in nearly every branch of medicine, understanding,
classification and treatment of these disorders have posed a considerable challenge.
As the DSM-V is in development, the proposed changes in comparison to the DSM-IV can be seen to reflect the current understanding of
non-organic physical symptoms. It is likely that somatization disorder, hypochondriasis, undifferentiated somatoform disorder and pain
disorder will be combined into a new category entitled “Complex Somatic Symptom Disorder” (CSSD) which emphasizes the symptoms
plus the patients’ abnormal cognitive processes. The term “complex” is intended to indicate that the symptoms must be persistent and
must include both somatic symptoms (criterion A) as well as dysfunctional cognitive processes (criterion B) for the diagnosis to be made.
Cognitive processes such as dysfunctional attention focusing, symptom catastrophizing, and symptom expectation that may be included
in criterion B also show the influence cognitive models have exercised in the understanding of these disorders.
These cognitive processes have to be evaluated against the background of possible psychiatric comorbidities, current life stressors,
possible past traumatic events and learning experiences that shaped emotion regulation in an unhelpful way. Contributing to the
maintenance of symptoms and resulting from dysfunctional cognitions are behaviours such as imbalanced level of activity, avoidance
and safety-seeking and reassurance-seeking behaviors.
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In cognitive behavioural therapy (CBT) of these disorders all the factors maintaining and contributing to the disorder are possible targets
for treatment. The first and possibly most important step is to develop, in cooperation with the patient, an alternative explanation of the
patient’s symptoms other than the presence of an organic cause. During the course of treatment the patient can then collect evidence
that supports the alternative explanation of symptoms.
The techniques that can be employed within the framework of the cognitive-behavioral approach are aimed at addressing the underlying
dysfunctional cognitive processes and behaviors. They may comprise cognitive restructuring, attention-training, behavioral experiments,
exposure, activity planning, and emotional-regulation techniques.
Conventionally, treatment can be conducted in individual and group sessions and usually comprises about 15 one-hour sessions. There is evidence
showing that CBT is effective in decreasing symptom severity and overall distress. However, there are limited number of studies comparing
different treatment modalities such as CBT and pharmacological interventions. Also it is not clear if combining CBT and pharmacological
treatment increases effectiveness. In addition different forms of therapy such as computer-based treatment have been developed.
The cognitive behavioral model has been influencing the current understanding of somatization and CBT has shown effectiveness in
its treatment although further studies are welcomed. Even if a full course of CBT cannot be offered, e.g. in an outpatient setting, and
pharmacological treatment is chosen, it appears promising to integrate at least certain parts of cognitive-behavioral treatment such
as developing an alternative explanation for the patient’s symptoms and exploring the role of processes such as attention, avoidance,
unbalanced activity levels and safety-seeking and reassurance-seeking behaviors.
Key words: Somatization, CBT, somatoform, hypochondriasis, treatment
[KC-04]
Mindfulness and acceptance based therapies
Kültegin Ögel
Acibadem University, Medical Faculty, Istanbul, Turkey
Mindfulness has reached far beyond the disciplines where it originated and has become an evidence-based psychotherapy method. In
particule, the application of mindfulness based therapies in addition to traditional methods for psychiatric disorders prevents relapses.
Mindfulness is concentrating with the aim of focusing at the moment in a nonjudgmental way. Mindfulness means being conscious of
the current experience and accepting it. In other words, mindfulness is a unique and receptive form of consciousness in which stimulants
are not evaluated, not classified and not analyzed.
Mindfulness and acceptance based therapies deal with the thought itself instead of the content of the thought. It may be said that they
help cognitive restructuring in this way. Mindfulness and acceptance based therapies differ from cognitive behavioral therapies in that
way and are accepted as third wave therapies.
Acceptance should not be confused with submission and giving up. Acceptance directs the person to turn to the current experience
(opening up) instead of running away from the experience (closing up). By this means, the person learns to be with and accept
experiences that are pleasant, unpleasant, or neutral. The person develops the skill of being fair to his or her own experiences. Being aware
of what is happenibg causes a willingness to let things that are pleasant or unpleasant happen just as they are.
Mindfulness acceptance therapies involves; Mindfulness Based Stress Reduction (MBSR), Mindfulnnes Based Cognitive Therapy (MBCT),
Acceptance and Commitment Therapy (ACT), and Dialectical Behavior Therapy (DBT).
The common basic strategies that all these therapies use are:
- Acceptance
- Focusing at the moment
- Cognitive defusion and decentering
- Being nonjudgmental
- Observing
Adaptation of the different viewpoints that are offered by mindfulness and acceptance based therapies by therapists, who have understood
them, is useful. However, understanding of the basic rationale of the therapy by all psychiatrists and psychologists is also useful.
Key words: Mindfulness, acceptance, psychotherapy
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[KC-05]
Eye movement desensitization and reprocessing method [EMDR]
Specifically designed for Turkish patient population in the Netherlands
Serdar Güner
Praktijk Voor Psychiatrie, The Netherlands
Dr. Serdar Guner reports that those behaviorally troubled Dutch patients with Turkish origin have not necessarily been benefitted by those
10-15 sessions of EMDR during their psychiatric evaluations necessitated by different conditions. The clinicians have reportedly been applying
traditional EMDR methods first to be objectifying relaxation through imagination and later on processing the completion of catharsis during
as well as after the said eye movements. The patients, however, have been reporting no benefits and even at times, worsened clinical
conditions after the given session. Dr. Guner has finally extracted the facts centered on this failure relevant to the given patient population.
Those Turkish-Dutch clients have not been acknowledged about the rationale relevant to which-treats-what phenomenon through the
catharsis. Lacking of explanation centralized around acknowledgement along with a possible language barrier has been hindering the
therapeutic process. This finding has eventually led him to develop a sister method specifically designed for this patient population. He
has slowly but steadily, started informing his patients about shock, repression of the feelings during it, and the effect of those repressed
emotions on the people in short as well as long term trajectories. He, later on, used metaphors in picturing the process through which
the said repressed emotions would be surfaced by means of EMDR. One of the interesting demographics has been the cultural difference
of this given patient population. Those Dutch clients with Turkish origins have not been motivated in processing anything if they had not
understood what they were doing. While this, in fact, is also true with the people from the other cultures, Dutch-Turks appeared to be a bit
more autonomous in directing themselves in comparison with the Western Europeans who have likely been more conformists with their
clinicians even when they have not necessarily been understanding what and why they were doing in any recommended method.
Dr. Guner reviews his methodology designed for this population during his presentation. Most of the work has been an “acknowledgement”
in his following up with his patients. This variant method has been helping PTSD patients’ feeling relaxation even after first two sessions.
Dr. Guner reports that about 150 of his patients have been very happy about the outcome of this EMDR variant.
Key words: EMDR, PTSD, psychotherapy
WORKSHOP
[WS-01]
Alternative CBT method of panic disorder treatment for Turkish patients
Serdar Güner
Praktijk Voor Psychiatrie, The Netherlands
I have been working as a psychiatrist and psychotherapist in the Netherlands for more than 20 years during which I have diagnosed and
treated many Turkish panic patients by the virtue of sharing the same language, culture, and other demographics of the native land,
Turkish Republic. The most important factor that led me to develop a different approach than that of a classical cognitive behavioral
therapy -- focusing on neuro-vegetative reactions, neutralizing them through psycho-education and home-work, generating an insight
into catastophic thoughts while “living” and finally easing up the panic attacks -- was the given patients’ thinking of the methods as
“ridicilous,” and not doing their homeworks or acting as if they completed them even they did not.
The alternative method I devised was related to use a lot of metaphors corresponding to the patients’ lives, generating an insight into
catastrophic thoughts while “understanding” their bodily dynamics, self-controlling neuro-vegetative reactions, and acknowledging
“the mechanism of panic reaction.” Since it is relatively short, not necessitating homework, and easy to understand for the panic stricken
patients, it promotes motivation leading to less relapses and even if relapses occur, achieving quicker and easier recovery.
The method appears to be effective among the native Dutch patients, as well as immigrants.
The presentation will be providing details of this newly applied successful panic treatment.
Key words: CBT, panic disorder, psychotherapy
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4th International
Antalya, Turkey
ABSTRACTS OF ORAL PRESENTATIONS
[SO-01]
Bacopa monniera: Current trends and future directions
Ref. No: 93
Chris Neale1, Andrew Scholey1, Matthew Hughes1, Patrick Johnston2
Brain and Psychological Sciences Research Centre (BPsyC), Swinburne University of Technology, Melbourne, Australia
1
Department of Psychology, University of York, York, England
2
Objectives: Bacopa monniera (BM) is an Indian herb used for centuries as a memory tonic in Ayurvedic medicine. Preclinical research has
shown that BM acts as an antioxidant, improves memory, and reduces amyloid plaque deposition in animal models of Alzheimer’s disease.
Human studies suggest that BM provides a fairly robust benefit to performance on certain attention, working memory, and learning tasks.
This talk will present a review of BM research through animal models to human clinical trials and what research is currently being undertaken on BM.
Methods: Two studies will be discussed further to the review of BM:
(1) An acute dose-ranging study of healthy young adults where participants were required to complete a multi-tasking framework (MTF)
and mood scales at baseline, 1hr and 3hrs post dose. The dosage was 300 or 600mg of BM or a matched placebo.
(2) The study utilized a double blind, placebo controlled crossover design where all participants completed a 90 day course of both
Bacopa (300mg daily) and placebo during the study. The participants were aged between 40 and 65 years and in good health. The
interventions were separated by a 120 day washout period. The scans were undertaken on a 3T Siemens TRIO magnet before and after
each 90 day intervention where participants would complete two runs of the task per scan visit.
Results: (1) There was a significant, dose-dependent effect of treatment on ratings of alertness favouring the 600 mg treatment at both
post-dose assessment times. There was a trend for dose-related effects on performance of the MTF, in particular for the Stroop task where
there was an advantage for the 300 mg dose.
(2) The data collection is still ongoing. The baseline data show a bilateral increase in BOLD activation in the precentral gyrus and precuneus
with activation extending to the left inferior frontal gyrus (n=7, p=.005) when compared with controls using a task greater than baseline mask.
Conclusions: The conclusions are speculative at this point for both studies, one being still in the data collection stage, one being
underpowered. However, the methodologies and the future directions of these studies will be discussed.
Key words: Bacopa monniera, human cognition, fMRI, nutraceuticals
[SO-02]
Association of the DRD2 TaqIA, 5-HT1B A-161T, and CNR1 1359 G/A polymorphisms
with alcohol dependence: A single center study in the Denizli Province of Turkey
Ref. No: 143
Ceyhan Balcı Şengül1, Mehmet Emin Erdal3, Cem Şengül2, Özlem İzci Ay3, Muharrem Efe2, Mustafa Ertan Ay3, Hasan Herken2
Psychiatry Clinic, Denizli State Hospital, Denizli, Turkey
1
Department of Psychiatry Pamukkale School of Medicine; Denizli,Turkey. 3 Department of Genetics Mersin School of Medicine, Mersin, Turkey
2
Background: Alcohol dependence is associated with genetic variants of alcohol-metabolizing enzymes and genes related to the
dopaminergic, gamma-aminobutyric acidergic, glutamatergic, opioid, cholinergic, and serotonergic systems. Genetic variations in the
endogenous cannabinoid system are also involved in alcohol dependence.
Objective: The present study was aimed at evaluating the association between three polymorphisms, DRD2 TaqIA, 5-HT1B A-161T and
CNR1 1359 G/A (rs1049353), and alcohol dependence.
Methods: One hundred and twenty three patients, who were admitted to the Alcohol and Substance Abuse Center of Denizli State Hospital
and diagnosed with alcohol dependence according to the DSM-IV criteria, and 125 healthy volunteers were included in the study.
Results: Of the three polymorphisms investigated, 5-HT1B A-161T was the only one found to be associated with alcohol dependence.
Conclusion: The 5-HT1B receptor A-161T polymorphism might be a promising marker for alcohol dependence; however, future studies
are needed to clarify these findings.
Key words: Alcohol dependence, DRD2 TaqIA, 5-HT1B A-161T, CNR1 1359 G/A, polymorphism
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[SO-03]
Treating psychotic substance abuse patients with opioid agonist therapy and
the atypical antipsychotic olanzapine
Ref. No: 102
Maria Chiara Pieri1
Department of Drug Addiction, Bologna Est, Italy
1
Objectives: The aims of the study were: 1. To evaluate the efficacy of olanzapine in patients on methadone maintenance treatment; 2. To
explore the time-course variation of cravings and weight at baseline and every 2 months for the first 6 months and then every 6 months until
the end of the study (30 months). 3. To compare the severity of the symptoms between patients on methadone and patients on buprenorphine.
Methods: The patients were enrolled from the Outpatient Addiction Unit in Bologna, Italy. All patients gave written informed consent. We
randomized 32 patients to treatment with methadone and 13 to treatment with buprenorphine. Based on inclusion and exclusion criteria,
36 patients were included in the study and they were divided into three treatment groups.
At the baseline and follow-up sessions the following rating scales were administered: The Minnesota Multiphasic Personality Inventory-2
(MMPI-2), the SCID-II (to identify and determine DSM-IV Axis II disorders i.e. personality disorders), Bech-Rafaelsen Mania and Melancholia
Scales (BRMAS, BRMES; Bech et al. 1988, to cover severity of manic and depressive symptoms, respectively), and a VAS (Visual Analogic
Scale, to quantify craving for drugs).
Also the body weight of the participants was registered and followed.
Results: After six months, no significant difference was found among the three subgroups, even though the olanzapine+methadone
group achieved better and quicker results and sustained them for longer periods. There was no significant difference at baseline and at
the end of the study in all patients.
Total and partial BRMES and BRMAS scores did not significantly change during the follow-up period (6th-30th month), eventhough the
curve displayed a downward trend. The VAS total scores were significantly lower both at the 6th and 30th month (p<0.0001) when
compared to the baseline condition. None of the three treatment subgroups showed a significant weight gain, both after 6 months (at
this follow up we observed better results in the treatment of mania and melancholia) and at the end of the study (eventhough there was
a small peak of weight gain). At the 30th month we considered the BRMAS and BRMES scores corresponding to the maintenance phase.
Three patients dropped out from the study just before the 30th month session because they stopped olanzapine due to weight gain (5kg
for one patient, and 3 kg for two patients).
Conclusions: We observed good adherence to antipsychotic treatment in this sample and we did not detect metabolic complications.
Buprenorphine was prescribed for younger patients and patients with lower severity of symptoms.
At the 30th month, all urine drug tests were negative. It is likely that the constant caregiving and clinical monitoring improved the patients’
motivation and adherence to the treatment. This point is important because the number of patients needing addiction treatment has
been increasing, while time and available resources are limited.
According to the results of this study, the use of methadone and olanzapine together in the treatment in psychotic substance abusers
improved treatment adherence, even in the presence of subthreshold psychiatric symptoms.
Key words: Heroin, addiction, therapy, dual diagnosis, psychiatry
[SO-04] A comparison of the effects of typical and atypical antipsychotics on the basolateral
amygdala of rats using deep brain EEG recordings
Ref. No: 111
Oytun Erbas, Saylav Bora
Department of Physiology, Ege University, School of Medicine, Izmir, Turkey
Objective: It is clinically known that compared to typical antipsychotics, the atypical antipsychotics are likely more efficient in the
treatment of psychosis with negative symptoms and cause fewer extrapyramidal side effects.
In the differentiation of receptors and extrapyramidal system (EPS) side effects, there are some medications which cannot be classified as
typical or atypical antipsychotics according to their activity at D2 receptors. There is not a clear method to classify antipsychotics.
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Materials & Methods: The experiments performed in this study were carried out according to the rules in the Guide for the Care and Use
of Laboratory Animals adopted by the National Institutes of Health (U.S.A) and received Ege University Animal Ethics Committee’s consent.
(Approval number: 2010-081)
In this study, 9 Sprague-Dawley (450-500 g) adult male rats (16-20 weeks old) were used. The rats were maintained under controlled
environmental conditions throughout the study: 21-25 °C ambient temperature, 12:12 light-dark cycle (light from 7:00-19:00h), and
Standard laboratory food and tap water available ad libitum. Under anesthesia, a small hole was drilled. Then by using the bregma as a
reference for the stereotaxic method (coordinates Anteroposterior: - 2.8 mm, Lateral: + 4.8 mm, Ventral: - 8.5 mm) (Paxinos Rat Brain), an
exterior insulated bipolar EEG electrode was placed in the basolateral amygdala.
The electrodes were fixed by using a dental acrylic (numerous alloys are used in the making of dental restorations). Rats were anesthetized
by using ketamine (40 mg/kg) and xylazine (4 mg/kg) intraperitoneally (IP).
Three days after the electrode was fixed, spontaneous amygdala EEG records were taken from the rats by injecting saline, when they
were awake and in their own box. Subsequently at 7 days intervals (5 times more than the half life of the drugs), olanzapine 1 mg/kg,
haloperidol 1 mg/kg, chlorpromazine 5 mg/kg or ziprasidone 1 mg/kg doses were IP administered. Before each drug injection amygdalar
EEG records were taken to observe the baseline rhythm of the amygdala. These drug doses were chosen after consideration of the
hypermetobolism of rats.
EEG recording was started 30 minutes after drug injection and each rat was recorded for 20 minutes. Signals were amplified by 10,000
times and filtered within a range of 1-60 Hz. System records were taken by a Biopac MP30 amplifier system and evaluated with FFT (Fast
Fourier Transform) and PSA (Power Spectral Analyses) methods. During this process Delta 1-4 Hz, Theta 4-8 Hz, alpha 8-12 Hz and beta
12-20 Hz waves in the EEG are accepted as the ratio of percentage in PSA (Power Spectral Analyses) methods. We confirmed electrode
locations histologically following euthanisation.
Results: According to the data obtained, the perceptibly dominant frequency in amygdala spontaneous activity was founded to be 1-4
Hz (Delta).
When we compared the EEG records in the 1-4 Hz (Delta) band of the groups which were given typical and atypical antipsychotic drugs to
the control group given isotonic saline, there was significant (p < 0.005) inhibition. On the other hand in the 4-8 Hz (Theta) and the 8-12
Hz (Alpha) (Figure 4) bands, a significant (p < 0.005) increase was observed.
When the EEG records of the group which was given atypical antipsychotics were compared to the typical antipsychotic administered
groups, in the 1-4 Hz band a significant increase (p< 0.05) and in the 4-8 Hz and 8-12 Hz bands significant inhibition (p<0.05) was
observed. In addition, the EEG records of the atypical antipsychotic groups were nearer to those of the saline administered group.
Conclusions: The results showed that there was less change in spontaneous electrical activity of the basolateral amygdala in the atypical
antipsychotic groups than in the typical antipsychotic ones. The EEG of deep brain recording may be used as a new method for classifying
antipsychotics into different groups.
Improvements in cognitive function in schizophrenia with atypical antipsychotics are known. This effect may be due to the impact of
atypical antipsychotics on the amygdala. This effect is probably related to the fast-off theory, meaning that the drug binds and leaves the
receptor quickly.
Although mesolimbic dopaminergic hyperactivation is inhibited with antipsychotics, the correction of mesocortical dopaminergic
hypoactivation and the recovery of cognitive capacity and normal affect are not completely clarified.
There are extensive connections between the prefrontal cortex and the amygdala. Typical antipsychotics in this study increased the
frequency of firing in the amygdala. This effect may be interpreted as being similar to the effects of Parkinsonism caused by the blockade
of striatal D2 receptors.
In this study typical antipsychotics increased the amygdalar frequency of the EEG. The breakdown of frequency of the amygdala was
more pronounced in chlorpromazine administration. This effect of chlorpromazine may be associated with non-selective blockade of the
histaminergic, adrenergic, serotonergic, and dopaminergic systems.
Atypical antipsychotics caused a very small change in the basal rhythm of the amygdala (Delta Frequency). This effect is thought to
be related to the recovery of normal cognitive function during use of the atypical antipsychotic drugs. In future studies, the effects of
antipsychotics in different brain regions may lead to a better differentiation of the typical and atypical antipsychotics.
Key words: EEG, amygdala, typical and atypical antipsychotics
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[SO-05]
The effect of cognitive-behavioral therapy in reducing the feeling of emotional
pressure and blood sugar control in patients with type 2 diabetes
Ref. No: 142
Shahnam Abolghasemi1, Ghahraman Mahmodi2, Mandana Zafari2
Department of Medicine, Islamic Azad university,Tonekabon, Iran
1
Department of Medicine, Islamic Azad university, Sari, Iran
2
Objective: The results of some studies show that diabetes patients experience some psychological problems, such as depression, stress, selfnegative labeling, and lack of self confidence. In this study, we investigated the effect of cognitive-behavioral therapy (CBT) in reducing the
feeling of emotional pressure and blood sugar control in type 2 diabetes patients, who were referred to the Tonekabon Society of Diabetes.
Methods: This feeling was measured by using Marghan’s Measure for Feeling of Emotional Pressure. In addition, the blood sugar levels
of all patients were tested and recorded. The 24 patients, who had the highest emotional pressure scores, were selected and randomly
divided into two groups, each consisting of 12 patients. They were provided CBT.
After the end of CBT, they were tested again. The collected data were tested by SPSS software, 10th edition and ANCOVA covariance
statistical test.
Results & Conclusions: There were some meaningful differences between the pre-and post-test levels of emotional pressure. The results
of the blood sugar test also indicated a reduction in the level of blood sugar and normalization of blood sugar control in some patients
with diabetes type 2.
Key words: Stress, blood sugar, lack of self confidence, CBT
[SO-06]
Acute effects of nicotine on working and reference memory in rats using
a 12-arm radial maze
Ref. No: 110
Mahsa Movahed Abtahi1, Hosein Molavi1, Jamal Moshtaghian2, Karim Askari1
University of Isfahan, Faculty of Education and Psychology, Department of Psychology
1
University of Isfahan, Faculty of Science, Department of Biology
2
Objectives: It has been shown that nicotine plays a significant role in improvement of memory. Based on this finding, nicotinic drugs are
being developed for possible use as co-treatments for cognitive impairment in some kinds of mental disorders. However, past studies
have mostly emphasized working memory function following acute administration of nicotine and the few studies concerned with
reference memory have shown no significant effects. As the 8-Arm Radial Maze, which has been used in most of the studies in this field,
provides a lower task difficulty, the present article aims to replicate previous studies with a specific emphasis on reference memory using
a 12-Arm Radial Maze which provides a higher level of cognitive task demands.
Methods: Three groups of male Wistar rats were used. The rats were subcutaneously injected with three doses of nicotine 20 min prior
to the start of each trial on the Radial- Arm Maze. The first group was injected with 0.1 mg/kg nicotine solution, the second group was
injected with 0.4 mg/kg , and the third group was the control which received saline.
The spatial memory of the rats was tested on a 12-Arm Radial Maze. The arm choices were recorded when the rat had placed all of its
paws beyond the threshold at the proximal end of the arm. Each session of the testing continued until the rat ate all 6 baits or until the
maximum time of 6 minutes was over. There was at least 24 hours between drug injections during which time the rats were not tested.
Results: The results of repeated analysis of variance showed a significant difference in working memory errors among the three groups,
but there was no significant difference in reference memory errors between the groups. An inverted U-shaped dose-effect curve was seen
for reference memory which showed that nicotine first results in increased reference memory errors and then, perhaps because of the
effect of training, the number of errors decreased.
Conclusions: The current study suggests a negative correlation between acute consumption of nicotine and long-term spatial
performance on a 12-Arm Radial Maze, which contradicts the former assumption on an 8-Arm Radial Maze. This finding also emphasizes
the different mechanisms underlying working and reference memory that should be considered in pharmacotherapeutic interventions
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with nicotinic drugs and other drugs for memory impairments in various mental disorders.
Key words: Nicotine, reference memory, learning, radial-arm maze
[SO-07]
The relationship between personality characteristics and internet addiction in adolescents
Ref. No: 243
Jalal Shafaie1, Sharooz Farjad2
Shafa jalal,Young Researchers Club, Islamic Azad University, Ardabil
1
Farjad Sharooz, Department of Educational Managment, Islamshar Branch, Islamic Azad University, Tehran
2
Introduction: Personality has been identified as a significant factor in internet addiction. The purpose of the present research was to
investigate the role of personality factors in the prediction of internet addiction in adolescents.
Materials-Methods: The research subjects consisted of 261 (146 females, 115 males) adolescents from the city of Ardabil. They were
selected by using the random clustering method. The data of the Young Internet addiction (IAT) test and the NEO-FFI Personality
Inventory were used together. The data were analyzed by Pearson’s correlation coefficient and multivariate regression analysis.
Results: The result of the Pearson correlation coefficients showed that there were significant relationships in adolescent girls between
neuroticism (r=0.42, P<0.01), extraversion (r=-0.19, P<0.05) and conscientiousness (r=-0.24, P<0.05) and internet addiction. In addition in
adolescent boys there were significant relationships between neuroticism (r=0.32, P<0.01), extraversion (r=-0.23, P<0.05), agreeableness
(r=-0.24, P<0.05), and conscientiousness (r=-0.17, P<0.05) and internet addiction. The result of multiple regression analysis demonstrated
that neuroticism, extraversion, agreeableness, and conscientiousness explained 32 percent of variance of internet addiction in adolescents.
Conclusions: The results were similar to findings in other studies and they indicated that low levels of neuroticism and high levels of
extraversion, agreeableness, and conscientiousness decrease internet addiction risk in adolescents.
Key words: Personality, addiction, Internet, adolescents
[SO-08]
Ref. No: 131
The sigma-1 receptor ligand, PRE-084, reduced infarct volume, neurological deficits,
pro-inflammatory cytokines, and enhanced anti-inflammatory cytokines after embolic stroke in rats
Mohammad Allahtavakoli, Bevyn Jarrott
Department of Physiology, Rafsanjan University of Medical Sciences, Iran
Objective: Sigma receptor agonists have been found to provide potent neuroprotection in rats and mice. This neuroprotection is thought to be mediated
through anti-excitotoxic mechanisms. Neuroprotective and immune modulatory effects of sigma ligands have not been investigated in embolic stroke.
Methods: In the present study, the rats were subjected to embolic stroke or sham stroke and were treated with the sigma-1 receptor
agonist, PRE-084 (5mg/kg i.p.), or saline vehicle 3 and 24hrs after stroke. The infarct volume and behavioural tests were conducted and
cytokine levels (ILs-1α and β, IL-2, IL-4, IL-6, IL-10, GM-CSF and TNF-α) were measured in ischemic and non-ischemic cortices. The axonal
damage was determined by using the pNF-H ELISA assay.
Results: The treatment with PRE-084 afforded neuroprotection following embolic stroke as evidenced by significantly reduced infarct
volume and improved behavioural outcomes. Remarkably, the treatment with PRE-084 reduced levels of pro-inflammatory cytokines and
enhanced anti-inflammatory cytokines. The levels of pNF-H were lower in rats treated with PRE-084 suggesting reduced axonal damage,
but this finding did not reach statistical significance.
Conclusions: The findings of the present study suggest that part of the neuroprotective effects of sigma-1 receptor agonists may be
mediated through a dual effect on cytokine release following stroke.
Key words: Cerebral ischemia, sigma receptor, neuroprotection
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[SO-09]
Comparison of the effects of bupropion and fluoxetine on reaction time in adults
with major depressive disorder in a 4-week, single-blind study
Ref. No: 254
Farshad Hashemian, Marjan Sadat Tabatabayi, Ali Sharifi, Marzieh Majd
Department of Clinical Pharmacy, Islamic Azad University, Pharmaceutical Sciences Branch,Tehran, Iran
Objectives: Some studies have shown that adults diagnosed with major depression have longer reaction time compared to the
healthy population. Longer reaction time may result in educational and occupational impairment and increased risk of fatal driving
incidents. Consequently, any impact on reaction time induced by drug therapy may have either positive or negative effects on treatment
outcome and quality of life of patients. Bupropion is an effective antidepressant, which clearly acts via different mechanisms than other
antidepressants. Its mechanism of action is thought to be dopamine and/or norepinephrine reuptake inhibition with negligible effects
on serotonin.
While bupropion is considered an antidepressant with minimal effects on alertness and cognitive function, the present study was
designed to evaluate the effects of bupropion on reaction time in comparison with fluoxetine, in adult patients with major depressive
disorder.
Methods: A total of 30 patients who met the DSM-IV criteria for major depression were recruited for this study. Patients were randomly
assigned to receive either bupropion (200 mg/day) or fluoxetine (20 mg /day) for 4 weeks. Reaction time was assessed at baseline, 2 and 4
weeks of treatment using validated computer-generated tasks and keyboard tapping tests in which the data was collected and analyzed
for auditory and visual stimuli. In addition, the participants were assessed using the Hamilton depression rating scale at baseline, 2 and 4
weeks of treatment. The number of correct responses, omissions, and substitution errors for each stimulus were calculated.
Results: No significant differences were observed between the groups regarding demographic characteristics and Hamilton depression
score at baseline.
In both groups, the number of correct responses to the visual stimuli increased significantly after 4 weeks of treatment (P<0.05). However,
significant improvement in the end point auditory task scores was observed solely in the bupropion group compared to the baseline.
Furthermore, the number of correct responses to visual stimuli was significantly greater in the bupropion group compared to the
fluoxetine group after 2 and 4 weeks of treatment.
Mean reaction times showed no significant differences between the two groups at the end of the study.
Conclusions: Results of this study showed that bupropion did not seem to change reaction times of the patients more than fluoxetine.
However, as the number of correct responses to visual stimuli improved, it may be suggested that bupropion treatment in this population
may enhance concentration more than fluoxetine.
Key words: Visual and auditory tasks, reaction time, bupropion, fluoxetine
[SO-10]
A placebo-controlled double-blind add-on study of Ginseng in opioid
withdrawal syndrome
Ref No: 294
Ofogh Bigdeli1, Farshad Hashemian1, Majid Shohrati2, Azarakhsh Mokri3, Marzieh Majd1
Department of Clinical Pharmacy, Pharmaceutical Sciences Branch, Islamic Azad University, Tehran, Iran
1
Department of Clinical Pharmacy, Baghyat Allah Medical University, Tehran, Iran
2
Department of Psychiatry, Tehran University of Medical Sciences, Tehran, Iran
3
Objectives: Pharmacological treatment of opiate withdrawal syndrome is used to facilitate a safe transition to a relapse prevention
program, while ameliorating signs and symptoms of withdrawal in the opioid-dependant individuals.
Ginseng, the root of the Panax species, is a well-known remedy in traditional medicine. Pharmacological studies have determined the
inhibitory effects of Ginseng Total Saponin (GTS) on morphine-induced tolerance and physical dependency. This effect might be due to
up-regulation inhibition of the cAMP pathway. Since conclusive human clinical data is missing, we performed this randomized, doubleblind, placebo-controlled study to assess the effects of ginseng augmentation therapy on withdrawal symptoms of opioid-dependent
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patients treated with methadone.
Methods: A total of 36 male opioid-dependent patients, aged between 18 and 50 years who met the DSM-IV criteria for opioid dependence,
were randomly assigned into two groups of 18 members, to receive either ginseng (two 250 mg capsules daily) or placebo for the first 15
days of detoxification. All patients were treated with a Methadone Maintenance Treatment (MMT) protocol. Opioid withdrawal syndrome
severity was measured by the Clinical Opioid Withdrawal Scale (COWS) on days 0, 1, 7, 10, and 15. In addition, the required daily methadone
dosage was recorded and compared between the groups. This trial was registered in the Iranian Registry of Clinical trials (IRCT) under ID of
IRCT201009063106N4 and was approved by the Ethics Committee of Azad University (approval number: 4115).
Results: Patients in the two treatment groups did not differ significantly in socio-demographic and clinical variables at the baseline.
As expected, a statistically significant decrease in the COWS total score and symptoms was observed from the first day to the end of the
study in both treatment groups.
As shown in figure 1, the required daily methadone dosage was lower in the ginseng group from day 5 to the end of the study (P<0.05).
Although no significant difference was observed in the COWS total score between the two groups, these scores were achieved with lower
methadone dosages in the ginseng group.
Conclusions: The differences in severity of symptoms were not statistically significant between two groups, but patients receiving
ginseng experienced similar withdrawal symptoms with lower methadone dosages.
Key words: Methadone, ginseng augmentation therapy, opioid withdrawal syndrome
[SO-11]
An in vitro analysis of disintegration times of different formulations of
orally disintegrating olanzapine
Ref. No: 114
Murat Altın1, Levent Alev1, Kübra Özbek1, David Hobbs2, Jamie Karagianis2, Tamas Treuer3, Joel Raskin4
Eli Lilly and Company, Turkey
1
Eli Lilly and Company, USA
2
Eli Lilly and Company, Hungary
3
Eli Lilly and Company, Canada
4
Objectives: Orally disintegrating tablet (ODT) forms of medications are sometimes used as alternatives to standard oral tablets for
patients who have difficulty swallowing, those who need to have ingestion verified, and those who may resist other drug product forms
(e.g. injection). ODTs are a tablet or wafer form of medication that disintegrates in the mouth, aided only by saliva. ODTs can disperse
in as little as 1 to 2 seconds or as long as 2 to 3 minutes, depending on the different fast dissolve/disintegration technologies used
to manufacture the tablets. Orally disintegrating olanzapine (ODO) is manufactured by several different companies, using different
formulations and processes. The objective of this study is to investigate differences in disintegration time of these tablets, which may
potentially impact clinical parameters such as patient acceptance and adherence to treatment.
Methods: Six types of ODO, along with Risperdal M-Tab as an external comparator, were evaluated for formulation composition,
manufacturing method, disintegration and dissolution characteristics, expiration dates, and packaging and formulation differences in
comparison with the freeze-dried Zydis/Velotab formulation of ODO. Automated dissolution test equipment, DISTEK DISBA0045 and
DISBA0046 with an Opt-Diss UV fiber optic SPEC0088 attachment, was used to capture the various ODT dissolution rates by measuring
real time release of the active ingredient. Additionally, a high speed video camera was used to capture disintegration times of ODO
products in simulated saliva held at 370C.
Results: 5-mg Tablets: Release for all tablets except Zoltrix was around 90% or above with 150 rpm for ten minutes at the end of the
analysis. In the first three minutes, Lilly’s Zydis formulation was the first to release with dissolution over 30% in less than 60 seconds. At
20 rpm only Zyprexa Zydis had instant disintegration. Other products required more than 30 seconds to dissolve even 10% of the active
ingredient. This is likely a function of formulation and compression vs. a freeze drying processing.
10-mg Tablets: Zydis (Velotab) was the first to show dissolution and showed a steady rate of dissolution. Procaps’ Prolanz FAST formulation
also had quick dissolution, but showed a longer delay to catch up to the Zydis formulation, taking 2 minutes before they were equivalent.
At a lower agitation rate of 20 rpm, Zydis 10 mg still had the fastest dissolution rate in the first 3 minutes. Zydis dissolution was not
significantly affected by dosage strengths (5, 10 mg).
15-mg Tablets and 20-mg Tablets: Lilly’s Zydis (Velotab) again provided the fastest disintegration and dissolution. Tablet mass and
formulation might slow the release of active ingredient from generic direct compressed tablets.
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Conclusions: The in vitro disintegration test is a proxy for the disintegration process in a patient’s mouth. Differences found in the
formulation and manufacturing processes of ODO products may be associated with different disintegration times, which may potentially
impact their use in clinical practice.
Key words: In vitro analysis, orally disintegrating olanzapine
[SO-12]
Effect of duloxetine on functional outcomes in patients with major depressive disorder
Ref. No: 118
Levent Alev1, Murat Altın1, Kübra Özbek1, David Sheehan2, Adam Meyers3, Jonna Ahl4, Apruva Prakash3, Tina Marie Myers Oakes4
Eli Lilly Turkey,
1
University of South Florida College of Medicine, Tampa, USA
2
Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, USA
3
Lilly, Indianapolis, USA
4
Objective: Patients with major depressive disorder (MDD) often have a reduced ability to function socially, maintain and enjoy
relationships and work. The aim of this analysis was to investigate the efficacy of duloxetine vs. placebo on improvement in functioning
after 8 weeks of treatment.
Methods: This was a pooled analysis of data from two separate 9-month studies conducted under the same protocol in patients with
MDD (DSM-IV-TR) to examine the efficacy of duloxetine 60 mg/day (n = 518) vs. placebo (n = 258) on impairment in functioning. Pooling
the data from these studies was specified a priori in the protocol to allow for increased power to detect differences between duloxetine
and placebo on secondary and exploratory objectives. The measures included in this analysis were: the Hamilton Depression Rating Scale
(HAMD) Item 7 (Work / Activities), the Sheehan Disability Scale (SDS), the Social Adaptation Self-evaluation Scale (SASS) to assess social
behavior, the Massachusetts General Hospital Cognitive and Physical Functioning Questionnaire (CPFQ) and the Profile of Mood States
-brief form (BPOMS) subscales Vigor / Activity (VA) and Fatigue / Inertia (FI) used as surrogate measures of function. Mean changes from
baseline were analyzed by using a mixed-effects model repeated measures approach (MMRM). An analysis of covariance (ANCOVA) using
a last observation carried forward (LOCF) approach was conducted as a sensitivity analysis. The endpoint for this analysis was at week 8.
Results: At baseline, patients had moderately severe levels of SDS global functional impairment scores (18.3±6.9). At the endpoint,
there was significant improvement from baseline (MMRM) with duloxetine treatment on the HAMD Work / Activities (p<.001), Sheehan
Disability Scale global (p=.002), SASS total (p<.001), Massachusetts General Hospital Cognitive and Physical Functioning Questionnaire
(p<.001) and BPOMS Vigor / Activity (p=.012) and Fatigue / Inertia (p=.006) subscales. At the endpoint (LOCF imputation), duloxetinetreated versus placebo-treated patients had significantly greater improvement from baseline on the HAMD Work / Activities, SDS global,
SASS total, CPFQ total and Profile of Mood States -brief form subscales VA and FI.
Conclusion: These results suggest that treatment with duloxetine may improve functional impairment in patients with major depressive
disorder.
Key words: Duloxetine, major depressive disorder
[SO-13]
Effect of vitamin D on zinc status, carbohydrate metabolism, and activities of some
enzymes in alloxan-diabetic rats fed on a zinc deficient diet
Ref. No: 92
Zine Kechrid, Malika Hamdikene
Department of Biochemistry, University of Annaba, Algeria
Objective: This study was carried out to investigate the effect of vitamin D on experimental diabetes in albino (Wistar) rats fed on a zinc
deficient diet.
Methods: Male alloxan-diabetic albino (Wistar) rats of ten weeks of age were divided into three groups. The first group was fed on a zinc
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adequate diet (AZ containing 5.4 mg zinc/100g). The second group was given a zinc deficient diet (ZD containing 0.12 mg zinc/100g),
and the third group received a zinc deficient diet and was treated orally with vitamin D (12.5µg/kg) (ZD + VD). Body weight gain was
recorded regularly during the experimental period. After three weeks, the animals were sacrificed and blood glucose, serum cholesterol,
serum triglycerides, serum total protein, serum urea, serum zinc, liver zinc, kidney zinc, pancreatic zinc, femur zinc, liver glutathione
concentrations, serum glutamic oxalic transaminase (GOT), serum glutamic pyruvic transaminase (GPT) and serum alkaline phosphatase
activities were determined.
Results: The body weight gain of the zinc deficient diabetic animals at the end of three weeks of dietary manipulation was significantly
lower than that of the zinc adequate diabetic animals. The zinc deficient diet significantly increased the blood glucose, serum cholesterol,
serum triglycerides, and serum urea of the zinc deficient diabetic rats as compared to their counterparts fed on an adequate zinc diet.
Meanwhile serum zinc, femur zinc, pancreatic zinc, liver zinc, kidney zinc, serum total protein, and liver glutathione levels were diminished.
The consumption of a zinc deficient diet led also to an increase in GOT and GPT and a decrease of serum alkaline phosphatase activities.
However, vitamin D treatment ameliorated all of the previous physiological and biochemical parameters.
Conclusion: In conclusion, this study demonstrated that vitamin D reduced the severity of diabetes development caused by zinc
deficiency. In other words, vitamin D probably increased zinc absorption which led to insulin synthesis and secretion and improvement
of insulin activity.
Key words: Zinc deficiency, diabetic rats, alloxan, vitamin D, GOT, GPT, alkaline phosphatase
[SO-14]
Ref. No: 152
Gabapentin in the treatment of opioid withdrawal
Gholam Reza Kheirabadi, Mehrdad Salehi, Mohammad Reza Maracy, Mansor Ranjkesh
Isfahan University of Medical Sciences, Iran
Objectives: To evaluate the efficacy of gabapentin (1600 mg/day) as an adjunct to methadone-assisted detoxification (MAD) in the
treatment of opioid withdrawal symptoms.
Methods: Design: A 3-week open label study (as the second phase) following a double blind placebo controlled study with 900mg/day of
gabapentin (as the first phase of this study). Setting: A specialized outpatient clinic for the treatment of patients with addictive disorders.
Participants: Twenty-seven opiate addicts, who met the DSM-IV-TR criteria for opioid dependency, randomly selected among outpatients
referred to our clinic. Intervention: The subjects received adjunctive treatment with gabapentin (1600 mg/day) in addition to MAD for
three weeks. Measurements: The Subjective Opiate Withdrawal Scale (SOWS) with a total score of 0 to 64 was administered at six timepoints during the study.
Results: The total SOWS score was significantly decreased after the intervention. Compared with our previous trial, an almost significant
difference was observed in total SOWS scores between groups treated with gabapentin 1600 mg/day and 900 mg/day at the end of the
intervention period (p = 0.06). Gabapentin at a dose of 1600 mg/day was significantly superior to a dose of 900 mg/day in decreasing the
severity of coldness, diarrhea, dysphoria, yawning, and muscle tension.
Conclusion: Add-on gabapentin at a dose of 1600 mg/day may be effective in reducing some of the withdrawal symptoms in opiate
addicts undergoing methadone-assisted detoxification.
Key words: Opium dependence, opioid withdrawal, gabapentin
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[SO-15]
The role of transcranial magnetic stimulation in cognitive processes and treatment
of psychiatric disorders
Ref. No: 103
Serwa Mohamadzadeh Ashna
Young Researchers Center, Islamic Azad University, Sanandaj Branch, Sanandaj, I.R. Iran
Background and Objectives: Transcranial magnetic stimulation (TMS) is a neurostimulation and neuromodulation technique, based on
the principle of electromagnetic induction of an electric field in the brain. This field can be of sufficient magnitude and density to depolarize
neurons. When TMS pulses are applied repetitively they can modulate cortical excitability, increasing or decreasing it depending on the
parameters of stimulation, even beyond the duration of the train of stimulation. This effect has behavioral consequences and therapeutic
potential. Due to its easy use and relatively minor side effects, transcranial magnetic stimulation is now widely used in neurosciences and
medicine. The main areas of transcranial magnetic stimulation application are:
1) the investigation of cortical and spinal excitability,
2) the investigation of neuronal plasticity,
3) the investigation of neuronal connectivity,
4) functional mapping, and
5) the treatment of some neurological and psychiatric disorders.
Transcranial magnetic stimulation alone or in combination with other noninvasive neuroimaging (PET – positron emission topography,
MRI – magnetic resonance imaging) and neurofunctional (EEG – electroencephalography, ERP – event-related potentials, FMRI – functional
magnetic resonance imaging) methods allows the conduction of research on brain functions. Thus, transcranial magnetic stimulation is
suitable as a diagnostic tool in neurological and neuropsychiatric brain investigations.
Method: The method of research in this paper was a review of the literature regarding publications that applied TMS for treatment and
investigation goals. A total of 104 relevant papers were identified and reviewed and the results are presented here.
Results: TMS is, through inducement of an electrical field, a useful instrument to visualize regional activities in response to stimulation.
The mechanism of effect of TMS is through inducing the depolarization of neurons that in turn activates other neurons and produces
behavioral and cognitive outcomes, depending on the stimulated area and its function. For example some of the observable TMS-induced
effects are: phosphene by stimulating the occipital cortex, interrupting working memory and speech processes by stimulating the
frontal lobe, or improving verbal memory in major depressive disorder through modulating effects on the dopamine system. TMS, unlike
electroconvulsive therapy (ECT), does not have any substantial cognitive side effects. TMS has effects on neurochemical and synaptic
processes in neurons. There are reports in the literature that depression, mania, schizophrenia, pain disorder, hallucinations, catatonia,
post traumatic stress disorder, obsessive compulsive disorder, Parkinson’s disease, epilepsy, neuronal plasticity studies, tick disorders,
migraine and dystonia are improved by TMS procedures.
Conclusions: Current published studies and meta-analyses have evaluated the efficacy of rTMS, given in treatment paradigms that were
almost certainly suboptimal (e.g. duration of two weeks), and found that TMS is a safe and tolerable intervention. These findings raise the
possibility of using TMS as a therapeutic device in psychiatric disorders and neuroscience research.
This study summarizes the mechanisms of effect, advantages, and side effects of TMS and reviews studies of the efficacy of transcranial
magnetic stimulation on psychiatric disorders.
Key words: Transcranial magnetic stimulation (TMS), neuromodulation, electromagnetic induction
[SO-16]
Oxytocin inhibition of pentylenetetrazole-induced convulsions and its identification
by behavioral measurement and thalamic EEG in the rats
Ref. No: 112
Oytun Erbas, Vedat Evren, Saylav Bora, Gonul O. Peker
Department of Physiology, Ege University, School of Medicine, Izmir, Turkey
Objective: In this study, our aim was to reveal the possible anticonvulsant effects of oxytocin (OX) in high doses, as oxytocin has inhibitory
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effects in brain. In addition, these effects were correlated with thalamic EEG recordings. To create the convulsions, pentilentetrazol (PTZ)
was used.
Materials-Methods: In this study sixty 8-12 weeks old Sprague-Dawley adult male rats, which were separated into 10 groups (n=6), were
used. In the first through the fifth groups 10, 20, 40, 80, and 120 U/kg OX was injected intraperitoneally (i.p) in order. In the sixth group
(control), saline was injected.
Five minutes after of each injection of OX, 70 mg/kg i.p. PTZ was injected into the all rats and seizures were induced.
We evaluated the seizure behaviors with the Racine Convulsion Scale and we determined the threshold seizure dose of PTZ, around 35
mg/kg, and the suppressive dose of OX, around 80 and 120 U/kg.
The rats, which were placed in a Plexiglas cage, were evaluated according to the severity of convulsions from 0 to stage 5.
The scale of convulsions was: (0):Normal,(1):Frozen,(2):Nodding,(3):Superficial clonic movements,(4): Bilateral clonus in front extremities
(piano play)(5):generalized tonic clonic seizures and falling sideways.
To show the anticonvulsant effects of oxytocin using the EEG, the seventh through the tenth groups were used. Under anesthesia a small
hole was drilled. Then by taking the bregma as a reference using the stereotaxic method (coordinates AP:-3.6 mm, L:+2.8 mm, V:-5.0 mm)
(Paxinos Rat Brain), an exterior insulated bipolar EEG electrode was placed in the left thalamic nucleus. In the seventh group thalamic EEG
records were taken after only saline injection.
The rats in the eighth and ninth groups were injected intraperitoneally (ip) with 80 and 120 U/kg OX , respectively. In the tenth group
(control), just saline was injected. Five minutes after each OX injection, 35 mg/kg i.p. PTZ was injected into the all rats.
EEG recordings were taken for 20 minutes. The signals were amplified by 10,000 times and filtered with a range of 1-60 Hz. System records
were taken by a Biopac MP30 amplifier system and evaluated with the FFT (Fast Fourier Transform) and PSA (Power Spectral Analyses)
methods. During this process Delta 1-4 Hz, Theta 4-8 Hz, alpha 8-12 Hz and beta 12-20 Hz waves in the EEG are accepted as the ratio of
percentage in PSA methods. We affirmed the electrode location histologically following euthanisation.
RESULTS: We observed that oxytocin has a powerful anticonvulsant effect, which appears at 40 U/Kg (Stage 3.14±0.69 ) and 80 U/kg (Stage
3.0±0.57) doses moderately and which shows the maximum effect at 120 U/kg (Stage 1.57±0.53) doses (p<0.005).
After injection of subconvulsive dose of PTZ (35mg/kg) and saline, the thalamic EEG delta frequency percentage was 54.6%±2.16 and
after injection of only saline the thalamic delta frequency percentage was 80.5%±3.08. We observed significant (p<0.005) diminution in
delta frequency and also augmentation in theta frequency. The augmentation of thalamic EEG frequency is linked to the GABA blocker
effects of PTZ.
After injection of a subconvulsive dose PTZ (35mg/kg) and saline, the thalamic EEG Delta frequency percentage was 54.6%±2.16 and in
the rats given PTZ and 120 U/kg oxytocin the thalamic delta frequency percentage was 94%±1.41. In comparison there was a significant
augmentation in delta frequency (p<0.005), and a diminution in theta frequency was observed.
In PTZ and saline injected rats, the EEG formed spike-wave complexes. In the 120U/kg oxytocin and PTZ injected rats, the spike-wave
complexes disappeared.
Conclusion: Our results indicate that Oxytocin has therapeutic potential similar to anticonvulsants in epilepsy.
Key words: Thalamic EEG, oxytocin (OX), racine scale, absence convulsion, generalized convulsion, pentylenetetrazol (PTZ)
[SO-17]
The effects of metoprolol and diltiazem in the prolonged QTc interval caused by
ziprasidone injection in rats
Ref. No: 128
Oytun Erbas
Department of Physiology, Ege University School of Medicine, Izmir, Turkey
Introduction: Antipsychotic drugs cause prolongation in the QTc interval and may cause sudden cardiac death in patients. The reason for
this prolongation in QTc interval is that cardiac repolarisation is made more difficult due to the blockade of potassium channels. Therefore,
antipsychotic medications predispose patients to torsades de pointes and ventricular tachychardia. The purpose of this study was to
reveal the effects of metoprolol and diltiazem on drug induced (ziprasidone) prolonged QTc (QT correct) interval.
Materials-methods: The experiments performed in this study were carried out according to the rules in the Guide for the Care and
Use of Laboratory Animals adopted by the National Institutes of Health (U.S.A) and received consent from Ege University Animal Ethics
Committee.
In this study 18 Sprague-Dawley adult male rats were used. Before administration of the anti-psychotic under anesthesia (ketamine (40
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mg/kg) and xylazine (4 mg/kg) intraperitoneally (IP)), an ECG was taken in derivation (D) I and the normal QTc interval was determined. To
calculate the QTc interval, Bazett’s formula was used.
The rats were divided into 3 groups (n=6). For the first group, 3 mg/kg ziprasidone and saline, for the second group, 3 mg/kg ziprasidone
and 1 mg/kg metoprolol and for the third group, 3 mg/kg ziprasidone and 2 mg/kg diltiazem were administered intraperitoneally.
Two hours later, under anesthesia, the QTc interval was calculated by taking the ECG in derivation I.
Results: In the first group of rats, given ziprasidone and saline the QTc interval (0.161±0.01 s) was significantly (p<0.05) prolonged
compared to the QTc interval (0.125±0.009 s) before the drug administration.
In the second group of rats, administered ziprasidone and metoprolol, the QTc interval (0.123±0.009 s) was significantly (p<0.05) shortener
than that of the group given ziprasidone and saline (the first group, QTc interval = 0.161±0.01 s)
In the third group of rats, injected with ziprasidone and diltiazem, the QTc interval (0.125±0.004 s) was significantly (p<0.05) shorter than
that of the group given ziprasidone and saline (the first group, QTc interval = 0.161±0.01 s).
Discussion: High dose ziprasidone causes prolongation in the QTc interval. Metoprolol and diltiazem prevent ziprasidone induced
elongation of the QTc interval. The prophylactic use of these drugs may be an option for reducing the risk for ventricular arrhythmias and
sudden cardiac death in patients taking antipsychotics.
Key words: Long QTc, ziprasidone, metoprolol, diltiazem, ventricular arrhythmias, sudden cardiac death
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4th International
Antalya, Turkey
POSTER PRESENTATIONS
Poster Presentations
[PP-001]
Visual hallucinations induced by bupropion: A case report
Ref. No: 133
Sevda Korkmaz1, Murat Kuloglu2, Sadullah Saglam3, Murad Atmaca2
Department of Psychiatry, 3Department of Neurology, Psychiatric Hospital
1
Department of Psychiatry Firat University School of Medicine, Elazig-Turkey
2
Bupropion is an antidepressant, which inhibits reuptake of norepinephrine and dopamine. It is a relatively reliable antidepressant in terms
of side effects and also is used in the treatment of nicotine deprivation (1, 2). Most frequent side effects are insomnia, dry mouth, and
headache (3). Here we present a case who developed visual hallucinations during bupropion treatment.
Case: F.Y: A 51 year old woman was admitted to the outpatient clinic with complaints of hump, horror, and seeing spider images. Visual
hallucinations, anxiety, irritability, insomnia, and anhedonia were noted on psychiatric examination. Except for the visual hallucinations,
there was no other perception abnormality nor other psychotic symptoms. History: she reported to a psychiatrist with complaints
of joylessness, weakness, fatigue, and anhedonia. She was diagnosed with major depressive disorder and subsequently was put on
bupropion 150mg/day. After a week, the dosage of bupropion was increased to 300mg/day. On the first day of the bupropion dose
increase to 300 mg/day, spider images developed in both of her eyes and in the following days these images increasingly continued. The
images lasted for days and scared the patient, ruined her sleep pattern, and increased her anxiety. The patient saw an ophthalmologist
with these complaints and at the medical examination there was no evidence of an organic or pathological disorder. Her blood pressure
was under control with treatment. The patient had been treated with escitalopram and duloxetine 6 years ago with a diagnosis of
depressive disorder, but the patient specified that she had not had any visual complaints. There were not any relevant symptoms at
that time and patient was not describing any clear stress factors. The family history was unremarkable. The patient did not have such
complaints as dizziness, tinnitus, or paraesthesia and there was not any pathological finding at the neurological examination. Also there
were no abnormal findings in the blood tests, urinalysis, and MR imaging. The Beck depression, Beck anxiety, and SCL-90 scales showed
high levels of anxiety and moderate depression. After the assessment of all these data, suspicion was focused on the bupropion as the
main cause of the spider images (visual hallucinations). The patient did not accept hospitalization, thus she was followed up periodically.
First the dosage of bupropion was decreased to 150 mg and bupropion treatment was stopped completely in a few days. Alprazolam 0.5
mg/day treatment was started to decrease the patient’s anxiety. Paroxetine 10 mg/ day was started and increased to 30 mg/day in two
weeks. Following the discontinuation of the bupropion, the visual hallucinations disappeared in a few days. The patient came for controls
monthly and at the end of the 6th month the symptoms of depression and anxiety had decreased considerably.
Comment: Bupropion has become a popular antidepressant in the treatment of depressive disorders in Turkey and is preferred frequently
because of its relatively low incidence of side effects. Nevertheless every kind of side effects including psychotic symptoms that appear
during treatment should be assessed carefully.
Key words: Bupropion, hallucination, antidepressant
References:
1.
Ascher JA, Cle JO, Colin JN, et al. Bupropion: A review of its mechanism of antideressant activity. J Clin Psychiatry 1995;56:395-401.
2.
Englisch S, Inta D, Eer A, Zink M (2010) Bupropion for depression in schizophrenia. Clin Neuropharmacol; 33(5): 257-259.
3.
Hurt RD, Sachs DPL, Glover ED, Offord KP, Johnston JA, Dale LC, et al. A comparison of sustained release bupropion and placebo. N Engl J Med 1997;337:1195-1202.
[PP-002]
Clinical features of patients with panic disorder in outpatient clinics of a psychiatric
training and research hospital
Ref. No: 139
Ramazan Konkan1, Erkan Aydın1, Oya Güçlü1, Ömer Şenormancı1, Mehmet Z. Sungur2
MD, Psychiatrist in Deparment of Psychiatry in Bakirkoy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, Istanbul Turkey
1
MD, Proffessor in Deparment of Psychiatry, Marmara University School of Medicine, Istanbul Turkey
2
Objective: Panic disorder is a disorder characterized by recurrent unexpected panic attacks where the patient may exhibit avoidance
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behavior by experiencing anticipatory anxiety for further attacks. According to the DSM-IV-TR, panic disorders are divided into two types:
with and without agoraphobia. Agoraphobia is an anxiety disorder in which there are repeated attacks of intense fear and anxiety, and
a fear of being in places where escape might be difficult, or where help might not be available, and it results in obvious avoidance of
feared places and situations. Panic attack is characterized by intense anxiety that occurs unexpectedly and spontaneously, accompanied
by somatic and cognitive symptoms. A marked deterioration can be observed in patients’ functions, particularly due to the anticipatory
anxiety and avoidance behaviors (1,2). The cognitive rationale of panic disorder is linked to a catastrophic interpretation of bodily
sensations. Negative and anxiety-related processes of thought such as heart attack, cerebral hemorrhage, and loss of control are effective
in the origin of panic attacks due to a catastrophic interpretation (3). The objective of our study was to identify clinical characteristics
involved in the onset and maintenance of this disorder in patients who presented to a training and research hospital.
Method: The study included 101 consecutive patients with panic disorder who presented to the clinics at the Bakirköy Hospital for
Mental and Neurological Disorders, met the inclusion criteria, volunteered to participate in the study, and provided informed consent.
The diagnosis was made by two psychiatrists, who were not involved in the study. The diagnosis was confirmed using the Structured
Clinical Interview Form for the DSM-IV Axis I Disorders (SCID-I). The patients filled in a sociodemographic form, which examined clinical
characteristics of the disease in detail, including the identifiable life events triggering the disease and the environmental conditions where
the attacks developed, taking the SCID-I clinical interview guide into consideration.
Results: The mean age of participants was 36.73 ± 9.42 years (min: 19, max: 58 years). The mean age of onset was 29.94 ± 9.17 years,
and the mean duration of disease was 6.73 ± 7.65 years. The sociodemographic characteristics of the participants are outlined in Table 1.
Distribution of the complaints listed in accordance with the DSM-IV-TR panic disorder criteria by their incidence is provided in Table 2 (only
the first 3 criteria among the DSM-IV-TR panic disorder criteria were included in the assessments). The clinical characteristics of patients
specific to panic disorder are shown in Table 3.
Discussion: Understanding the clinical characteristics specific to panic disorder, which have a significant impact on the functioning
of a person due to escape, avoidance, and safety seeking behaviors as a result of a catastrophic interpretation of bodily sensations, is
important in conceptualization and therapeutic interventions of the disorder.
In the present study, the population was not well reflected in terms of gender as participants were consecutively enrolled from the clinics
of a training and research hospital. It was a single-center study, and Axis I and II comorbidities were not evaluated. We believe that further
studies eliminating such limitations would be beneficial.
Key words: Panic disorder, panic symptoms, avoiding behavior
[PP-003]
Effect of calcium in treatment of premenstrual syndrome
Ref. No: 141
Mandana Zafari, Azar Aghamohammadi
Department of Midwifery Group, Islamic Azad University, Sari Branch, Sari, Iran
Purpose: The occurrence of menses is a natural and biological event, which is experienced by half of the human race for about 30 years of
life. This natural phenomenon is often surrounded by vagary, delusions, and negative views, and for some women menses means disorder,
wound or mental and physical impurity. This feeling is matched with premenstrual stress and its destructive complications overshadow
the lives of these women. This syndrome as an unsolvable problem lasting during a significant portion of human life and causes family
problems, misbehaviour with children, problems at work, or absences from work. All of these consequences have caused the public media
to pay much attention to this syndrome in recent years. The purpose of this study was to determine the effect of calcium in the treatment
of premenstrual syndrome.
Method: This study was done using a semi-experimental method, among all of medical students at the Medical School of Mazandaran,
who filled in the questionnaire to diagnose this syndrome (Rosignol Bonlender Questionnaire) during a period of 3 months. This
questionnaire included demographic information, entrance and omission criteria, check paper, and a symptom list of Rosignol Bolender.
A total of 200 girls who suffered from the moderate or severe form of this syndrome were selected randomly and divided in two groups.
The first group (100 girls) took 100 mg /day of calcium for 7 days at the end of their cycle and the second group (100 girls) took placebo
for 7 days at the end of their cycle. The duration of the treatment was 3 months. After the treatment, the severity of physical and mental
symptoms was compared. Also the comparison after the intervention was done in two groups.
Results: Based on the independent sample test, these two groups were homogeneous with respect to age (p = 0.233, based on
independent sample test ), education level (p = 0.328, based on x2 tests , length of menstrual cycle (p = 0.245), based on independent
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sample test ), severity of physical symptoms before intervention (p = 0.141), severity of mental symptoms before the intervention (p =
0.132), severity of physical and mental symptoms altogether before the intervention (p = 0.144). In the first group there was a meaningful
difference between the severity of physical (p= 0.000), mental (p= 0.000) and physical & mental symptoms combined (p= 0.000 ) between
before and after the intervention measurements. The reduction in severity of physical, mental, and physical and mental symptoms
altogether after the intervention were meaningful between the two groups (p= 0.000).
Conclusion: Based on our results calcium may improve the symptoms of premenstrual syndrome.
Key words: Premenstrual syndrome, calcium, placebo, physical symptoms, mental symptoms
[PP-004]
Eye movement desensitization and reprocessing (EMDR) treatment in a patient
with post-traumatic stress disorder: A case report
Ref. No: 203
Hakan Balibey1, Adem Balikci2
Department of Psychiatry Ankara Military Hospital, Ankara, Turkey
1
Department of Psychiatry Samsun Military Hospital, Samsun, Turkey
2
Post-traumatic stress disorder (PTSD) is a psychiatric disorder that is characterized by autonomic, dysphoric, and cognitive signs together
with affective numbing and distressed re-experiencing and avoidance of previous traumatic events in a person who has encountered,
lived, or heard an excessively traumatic event.
EMDR is a psychological method, which has proven to be effective bringing together elements of well-established approaches such as
psychodynamic, cognitive, behavioral, and client-centered approaches.
In recent years, there has been an interest in using the EMDR (Eye Movement Desensitization and Reprocessing) therapy. One of the
reasons for this interest may be its effectiveness shown by numerous studies, especially, conducted with individuals who suffer from Post
-Traumatic Stress Disorder (PTSD). EMDR is known to be an innovative approach that accelerates information processing and facilitates
the integration of fragmented traumatic memories. This process is stated to allow better integration of the information that a person
has to handle in the future. Recent practice guidelines and meta-analyses have designated EMDR as a first-line treatment for trauma.
Although the prevalence of trauma and trauma related disorders is high in Turkey, there have been a limited number of published studies
highlighting treatment options (6-8). Given the effectiveness of EMDR regarding trauma and related disorders, the utilization of the
technique by a broad number of mental health professionals may not only increase the professionals’ competency in treatment of these
disorders, but also may provide patients suffering from the mentioned disorders a chance to recover in a relatively short period of time.
In this paper, the treatment process with Eye Movement Desensitization and Reprocessing (EMDR) of a case, who showed signs of posttraumatic stress disorder after a car accident and the need to use this effective method by clinicians more frequently and broadly in posttraumatic stress disorder patients will be discussed.
Key words: Eye movement desensitization and reprocessing, therapy, trauma, post-traumatic stress disorder (PTSD)
References:
1.
Sadock BJ, Sadock VA. Kaplan & Sadocks’s Synopsis of Psychiatry: Behavioral Sciences, Clinical Psychiatry. Ninth ed., Philadelphia, Lippincott Williams & Wilkins,2003
p.623-31.
2.
Amerikan Psikiyatri Birliği. Psikiyatride Hastalıkların Tanımlanması ve Sınıflandırılması El Kitabı. Yeniden gözden geçirilmiş dördüncü baskı (DSM-IV-TR),Washington
DC, Amerikan Psikiyatri Birliği, 2000’den çeviren E Köroğlu, Ankara, Hekimler Yayın Birliği, 2001.
3.
Shapiro, F., Eye Movement Desensitization and Reprocessing: Basic Principles, Protocols and Procedures, 2nd Edition, Guilford Press,Newyork, 2001.
4.
Bisson J, Andrew M. Psychological treatment of post-traumatic stres disorder(PTSD). Cochrane Database Syst Rev 2007;18(3):CD003388.
5.
Seidler GH, Wagner FE. Comparing the efficacy of EMDR and trauma-focused cognitive-behavioral therapy in the treatment of PTSD: a meya-analytic study. Psychol
Med 2006;36(11):1515-22.
6. Kavakcı Ö, Doğan O, Kuğu N. EMDR (eye movement desensitization and reprocessing): a different option in psychotherapy. Düşünen Adam The Journal of
Psiychiatry and Neurological Sciences 2010;23(3):195-205.
7.
Hocaoğlu Ç, Sağlam D. Post-traumatic Stress Disorder in the Elderly: A Case Report. Klinik Psikiyatri 2007;10:223-27.
8.
Kavakçı Ö, Yıldırım O, Kuğu N. EMDR for Post Travmatic Stress Disorder and Test Anxiety: A Case Report Klinik Psikiyatri 2010;13:42-47.
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[PP-005]
Ref. No: 208
Cabergoline induced manic episode: A case report
Rabia Nazik Yuksel, Zeynep Elyas Kaya, Nesrin Dilbaz
Department of Psychiatry, Ankara Numune Training and Research Hospital, Ankara, Turkey
Cabergoline is an orally administered synthetic dopamine agonist, which is used for the treatment of hyperprolactinemia, Parkinson
Disease, and antipsychotic-induced prolactin elevation.
One major characteristic of cabergoline is its long duration of effect. It is highly effective in suppressing prolactin levels up to 21 days after
a single 1 mg oral dose. The prolonged elimination half-life offers an advantage of once daily dosing but it might be a handicap in terms
of wash-out of adverse effects like psychosis.
Cabergoline has been associated with adverse reactions consistent with other dopaminergic agonists including cardiovascular,
gastrointestinal, and neuropsychiatric effects. It is known that dopaminergic treatment is a remarkable risk factor for psychosis. A number
of reports implicate dopamine agonists in the development of psychosis. But there is no report in the literature on dopamine agonistinduced mania. In this case, we report the first manic episode occurring after cabergoline use for hyperprolactinemia treatment. In
susceptible individuals, cabergoline can cause manic episodes and cabergoline should be used more carefully considering the risk-benefit
ratio.
Key words: Cabergoline, manic episode, bipolar disorder, dopamine agonists, hyperprolactinemia
[PP-006]
Substance use and eating patterns of female adolescent students
Ref. No: 218
Joung Sook Ahn, Jongho Shin, Ki Chang Park, Seongho Min, Min Hyuk Kim
Department of Psychiatry, Wonju Medical Center, Yonsei University, Wonju, South Korea
Introduction: The problems of smoking and/or drinking among female adolescents come to the front as a serious social problem, as
the rate of occurrence of these behaviors among female adolescents is on the increase. Substance use disorders and eating disorders
frequently co-occur in the presence of other psychiatric disorders. Although this co-occurrence suggests the possibility of shared factors
in the etiology of these two problems, research to date has not established such links. Regardless of the meaning of the association, the
reality that substance use disorders and eating disorders frequently co-occur has important implications for assessment, treatment, and
future research, especially for female adolescents.
Objectives: The first objective of this research was to estimate the rates of smoking and drinking problems among female adolescent
students and the second was to examine their association with psychopathologies and eating behaviors.
Methods: We surveyed 861 female adolescents, 405 students in the 8th grade of one middle school and 456 students in the 10th grade
from two high schools in Wonju, South Korea. Each student completed a questionnaire that consisted of demographic data, parental
monitoring, her attitude toward her parents (CATP), her own attitude toward alcohol, tobacco, and foods, BMI, and the difference between
perceived and ideal body images (DoBI). The TFEQ (Three Factor Eating Questionnaire) for eating patterns and the self-report version of
SDQ (Strengths and Difficulties Questionnaire-self report) for psychopathology were also administered.
Results: 1) For the 8th graders, the prevalence of smoking and drinking were 8.6% and 18.4%, respectively. These prevalences were
14% and 48.3% correspondingly in the 10th graders (Table 1). 2) Female adolescents with smoking and/or drinking habits, except for
the 10th graders with smoking, showed inattention-hyperactivity and conduct problems more frequently than the students without
substance use habits. 3) The 10th graders who reported drinking had eating patterns characterized by dietary restraints, and the 8th
graders with drinking problems showed disinhibition of eating patterns (Table 2). 4) The female adolescents with a high score in the
difference between perceived and ideal body image showed inattention-hyperactivity and emotional problems more frequently
(Table 3).
Conclusions: From these results, we suggest that middle-school girls may start smoking to reduce their weight. The lower the disinhibition
score is, the higher the risk of smoking and drinking. For the high-school girls, the lower the dietary restraint score is, the higher the risk
of drinking. In conclusion, smoking and drinking behaviors are closely related to externalizing problems such as inattention-hyperactivity
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and conduct problems and eating behavior is mainly related to drinking rather than smoking. The association of eating behavior and
drinking is likely correlated through the medium of various psychopathologies.
Key words: Substance use, eating pattern, psychopathology, female adolescents.
[PP-007]
Neuroleptic malignant syndrome: A case report
Ref. No: 219
Hale Yaci1, Esra Kaymak Koca1, Yasemin Uz1, Aysun Demir1, Aygun Akbay Ozşahin2, Fusun Mayda Domac2
Department of Psychiatry, Erenkoy Mental Research and Training Hospital, Istanbul, Turkey
1
Department of Neurology, Erenkoy Mental Research and Training Hospital, Istanbul, Turkey
2
Summary: Neuroleptic Malignant Syndrome (NMS) is a state, which commonly presents with autonomic changes like fever exceeding
40 degrees Celsius, muscle rigidity, changes in mental status, tachypnea, and fluctuations in blood pressure. It occurs mostly due to
classical antipsychotic drugs with high potency. However, atypical antipsychotic drugs, such as fluoxetine, reserpine and phenothiazinelike antiemetics, can also cause NMS. We present a case of a 38 year-old patient with chronic schizophrenia, who developed NMS after
ingestion of the intramuscular form of zuclopenthixol acetate 50 mg/ml twice, two days apart.
Case: A 38 year-old, single, male patient with a diagnosis of chronic schizophrenia for 18 years. While being followed up with clozapine
300 mg/d, amisulpride 200 mg/d for the last 6 months, upon oral administration of zuclopenthixol acetate 50 mg/ml (im) twice, two days
apart, by his family for an acute psychotic flare, he presented to the emergency room with sweating, progressive dysphagia, refusal of
food intake, hypersalivation, slowing of speech, dysuria, and muscle cramps. On examination, his body temperature was 39.3 degrees
Celsius, heart rate was 110 bpm, blood pressure was 120/70 mm-Hg, and the patient was tachypneic (32/min). There were no pathological
findings apart from urinary incontinence. On laboratory work-up: WBC=12700/mm3, CPK=3226 U/l, urea=74 mg/dl, creatinine=1.4 mg/dl,
Fe=19 U/dl. On follow up, a mild to moderate increase in leukocytosis was seen. For hydration, 2000 cc IV fluid was given as a replacement
with regards to his urinary output. All antipsychotic drugs were stopped. He was put on lorazepam 1 mg/dl because of agitation. On follow
up, his leukocyte count went back to normal, CPK level was down from 3226 to 102 consecutively. Urea and creatinine levels were 20 mg/
dl and 1.4 mg/dl, respectively. His oral intake returned to normal in 5 days; fluid replacement was continued for 3 more days. His rigidity
was still present but to a lesser extent and after 10 days the patient was discharged with clinical recovery.
Conclusion: NMS is often seen within 10 days following antipsychotic use; however, regardless of dose and duration of usage, it can
be seen at any stage of therapy. There are no cases reported in the literature like ours on oral ingestion of the intramuscular form of an
antipsychotic drug. We believe that as the number of case reports on NMS increase, this issue will be better understood.
Key words: Neuroleptic malignant syndrome, chronic schizophrenia, zuclopenthixol acetate.
[PP-008]
Treatment of clozapine induced obsessive compulsive behavior in a schizophrenic
patient with valproic acid augmentation: A case report
Ref. No: 223
Fatih Canan1, Unsal Aydınoglu2, Gjergji Sinani3
Bolu İzzet Baysal Ruh Sağlığı ve Hastalıkları Hastanesi, Bolu, Turkey
1
Atatürk Üniversitesi, Psikiyatri Anabilim Dalı, Erzurum, Turkey
2
Marmara Üniversitesi, Psikiyatri Anabilim Dalı, İstanbul, Turkey
3
Introduction: The comorbidity of obsessive-compulsive disorders (OCD) and schizophrenia has been documented by epidemiological
investigations. Within the multiple pathogenetic factors leading to OCD in schizophrenic patients, treatment with atypical antipsychotics
has been proposed for a significant subgroup of these patients. Herein, we report the case of a schizophrenic patient who developed
clozapine-induced obsessive compulsive symptoms that responded to valproic acid augmentation.
Case Report: A 51-year-old male patient first developed paranoid delusions and auditory and visual hallucinations at the age of 23,
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fulfilling the diagnostic criteria of the DSM-IV for schizophrenia. He had been hospitalized several times and underwent various treatment
regimens (including electroconvulsive therapy) in the past for acute schizophrenic episodes. He had been in remission with clozapine 500
mg/day for approximately one year before relapse occurred as a result of treatment noncompliance. He was admitted to hospital with
exacerbation of positive symptoms. He was started on clozapine 50 mg/day and titrated up to 500 mg/day. A significant improvement
was observed in positive symptoms. However, he developed compulsive hand washing behavior in the 3rd week of the treatment. He had
been spending 5 to 8 hours a day washing his hands although he recognized that it was senseless. He did not have a history of obsessivecompulsive disorder. We assumed clozapine-induced obsessive compulsive symptoms and gradually decreased the dosage of clozapine
which resulted in aggravation of positive symptoms and elevated mood. Therefore, valproic acid 1000 mg/day was added to the regimen
of clozapine 500 mg/day. Two weeks after starting valproic acid, the patient`s positive symptoms and elevated mood were significantly
reduced and his compulsive hand-washing disappeared. He was discharged and in a 3 month-follow-up, he was maintained well under a
combined treatment with clozapine and valproic acid.
Discussion: Our patient developed hand-washing compulsion during treatment with clozapine,an atypical antipsychotic, which
disappeared after augmentation of valproic acid. Although a few case reports have mentioned the efficacy of valproic acid in the treatment
of OCD, there is only one case report showing alleviation of clozapine-induced OCD symptoms with valproic acid augmentation in a
patient with schizophrenia. In light of our case report, we suggest that valproic acid may be a choice when treating OCD symptoms which
may appear as an adverse effect of atypical antipsychotics in patients with schizophrenia. Case-controlled studies are required to establish
the efficacy of valproic acid in the treatment of antipsychotic-induced OCD symptoms before definitive conclusions can be reached.
Key words: Clozapine, obsessive compulsive behavior, schizophrenia, valproic acid, augmentation
[PP-009]
Treatment of bipolar disorder in adolescents: A case report
Ref. No: 227
Çagdas Hunkar Yeloglu1, Hulya Guveli1, Kadir Sarp3, Bulent Bahceci2, Cicecek Hocaoglu2
Psychiatry Clinic, Rize Training and Research Hospital, Rize-Turkey
1
Department of Psychiatry, Rize University, Faculty of Medicine, Rize-Turkey
2
Gynecology and Pediatrics Hospital, Trabzon-Turkey
3
Bipolar disorder in adolescents is a chronic and recurrent psychiatric disorder with significant short-term and long-term morbidity. Bipolar
disorder can occur with different clinical manifestations in the adolescent stage compared to the adult form and usually results in a wrong
diagnosis. Mixed and rapid cycling type mania can be seen more frequently in adolescents than adults. This disorder often results in poor
academic and social-family performance, legal problems, and increased risk of suicide. For these reasons, it should be treated in a timely
and effective manner. However, information on the treatment of bipolar disorder in children and adolescents is limited. We discussed
prospective studies with more reliable methods that have been published in the last 10 years. With the recent indication of risperidone,
aripiprazole, quetiapine and olanzapine for treatment of bipolar disorders in children and adolescents, the atypical antipsychotics are
rapidly becoming a first-line treatment option. The effectiveness of lithium and other mood-stabilizing drug are also supported in
monotherapy and combination treatment. Studies concerning the pharmacological treatment of bipolar disorders in adolescents have
commonly focused on the treatment of manic episodes, and very few data are available regarding the treatment of bipolar depression,
maintenance treatments, and comorbid diseases. Also, further studies examining the safety, efficacy, tolerability and neurobiological
effects of psychotropic medications in children and adolescents with or at familial risk for developing bipolar disorder are needed. In this
case report, we will review clinical manifestations, differential diagnosis, and current treatment approaches of bipolar mood disorder. To
this end, we will present and discuss the case, and the relevant literature, of a 16 year old female inpatient, who has received treatment at
our clinic, has had a bipolar mood disorder diagnosis for 2 years and has been taking an atypical antipsychotic medication with lithium.
Key words: Bipolar disorder, treatment, adolescents
References:
1.
Kılınçaslan A, Savaş HA. Çocuk ve Ergenlerde İki Uçlu Bozukluğun İlaçla Tedavisinde Yeni Gelişmeler Güncel Psikiyatri ve Psikonörofarmakoloji 2011;1(1):24-36.
2.
Taylor E. Managing bipolar disorders in children and adolescents. Nat Rev Neurol 2009;5(9):484-91.
3.
Sayar K, Öztürk M, Özer AÖ. Üç Olgu Nedeniyle Ergenlik Döneminde Bipolar Bozukluk Van Tıp Dergisi, 2000; 7(2):66-77.
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[PP-010]
Leukopenia and neutropenia due to venlafaxine use: A case report
Ref. No: 273
Erdem Onder Sonmez, Nazmiye Kaya
Department of Psychiatry, Selçuk University, Meram School of Medicine, Konya-Turkey
Background: Neutropenia is a serious side effect of psychopharmacological treatment. Neutropenia is defined as less than 0.5 x 109/L
mature neutrophil cells. Patients with such severe acute neutropenia are likely to experience life-threatening and sometimes fatal infections.
This report includes a case, who developed leukopenia and neutropenia due to venlafaxine use and a review of the relevant literature.
Case: A 27 year-old, married female patient, who had a history of major depression and used venlafaxine 75mg/day for 6 months 5 years
ago. The patient reported a significant decrease in psychiatric symptoms and no side effects due to the treatment in this period. The
patient reported that the symptom remission had been sustained for 4 years. She reported that complaints including anxiety, palpitation,
dyspnea, paresthesia, and fear of death started recently following a psychosocial stress. A psychiatrist prescribed venlafaxine 75mg/day
with a diagnosis of panic disorder. After one month a complete blood count test was performed because the patient complained of
fatigue. It indicated neutropenia and leukopenia (neutrophil count, 1.2K/uL; leukocyte count, 3.26K/uL). The same test was repeated after
2 weeks and it indicated a progression in severity of neutropenia and leukopenia (neutrophil count, 0.37K/uL; leucocyte count,2.38K/
uL). She had no other concerning pharmacological agent. Because medical evaluations found no other medical problem associated with
neutropenia, venlafaxine was stopped. Two weeks later, the neutrophil count was 2.54K/uL and the leukocyte count was 4.77K/uL. The
patient’s hematological table recovered within one month.
Conclusion: Neutropenia and leukopenia have never been reported during treatment with venlafaxine. A case presentation of
neutropenia is reported with combined treatment of mianserin and venlafaxine. When neutropenia and/or leukopenia develop during
a drug treatment the drug should be stopped immediately. Blood cell counts can return to normal after stopping the drug. In our
case blood cell counts were completely normal in 2 weeks after stopping venlafaxine. It is important to consider routine blood tests in
psychopharmacological treatments.
Key words: Leukopenia, neutropenia, side effect, venlafaxine
References:
1.
Anghelescu I, Klawe C, Dahmen N. Venlafaxine in a patient with idiopathic leukopenia and mirtazapine-induced severe neutropenia. J Clin Psychiatry 2002; 63(9):838.
2.
Andrès E, Maloisel F. Idiosyncratic drug-induced agranulocytosis or acute neutropenia. Curr Opin Hematol 2008; 15(1):15-21.
3.
Lucht MJ, Kleinschmidt R, Maier W, Rietschel M. Agranulocytosis during treatment with mianserin and venlafaxine. J Clin Psychopharmacol 2000; 20(4):490-1.
[PP-011]
EMDR treatment for a sexual rape victim: A case report
Ref. No: 138
Mehmet Ak, Ebru Sinici, Ozgur Maden, Ali Bozkurt, Aytekin Ozsahin
Department of Psychiatry, Gulhane School of Medicine, Ankara, Turkey
Almost anyone who has had a traumatic experience might show intense stress symptoms. It is possible to see post-traumatic stress symptoms
especially among people who have been raped. Recently, efforts to provide counseling for rape victims have become common. The EMDR
treatment focuses on the sensorial units of the memory (emotional, cognitive, and physical) to reach the disturbing events, accelerate
functions, and improve the learning process. It is thought that EMDR treatment relieves post-traumatic stress symptoms for rape victims. In
this case 90 minute EMDR sessions were applied. The Beck Depression Inventory (BDI), Beck Anxiety Inventory (BAI), State and Trait Anxiety
Inventory-I (STAI-I), and Impact of Events Scale- Revision (IES-R) were completed before and after treatment and 1 month later in a follow up
session. It was observed that the stress symptoms of the patient decreased shortly after the EMDR treatment and 1 month later in the follow
up session. Although the study was conducted with one individual, in patients with sexual trauma, the EMDR application might be beneficial.
Key words: Trauma, rape, EMDR
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[PP-012]
Influence of family and education factors on the inclination to commit crimes in
Soviet times and today
Ref. No: 124
Elena Valzdorf
Irkutsk Regional Psychoneurologic Dispensary, Irkutsk, Russia.
Objective: The objectives of the research were to study the influence of education level and some family factors (alcohol addiction of
parents, upbringing in a one-parent family) on the inclination to commit criminal offences in the examined individuals in Soviet times in
comparison to the current situation. Material and methods: 35 reports of the Commission of forensic psychiatric experts over the period
of January - March 2010 (the examined individuals of group 1) and 35 archive acts of outpatient forensic psychiatric examination that
covered the period of January-March 1991 (the examined individuals of group 2) were analyzed. In total 70 men aged between 15 and 75
were considered. The statistic method, comparative analysis, in combination with the data on the somatoneurological state and the data
of an experimental psychological study were applied.
Results: The study found out that 20 patients of group 1 were held criminally responsible under article 131 of the RF Criminal Code (CC),
13 under article 132 of the RF CC, and 2 individuals were held criminally responsible under article 135 of the RF CC. Out of total 20 patients,
14 had received incomplete secondary education, 7 did not receive any education at all, 6 individuals received full secondary education,
4 incomplete secondary vocational education, 4 higher vocational education, and 1 patient received education in the form of 8 years of
special school. The family history data showed that 10 patients were brought up in the family in which either 1 or both parents abused
alcohol, 9 individuals were raised and developed in a one-parent family, 8 individuals did not have parents at all, and only 8 out of the
35 patients of group 1 were brought up in secure families. The 35 patients of group 2 included 9 individuals that were held criminally
responsible under article 144 of the RSFSR CC, 5 under article 108 of the RSFSR CC, 4 under each of articles 103, 145 of the RSFSR CC, 2
under each of articles 117, 206, 246 of the RSFSR CC, 1 under each of articles 89, 102, 120, 148, 188, 212, 224 of the RSFSR CC. In group
2 there were 15 individuals with incomplete secondary education, 13 with incomplete secondary vocational education, 5 with full
secondary education and 2 with full secondary vocational education. The family history data showed that 18 patients from group 2 were
brought up in the family where either one or both parents abused alcohol, 28 were raised in a two-parent secure family and 7 individuals
were raised in a one-parent family.
Conclusion: The study demonstrated a clear relationship between the education level and some family factors affecting the inclination
to commit criminal offences. Now the number of criminal offenses against the person that are committed by uneducated individuals
has increased, as well as crimes committed by those who have higher vocational education, while the number of secure families has
decreased, which in turn has exacerbated the criminal situation in the country.
Key words: Education factors, Soviet times, forensic psychiatric examination
[PP-013]
Survey of referral pathways to a crisis team
Ref. No: 108
Mahesh Nachnani, Stuart Beatson
Department of psychiatry, Pilgrim Hospital, NHS, Boston, United Kingdom
Introduction: Crisis Teams are well established in many trusts in the departments of psychiatry around the UK. The crisis team based
at Pilgrim Hospital, Boston receives 1300 referrals per year approximately. Not only is it important to know what the sources of referrals
to a crisis team are, but it is helpful to survey where the patients are discharged to at the time when a case is closed by the crisis team.
This information will have implications in terms of service provision, as well as targeting potential sources of referrals in terms of psychoeducation of not only service users, but also of referring agencies at different tiers of mental health services, from a general practitioner
to a care provider in the community.
Objectives and Methods: To ascertain sources of referrals to a crisis team and the destination to which service users were discharged at
the time of closure of a case by the crisis team.
Results and Conclusion: N = 92 records of service users were randomly selected. They all completed their journey through the crisis team
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from triage to discharge.
Key words: Crisis team, referral pathways, community care
[PP-014
Fluanxol and haloperidol efficacy evaluation in treatment of schizophrenic patients
Ref. No: 122
Elena Valzdorf
Irkutsk Regional Psychoneurologic Dispensary, Irkutsk, Russia.
Objective: The purpose of the research was to study the efficacy of Fluanxol in the treatment of schizophrenic patients compared with haloperidol.
Method: Research subjects were 23 paroxysmal progredient schizophrenia patients, who were stationary examined. There were 18 men
and 5 women among them, 6 patients of 16 to 20 years of age and 17 patients aged between 20 to 40 years.
A clinical-psychopathological research method with a psychopharmacological approach was used.
Results: Three groups of patients were picked out. The first group of 9 patients included patients with an acute and subacute exacerbation,
Kandinski-Klerambo syndrome, acute sensitive delusions of grandeur, of influence, of persecution with imperative pseudo hallucinations,
and open thought symptoms.
The second group of 4 cases included patients with paraphrenia acute exacerbations, expansive delusions, and auditory pseudo
hallucinations with oneric inclusions.
In both groups the therapy began with traditional neuroleptics. Haloperidol depot 5 mg was prescribed intramuscularly once every 2
weeks, but haloperidol intravenously from 5 to 10 mg a day. During 7-10 days of treatment, productive psychotic symptoms were reduced
only through intensity in order to change preparation closed to atypical antipsychotic drug. So Fluanxol depot from 10-20 mg was
prescribed intramuscularly once every 2 weeks and at the same time patients took it from 3 to 10 mg twice a day inside. During Fluanxol
therapy, psychotic symptoms were reduced after 5-7 days of treatment.
The third group of 10 people included less progredient schizophrenia patients with neurosis-like negative symptomatology. Haloperidol
from, 1.5 to 5 mg a day inside for 3-4 weeks of treatment, didn’t have a positive effect on the negative symptoms. Fluanxol, from 1 to 3 mg
twice a day inside for 7-12 days of treatment, caused a decrease in intensity or a complete reduction in negative symptomatology, so as
mimics, mood, emotions were improved. This Fluanxol effect was shown by the two first groups having negative symptoms. Most patients
took it without any corrector-preparation.
Conclusion: Fluanxol is more effective in the treatment of schizophrenic patients.
In comparison with haloperidol it decreased positive symptomatology more quickly, decreased or completely reduced negative
symptoms and only in some cases caused drug side effects.
Key words: Fluanxol, haloperidol, schizophrenia
[PP-015]
Anorexia nervosa and cannabis abuse: A case report
Ref. No: 241
Semra Karayılan, Atila Erol
Department of Psychiatry, Sakarya University School of Medicine, Sakarya, Turkey
Rates of comorbidity are higher in patients with eating disorders and also the number of comorbid disorders is numerous. Most
comorbidities associated with eating disorders are mood disorders, anxiety disorders, personality disorders, and substance use disorders.
According to past research, there is a high rate of comorbidity of alcohol-substance abuse and eating disorders. Although the majority of
studies in this area are focused on the use of alcohol, studies that have identified an association between illegal substance use and eating
disorders are also available. In a study in the USA, the use of cannabis with anorexia nervosa (AN) and bulimia nervosa (BN) disorders is
reported to be 6-7%. In Turkey, in a study that investigated the comorbidity of eating disorders and substance use, the use of alcohol and
cannabis was reported in cases of BN, but the use of psychoactive substances and cannabis was not established in cases of AN. Among
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eating disorders, alcohol or drug abuse are most often found in individuals with bulimia nervosa and bulimic behaviors. Also, binge eating/
purging anorexics appear to be more likely than restricting anorexics to indulge in substance use. Patients with bulimia nervosa have
significantly higher rates of use of amphetamines, barbiturates, marijuana, tranquilizers, and cocaine than patients with anorexia nervosa.
Compounds of cannabis like tetrahydrocannabinol activate endogenous cannabinoid receptors (CB1 and CB2) in brain. Stimulating the CB1
receptor is known to cause increased appetite and an antiemetic effect and because of these effects cannabinoids are included in clinical
use. In this case report, an anorexia nervosa case, who was a young female patient using cannabis, will be presented. The patient, a 17 yearold, high school student, lived with her family, had complaints of weight loss and had used cannabis for three years. Before beginning to
use cannabis her BMI was approximately 22, when referred to our clinic it was 15.6. She indicated that at first cannabis caused increased
appetite, but excessive vomiting occurred in the first few months and then she started to exercise excessively. Although she noticed losing
weight in this way, she did not stop the use of cannabis. According to a review of the literature in Turkey, such a case of cannabis use and
anorexia nervosa comorbidity hasn’t previously been reported. In this respect, discussion of the case in detail is important.
Key words: Anorexia nervosa, cannabis, substance abuse, eating disorders
[PP-016]
Fluoxetine-induced thrombocytopenia: A case report
Ref. No: 249
Atakan Yucel1, Mustafa Gulec1, Adem Aydin2
Department of Psychiatry, Atatürk University, School of Medicine, Erzurum-Turkey
1
Department of Psychiatry, Yuzuncu Yil University, School of Medicine, Van-Turkey
2
Case: A 44 year old, university graduate, married male with 2 children was diagnosed with a first episode major depressive disorder
and no abnormalities were observed in the routine tests, including the total blood count test carried out prior to commencing drug
therapy. Afterwards the patient was prescribed fluoxetine and the daily total drug dose was set at 10 mg for the first week of treatment
and 20 mg for the following 3 weeks. During the first follow up visit after thirty days, it was observed that the patient had gone into a
total remission and no change was made in the pharmacotherapy. However, it was learned that thrombocytopenia was detected in the
total blood count test requested by the family doctor because of a suspicion of a urinary tract infection. Since no pathology that could
account for the thrombocytopenia that was detected by a hematology expert following standard consultation and further tests, the
patient was transferred back to us with a suspicion of fluoxetine induced thrombocytopenia. Fluoxetine was immediately discontinued
and replaced with reboxetine and similarly reboxetine was prescribed as 4 mg/day for the first week and as 8 mg/day after the first week.
The thrombocytopenia of the patient went into total remission within 7 days and no problem was observed during the total blood count
tests for the next 6 months.
Even though the most common side effects of fluoxetine are nausea, nervousness, and insomnia, side effects of the hematological
system have also been noted. To this end, there are publications which suggest possible negative effects on the number and function of
thrombocytes. It is thought that the mechanism behind these hemostasis related side effects of fluoxetine is the depletion of serotonin
stores by preventing the reuptake of serotonin into thrombocytes. Starting from this hypothesis, the presumption is that reboxetine,
which is a pure noradrenaline reuptake inhibitor, will have no effect on these processes. In fact, there have been no reports that relate
reboxetine with thrombocytopenia and/or thrombocyte functional disorders. However it should be clarified with further studies whether
this is purely coincidental or if reboxetine has no effect on serotonergic systems.
Conclusion: Reboxetine may be a good alternative for patients with thrombocytopenia and/or with functional thrombocyte disorders in
the treatment of major depressive disorders. However, more research is required in order to reach more certain conclusions.
Key words: Depression, hematological, side effect, switching, reboxetine, fluoxetine, thrombocytopenia
References:
1.
Pai VB, Kelly MW. Bruising associated with the use of fluoxetine. Ann Pharmacother 1996; 30(7-8):786-788
2.
Mirsal H, Kalyoncu A, Pektaş O. Ecchymosis associated with the use of fluoxetine: case report. Turk Psikiyatri Derg 2002; 13(4):320-324
3.
Halperin D, Reber G. Influence of antidepressants on hemostasis. Dialogues Clin Neurosci 2007; 9(1):47-59
4.
Lewis G, Mulligan J, Wiles N, Cowen P, Craddock N, Ikeda M, et al. Polymorphism of the 5-HT transporter and response to antidepressants: randomised controlled
trial. Br J Psychiatry 2011; 198(6):464-471
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[PP-017]
Interethnic differences in UGT1A4 genetic polymorphisms in Mexican and
Spanish populations
Ref. No: 312
Marisol López1, Pedro Dorado2, Alberto Ortega1, Eva Peñas Lledó2, Nancy Monroy3, Esther Machín2, María Elisa Alonso3, Adrián Llerena2
Department of Biological Systems, Universidad Autónoma Metropolitana-Xochimilco, Mexico City, Mexico
1
CICAB Clinical Research Centre. Extremadura University Hospital and Medical School. Servicio Extremeño de Salud, Badajoz, Spain
2
Department of Neurogenetics and Molecular Biology, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City, Mexico
3
Clinical treatment with antiepileptics exhibits large interpatient variability. The UDP-glucuronosyltransferase (UGT) 1A4 is an enzyme
responsible for the conjugation of glucuronic acid in diverse functional groups included in various antiepileptic drugs, such as lamotrigine
and phenytoin. Several genetic polymorphisms of UGT1A4 have been described in different populations; among them, two nonsynonymous single nucleotide polymorphisms (SNPs) 70A>C (P24T; UGT1A4*2) and 142T>G (L48V; UGT1A4*3b), as well as a synonymous
variant SNP 471T>C (C157C; UGT1A4*1b). P24T and L48V polymorphisms reduce the glucuronidation activity on various substrates.
Recently, it has been shown that L48V polymorphism decreases the serum concentration of lamotrigine in patients on monotherapy or
polytherapy, resulting in clinical outcome variability.
The main goal of this study was to determine the allelic frequencies of UGT1A4*1b, UGT1A4*2 and UGT1A4*3b in a sample of Mexican
Mestizo (MM) and Spaniard (SP) healthy volunteers. UGT1A4 genotyping is clinically important in order to identify patients who may be
at an increased risk for failure of therapy and/or adverse effects to anticonvulsants such as phenytoin and lamotrigine.
In this study, the allelic frequencies of these three UGT1A4 variants were determined by combined methodology of RFLPs and RT-PCR in
MM and SP populations. The allelic frequencies of the three UGT1A4 polymorphisms analyzed showed interethnic differences between
MM and SP, that was statistically significant for UGT1A4*1b (0.17 and 0.08, respectively; p=0.002).
These data could help clinicians to improve clinical response during treatment with UGT1A4 antiepileptic drug substrates in these
populations.
Key words: Interethnic differences, UGT1A4, genetic polymorphism.
[PP-018]
Influence of CYP2C9 genetic polymorphism on losartan oxidation in an
Ecuadorian population
Ref. No: 315
Pedro Dorado, Eva Peñas Lledó, Esther Machín, Adrián Llerena, Enrique Terán, Leonardo Beltrán
CICAB Clinical Research Centre. Extremadura University Hospital and Medical School. Servicio Extremeño de Salud, Badajoz, Spain. Biomedical Centre, Central University
of Ecuador and Health Science College, Universidad San Francisco de Quito, Quito, Ecuador
Background: Cytochrome P450 2C9 (CYP2C9) is a polymorphic enzyme catalyzing the metabolism of several important drugs. CYP2C9
metabolizes a number of therapeutically important drugs, including most nonsteroidal anti-inflammatory drugs, S-warfarin, phenytoin,
and losartan. CYP2C9 is also involved in the metabolism of several important psychoactive substances (tetrahydrocannabinol, fluoxetine,
amitriptyline, phenytoin, etc.). It has been reported that CYP2C9 activity is modulated by endogenous substrates such as adrenaline and
serotonin. The involvement of CYP2C9 in the metabolism of melatonin has also been suggested.
Losartan has recently been suggested as a selective probe for CYP2C9 metabolic activity.
Objective: The aim of the study was to determine the activity of CYP2C9, using losartan as a probe drug, in relation to CYP2C9 genotype
in healthy Ecuadorian subjects.
Methods: A single oral dose of 50 mg losartan was given to 194 Ecuadorian unrelated subjects. Concentrations of losartan and its
carboxylic acid metabolite, E3174, were analyzed by means of high-performance liquid chromatography in urine collected for 8 h. The
CYP2C9 genotypes were determined in 194 subjects using specific methods for CYP2C9*2 and CYP2C9*3.
Results: The frequencies of the allelic variants CYP2C9*2 and CYP2C9*3 were 0.054 and 0.015, respectively. The urinary losartan/E3174
ratio was significantly higher (p=0.027) in subjects with the CYP2C9*1/*3 genotype (mean±SD, 12.4±13.8; n=6) than in subjects with the
CYP2C9*1/*1 (4.9±7.0; n=167).
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Conclusion: This is the first most extensive population where losartan has been used as a probe drug to evaluate the CYP2C9 activity in
vivo. The urinary losartan to E3174 metabolic ratio after a 50mg losartan dose was found to be a safe and useful phenotyping assay for
CYP2C9 activity in vivo. The CYP2C9*3 variant allele is a major determinant of the enzyme activity, and it decreases losartan metabolism
significantly, while the CYP2C9*2 allele has less impact on enzyme function.
Key words: Cytochrome P450 2C9, genetic polymorphism, losartan, ecuadorian population
[PP-019]
Efficacy of progressive muscle relaxation training on anxiety, depression and
quality of life in cancer patients under chemotherapy
Ref. No: 194
Sepideh Ershadmanesh Herizchi1, Isa Tt Piri2, Iraj Tt Asvadi3, Zohreh Tt Sanaat4, Mrs Tt Golchin5, Reza Tt Shabanloui5
Assistant Professor of Psychiatry, 2Psychologist, 3Professor of Oncology,
1
Z.Sanaat, Assistant Professor of Oncology, 5MS of Nursing, Hematology & Oncology Research Center-2010, Tabriz, Iran
4
Introduction: Chemotherapy is one of the common treatment methods for cancer. However, many side effects can be seen among
patients and some of them are very serious and painful. Alopecia, anorexia, vomiting, pain in the limbs, headache, and backache are some
unwanted effects. On the other hand many patients suffer from psychiatric disorders especially anxiety and depression probably due to
the drugs or coping with the disease state. These disorders can cause some problems in the treatment process and the Quality of life.
Patients with anxiety and depression can be treated with drugs or psychotherapy.
Progressive Muscle Relaxation [PMR] training is a cost effective self-help method promoting mental health in healthy participants.
The aim of this study was to determine anxiety, depression, and quality of life dimensions of cancer patients undergoing chemotherapy
and the effect of progressive muscle relaxation training in improving their mental health and quality of life.
Materials and Methods: This research was designed as a randomized clinical trial. Sixty cancer inpatients undergoing chemotherapy
in the Tabriz Hematology & Oncology ward in 2009 were randomly selected and divided into two groups, intervention or control. All
participants provided a written formal consent.
Anxiety, depression, and quality of life dimensions were determined with HADS and EORTC QLQ-C30 questionnaires. SPSS 16 software
was employed for the data analysis.
After completion of the 1st questionnaires by all participants, the case group was trained in progressive muscle relaxation in 3-6 person
groups, with the aim of doing it by themselves in the hospital and after discharge 2-3 times a day. At 2 weeks and one and three months
after the intervention, questionnaires were completed again by both groups, and the results were compared.
Results: After initial data analysis almost all of the participants were satisfied with the learning and the experience of this technique.
There was no significant difference between the scores of the case and control groups after PMR after 2 weeks and 1 month (p >0.05).
However, after 3 months, anxiety, depression and quality of life dimensions were significantly improved (p <0.05).
Discussion and Conclusion: Almost always side effects of chemotherapy were so terrible that participants could not benefit from PMR
in the first weeks.
However, after a decrease in the side effects of the chemotherapy and by practicing more and doing PMR better, this technique improved
anxiety, depression, and quality of life in patients with cancer.
Key words: Anxiety, depression, quality of life, chemotherapy, progressive muscle relaxation
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[PP-020]
Anxiety reducing effects of oxytocin on the basolateral amygdala by using
an electrophysiological method
Ref. No: 127
Oytun Erbas, Saylav Bora, Serdar Demirgoren, Gonul Peker
Physiology Department, Ege University, School of Medicine, Izmir, Turkey
Objective: It has been shown by behavioral studies that oxytocin has anxiolytic effects and that oxytocin in nasal spray form suppresses
amygdala activity, which is powered by anxiety as demonstrated in functional MRI studies in humans. The amygdala is a part of the
limbic system and is activated in case of fear and anxiety. This study evaluated the effects of oxytocin on the basolateral amygdala using
a spontaneous EEG.
Material and Methods: The experiments performed in this study have been carried out according to the rules in the Guide for the Care
and Use of Laboratory Animals adopted by National Institutes of Health (U.S.A) and have received consent from Ege University Animal
Ethics Committee.
The rats were maintained under controlled environmental conditions throughout the study: 22-24 °C ambient temperature, 12:12 lightdark cycle (light from 7:00-19:00), and standard laboratory food and tap water available ad libitum.
In this study 7 Sprague-Dawley adult male rats were used, which were 8-12 weeks old. Under anesthesia a small hole was drilled. Then by
taking the bregma as a reference using the stereotaxic method (coordinates Anteroposterior: - 2.8 mm, Lateral: + 4.8 mm, Ventral: - 8.5
mm) (Paxinos Rat Brain), an exterior insulated bipolar EEG electrode was placed in the basolateral amygdala.
Electrodes were fixed by using a dental acrylic (numerous alloys are used in the making of dental restorations). The rats were anesthetized
using ketamine (40 mg/kg) and xylazine (4 mg/kg) intraperitoneally (IP).
Electrodes were placed and 3 days later, while the animals were awake in their cages, spontaneous EEG recordings were taken from
the amygdala. Then, 0.9% isotonic NaCl solution was injected intraperitoneally into the rats (n = 7), and the EEG was recorded from the
amygdala while they were in their cages.
One day later to the same rats (n=7) oxytocin 10 IU/Kg (Synpitan 5 IU) was given IP, and 5 minutes later the oxytocin EEG records were
taken in their own cage.
The system recordings were taken for 20 minutes by a Biopac MP30 amplifier system in the range of the 1-60 Hz band, with 10,000
amplification. During this process Delta 1-4 Hz Theta 4-8 Hz, alpha 8-12 Hz and beta 12-20 Hz waves in the EEG were accepted as the ratio
of percentage in PSA (Power Spectral Analyses) methods. We affirmed electrode location histologically following euthanisation.
Results: There was significant (p<0.05) diminution in delta frequency (64.4 ± 10.9) in the rats given normal saline than in the spontaneous
EEG records (79.5% ± 12.8).
There was a significant (p<0.05) increase in delta frequency (76.8 ± 12.5) in rats given oxytocin one day after the normal saline was injected
(64.4% ± 10.9)(Figure I)
Conclusion: Anxiety caused by injection of a normal saline solution augmented EEG frequency when compared with resting EEG records.
Oxytocin diminished the EEG frequency of rats that had injection anxiety. This results show electrophysiologically that oxytocin is a
powerful anxiolytic.
Key words: Amygdala, anxiety, EEG, oxytocin
[PP-021]
Genital mutilation in a patient with schizophrenia: A case report
Ref. No: 134
Fulya Maner, Ozge Hisim, Ozge Sahmelikoglu, Ozlem Cetinkaya Girit, Aysegul Ermis, Mehmet Emin Ceylan
Fourth Psychiatry Unit, Bakırköy Nueropsychiatry Research & Training Hospital, Istanbul-Turkey
Genital mutilation, which is quite rare, is generally seen in young male patients. The presented patient was a 23 year old male who was
brought by his brother to our psychiatry hospital from an urology clinic. He had extracted one of his testicles with a knife without any
anesthetic and put three cherry seeds inside the injured part, then sewed up the injury. He chewed the extracted testicle and vomited the
material when his brother saw what had happen. His life history revealed that the disorder began insidiously in his late adolescence; he
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had no treatment up to then, and stayed in prison for three years due to injuring his chief with a knife because of delusions of persecution.
Autism, flattening of affect, incoherent speech and bizarre, somatic, nihilistic delusions were found in the psychiatric examination.
Flupentixol decanoate 20 mg every 15 days IM, haloperidol 20 mg/day and biperiden 10mg/day were administered first IM then orally.
There was no remission even after adding ECT for ten sessions. Then clozapine was begun at 25mg/day and titrated to 500mg/day. He
was discharged with symptoms which were much improved by using clozapine 500 mg/day, haloperidol 10 mg/day, biperiden 4mg/day,
quetiapine 300 mg/day.
In this paper a schizophrenic patient with testicular mutilation was presented and genital amputation was discussed along with reports
in the literature.
Key words: Schizophrenia, testicular mutilation
[PP-022]
Ref. No: 135
Hoarding and mood disorder: A case report
Özlem Çetinkaya Girit1, Fulya Maner1, Emine Kılınç2, Derya İpekçioğlu1, Mehmet Emin Ceylan1
Psychiatry Unit, Bakırköy Nueropsychiatry Research & Training Hospital, Istanbul-Turkey
1
NPİ Nueropsychiatric Hospital , İstanbul
2
Hoarding is the excessive acquisition of possessions and failure to use or discard them even if the items are worthless or hazardous. The
hoarder may believe that the hoarded items are very valuable, know that the accumulated items are useless, or attach a strong personal
value to items. It is not clear whether hoarding is an isolated disorder or rather a symptom of another condition such as obsessive
compulsive disorder. Hoarding seems to involve some neurological mechanisms which are detected by brain imaging studies. In this case
report a patient with mood disorder whose predominant symptom was hoarding is presented and the status of literature about hoarding
is reviewed.
Key words: Hoarding, obsessive compulsive disorder, mood disorder, dementia
[PP-023]
Effect of fish oil on treatment of premenstrual syndrome
Ref. No: 140
Mandana Zafari, Azar Aghamohammadi
Department of Midwifery Group, Islamic Azad University, Sari Branch, Sari, Iran
Objective: Women go through many hormonal changes throughout their lives from birth to death and this causes many physical and
mental challenges that are directly related to their unique reproduction delicacy. Premenstrual syndrome refers to a cyclic appearance of
somatic and psychiatric symptoms in some women. Different theories and hypotheses have been proposed and discussed on this issue.
Finding an effective and safe solution for the treatment of PMS has always been under consideration. The purpose of our study was to
determine the effect of fish oil on treatment of premenstrual syndrome.
Methods: This study was a double blind randomized placebo controlled trial. All of the medical students at the Medicine School of
Mazandaran filled in the Rosignol Bonlender Questionnaire for 3 months. This questionnaire included demographic information, inclusion
and exclusion criteria, check paper and the symptom list of Rosignol Bolender. A total of 200 girls suffering from the moderate and severe
forms of this syndrome were selected randomly and assigned in two groups. The first group (100 girls) took a 1000 mg /day capsule of fish
oil for all days of their cycle and the second group (100 girls) took placebo for all days of their cycle. The duration of this treatment was 3
months. After treatment, the severity of physical, mental, and combined physical-mental symptoms were compared before and after the
intervention. Also the comparison after intervention was done in two groups.
Results: Based on this and based on the independent sample test, these two groups were homogeneous from the point of view of age
(p = 0.287, based on independent sample test ), education level (p = 0.954, based on x2 tests), length of menstrual cycle (p = 0.305),
based on independent sample test ), severity of physical symptoms before intervention ( p = 0.039 ), severity of mental symptoms before
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intervention (p = 0.144), severity of combined physical-mental symptoms before intervention (p = 0.242) in the first group. There was a
significant difference among the severity of physical (p= 0.000), mental (p= 0.000), combined physical-mental symptoms (p= 0.000) before
and after intervention. The reduction in severity of physical, mental, and combined physical-mental symptoms after intervention was
significant between the two groups (p= 0.000).
Conclusion: Based on our results 1000mg/day fish oil may reduce the severity of physical, mental, and combined physical-mental
symptoms of PMS.
Key words: Premenstrual syndrome, fish oil, placebo, physical symptom, mental symptom
[PP-024]
Improvement of risperidone-induced hyperprolactinemia with the addition
of aripiprazole: Case report
Ref. No: 145
Medine Gıynaş Ayhan, Faruk Uguz, Nazmiye Kaya
Department of Psychiatry, Selcuk University,Meram School of Medicine, Konya, Turkey.
Objective: Hyperprolactinemia is an important side effect of antipsychotic treatment. All typical antipsychotics and some atypical
antipsychotics such as risperidone and amisulpiride have been shown to cause marked elevation in serum prolactin levels, whereas most
other atypical antipsychotics such as quetiapine, olanzapine, clozapine, ziprasidone, and aripiprazole appear to have little or no effect on
serum prolactin levels. Hyperprolactinemia can lead to gynecomastia, galactorrhea, sexual dysfunction, infertility, oligomenorrhea, and
amenorrhea. It also reduces the bone mineral density and contributes to osteoporosis in the long term. These important side effects cause
patients in remission not to continue treatment.
Case: We report two clinical cases of risperidone-induced hyperprolactinemia and amenorrhea, who with treatment by the partial
dopamine agonist aripiprazole, showed prolactin normalization.
Conclusion: Addition of aripiprazole to treatment may be considered as a first option in hyperprolactinemia cases with significant
improvement in psychotic symptoms.
Key words: Hyperprolactinemia, amenorrhea, antipsychotic, risperidone, aripiprazole
[PP-025]
Atomoxetine for the treatment of ADHD in young adults with an assessment
of associated functional outcomes
Ref. No: 146
Murat Altın1, Levent Alev1, Todd M. Durell2, Leonard A. Adler3, Dave W. Williams2, Ahmed Deldar2, James J. Mcgough4,
Paul E. Glaser5, Richard L. Rubin6, Elias S. Sarkis7, Teresa A. Pigott8, Bethany K. Boardman2
Eli Lilly and Company, Istanbul,Turkey
1
Eli Lilly and Company and/or one of its subsidiaries, Indianapolis, IN, USA
2
Department of Psychiatry, NYU School of Medicine; and Psychiatry Service, New York VA Harbor Healthcare System, New York, NY, USA
3
UCLA Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA, USA
4
University of Kentucky, Department of Psychiatry, Lexington, KY, USA,
5
Vermont Clinical Study Center, Burlington, VT, USA
6
Division of Child and Adolescent Psychiatry, University of Florida, Gainesville, FL, USA
7
Department of Psychiatry, University of Florida, Gainesville, FL, USA
8
Objectives: ADHD in young adults is associated with significant impairment in multiple functional domains. This trial examined the
efficacy of atomoxetine (ATX) in young adults and evaluated improvements in core ADHD symptoms and associated functional outcomes.
Method: Patients aged 18-30 years were randomized to 12 weeks of double-blind treatment with ATX (n=220) or placebo (PBO, n=225).
Patients in the atomoxetine treatment arm began treatment with 40 mg/day (dosed 20 mg BID) for a minimum of 7 days followed by
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80 mg/day (dosed 40 mg BID) for a minimum of 7 days. At Visit 5, or any visit thereafter, the dose could be increased to the maximum of
100 mg/day (dosed 50 mg BID) depending upon continued ADHD symptoms. One unscheduled dose change was allowed if needed for
tolerability or safety. The Conners’ Adult ADHD Rating Scale- Investigator Rated, Screening Version Total ADHD Symptoms score (CAARS
– Inv:SV) with adult ADHD prompts, assessed core ADHD symptoms and was the primary efficacy measure. The adult ADHD Quality of
Life-29 (AAQOL-29) scale evaluated functional outcomes in various life domains. Other assessments included Clinical Global ImpressionADHD-Severity (CGI-ADHD-S), CAARS Self Report (CAARS-S:SV), Patient Global Impression-Improvement (PGI-I), Behavior Rating Inventory
of Executive Function-Adult Version Self Report (BRIEF-A), and measures for depression, anxiety, sleepiness, driving behaviors, social
adaptation, and substance use. Reported means are least-squares means from last-observation-carried-forward ANCOVA models. A
mixed-model repeated measures visit-wise analysis was also conducted.
Results: Significant improvement (mean±SE) after ATX treatment was demonstrated on CAARS-Inv:SV (ATX [-13.6±0.8] vs. PBO [-9.3±0.8],
p<.001), AAQOL-29 (ATX [14.8±1.1] vs. PBO [10.6±1.1], p<.001), CGI-ADHD-S (ATX [-1.1±0.1] vs. PBO [-0.7±0.1], p<.001), CAARS-S:SV (ATX
[-11.9±0.8] vs. PBO [-7.8±0.7], p<.001), and on most components of BRIEF-A, but not PGI-I. Additional assessments were not significant
(p>0.05). The adverse event profile in this study was similar to that observed in other ATX studies.
Conclusion: ATX improved core ADHD symptoms with respect to PBO in young adults. Several functional outcomes and executive
functioning measures improved significantly with ATX treatment. ATX was generally well-tolerated.
Key words: ADHD, atomoxetine, efficacy, functional outcomes.
[PP-026]
Role of psychopharmacological intervention in cognitive and psychological
recovery in hemorrhagic brain injury
Ref. No: 136
Rafat Mohammed Alowesie
Sultan Bin AbdulAziz Humanitarian City, Saudi Arabia
Cognitive impairment is the most common chronic sequela of brain injury, which can result in more persistent disability than the physical
injury. However, there are no medications with an approved indication for treating brain injury related cognitive impairment.
The purpose of this poster is to present a case study of a patient who sustained a severe hemorrhagic brain injury and who subsequently
experienced cognitive recovery to an unexpected degree.
Based on all criteria, this patient’s prognosis was extremely poor. Initially, he had GCS of 7/15. Upon admission to our facility for rehabilitation,
4 months after injury, he had a Rancho Los Amigos score of II, meaning that he had nonspecific non- purposeful reactions to stimuli.
Despite this, he survived his brain injury in far more than a minimally responsive state and today can reasonably be assigned the highest
Rancho Los Amigos score of VIII, meaning that he is able to learn new things and compensate for his problems. He exhibits more flexibility
in thinking and realizes that he has a problem in his thinking and memory.
The patient’s remarkable recovery can be attributed to the team effort; however, in this presentation I will focus on the psychopharmacological
intervention, which played a significant role in the patient’s cognitive and psychological recovery.
Key words: Brain injury, cholinesterase inhibitors, antidepressants, cognitive functions.
[PP-027] Ref. No: 148
Obsessive beliefs in patients with panic disorder
Ramazan Konkan1, Erkan Aydın1, Oya Güçlü1, Ömer Şenormancı1, Mehmet Z. Sungur2
Bakirköy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, İstanbul, Turkey
1
Marmara Universty School of Medicine, İstanbul, Turkey
2
Objective: A growing emphasis is given to beliefs of a person by cognitive models of anxiety disorders. Consensus ratings indicate that
6 belief domains are likely to be important in OCD. The objective of the present study was to investigate whether or not these belief
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domains, considered to be important in OCD patients, are also valid for Panic Disorder.
Method: Our sample group included 101 Panic Disorder group, and 155 healthy volunteers with similar sociodemographic characteristics.
The instruments used included the Beck Depression Inventory (BDI), State-Trait Anxiety Inventory (STAI), Panic Agoraphobia Scale (PAS), and
Obsessive Beliefs Questionnaire (OBQ-44). Total and sub-scale scores of obsessive beliefs as assessed by the Obsessive Beliefs Questionnaire-44
(OBQ-44) were compared between the groups. Total and sub-scale scores in the panic disorder group were re-evaluated against the state,
trait, and depression factors of the State-Trait Anxiety Inventory (STAI). SPSS 18.0 for Windows was used for statistical analysis.
Results: The mean age was 36.73±9.42 years in the patient group, and 34.74±12.46 years in the control group. The State Anxiety Scale
total score, Trait Anxiety Scale total score, Beck Depression Inventory total score, OBQ-44 total, and subscale scores in patients with a PAS
score of 12 or more were statistically significantly higher compared to the control group (p<0.01). No statistically significant difference was
observed in the OBQ-44 total and subscale scores in 33 patients with a PAS score of 11 or less. The group with a score of 12 or more, which
is the cut-off value in the Turkish version of PAS, had statistically significant higher scores in “perfectionism/intolerance of uncertainity”
compared to those with a PAS value of 11 or less. The ”inflated responsibility/ overestimation of threat” scores (p<0.05), ”overimportance
of thoughts/controlling thoughts” scores (p<0.05) and ”OBQ total scores” (p<0.01) were statistically significantly higher.
Comparison results for those patients with a PAS score of 12 or more with the control group in obsessive beliefs after the STAI state anxiety
level was controlled are shown in Table 1; for those with a PAS score of 12 or more with the control group in obsessive beliefs after the
STAI trait anxiety level was controlled are listed in Table 2; and for those with a PAS score of 12 or more with the control group in obsessive
beliefs after the STAI depression level was controlled are illustrated in Table 3 as OBQ-44 total and subscale scores.
Discussion: We thought that as obsessive beliefs of panic disorder are present in the active period of the disease, and they disappear
during remission, they are likely to be associated with severity of the disease. ”Overimportance of thoughts/controlling thoughts” was
considered to be a constant feature of panic disorder even when depression and trait anxiety levels of belief domain are controlled. This
common feature of OCD and panic disorder should be supported by further studies. It has been also found that depression and trait
anxiety contributed to the obsessive beliefs in panic disorder patients.
Key words: OCD, panic disorder, obsessive beliefs
[PP-028]
Erectile dysfunction in patients on methadone maintenance therapy in Malaysia
Ref. No: 151
Nik Ruzyanei Nik Jaafar1, Noormazita Mislan2, Azlin Baharudin1, Normala Ibrahim3, Salina Abdul Aziz4, Hatta Sidi1
Dept. of Psychiatry, Faculty of Medicine, Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia
1
Dept. of Psychiatry, Hospital Batu Pahat, Johor Bahru, Malaysia
2
Dept. of Psychiatry, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Kuala Lumpur, Malaysia
3
Dept. of Psychiatry, Hospital Kuala Lumpur, Kuala Lumpur, Malaysia
4
Objective: The main objectives of this study were to determine the prevalence of erectile dysfunction (ED) and its predictive factor(s) in
male patients on methadone maintenance therapy (MMT) attending the Drug Clinic, Hospital Kuala Lumpur.
Methods: This is a cross-sectional study conducted between October 1 and December 30, 2008. A total of 108 subjects participated in the
study. The instruments used include the Structured Clinical Interview for the DSM-IV Axis-I Disorder (SCID-I), Beck Depression Inventory
(BDI) and International Index of Erectile Function-15 (IIEF-15).
Results: The mean age of the participants was 44.6 ± 9 years. The rate of ED among men on MMT was 68.5% (mild ED was 36.1 %, mild
to moderate was 22.2% and severe ED was 3.7%). There were significant associations between age of respondents (p=0.002), concurrent
illicit heroin use (p=0.024), and age of the respondents’ partners (p=0.039) with ED. After multivariate analysis, it was found that increased
age is the only significant predictor of ED with an adjusted odds ratio of 1.07 (1.02-1.16). The methadone dose and duration of methadone
treatment were not significantly associated with ED.
Conclusions: ED was highly prevalent among male patients on MMT. While current practice in dosage and duration of MMT in Malaysia
did not have any significant impact on ED, sexual function needs to be routinely assessed in patients on methadone.
Key words: Erectile dysfunction, risk factors, methadone substitution therapy
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[PP-029]
Cerebellar contusion presenting with pure psychiatric symptoms and cerebellar
cognitive affective syndrome: A case report
Ref. No: 154
Baise Tıkır, Erol Göka, Makbule Çiğdem Aydemir, Sinem Duran
Ankara Numune Education and Research Hospital, Department of Psychiatry, Ankara, Turkey
The cerebellum is known to be responsible for posture and motor coordination of the body. Recent studies indicate that the cerebellum
has a role in conduction of higher brain functions, such as perception, affect, capacity to analyze, and memory, via neuronal connections
between the cerebellum and the other regions of the brain. Schmahmann and Shermann described a new syndrome called “the Cerebellar
Cognitive Affective Syndrome” (SCAS) and drew attention on cognitive functions of cerebellum. The syndrome was described in a group
of patients who had impairment of executive functions, difficulties with spatial cognition, personality changes, blunt affect and language
deficits in addition to primary neurological symptoms. In this case report we present a rare case of cerebellar cognitive affective syndrome
presenting with pure psychiatric symptoms,who had a posterior cerebellar lobe lesion due to a contusion at the back of the skull.
Key words: Cerebellar cognitive affective syndrome, cerebellum, cognitive functions
[PP-030]
Self-perception and anger with chest pain without cardiac etiology
Ref. No: 226
Esra Aydın Sünbül1, Murat Sünbül2, Fatma Feriha Cengiz1
Erenkoy Ruh ve Sinir Hastalıkları Eğitim ve Araştırma Hastanesi, Istanbul, Turkey
1
Department of Cardiology, Marmara Universitesi, Istanbul, Turkey
2
Objective: Physical symptoms are the most common expressions of social problems and emotional inconvenience. This problem is
usually medically unexplained in patients with chest pain. ‘Chest Pain without Cardiac Etiology’ is diagnosed in more than fifty percent
of patients with chest pain. Anger and suppressed hostility are important factors the development of somatic symptoms. It is important
to point out that somatization in depressive disorders is due to expression of anger while somatization in anxiety is due to anger
suppression. It is known that, while patients with chronic pain experience anger, they do not care enough to express it because they are
in denial of this situation. The form of anger expression in patients with chronic pain may be effective in the disease process and is one of
the subjects to be emphasized. Suppression of intense anger leads to the development of chronic pain and suppressed anger scores are
higher than healthy controls. In this study, we compared patients with chest pain without detected cardiac etiology and healthy controls
in terms of anger and self perception.
Methods: Twenty five patients were included in the study. They all presented to the cardiology clinic with complaints of chest pain, but
did not have any detected cardiac etiology. The healthy control group of 80 persons was organized by matching them with the patients
according to their age, gender, and education. The Socio-demographical data collection form, Multidimensional Anger Scale, and Social
Comparison Scale were given to both of the groups.
Results: There was no significant difference between the socio-demographic features of the two groups. The non-cardiac chest pain
group scored higher on the Social Comparison Scale. The healthy control group scored higher on calm behaviour and nonchalant
response. Revenge for the reaction and inward looking responses were significantly higher in the non-cardiac chest pain group.
Conclusions: The non-cardiac chest pain group had more negative perception of self as compared to healthy individuals, further they
were found to be more negative in their forms of expressing anger. Repressed anger and hostility are important factors in the development
of chronic pain. Work on the relationship between mind and body has been a topic of interest in recent years. Not just how an individual
perceives himself, but also how other people perceive and relate to him, probably effects the physiological system of that individual.
Key words: Chest pain without cardiac etiology, self-perception, anger
References:
1.
Kirmayer lj, Young A. Culture and somatization: clinical, epidemiological and ethnographic perspectives. Psychosom Med 1998; 60: 420-430.
2.
Mayou R. Invited review: atypical chest pain. J Psychosom Res 1989; 33: 393-406.
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3.
Koh KB. Anger and somatization. J Psychosom Res 2003; 55:113.
4.
Sayar K, Bilen A, Arıkan M. Kronik ağrı hastalrında öfke, benlik saygısı ve aleksitimi. Türkiye Klinikleri Psikiyatri 2001; 2: 36-42.
5.
Güleç MY, Hocaoğlu Ç, Gökçe M, Sayar K. Anadolu Psikiyatri Derg 2007; 8:14-21.
[PP-031]
Mirtazapine treatment for weight loss and insomnia associated with methylphenidate:
A chart review
Ref. No: 155
Sabri Hergüner, Arzu Hergüner
Meram Faculty of Medicine, Department of Child and Adolescent Psychiatry
Introduction: Stimulants are used as first-line treatment for children with attention deficit hyperactivity disorder (ADHD), and their safety
and efficacy are well established. Their most frequent adverse effects are sleep disturbance and decreased appetite which may limit
optimal dosing and compliance. The aim of this study was to investigate the efficacy of mirtazapine on OROS methylphenidate (MPH) induced weight loss and insomnia in children and adolescents with ADHD.
Methods: We reviewed the charts of children and adolescents diagnosed with ADHD and identified 18 individuals prescribed mirtazapine for weight
loss and/or insomnia while on OROS – MPH treatment. Of these, 2 discontinued mirtazapine within the first week due to excessive daytime sedation.
Results: Mirtazapine was well tolerated by the remaining 16 subjects and no other side effects were reported. All subjects gained weight
during concomitant mirtazapine treatment, with a mean gain of 2.1 kg. Fourteen of 16 children who had reported insomnia on MPH alone
noted significant improvements in sleep after initiation of mirtazapine.
Conclusion: In this chart review, mirtazapine was found to be beneficial for weight loss and insomnia associated with MPH treatment in
children and adolescents with ADHD.
Key words: Attention-deficit/hyperactivity disorder, children, methylphenidate, mirtazapine, insomnia, weight loss
[PP-032]
Rapid-onset hyponatremia induced by duloxetine in a middle-aged male with
depression and somatic symptoms
Ref. No: 157
Jung Seok Choi, Hae Woo Lee, Jun Young Lee, Hee Yeon Jung
Department of psychiatry, Smg-Snu Boramae Medical Center, Seoul, Korea
Duloxetine is a relatively balanced selective serotonin and noradrenaline reuptake inhibitor. We report a case of hyponatremia induced by
duloxetine that developed rapidly after starting the medication in a middle-aged male with multiple somatic symptoms and depression.
Two days after discontinuation of duloxetine and management with hypertonic saline as well as fluid restriction, the serum sodium level
normalized. The patient had two risk factors for developing hyponatremia, namely severe weight loss and pneumonia. Therefore, when
treating patients with depression and somatic symptoms, especially with risk factors for developing hyponatremia, close monitoring for
clinical and laboratory evidence of hyponatremia may be essential.
Key words: Duloxetine, hyponatremia, middle-aged male, somatic symptoms, depression
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[PP-033]
Gender specific metabolic adverse effects in bipolar patients: A comparison
between lithium, quetiapine and olanzapine
Ref. No: 192
Sermin Kesebir, Burak Baykaran, Burak Toprak, Ahmet Ertan Tezcan
Erenkoy TEHMND, Istanbul, Turkey
Objective: There is some evidence showing gender based differences in the side effects of atypical antipsychotic drugs. The aim of this
study was to determine the differences between lithium, quetiapine and olanzapine with regard to their effects on metabolic variables in
bipolar disorder and to assess the findings in terms of gender differences.
Method: Twenty-eight female and 29 male cases diagnosed with bipolar disorder type I according to the DSM-IV, taking lithium or
quetiapine or quetiapine+lithium or olanzapine or olanzapine+lithium, were evaluated consecutively. For evaluation, being in a remission
period was set as a criterion for these cases. Patient interviews were carried out with SCID-I and SKIP-TURK. Blood samples were taken from
the patients in order to determine PRL, blood lipids and HbA1c levels.
Results: Mean age, mean age of onset, number of manic, depressive, and total episodes, functionality, and PRL levels were similar between
female and male patients. BMI, HbA1c, cholesterol, triglycerides, LDL and HDL levels are found to be similar between the two groups. Both
in female and male patients, no difference was found between the lithium, quetiapine and quetiapine+lithium and the olanzapine and
olanzapine+lithium groups in terms of BMI, HbA1c, cholesterol, triglyceride, LDL and HDL levels. The only difference (although not significant)
among the three groups was the level of cholesterol in women treated with lithium, which was found to be lower than in the other two groups.
Conclusions: This insignificant difference was found while the clinical properties and PRL levels were similar among the lithium,
quetiapine and quetiapine+lithium and the olanzapine and olanzapine+lithium groups. Future studies with a specific focus on this topic
are needed in order to have a better understanding of the basic mechanisms of gender differences.
Key words: Gender, metabolic side effect, psychotropics, bipolar disorder
[PP-034]
New model of psychogenic stress-induced depression and antioxidant system of rat brain
Ref. No: 161
Konstantin Chichinadze1, Tamar Domianidze1, Tamar Matitaishvili1, Ia Labadze1, Ann Lazarashvili2, Mikhail Khananashvili1
Laboratory of Behavior and Cognitive Functions, Life Sciences Research Center, Tbilisi, Georgia
1
Department of Pathology, Tbilisi State University, Tbilisi, Georgia
2
The present article describes results of investigation of lipid peroxidation and antioxidant enzyme activity in the brain cells of laboratory
rats, that were subjected to a depression-like state. The above-mentioned state was achieved by means of a new model of depression
elaborated by us. The model is based on the application of stressors of psychogenic nature.
Our investigations demonstrated that in the depression-like state activity of lipid peroxidation processes increase, which was confirmed
by increase of concentration of its end product – malondialdehyde, both in mitochondrial and cytosolic fractions of brain cells. In
response to oxidative stress in mitochondria, activity of antioxidant system –namely the leading intracellular antioxidant superoxide
dismutase (SOD) – increased. On the other hand, concentration of another important antioxidant –catalase– decreased. Most probably,
the depletion of antioxidative potential of the cell, related to depression, proceeds at various speeds in various enzymatic systems.
Administration of the antidepressant drug –fluoxetine– led to the normalization of intensity of lipid peroxidation and overall activity of
antioxidative systems. Thus, if activity of these processes increases, antidepressants cause their down-regulation and in they decrease
–antidepressants lead to their up-regulation. As a final result, this leads to normalization of cell functioning.
Key words: Animal model of depression, lipid peroxidation, antidepressants
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[PP-035]
Effects of strawberry leaf and celery seed extracts in terlipressin-induced chronic
hyponatremia in rats
Ref. No: 216
Rehab R. Hegazy1, Hala F. Zaki2, Ola A. Sharaf1, Ismail E. Ismail1, Sanaa A. Kenawy2
Departement of Pharmacology, Medical Division, National Research Center, Giza, Egypt
1
Departement of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt
2
Hyponatremia (HN) is associated with mortality and morbidity risks due to development of encephalopathy and neurogenic pulmonary
edema. Moreover, its rapid correction carries a high risk of development of the serious cerebral disorder known as osmotic demyelination
syndrome (ODS).
In the present study, chronic HN was induced in rats using a single daily administration of terlipressin (TP), a synthetic, long-acting analogue
of vasopressin, for 3 days. TP-induced HN was then used to study the possible therapeutic effects of strawberry leaf extract (StrwLE) and
celery seed extract (CelrSE), and to compare their effects with that resulting from rapid correction using hypertonic saline (HtNaCl). Serum
sodium level, as a marker of HN, was measured following induction and treatment, respectively. The study was extended to investigate
changes in locomotor activity, pain reflex and lung function using an activity cage, hot-plate test, and spirometer, respectively. Furthermore,
assessment of brain nitric oxide (NO) content, that has been shown to play a role in the pathogenesis of ODS, was carried out.
It was found that TP induced a profound (<115 mmo/l) chronic (>48 h) HN that was coupled by decreased locomotor activity, delayed pain
reflex and impaired lung function. Administration of StrwLE resulted in a correction of HN with its subsequent neurological dysfunction
without elevation of the brain content of NO; however, it resulted in deterioration of the lung function parameters of hyponatremic rats. These
findings suggested that StrwLE is useful for treatment of chronic HN, yet, further investigations are required to study its effect on the lungs.
Key words: Hyponatremia, terlipressin, rats, locomotor activity, pain reflex, lung functions
[PP-036]
Post traumatic stress disorder in patients with spinal cord injury and relevant factors
Ref. No: 165
Murat İlhan Atagün1, Ünal Altınok1, Özlem Devrim Balaban1, Zeliha Atagün2, Latif Ruhşat Alpkan1, Kadriye Öneş2
1
İstanbul Physical Therapy and Rehabilitation Research and Training Hospital, İstanbul, Turkey
2
Objective: Although spinal cord injury (SCI) was thought to be a fatal case, development of rehabilitation approaches in the early 20th
century prolonged survival rates and longevity. Physical and psychological trauma and permanent results of the injury are difficult to cope
with. Post traumatic stress disorder rates following SCI range from 10 to 44%. In this study we aimed to assess PTSD frequencies in patients
with SPI in Turkey and the association of PTSD to factors like depression, anxiety and caregiver burden.
Methods: Eighty four patients with SCI (mean age= 40.5±15.97; 40 female, 44 male) and caregivers (n=83; mean age=43.72±14.37; 67
female, 16 male) were enrolled. Patients with mental retardation, premorbid psychiatric disorder, comorbid central nerve system disease
and patients with professional caregivers were excluded. Clinican administered post traumatic stress disorder rating scale (CAPS), the Beck
depression and anxiety, and Zarit caregiver burden scales were assessment tools.
Results: Although they had experienced traumatic events, 32.1% (n=27) of the patients did not have PTSD, while 40.5% (n=34) had
PTSD. About 28.6% of these had acute PTSD symptoms and 11.9% (n=10) had had PTSD symptoms in the past. Patients with PTSD had
statistically significant higher scores of depression, anxiety and caregiver burden.
Discussion: Perception of stress may be influenced by several factors including personality and economical factors. Expression of feelings
may increase stress tolerance. The differing results may be due to the factors above as well as methodologies, different stages of assessed
samples, social and cultural differences, and tolerance to stress. On the other hand, some negative effects of PTSD are screened in this
study. These negative factors may influence adjustment of the disabled person and thus may cause a vicious circle.
Key words: Spinal Cord Injury, post traumatic stress disorder, depression, anxiety, caregiver burden
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[PP-037]
A comparison before and after using lamotrigine in long term continued treatment:
the effect of blood levels
Ref. No: 230
Sermin Kesebir1, Fisun Akdeniz2, Aysun Demir1, Mustafa Bilici1
Erenkoy TEHMND, Istanbul, Turkey
1
Ege University, Psychiatry, Izmir, Turkey
2
Objective: The purpose of this study is that determine whether or not the efficacy of lamotrigine, which is an anticonvulsant with a
stabilizer quality in neuronal membranes and has inhibitor activity in sodium and calcium channels and presynaptic neurons, is related
to blood levels in bipolar disorder. We compared the period before and after lamotrigine use in bipolar cases and studied if there was any
relationship between lamotrigine blood levels and clinical progress.
Method: Forty cases, diagnosed with bipolar disorder type I according to the DSM-IV, and taking lamotrigine for at least two years
together with any mood stabilizer (lithium, anticonvulsants or atypical antipsychotics), were evaluated consecutively. For evaluation,
being in remission period was set as a criterion for these cases. Patient interviews were carried out with the SCID-I in bipolar cases. Before
or after protective treatment, the SCIP-TURK Mood Disorders Diagnosis and Patient Registration Form were filled in by the patients and
their relatives. Later blood samples were taken from the bipolar cases in order to analyze lamotrigine blood levels.
Results: In the bipolar cases, when comparing before and after long term maintenance of lamotrigine, it was determined that after using
lamotrigine, total episode and depressive episode frequency decreased, episode severity was less (p< 0.001, 0.039, and 0.04, respectively)
and the fast onset and termination ratio decreased (p= 0.027). When evaluated according to these variables, in long term maintenance,
the ratio of good treatment response to lamotrigine among bipolar cases was 77.5%. In cases with good treatment response to
lamotrigine, while lamotrigine doses were found to be similar to the others (135.5±52.7/155.6±69.7 mg/day), lamotrigine blood levels
were found to be higher (3.8±1.9/2.0±1.1 µg /ml) (p= 0.005). No correlation was shown between lamotrigine dose and lamotrigine blood
levels (r= 0.185, p= 0.254).
Conclusion: As a result, lamotrigine is an efficient choice in long term maintenance treatment of bipolar disorder. The relationship of this
efficacy to lamotrigine blood levels must be explored in future studies.
Key words: Lamotrigine, bipolar disorder, blood level
[PP-038]
ICAM, VCAM and E-selectin levels in first episode schizophrenic patients
Ref. No: 172
Semine Özdoğan Kavzoğlu, Aytül Gürsu Hariri
Erenköy Research and Training Hospital for Neuropsychiatry, Istanbul, Turkey
Objective: It is known that mortality rates in schizophrenic patients with cardiovascular diseases are twice as high as other diseases.
Some of the research has revealed that the risks of cardiovascular disease were dependent on adhesion molecules. The main adhesion
molecules are intracellular adhesive molecule (ICAM-1), vascular cell adhesive molecule (VCAM-1) and E-selectin. The aim of this study
was to determine whether or not ICAM-1, V-CAM-1 and E-selectin levels, which are considered as possible biological determinants in the
prognosis and progression of atherosclerosis, change with treatment in schizophrenic patients with respect to controls.
Method: In the Erenköy Research and Training Hospital for Neuropsychiatry, 50 patients who were diagnosed with first episode
schizophrenia according to the DSM-IV-TR diagnostic criteria and had never received antipsychotic treatment and a control group
consisting of 50 healthy volunteers were enrolled the study. At the beginning of the study (n=50) and after the third month (n=39), ICAM,
VCAM, E-selectin, Fasting Blood Glucose, Total Cholesterol, LDL Cholesterol, HDL Cholesterol and Triglyceride levels were checked in the
plasma of each patient and compared with each other. For the control group, the same biochemical parameters were investigated only at
the beginning of the study. In order to assess the termination of the acute episode, the patient group was given the Positive Symptoms
Assessment Scale (SAPS) and Negative Symptoms Assessment Scale (SANS) in the beginning and at the end of the third month.
Results: In the first episode schizophrenic patients, the average age was 30.14±7.50 years. In the patients, the beginning ICAM-1 levels
were lower than the control group (t= 3.41, p=0.001) and increased during treatment (t=-6.73 p<0.001), while VCAM-1 and E-selectin
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levels were similar to the control group (t=-1.23, p=0.223; t=-0.32 p=0.750, respectively). In addition, after treatment the VCAM-1 level was
determined to be lower than the pretreatment level (t=7.17, p<0.001). Whereas the averages of Fasting Blood Glucose, Total Cholesterol,
LDL Cholesterol, HDL Cholesterol and Triglycerides were similar in the control and patient groups, a significant increase was observed in
the triglyceride levels of the schizophrenic patients after treatment (t=-3.19, p=0.003). According to the statistics, a significant positive
correlation was found between ICAM and triglyceride values (r= 0.351, p<0.001).
Conclusion: When compared with the control group, it was observed that the levels of cellular adhesion molecules of individuals with first episode
schizophrenia were not different, except for ICAM-1. Whereas according to the information retrieved from levels determined in plasma during
treatment, cellular adhesion molecules act differently. It was observed that the antipsychotics used for treatment had an effect on increasing
ICAM-1 and decreasing VCAM-1. It is possible that the number of patients was not enough, the disease does not have a homogenous structure,
and some other unknown confounding factors could be present. Our findings need to be replicated by other clinical groups in larger studies.
Key words: Atherosclerosis, E-selectin, ICAM-1, schizophrenia, VCAM-1
[PP-039]
Body dysmorphic disorder incidentally treated with bupropion
Ref. No: 175
Fatih Canan1, Gjergji Sinani2, Ünsal Aydınoğlu3
Bolu Izzet Baysal Mental Health Hospital, Bolu, Turkey
1
2
3
Introduction: Bupropion is a preferential dopamine and norepinephrine reuptake inhibitor. It has been shown to be effective in patients
with depression and socialphobia, however data on its efficacy in body dysmorphic disorder (BDD) are lacking.
So far, only two BDD cases have been reported to respond bupropion treatment. Herein, we report another case of a patient with BDD
incidentally treated with sustained-release bupropion.
Case Report: Mr. H., a 26-year-old factory worker, visited a psychiatric outpatient clinic with the intent to quit smoking by seeking
professional help. Bupropion sustained-release was initiated at 150mg/day during the first week and then raised to 300 mg/day, along
with behavioral counseling. He was able to remain smoke free in the sixth week of the treatment.
During his control visit on the 8th week, Mr. H. stated that his preoccupation about his face had also disappeared. Mr. H. looked normal but
had been preoccupied with the appearance of his face since age 16. He reported thinking about his appearance for at least 5 to 6 hours a
day and he worried that other people would notice him or judge him negatively because his skin looked so ‘deformed’. For 3 to 7 hours a
day, Mr. H. checked his face in mirrors and other reflecting surfaces and compared his face with the faces of other people. Because he was
so preoccupied with, and distressed by his face, Mr. H. was often late for work, and his productivity suffered, which resulted in conflicts
with his employer. Previously, he had been fired from three jobs because of these symptoms. As Mr. H. was so embarrassed about how he
looked, and feared that other people would judge him negatively, Mr. H. avoided all contact with friends and saw his family only on special
occasions. He did not seek help about his symptoms and he avoided mentioning his complaints because he felt ashamed of talking about
his appearance. He was diagnosed as body dysmorphic disorder according to the DSM-IV criteria. Mr. H. reported that his preoccupation
had diminished gradually during treatment and that he had been peaceful about his face for 2 weeks. During 3 months of follow-up, he
was well maintained on sustained-release bupropion and there was no re-emergence of his symptoms.
Discussion: Currently, selective serotonine reuptake inhibitors (SSRI) are recommended as the first-line medication for BDD, including
delusional BDD. SSRI antidepressants have been reported to be more efficacious for BDD than non-SSRI antidepressants or other types
of psychotropic medications.
The literature regarding the efficacy of bupropion in the treatment of BDD is restricted to a single report. Nardi et al have reported two
cases with coexisting BDD and major depressive disorder (MDD) who were resistant to antidepressant pharmacotherapy and were treated
with bupropion 300 mg/day. Our case responded well to bupropion treatment although he did not have comorbid MDD.
According to our case report, bupropion may be a treatment option for some patients with BDD. Further studies and case reports are
required to explore the efficacy of bupropion in the treatment of BDD.
Key words: Body dysmorphic disorder, bupropion
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[PP-040]
Ref. No: 176
Tardive akathisia with aripiprazole: A case report
Ömer Şenormancı, Oya Gönüllü Güçlü, Ramazan Konkan, Yavuz Altunkaynak, Güliz Şenormancı
Bakırköy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, İstanbul, Turkey
Tardive akathisia is characterized by feelings of restlessness, discomfort, and tension causing the patient to be unable to settle down and
sit still. The patient should also be taking a long term antipsychotic medication without any recent changes in dosage or type, and no
withdrawal of antiakathisic drugs. Aripiprazole is a potent partial agonist that shows high affinity binding to dopamine (D2) and serotonin
(5HT1a) receptors and is an antagonist at 5HT2a, 5HT2b receptors. Although there are a number of case reports about arippiprazole
causing acute akathisia, only one tardive akathisia case, who was a nonpsychotic female patient, has been reported so far. In this case
tardive akathisia with aripiprazole developed in a patient who had diagnoses of mental retardation and psychotic disorder not otherwise
specified and who was treated by supplementary drugs without stopping aripiprazole.
Key words: Antipsychiotics, aripiprazole, extrapyramidal side effects, atypical antipsychotics, tardive akathisia, tardive syndromes
[PP-041]
Comparing mental disorders between divorced couples and normal
couples in a city of Iran
Ref. No: 178
Majid Kazemi1, Sima Karimi2, Hadi Hasankhani3, Somayeh Kazemi4
Rafsanjan University of Medical Science, Iran
1
Islamic Azad University- Sirjan Branch, Iran
2
Tabriz University of Medical sciences, Iran
3
Islamic Azad University- Mashhad Branch, Iran
4
Background: The family is the first and the most important source for fulfilling needs of human beings including love, satisfaction and
peace. One serious difficulty in couple’s lives is the phenomenon of divorce, which recently has been increasing in Iran. Divorce has a lot
of negative effects, both physical and psychological, on couples.
Objective: The aim of this study was to compare mental disorders between the couples who were divorced and normal couples in a town
in Iran.
Method: This research was causal –comparative on couples in Sirjan in 2010. Seventy couples were chosen voluntarily and randomly
based on the duration of their marriage from couples applying for divorce and refereeing to the administration of justice and normal
couples. The questionnaire symptom checklist-90-revised (SCL-90-R) was used. The data were collected and analyzed.
Results: The averages of mental disorder scores between two groups in nine dimensions were compared and showed different
significances. People who had gotten divorced had more high scores comparing the total coefficient of global severity index (GSI).
The findings revealed that the divorced couples had higher GSIs and a significant correlation was observed (p<0.05). In addition the
average Positive Symptom Total (PST) was higher (59.03±24.09) for divorced couples compared to normal couples (40.9±24.25) There
was a significant correlation, too (p<0.05). Comparing positive symptom distress indexes (PSDI) between the two groups using the t-test
showed a different significance (p<0.05).
Conclusion: The results of the present study illustrated that divorced couples had higher GSI, PST and PSDI (P<0.05). In order to deal
with divorce complications, background factors and variables must be considered that lead to the increase in divorce in the community.
Key words: Mental disorder, marital conflict, divorce, SCL-90
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[PP-042]
Suicide rate in Oman in the period between January 2000 and December 2010
Ref. No: 238
Saif Salam Al Hashmi, Ahmed Ali Al Sabri, Nasser Mubarak Al Felati
Armed forces hospital, Muscat, Oman
Background: Suicide rates have been explored in different parts of the world, including many Arab /Islamic countries. To our knowledge,
no study has been conducted in Oman so far.
Objective: To examine the rate of suicide in the Sultanate of Oman in a ten year period (2000-2010).
Method: The data kept at the Royal Oman Police Forensic Department were queried for the presence of suicide as a cause of death for a
10 year period (2000-2010)
Results: The total number of suicide cases in Oman in that period was 599, with 59.9 cases every year. Omanis account for 8.7 cases every
year.
Conclusion: Based on our data the suicide rate in Oman was found to be 2 /100,000 /year. This puts Oman in the group of low suicide
rate countries in the world.
Key words: Suicide rate, Oman, ten year period
[PP-043]
The effect of the recitation of the Quran on depressed patients in the psychiatry
department of Moradi hospital in Rafsanjan (IRAN)
Ref. No: 179
Ali Ansari, Tayebeh Negahban, Ahmad Reza Sayyadi
Rafsanjan University of Medical Sciences
Background and Objective:: Depression is a common psychiatric disorder and has a huge impact on human life. Data published in
scientific sources suggest that about one hundred million cases are diagnosed annually. Depression comprises about 35 to 45% of
all mental disorders in Iran. Unfortunately, this figure is rising day by day and it is necessary to look for new and modern methods for
treatment and prevention of this psychiatric disorder. One of the non- medicinal methods of treatment is music therapy, which seems to
be a safe and effective therapeutic method. Reading the Koran with a pleasant voice can be regarded as a kind of agreeable Gnostic music.
The main purpose of this research was to determine the effect of the recitation of the Koran on depression.
Methods: This study was a semi-experimental one and included all the depressed patients who had been hospitalized in the psychiatry
department of the Rafsanjan Moradi Center. The sampling time period was one year. The patients were divided into two groups randomly,
(30 people in the experimental and 30 in the control group). The selection of the subjects was based on the psychiatrist’s diagnosis, Beck’s
depression scale and the condition of the patients. The questionnaires were filled out for the case group. Recitation of Yousof Verse of
the Koran by Abdolbaset, was transmitted for the case group, for 15 minutes every other day for 7 sessions. At the end of the first two
weeks of hospitalization, both of the groups were retested by another questionnaire and the results were analyzed by paired t- test and
Student’s t test by EPI6.
Results: The result of this research showed that the Koran reciting had a beneficial effect on the depressed patients (p<0.0001). In our study the
patients who expressed a strong belief in the Koran had a greater decrease in median depression scores before and after this kind of therapy.
Conclusion: According to the results of this research and because of the rhythmic agreeable intonation of the Koran as a Gnostic music
and its miracle aspect, we can use the Koran tone as a non-medicinal method of therapy in the treatment of depressed patients.
Key words: The Quran reciting, depression
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[PP-044]
Dissociative symptoms associated with piracetam use: a case report
Ref. No: 239
Adem Aydın1, Pınar Güzel Özdemir1, Yavuz Selvi1, Faruk Uğuz2
Department of Psychiatry, Yuzuncu Yıl University, Van, Turkey
1
Department of Psychiatry, Selcuk University, Konya, Turkey
2
Piracetam is a cyclic derivative of a gamma-aminobutyric acid drug that is often used in neurology practice (1). It has antithrombotic and
neuroprotective properties and improves cognitive performance (2).
In this article, a case report, piracetam is used for combined therapy, but after piracetam use, dissociative symptoms like depersonalization
and derealization were detected.
Case: A 29-year-old female patient applied to the psychiatric clinic with the following complaints: Intense discomfort, alienation from herself,
perceiving herself odd , that perception that her hands and feet were bigger, feeling like not living in the society, the feeling that colors and
sizes of objects seemed abnormal, and feelings of alienation from objects and people in her surroundings. These complaints continued for
10 days and she had never had any psychological complaints before. She also expressed that these complaints bothered her greatly. Except
for these complaints, she did not describe any other abnormality in perception and thought content. She did not have prominent depressive
symptoms and psychosocial stress in her history. One month ago, she had seen a neurologist for vertigo. She was diagnosed with peripheral
vertigo and prescribed betahistine 16mg/day. After this medication, she described a marked reduction in the vertigo, however since she did
not get rid of her complaints completely, after 12 days she was prescribed piracetam 2400mg/day as combination treatment.
On psychiatric examination, she was conscious, oriented normally, anxious,appeared ready to cry, thought contents were normal, positive
depersonalization and derealization in the perception, psychomotor activation was normal. Nothing abnormal was detected in her
hemogram, biochemistry, serum B12, thyroid function tests, EEG, and brain MRI.
In clinical follow-up, since there was a connection between the patient’s administration of piracetam and the dissociative indications,
piracetam was stopped. Betahistine was continued in the same dosage. It was observed in daily observation that after a day, a decrease
in her dissociative symptoms began and in 5 days they had totally disappeared. In further follow up visits dissociative symptoms were
not observed in a month.
The dissociative symptoms like derealization and depersonalization were started with addition of piracetam to the treatment, and
diminished quickly after piracetam was stopped. This directed us to think that those dissociative symptoms were related to the piracetam
administration. This relation is not established in literature (3).
Trauma is usually reported as the origin of dissociative symptoms. There generally is childhood period trauma and dissociative symptoms
come up in later life. There is still no etiopathogenesis described related to development of dissociative symptoms. Traumatic stress and
neurobiological theories are basic models suggested in etiology (3). In the medication studies, depersonalization is the basic dissociative
symptom in dissociation’s neurobiological theories. In those studies, it is also shown that serotonergic and glutamate receptors have a
role in depersonalization (3).
We think that this case report which shows the administration of piracetam and development of dissociative indications may contribute
to the neurobiological theories on dissociative disorder’s etiology.
Key words: Dissociative symptoms, piracetam
References:
1.
Değirmenci E, Şahiner T, Erdoğan Ç. Long Term Effects of Piracetam on Spectral Analysis of EEG in Alzheimer’s Disease and Minimal Cognitive Impairment. Klinik
Psikofarmakoloji 2006;16:93-7
2.
Winbland B. Piracetam: a review of pharmacological properties and clinical uses. CNS Drug Rev 2005;11:169-82
3.
Wınnica K, Tomasiak M, Bielawska A. Piracetam-an old drug with novel properties? Acta Poloniae Pharmaceutica- Drug Research 2005;62:405-409
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[PP-045]
Reversible normoprolactinemic galactorrhea induced by fluoxetine
Ref. No: 181
Fatih Canan1, Ünsal Aydınoğlu2, Gjiergji Sinani3
Bolu Izzet Baysal Mental Health Hospital, Bolu, Turkey
1
2
3
Introduction: Several drugs can cause galactorrhea and it’s etiology needs to be differentiated from other local or neuroendocrinological
causes. All conventional antipsychotic drugs block D2 receptors on lactotroph cells and thus remove the main inhibitory influence on
prolactin secretion. Tricyclic antidepressants, selective serotonin reuptake inhibitors, and monoamine oxidase inhibitors are less frequent
causes. There is evidence that serotonin may stimulate prolactin release directly via postsynaptic 5-HT receptors in the hypothalamus or
indirectly via 5-HT mediated inhibition of tubuloinfundibular dopaminergic neurons. However, galactorrhea due to antidepressants is
not consistently associated with elevated prolactin levels, which may suggest still unexplained mechanisms of antidepressant-induced
galactorrhea.
We report a case of euprolactinemic galactorrhea in a woman with generalized anxiety disorder while on treatment with fluoxetine.
Case Report: A 29-year-old woman visited a psychiatric outpatient clinic with complaints of excessive and uncontrollable worry about
minor life events, feeling restlessness, irritability, muscle tension, tiring easily, and poor sleep that started 8 months prior to admission. She
had no history of endocrine or reproductive pathology or psychiatric problems. She was diagnosed as having generalized anxiety disorder
according to the DSM-IV criteria and was started on fluoxetine 20 mg per day. After 4 weeks of medication, her symptoms diminished.
However, she developed unilateral galactorrhea (the nonpuerperal discharge of milk-containing fluid from the breast). She had no history
of galactorrhea. She first noticed the discharge on treatment day 21 and described it as white-creamy and from the right nipple. She did
not notice any bloody, greenish, or foul-smelling discharge, nor did she report any sexual dysfunction. She consulted her gynecologist,
who recommended a mammogram and breast ultrasonography. The pregnancy test was negative. The results of these tests and breast
examination were normal. Serum prolactin level on treatment day 28 was 18.18 ng/mL (reference range: 2.5-29 ng/mL). Because her
galactorrhea developed after the initiation of fluoxetine, her medication was discontinued. Buspirone 5 mg/day was started and gradually
raised to 20 mg/day. Eight days after stopping fluoxetine, the patient reported reduction and cessation of galactorrhea. At the 3 month
follow-up visit, the patient was well maintained on buspirone and there was no re-emergence of galactorrhea.
Discussion: Although galactorrhea caused by the use of fluoxetine has been reported earlier, the commonly perceived cause is
hyperprolactinemia. Fluoxetine has been shown to potentiate elevation of prolactin levels from other stimuli, including insulin,
fenfluramine, and 5-HT. However, hyperprolactinemia is not the only mechanism responsible for the development of SSRI-induced
galactorrhea. The exact mechanism of galactorrhea remains unknown in many cases.
Our patient developed galactorrhea without hyperprolactinemia after beginning fluoxetine therapy. The strict temporal relationship
between the use of the drug and the onset of galactorrhea, as well as the resolution once treatment was discontinued, suggests a causal
link between the two phenomena.
To the best of our knowledge, we are the first to report an association with fluoxetine use and galactorrhea without elevated prolactin
levels. Clinicians should consider fluoxetine as a possible cause of galactorrhea even with normal prolactin levels. Future research should
investigate the precise mechanisms of antidepressant-induced normoprolactinemic galactorrhea.
Key words: Fluoxetine, galactorrhea
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[PP-046]
Influence of polymorphism of the norepinephrine transporter gene (SLC6A2) and
alpha-2 adrenergic receptor gene (ADRA2A) on regional cerebral blood flow
in a Korean ADHD sample: a preliminary study
Ref. No: 240
Younghui Yang1, Jaewon Kim2, Boongnyun Kim2, Minsup Shin2, Soochurl Cho2
Department of Psychiatry, Pusan National University Yangsan Hospital, Yangsan, Republic of Korea
1
Division of Child and Adolescent Psychiatry, Seoul National University Hospital, Seoul, Republic of Korea
2
Some genes related to the noradrenergic system have been investigated as candidate genes in Attention Deficit Hyperactivity Disorder
(ADHD). Through functional brain imaging studies, it has been reported that brain areas such as the prefrontal cortex (PFC), dorsal
anterior cingulate cortex, and striatum show abnormal findings in ADHD patients. We have investigated whether there was an association
between polymorphism of the noradrenergic system related genes (SLC6A2 and ADRA2A) and regional cerebral blood flow (rCBF) in a
Korean ADHD sample.
Methods: A total of thirty-six children (31 boys and 5 girls, mean age: 8.9 (± 1.84) years) participated in this study. Subjects were recruited
from the outpatient’s clinic of child and adolescent psychiatry in the Seoul National University Hospital. The diagnosis of ADHD was made
based on the DSM-IV-TR. All patients were drug naïve at the time of image acquisition. Genotyping of SLC6A2 (G1287A, -3081(A/T)) and
ADRA2A (Dral, Mspl) was done. SPM8 (Statistical parametric mapping 8) was used to compare images between the two groups divided
by each genotype.
Results: Children with the G/A and A/A genotypes at the SLC6A2 G1287A polymorphism showed decreased rCBF in the right inferior
temporal gyrus and the left middle temporal gyrus compared to children with G/G genotype (uncorrected p-value< 0.001). In ADRA2A
Mspl polymorphism, children with the C/G and C/C genotypes showed increased rCBF in the left striatum and the left cingulate gyrus and
decreased rCBF in the left cerebellar vermis compared to children with G/G genotype.
There were no significant rCBF alterations across genotypes in the SLC6A2 -3081(A/T) and ADRA2A Mspl genes.
Conclusion: This study showed that the noradrenergic system related genes might be associated with functional brain abnormalities in
children with ADHD.
Key words: ADHD, neuroimaging, SLC6A2, ADRA2A
[PP-047]
Do we need specialist clinics to monitor metabolic side effects on chronic
bipolar patients in Treatment? – Audit of management of bipolar disorder against
NICE guidelines in South Staffordshire NHS Trust, UK
Ref. No: 129
Fiesal Jan, Vanathi Kennedy
Foundation House, St. Georges’ Hospital, Corporation Street, ST16 3AG, Stafford
Objective: To highlight the pharmacological management of patients with Bipolar Affective Disorder and to evaluate whether the
management meets the current standards as set up by recognised guidelines, especially those underlined by NICE guidelines.
Method: The audit data were collected from a patient population from the West patch of South Staffordshire and focussed on inpatients
from the 2 adult units based at Stafford and a psychiatric ICU. It also included a minimum of 5 patients of both genders from all the
community teams. The selection was random and not based on severity or duration of the disorder, co-morbidity or other accompanying
diagnoses, for e.g, Personality disorder.
The audit tool was devised by the clinical audit coordinator in conjunction with clinicians.
Results: Twenty of twenty-eight 28 patients (72%) were on mood stabilizers, either lithium or sodium valproate, with sodium valproate
the more preferred drug.
Twelve of twenty-eight (43%) were on antipsychotics. Three of seven (43%) patients, who did not respond to combination treatment,
were started on lamotrigine.
In 21/22 (95%) of the patients, antidepressants were stopped.
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Nine of the twenty-eight (32%) patients continued to be on antidepressants even after resolution of the depressive episode.
The compliance of monitoring for physical side effects during the initial period of starting medications was not satisfactory with only:
19/24 (79%) monitored for renal disease,
18/24 (75%) monitored for diabetes,
15/24 (63%) monitored and advised about obesity and
15/24 (63%) drug levels checked regularly.
In 4/28 (15%), there was no documentation about any physical health monitoring.
Only in 50-60% of patients had the monitoring been done annually, but it was regardless of any recognised guidelines.
In 19/26 (73%) the patient’s preference of drug choices was recorded.
In 21/28 (75%) patients, there was documentation about discussion of potential benefits and side effects of the medications.
Five of twenty-eight (18%) patients who were prescribed valproate were of child bearing age; 4 were advised to use contraception and
one had been sterilized.
Clinical implications: Monitoring cognitive function tests is often dependent on patient mental health, illness, age, and lack of side
effects.
Patient preference for drugs should be taken into consideration.
Evidence should be documented regarding clinical need or history of risk on antidepressant medication.
Evidence of long term treatment with antidepressants after resolution of a depressive episode should be documented in the patient
notes.
Annual check-ups of parameters should be documented by either the GP or Mental Health Team. However, weight and BP machines may
not be available at clinic appointments. There is a need for closer understanding among clinicians about the responsibility for initiation
and maintenance of close physical monitoring.
Discussions should be held with women of child bearing age regarding contraception.
Teams to monitor the need for referral to specialist Bipolar Units should be available, regardless of any cost implications.
Key words: Bipolar, mood disorder, mood stabiliser, antipsychotics, physical health monitoring, serum drug levels, cognitive side effects, relapse,
pregnant women
[PP-048]
Assessment of risk of absenteeism in elemantary school students
Ref. No: 186
Kültegin Ögel1, Gülşah Karadayı2, Zeynep Karaman3, Hediye Atıcı Arıcan3, Niyazi Kaya3, Uğur Karaman3, Ahmet Murat Altuğ3
Acibadem University Medical Faculty
1
Yeniden Society
2
Ministry of National Education Primary School Department
3
Finding a resolution to the absenteeism problem is important in terms of children’s development. It is necessary that the risk of
absenteeism is determined in an early stage and an early warning system is established to prevent absenteeism. For this reason,
development of an assessment tool was targeted.
Methods: A qualitative research design was carried out at the first stage of the study. During this research procedure, 97 teachers, 53
administrators, 73 elementary school students who hadleft school, and 76 of their parents who were selected to represent the overall
structure of the population in Turkey were included in the study. With the information retrieved from this research, a scale named the Risk
Assessment Form (RIDEF) was developed. RIDEF consists of 111 questions within 9 risk categories.
The second stage of the study was carried out with 3871 students studying in 21 schools from 5 different cities, which were selected at
the first stage. While 49.5% (n=1924) of the students were between the ages of 7 and 12, 48% (n=1859) of the students were between 13
to 16 years of age. The mean age was 12.27±1.87 years. The mean of days of unexcused absences of those students within the 2009-2010
academic year, during which time this research was implemented, was 6.62±8.93 days and the mean of days of their unexcused absences
the year before was 6.08±7.21 days.
At the second stage, the RIDEF was applied to the same students 15 days after the first application and also a different interviewer filled
the form for half of the students. The School Atmosphere Scale was applied during the study, as well.
Results: When the total score derived from the scale was compared with the Pearson correlation analysis the interrater reliability was
found as r= 0.96 (p<0.01). Test – re-test reliability was determined as r= 0.85 (p<0.01).
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Based on the risk indicators obtained from RIDEF, the Cronbach alpha validity of the scale was calculated as 0.79. When any item is
removed from the scale, the value of the internal consistency coefficient varies between 0.77 and 0.79.
It has been observed that there is a statistically significant level of correlation between the School Atmosphere Scale and RIDEF sub-scales
(r=0.51, p=0.001).
As a result of the analysis, categorized risk indicators were grouped under two factors, which accounted for 44.73% of the total variance
with eigen values over one. The first factor, consisting of 4 items grouped under the title of individual problems related to childhood,
explains 30.98% of the variance and the second factor, consisting of 5 items with the title social and economic problems related to the
family, accounts for 13.75% of the variance.
The mean scores of the risk points derived from all of the categories showed a statistically significant difference between students with
high and low levels of absenteeism.
Discussion: This research study showed that the RIDEF is a reliable and valid scale in determining the risk of absenteeism.
Key words: Absenteeism, assessment
[PP-049]
Effectiveness of an addiction treatment program called SAMBA: A pilot study
Ref. No: 185
Kültegin Ögel1, Ceren Koç2, Bircan Karalar2, Aslı Başabak2, Alper Aksoy2, Mebrure İşmen3, Romina Yeroham2
1
Yeniden Society
2
Umraniye Prison
3
Description of SAMBA program: SAMBA (Sigara, Alkol ve Madde Bağımlılığı Tedavi Programı / Tobacco, Alcohol, and Drug Addiction
Treatment Program) is a treatment program which is designed to treat tobacco, alcohol, and drug addiction problems.
Development of SAMBA: Before developing this program, a comprehensive literature review was done. Addiction treatment programs
that are still applied in addiction centers in Turkey were reviewed. Necessary meetings with the specialists working in the addiction field
were conducted. The weaknesses and strengths of the programs were discussed with the specialists and expectations from an addiction
program were reviewed. SAMBA was developed according to the findings of the literature review and suggestions made in the meetings
with professionals.
The Content of SAMBA: SAMBA is a program that is based on Cognitive Behavioral Theory. In some sessions, some interventions that are
based on Mindfulness and Acceptance Therapy are used. In addition, in some sessions, some techniques of Dialectical Behavior Therapy
and Emotion Regulation are applied.
The Structure of SAMBA: SAMBA is composed of 7 modules and 13 sessions. The modules of SAMBA are:
1. The Effects of Drugs, Alcohol, and Tobacco
2. Motivation
3. Mindfulness
4. Anger and Stress Management
5. Relapse Prevention
6. Communication Skills
7. Thinking Errors
Each session lasts around one and half to two hours. All sessions are designed in an interactive mode. It contains activities and didactic
lectures.
SAMBA should be applied in group format and by professionals such as psychologists, social workers and psychiatrists.
Pilot Study: The pilot Study of SAMBA was carried out at Ümraniye T-Type Prison. The first pilot scheme was applied with a group that
consisted of members who are alcohol and drug addicts. After all the modules were applied, feedback from the group members was
collected. According to the feedback, necessary changes were made. Afterwards, the second pilot scheme was done with other members
who were again alcohol and drug addicts from the same prison. Based on the feedbacks, SAMBA was reviewed and reached its final form.
The results showed that there was a significant difference between the pre-test and post-test of the dimensions of Anger and Stress
Management (Z= -1.919, p<0.5), Relapse Prevention (Z= -2.557, p<0.5), and Craving (Z= -2.874, p<0.5).
The results of the dimension of “Information about Drugs, Alcohol, and Tobacco” were not found to be significant. However, there was a
difference between mean scores of pretest and post-test. One possible reason for this result might be the sample size.
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There was not a significant difference between the results pre-test and post-test of the dimension of Motivation. The results showed that
the participants were not well-informed about relapse prevention. Therefore, it is suggested that the focus of the program should be on
relapse prevention.
According to the results of the feedback form, 66.6% of the participants claimed that they have learned moderate or very much information
from the SAMBA program. 91.6% of the participants claimed that the trainers were moderately or very much successful. Lastly, 75% of the
participants reported that they had the opportunity to participate and share ideas during the sessions again moderately or very much.
Key words: Addiction, psychotherapy, treatment, effectiveness
[PP-050]
Psychometric properties of different forms of the Addiction Profile Index (BAPI)
Ref. No: 187
Kültegin Ögel1, Aslı Başabak2, Ceren Koç2, Alper Aksoy2, Gülşah Karadayı2
1
Yeniden Society
2
The Addiction Profile Index (BAPI) is composed of 37 items and 5 subscales assessing the characteristics of substance use, dependency
diagnosis, the effect of substance use on the person’s life, craving, and the motivation to quit using substances. The reliability and validity
of the scale were reported in a very recent study.
In these current studies, we aimed to develop a clinician-administered form (BAPI-U), clinical form (BAPI-II) and a short form of BAPI (BAPI-K).
Study 1: Psychometric properties of clinician-administered form of BAPI
Items of the BAPI were changed to a clinician asked type. In the original BAPI 5-point likert ratings were used. In this questionnaire we
used 3-point likert ratings.
A total of 150 male inmates were recruited from the Umraniye, Istanbul T-type prison. Cinical Psychologists and guardians of the prison
conducted face-to-face interviews with inmates to complete the BAPI.
The BAPI-U items were found to be significantly correlated with the self-reported form (0.89). High correlations between interviewer
ratings in all subscales were found. Factor analyses yielded four factors for the BAPI-U, which were similar to the BAPI.
It was concluded that the BAPI-U has similarities with the BAPI and therefore it may be applied by non-clinical professionals (such as
nurses, guardians etc) after a short training period.
Study 2: Development and psychometric properties of the clinical form of the BAPI
It is important to know the factors causing alcohol or substance dependence disorders in order to choose the treatment modality and to
prevent relapses.
In order to assess depression, anxiety, anger, and assertiveness, new items were added to the original BAPI items. This new instrument
was named the BAPI-II.
The research sample was similar to study 1. The Beck Depression Inventory, Rathus Assertiveness Inventory, Multi-dimensional Anger
Scale and STAI-1 were used in this study.
The Cronbach Alpha value of the whole scale was found to be 0.79. The self and clinican administered rating correlations were statistically significant.
The correlation of the BAPI-II with the other scales was high. One factor was obtained and 54.34% of the variance was explained by this factor.
High correlations were found between the ratings of psychologists and prison guardians in all subscales. This shows that the BAPI may be
administered by non clinical professionals efficiently.
Study 3: Development and psychometric properties of the short form of the BAPI
This study was conducted to develop a shorter version of the BAPI to be used as a screening tool. The study was carried out with 1200
people in 7 different prisons. Based on the results of the statistical analyses, some questions were removed. The short version of the BAPI
is composed of 23 questions and is named as BAPI-K.
The correlation between the original form and the short version of the form was found to be very high (0.96). Both subscales of the two
scales were found to be correlated. The scores of the correlations of the BAPI with CAGE and AUDIT were also found to be statistically
significant. The internal consistency of the new scale was found to be satisfactory (0.89).
The results have shown that the BAPI-K is a valid and reliable instrument, and can be used as a screening tool.
Key words: Addiction, assesment, questionnaire
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[PP-051]
Aripiprazole treatment for the choreoathetoid movements and psychotic
symptoms of Huntington’s disease: A case report
Ref. No: 199
Sevinç Ulusoy, İzgi Alnıak, Kasım Fatih Yavuz, Tuğba Kara
Bakirkoy Research and Training Hospital for Psychiatry and Neurology, Istanbul, Turkey
Introduction: Huntington’s Disease, that is caused by CAG trinucleotide repeat expansion in the IT15 gene located on the short
arm of chromosome 4, is an autosomal dominant, progressive neurodegenerative disorder characterized by motor, cognitive, and
psychopathological symptoms (1). The disease is accompanied by a variety of psychiatric disorders and its incidence rates range from 33
to 76%. Although depression is the most common accompanying psychiatric disorder, anxiety, obsessive-compulsive disorder, irritability
and manic and psychotic symptoms may be associated with Huntington’s Disease (2).
In this case report, we discuss the effectiveness of aripiprazole on the motor and psychiatric symptoms of a patient with Huntington’s
disease, who had psychotic symptoms.
Case: Two years ago, psychotic symptoms developed in addition to existing neurological symptoms in a fifty-year-old patient who was
known to have had Huntington’s disease for twenty years.
After one month of 30 mg/day aripiprazole treatment for a diagnosis of ‘Psychotic Disorder Due to a General Medical Condition’, a
significant decline was observed in the motor and psychotic symptoms that had been present at the beginning of the disease.
Discussion: Although the pathogenesis of the Huntington’s disease has not been exactly solved, the glutamatergic and dopaminergic
systems with striatal neurodegeneration are thought to be responsible for the clinical signs of the disease (3).
By the consideration of this process it is conceivable that aripiprazole, which is used in the treatment of psychosis and chorea, may be a
well-tolerated agent for its effects on the negative and positive symptoms with low metabolic and extrapyramidal side effects.
Key words: Aripiprazole, choreoathetoid movement, Huntington’s disease
References:
1.
Walker FO: Huntington’s disease. Lancet 2007; 369:218–228
2.
van Duijn E, Kingma EM, van der Mast RC: Psychopathology in verified Huntington’s disease gene carriers. J Neuropsychiatry Clin Neurosci 2007, 19:441-8.
3.
Paoletti P, Vila I, Rife´ M, et al: Dopaminergic and glutamatergic signaling crosstalk in Huntington’s disease neurodegeneration: the role of p25/ cyclin-dependent
kinase 5. J Neurosci 2008; 28:1090–1101
[PP-052]
Acute effects of Bacopa monnieri on mood in healthy young adults
Ref. No: 189
Chris Neale, Sarah Benson, Con Stough, Andrew Scholey
Centre for Human Psychopharmacology, Swinburne University, Melbourne, Australia
Objectives: Previous research has identified that Bacopa monnieri (BM) improves aspects of cognitive functioning such as attention,
speed of information processing and verbal learning with chronic dosing (300mg daily). To date there have been no reports of acute
neurocognitive benefits of BM where acute testing has been evaluated; only one known study has reported on acute Bacopa measures[1].
It is possible that in this previous study the cognitive instruments were not demanding enough to detect acute effects. This study is the
first acute dose ranging study of BM using multi-tasking cognitive assessment and measurement of mood.
Methods: Seventeen healthy young adults took part in this double-blind, placebo-controlled three-period crossover study. They were
administered 300 mg BM, 600 mg BM, or a matching placebo on different days with a seven-day washout period between visits. The
treatment order was determined using a Latin Squares design. Following baseline assessment, participants were administered the day’s
treatment and further assessment took place 1 h and 4 h later. The assessments included the Purple multi-tasking framework (MTF) and
the Bond-Lader mood visual analogue scales (administered before and after each 20 min MTF session). The MTF is a 20 minute framework
where participants are required to complete four tasks simultaneously. Tasks include Stroop, maths, tracking and working memory.
Results: There was a significant, dose-dependent effect of treatment on ratings of alertness favouring the 600 mg treatment at both
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post-dose assessment times. There was a trend for dose-related effects on performance of the MTF, in particular for the Stroop task, where
there was an advantage for the 300 mg dose.
Conclusions: This is the first demonstration of acute neurocognitive effects of BM. The combination of increased alertness for 600 mg and
better selective attentional performance for 300 mg suggests that mood and cognitive processes can be dissociated and that different
doses of Bacopa may benefit different neural mechanisms.
Further participants are needed for this cohort to increase the statistical power of these findings.
Key words: Bacopa monnieri, nutraceuticals, mood, cognition
References:
1.
Nathan, P.J., et al., The acute effects of an extract of Bacopa monniera (Brahmi) on cognitive function in healthy normal subjects, in Human Psychopharmacology:
Clinical & Experimental. 2001, John Wiley & Sons Ltd. 1996. p. 345-351.
[PP-053]
Anxiety and depressive symptom levels among adolescents with risk taking behaviour
Ref. No: 201
Nuray Sarp1, Aylin Aksoy Çoban2, Kültegin Ögel3
Acıbadem Fulya Hospital, Psychiatry service, Psychology Department, İstanbul, Turkey
1
Acıbadem Fulya Hospital, Psychiatry service, Istanbul, Turkey
2
Acıbadem University School of medicine, Department of Mental Heath Disease, Istanbul, Turkey
3
Background: In our country, risk taking behavior has increased among adolescents in recent years. Risky behaviours are defined as
behaviors that affect an adolescent’s health and wellness and daily life directly or indirectly. These behaviours can cause potential
negative results. Bullying, smoking, using alcohol or drugs, early or unprotected sexual activity, skipping school, elopement, damaging
friends and self destruction are the most frequent risky behaviors among adolescents. Through previous research, it has been shown that
the moods of adolescents with risky behaviors differ from other adolescents. Thus it is thought that there may be an association between
risky behavior and depression and anxiety.
Objective: This study investigated the differences between adolescents with risky behaviour and the ones with non-risky behaviour in
terms of depressive and anxiety symptom levels.
Methods: The participants were from different regions and different socio-economic statuses. A total of 3483 students from forty-three
schools (12 vocational high schools, 23 state schools and 6 private high schools ) and104 classes were included in this study. The multistage cluster sampling method was used for the selection of the sample. In the study, YSR 11-18 (Youth Self Report) and a questionnaire,
which was developed by the researchers, were used. The research survey consisted of 238 items; The questions covered demographical
information, parent and region features, problems about school life, risky behaviours, neglect and abuse, disease, trauma, and health.
Results: In this study, 45.5% of participants were female, 54.5% were male. According to the analysis of each risky behaviour, significant
differences were found for depressive and anxiety symptom levels between groups.
Adolescents who exhibit bullying, elopement, self destruction, commit crimes, and have damaging friends are more likely to show
anxiety and depressive symptoms compared to non-risky behavior adolescents.(p=0.000). In addition, the level of depressive and anxiety
symptoms of drug users were higher than the level of depressive and anxiety symptoms of non-users (depressive; p=0.000, anxiety;
p=0.019).
Adolescents who are carrying a weapon, using alcohol, working in a job and skipping school had a higher level of only depressive
symptoms (p=0.0000). On the other hand, only the high level anxiety group had unprotected sexual activity (p=0.092).
Conclusions: A comparison of non-risky behavior adolescents to risky behavior adolescents showed significant differences in terms of
anxiety and depressive symptom levels and these symptom levels changed according to the risky behaviour type.
Key words: Adolescents, anxiety symptom levels, depressive symmptom levels, risky behavior
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[PP-054]
The relationship between mental health and academic achievement among
Kordestan high school students
Ref. No: 153
Fayegh Yousefi, Srwa Mohamadzadeh
Department of Psychiatry at Kordestan University of Medical Sciences, Sanandaj, Kordestan, Iran
Objective: Academic achievement is one of the important factors to which parents, teachers and society pay attention and also, it is
related to students’ mental health. The main objective in the present study was to determine the relationship between students’ mental
health and their academic achievement.
Method: The sample of this study was 1662 high school students (765 males and 908 females) in the age range of 14-19 years. The
sampling method of this study satisfied random sampling. Also, data were gathered by using the GHQ-28. The GHQ-28 is an instrument
to determine mental health and it includes four scales measuring depression, anxiety, somatization and social function. The reliability of
this scale is 0.91 by Cronbach’s alpha.
Results: The results of the present study showed that 45.4% of the respondents had a lack of mental health. Based on the results of the
current study, the low rate of lack of mental health (42.2%) was in the first grade of high school while, the high rate of loss of mental health
were among Pre-University students.
In addition, the results from the present study indicated that there is significant relationship between the education of the respondents’
father and students’ mental health (p<=.0.001). According to the present study, there was a significant difference between gender and
mental health (p<=.0.001).
Conclusions: Various factors such as self-esteem, motivation, anxiety, attention and concentration, gender, study curriculum and mental
affective situations impact on academic achievement. As a result all of the mentioned factors are related to mental health directly or
indirectly. So, it is suggested to investigate the mental health and also types of mental disorders among students in of Iranian schools
especially among high school students.
Note: The sponsor of present study is the Education Office in Kurdistan Province.
Key words: Mental health, academic achievement
[PP-055]
Does the profile of addiction change according to the type of the substance used?
Ref. No: 195
Kültegin Ögel1, Figen Karadağ2, Cüneyt Evren3, Defne Tamar Gürol3
1Acibadem University Medical Faculty, İstanbul, Turkey
2Maltepe University Medical Faculty, İstanbul, Turkey
3Bakirkoy mental hospital AMATEM, İstanbul, Turkey
Objective: The Addiction Profile Index (BAPI) is a self-report scale that has been developed in order to assess addiction severity and
different dimensions of addiction. The BAPI is composed of 37 items and 5 subscales. The subscales assess substance use characteristics,
addiction diagnosis criteria, the effects of substance use to the person’s life, craving, and motivation to quit. The aim of this study was to
investigate the psychometric properties of the scale in people using alcohol and substances.
Methods: A total of 345 alcohol and/or substance abusers participated in the study from two addiction treatment clinics and a prison.
The validity of the questionnaire was tested with the Michigan Alcoholism Screening Test (MAST), Readiness to Change Questionnaire
(SOCRATES), Penn Alcohol Craving Scale (PACS), Structured Clinical Interview for the DSM-IV Axis I Disorders (SCID I) and Addiction
Severity Index (ASI).
Results: The Cronbach alpha coefficient was found to be 0.89. The Cronbach alpha coefficient for alcohol abusers was 0.76, whereas it was
0.70 for substance abusers. The Cronbach alpha coefficients for the subscales ranged from 0.63 to 0.86. This coefficient ranged from 0.57
to 0.83 for alcohol abusers and from 0.67 to 0.86 for substance abusers.
Four factors were obtained according to the explanatory factor analysis and these 4 factors represented 52.39% percent of the whole
variance. Two factors represented 48.5% of the variance for alcohol abusers and two factors explained 50.9% of the variance for substance
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abusers. In the ROC analyses, the area under the curve was found to be 0.90. The ROC analysis has shown that the area under the curve
for alcohol abusers was 0.81 and for substance abusers was 0.93 (Graph 1 and 2).
The BAPI craving subscale was found to be consistent with the PACS and the motivation subscale was found to be consistent with the
SOCRATES. The BAPI total score showed a significant correlation with the MATT average score and the composite score of the Medical
Condition, Substance Use, and Legal Status and Family Social Relations subscales of the ASI questionnaire.
Discussion: The results have shown that psychometric properties of the BAPI are satisfactory for alcohol and substance abusers. The
psychometric properties of the total scale and the data of alcohol and substance abuse are similar. Finally, we can say that the BAPI can
assess both alcohol and substance abuse rather than just alcohol use.
Key words: Addiction, alcohol, assessment
[PP-056]
Death anxiety among terminally ill inpatients
Ref. No: 160
Marjan Anvar Abnavi, Ali Javadpour, Sahand Mohamadzadeh
Department of Psychiatry, Shiraz University of Medical Sciences, Shiraz, Iran
Objective: In spite of the certainty of death, people seem unable to escape anxiety at the prospect of it. Death anxiety contributes
to important emotional and behavioral consequences. The aim of this study was to investigate the relationship of death anxiety with
variables such as severity of illness, depression, and religious beliefs.
Methods: The study is a cross-sectional descriptive study. The data were collected by using a demographic questionnaire, the Templar
Death Anxiety Scale, the Beck Depression Questionnaire, the Cumulative Illness Rating Scale and the Religious Attitude Questionnaire.
Stepwise multiple regression analysis was conducted to identify the factors that influenced the degree of death anxiety.
Results: A group of one hundred and fifty persons, (50 severely ill patients, 50 relatives, and 50 normal controls) completed the
questionnaires. Death anxiety score was 7.2 in attendants, 5.3 in patients, and 4.4 in the control group. Depression and severity of illness
had a positive correlation with death anxiety (p<0.05). Religious beliefs had a negative correlation with death anxiety (p<0.05). Religious
beliefs and depression had stronger predictive value esspecially in severely ill patients.
Conclusions: Among the factors studied depression and severity of illness had a significant positive and religious beliefs had a significant
negative correlation with levels of death anxiety.
Key words: Death, anxiety, religious beliefs, depression
[PP-057]
The effective features of access to medical care in Iran
Ref. No: 188
Amir Ashkan Nasiripour1, Ghahraman Mahmodi2, Mandana Zafari3
Department of Health Services management, Science and Research Branch, Islamic Azad University, Tehran, Iran
1
Department of Research Methodology, School of Management and Medical Information Services, Tehran University of Medical Science, Tehran, Iran
2
Department of Midwifery, Sari Branch,Islamic Azad University, Sari,Iran
3
Objective: Access to medical care is recognized as a fundamental requirement in the health system. The purpose of this study was to
improve people’s access to medical care through determining the features influencing the access to medical care and its subcomponents
and preparing a proper model for public hospitals in Iran.
Methods: The sample size was 406 patients and 401 experts of Iran’s public hospitals chosen by a multistage sampling method, in which
the country was divided in to 5 regions of the North, South, Center, West, and East. By giving two shares to each region, two hospitals
were chosen from each region, then from each hospital 40 patients and experts were chosen separately. To collect data, the researcher
prepared a questionnaire to be used. To evaluate the validity of the questionnaires, expert tips, content validity and the factorial analysis
method were utilized and in order to evaluate the reliability of the questionnaire the Cronbach alpha coefficient was used. In this
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study, the Cronbach alpha coefficient of the questionnaire was calculated to be 0.88 for patients and 0.80 for experts, which was very
satisfactory. The data were analyzed by the SPSS software and Lisrel through the factor analysis method.
Results: Based on the responses of 401 patients and 406 experts, the current situation of access to medical care in the public hospitals
of Iran has lower than average quality and most of the patients and experts gave a low rating to each of the 5 factors of accessibility
in the current situation. In addition, the findings showed that the structure of access to medical care in Iranian public hospitals has a
5-dimensional structure containing individual characteristics, service providing system, social-geographic features, health policy making
and management strategies. The relationship among the 5 dimensions was meaningful from 0.13 for the correlation of health policy
making with the individual characteristics to 0.40 for the correlation of health policy making with the management strategies.
Conclusions: The findings show that the service providing system had the highest quality and was the most effective factor on having
access to medical care structure. It seems that it can be helpful to pay attention to the above factors especially in programming and policy
making to improve access to medical care by distributing the standardized number of beds and specialists based on the population of
each region, training, organizing, and managing the human resources, and improving the service providing system process.
Key words: Feature, access, access to health care, medical care
[PP-058]
Smoking behaviour during the course of paroxetine treatment: A case report
Ref. No: 174
Neslihan Akkişi Kumsar, Atila Erol
Sakarya Training and Research Hospital, Sakarya, Turkey
Selective serotonin reuptake inhibitors are used for the treatment of a wide range of psychiatric disorders, although nicotine craving
attributed to the use of serotonin reuptake inhibitors especially paroxetine has not yet been reported in the literature. Here we present
a case, who developed nicotine craving and started to smoke cigarettes after initiation of 20mg/day paroxetine, and discuss possible
mechanisms of this side effect while reviewing current status of the literature. A 25 year-old female patient was evaluated at our outpatient
clinic and diagnosed with generalized anxiety disorder. She was given paroxetine 20mg/day for four weeks. While her symptomatology
improved by the second week of the treatment, she complained of nicotine craving at the fourth week. During psychiatric assessment
there was not any history of smoking, alcohol or any other substance use disorder. She mentioned that she started smoking one package/
day after starting the paroxetine treatment. The craving for nicotine decreased after the drug was discontinued and she quit smoking
within two weeks. We did not find any report of smoking behaviour attributed to SSRIs in the literature, although there is a study about
decreased smoking behaviour during paroxetine treatment. To the best of our knowledge this case is the first one in the literature. More
research is needed to exlore nicotine craving and SSRIs.
Key words: Craving, cigarette, paroxetine
[PP-059]
Development of a SNP genotyping panel and a medical decision support algorithm
to predict drug response in schizophrenia
Ref. No: 190
Hüseyin Alper Döm1, Mehmet Ali Döke2, Yemliha Yener Tuncel1, Gürkan Üstünkar3, Yeşim Aydın Son4
Middle East Technical University, Bioinformatics Graduate Program Ankara, Turkey
1
Middle East Technical University, Department of Biological Sciences, Ankara, Turkey
2
Middle East Technical University, Informatics Institute, Department of Information Science, Ankara, Turkey
3
Middle East Technical University, Informatics Institute, Department of Health Informatics, Ankara, Turkey
4
Genome Wide Association Studies (GWAS) of Single Nucleotide Polymorphisms (SNPs) is leading the development of personalized
medicine approaches to predict and diagnose diseases or to determine drug response in individual patients. As the basic research
provides all the genomic information and interpretation of these data, translational research has to be conducted in order to develop
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genomic diagnostics to apply this information into practice in medical clinics. In this perspective, our goal is to design a diagnostic assay
for the Prediction of Drug Response for Schizophrenia to especially guide the initial selection of antipsychotics based on the individual
genomic information of the patients.
Initially a literature search has been done to identify previously described SNPs associated with schizophrenia that are known to effect
the response to antipsychotics or predict the side effects of antipsychotic drugs. Twenty-two SNPs are identified, that map to 8 genes.
Next, we have applied the novel AHP based SNP prioritization approach implemented in the METU-SNP software for GWAS to the SNP
Genotyping data for the European American population (from dbGAP database), with 1351 patients and 1378 controls genotyped for
over 729454 SNPs. The 22 SNPs selected based on the literature were cross-checked with the results of GWAS and prioritized in order to
finalize the pharmacogenomics of the SNP (p-SNP) panel for schizophrenia and to determine the order of SNPs to be targeted in the assay
development process. The pyro-sequencing approach was used during the development of the assay to determine the genotypes of the
patients for the SNPs selected for the panel. After the next phase of our project, which is the development and optimization of primer
sets, is completed a validation study will be designed in collaboration with psychiatric clinics for the described p-SNP kit panel and the
supporting software that is in-line, for development of easy translation of the genotyping results to support the clinical decision of the
choice of therapy.
Application of personalized medicine approaches and utilizing genomic diagnostic assays as presented here will eliminate or decrease
the number of trials-and-errors in selecting sthe right treatment and dosage for particuler patient, and will also minimize emergency
visits due to side effects of the drugs. In addition, the prescription of the right medicine and treatment plan at the initial diagnosis
of schizophrenia will increase trust between healthcare professionals and patients, which in return is expected to provide higher
cooperation and adherance rates of patients to their treatment. Overall the personalized medicine approach is expected to decrease the
cost of healthcare in psychiatry and other disciplines, while offering higher quality healthcare.
Key words: Pharmacogenomics, personalized medicine, translational medicine, genomic diagnostics, medical decision support systems, GWAS,
SNP genotyping, METU-SNP, schizophrenia
[PP-060]
Basal ganglial hemorrhage induced mania
Ref. No: 200
Barış Yılbaş1, Murat Gönen2
Department of Psychiatry, Elbistan State Hospital, Elbistan-K.Maraş, Turkey
1
Department of Neurology, Elbistan State Hospital, Elbistan-K.Maraş, Turkey
2
Neuroimaging studies on mood disorders concentrate on the limbic system, especially on the hippocampus and amygdala. Accumulating
evidence suggests an association between abnormalities of the basal ganglia and mood disorders. We present a case of mania following
basal ganglial hemorrhage.
A 30-year old male, with no history of bipolar disorder, was admitted to the emergency room with complaints of euphoria and decreased
need for sleep. During psychiatric assessment, he exhibited grandiosity, psychomotor activation, irritability, and flight of ideas. The
patient,whose cranial MRI showed hemorrhage in the basal ganglia, was hospitalized with a diagnosis of mood disorder due to a general
medical condition. Lorazepam 5mg/day and olanzapine 10mg/day was started. On the tenth day of treatment his episode ended.
The basal ganglia are interconnected with the limbic system and prefrontal cortex and therefore are implicated in bipolar disorder.
Key words: Basal ganglia hemorrhage, mania
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[PP-061]
Evaluation of cognitive functions in euthymic bipolar patients using
mono- and multi- drug treatments
Ref. No: 233
Birgül Elbozan Cumurcu1, Rıfat Karlıdağ1, Şükrü Kartalcı1, Işıl Göğcegöz Gül1, Süleyman Demir2, Bahar Yeşil1
Inonu University Medical Faculty, Turgut Ozal Medical Center, Department of Psychiatry, Malatya, Turkey
1
Gaziosmanpasa University School of Medicine, Department of Psychiartry, Tokat, Turkey
2
Objective: Some studies on patients suffering from bipolar disorder show that in active and remission periods of the disorder there are
cognitive insufficiencies (1,2,3). The causes of cognitive insuffuciencies in bipolar disorder is not understood yet. We anticipate that multidrug usage has more adverse effects on cognitive functions than mono- drug usage and our aim in this study was to investigate effects of
drugs used in treatment of bipolar disorder on cognitive functions. In this study we evaluated the cognitive functions of bipolar patients
who were in their euthymic period taking mono- and multi-drug regimens and compared them with a healthy control group.
Methods: Eighty bipolar I and II patients diagnosed based on the DSM-IV criteria and 80 healthy controls were included in the study and
two groups matched according to age, sex, and education aspects. The patients and controls gave written informed consent to participate
in the study. The necessary approval and ethic committee reviews and permits were obtained prior to the study. The patients were
evaluated using a psychiatric interview, the Young Mania Scale and the Hamilton Depression Rating Scale. A large neurocognitive battery
(Wechsler Memory Scale-Revised, Stroop,Verbal Memory Processes Scale) was used for neurocognitive assessment.
Results: In most cognitive tests the results of the patient group were worse than the control group. The Verbal Memory Processes
Scale-learning scores and long term memory scores were higher in the patients on a mono-drug regimen. All other tests did not show
significant differences.
Conclusions: Our study showed that the cognitive function of bipolar patients had deficiencies not only in active periods of bipolar
disorder but also in remission periods, like previous studies (4,5,6).
The Verbal Memory Processes Scale learning scores and long term memory scores showed better results in patients using a mono-drug
compared to the ones on a multi-drug regimen. Other tests did not show significant differences. Future studies with larger number of
patients may show different results. Also other studies to investigate the effects of each drug group on cognitive functions in bipolar
patients are needed.
Key words: Bipolar disorder, cognitive functions, euthymia
[PP-062]
Adult ADHD symptoms in cannabis dependence and the importance of
comorbidity in Adult ADHD
Ref. No: 247
Umut Mert Aksoy, Şennur Günay Aksoy, Fulya Maner
Bakirkoy Research And Teaching Hospital For Neuropsychiatry, İstanbul, Turkey
Background: Adult Attention Deficit Hyperactivity Disoeder (A-ADHD) is one of the most important neuropsychiatric disorders originating
in childhood. According to the last epidemiological studies, ADHD can be persistent into adulthood. Sixty percent of childhood ADHD
cases present with at one or more symptoms in adulthood (Biedermann 2000, Wilens 2006). A prevalance rate of 4.4% of adults has been
reported for ADHD (Fayyad 2007, Kessler 2006).
Comorbidity with alcohol and substance use disorders in A-ADHD is also common and reported as 50%, which is 2-3 times more common
than in the normal population (15%) (Katusic 2005). A-ADHD is reported to be an independent risk factor for substance abuse. Comorbid
substance use disorders have been observed at rates of 9-30& (Wilens 2006).
Individuals with substance use dişorders comorbid with A-ADHD do not differ in substance preference from individuals without A-ADHD
comorbidity. Cannabis is the most abused substance.
Objective: We aimed to demonstrate the existence and intensity of Adult ADHD symptoms in cannabis dependent individiuals and
discuss the importance of comorbid A-ADHD.
Methods: Seventy patients participated and gave informed consent. The participants were selected from patients who underwent
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inpatient treatment in the Department for Addiction at Samsun Neuropsychiatry Hospital. Diagnostic interviews were conducted for
cannabis dependence syndrome (ICD 10; DSM-IV); the earliest interview was after 21 days of detoxification therapy. For assesment, the
Adult ADD/ADHD DSM IV based Diagnostic Screening and Rating Scale was used. The reliability, validity, and transliteral equivalance study
had been performed by Günay et.al in 2005 (Günay 2006). The scale was developed by Prof. Dr.Turgay, former Director of the Toronto
ADHD Clinic, Ontario,Canada. It is a self assessment scale.
General total and subscale mean scores and standard deviation of the ADHD scale according to group factors were calculated. Mean
ADHD total and subscale scores were compared by using the group variable independent t test. The analyses were conducted using SPSS
for Windows 16.00.
Results: The ADHD general total mean scores and subscale mean scores were compared between the groups. Considerably higher scores
were observed in cannabis dependent individuals.
Twenty-two patients met the criterion of inattention whereas 24 patients met both the criteria of hyperactivity and inattention. Twentyfour patients were re-evaluated and interviewed and Adult ADHD was diagnosed.
Five individuals in the control group met the criterion of inattention, and there were no individuals who met the criteria for both
hyperactivity and inattention.
All three subdimensions of the Turgay Adult ADHD Scale were found to be statistically higher in the cannabis dependent patients.
Conclusions: As this study shows, Adult ADHD is highly represented in cannabis dependent patients.(in our sample 35% of patients were
diagnosed with Adult ADHD).
The awareness of the ADHD diagnosis in Turkey has rapidly increased over time. However it is not commonly researched, diagnosed, or
treated in adult psychiatric units. A major difficulty may be that ADHD has been misdiagnosed because comorbidity is common and 90%
of A-ADHD patients present with another psychiatric disorder in clinical practice. Recent studies clearly show a strong relation between
ADHD and addiction, which supports the idea that a high percentage of drug dependent individuals are also suffering from undiagnosed
A-ADHD. Individuals who are diagnosed and treated are less vulnerable to addiction (Biedermann 1999)
Key words: Adult ADHD, cannabis dependency, substance use
References:
1. Biederman J, Mick E, Faraone SV (2000) Age-de¬pendent decline of symptoms of attention deficit hyperactivity disorder: impact of remission definition and
symptom type. Am J Psychiatry 157:816–818
2.
Wilens TE (2006) Attention-deficit/hyperactivity disorder and the substance use disorders: the nature of the relationship, subtypes at risk, and treatment issues.
Psychiatr Clin North Am 27:283–30.
3.
Fayyad J, De GR, Kessler R et al (2007) Cross-national prevalence and correlates of adult attentionDeficit hyperactivity disorder. Br J Psychiatry 190:402–409
[PP-063]
Ganser syndrome as a dissociative disorder: A case report
Ref. No: 270
Beliz Soyer, Jülide Kenar, Kader Semra Karataş
Erenkoy Mental and Nervous Diseases Training and Research Hospital, Istanbul, Turkey
Ganser syndrome was first described in 1898 by Sigbert Ganser in 4 prisoners. Initially, it was believed to be rare, occurring mainly in
forensic settings. Hence, it was referred to as prison psychosis. Later, such cases were reported more frequently in non-forensic settings.
The syndrome has found a place in both the ICD-10 and DSM-IV, despite controversy about its existence and distinctiveness. This disorder
was previously classified as a fictitious disorder; currently, it is classified under ‘dissociative disorder not otherwise specified.’ We report a
case of a 38 year old woman with Ganser syndrome. The symptoms started 9 months after the death of her brother’s children.
Key words: Ganser Syndrome, vorbeireden, dissociative disorder
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[PP-064]
Escitalopram induced galacthorrea: Phenomenon presentation
Ref. No: 272
Aslı Aktümen Bilgin1, Birmay Çam2
Zonguldak Atatürk Devlet Hastanesi Psikiyatri Kliniği, Zonguldak, Turkey
1
Gönen Devlet Hastanesi Psikiyatri Kliniği Balıkesir, Turkey
2
Hyperprolactinemia can present with many physical symptoms such as galactorrhea, amenorrhea, infertility and osteoporosis and
can also cause psychological problems like depression and anxiety. Hyperprolactinemia is mostly seen as a side effect of antipsychotic
medications and rarely can also occur as a side effect of an SSRI. Hyperprolactinemia and galactorrhea as adverse effects of escitalopram
are rarely encountered. In this text we present a case, who developed hyperprolactinemia and galactorrhea on the sixth day of treatment.
The prolactin level decreased to normal after stopping the medication.
Key words: Escitalopram, galactorrhea, hyperprolactinemia
[PP-065]
Amisulpride use in treatment of Tourette’s disorder
Ref. No: 276
Yasemen Taner, Hande Ayraler Taner
Departmant of Child and Adolescent Psychiatry, Gazi University, Ankara, Turkey
Tourette’s disorder is a neuropsychiatric disease characterised by chronic vocal and motor tics that leads to severe psychosocial disability.
Many old and new generation antipsyshotics had been used in the treatment of Tourette’s Disorder, especially antipsychotics which have
strong effects on D2 receptors. Amisulpride is an antipsychotic which has strong effects on D2 and D3 receptors. Parkinsonism, endocrine
system side effects, and weight gain are less frequent than with the other antipsychotics. Amisulpride is safely used in the treatment of
schizophrenia and the other psychoses in adults. In this case report we discuss amisulpride use in 3 cases with Tourette’s disorder. These
cases previously used other antipsychotics for Tourette’s disorder treatment. Amisulpride was used at a dose of 75-200 mg/day. After
treatment in all three of these cases, the Yale Global Tic Severity Scale score decreased.
Key words: Tourette’s disorder, amisulpride
[PP-066]
Lithium associated glossodynia syndrome: A case report
Ref. No: 299
Hasan Toğul
Gata Haydarpasa Training Hospital, İstanbul, Turkey
Lithium revolutionized the treatment of bipolar disorder and continues to be the most widely used treatment for this disorder. There
are several side effects that result from lithium carbonate therapy and among the most commonly reported are polydipsia, polyuria,
tremor and weight gain. There have also been reports of various skin lesions with lithium treatment. The following case report suggests
that mucosal lesions may possibly result from lithium therapy. Glossodynia is commonly seen in old female patients. In our case, a 45
year old male had glossodynia after lithium carbonate therapy. The patient’s symptoms were under control with a lithium regimen for a
year. He stopped using lithium in January 2011 and one and a half months later he was hospitilazed because of dysphoric mania. After
his hospitalization, lithium therapy was started again. Three weeks later he reported mucosal ulcerations in the mouth, with associated
soreness of the tongue. The tongue appeared inflamed, with cracks or irregular reddish areas. He was evaluated by a dermatologist, who
diagnosed him with glossodynia. No other medical causes for the lesions were found; the lesions were presumed to be secondary to
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lithium treatment. His lithium treatment was stopped and glossodynia treatment begun. Shortly thereafter, his glossodynia symptoms
disappeared. Psychotropic medications can cause mucosal ulcerations and it is important to consider these side effects in the differential
diagnosis and and begin treatment as soon as possible.
Key words: Lithium carbonate, glossodynia, side effects
[PP-067]
Two cases of affective disorder due to immunosuppresive treatment
that followed renal transplantation
Ref. No: 300
Hüseyin Ünübol, Başak Ünübol, Jülide Güler, Alper Ünal
Erenkoy Mental Health Education and Research Hospital, İstanbul, Turkey
The advent of effective immunosuppressive medicines in the mid-1980s, most notably cyclosporine, revolutionized solid-organ transplant
surgery. For the first time, survival rates reached acceptable levels and rendered organ transplantation a reasonable, non-experimental
standard of medical practice. From the beginning, the immunosuppressive medications were noted to have significant neurological and
psychiatric side effects. From that time to this, the neuropsychiatric side effects such as subjective anxiety or jitteriness, along with tremor,
have served as endpoints in the clinical titration of the the most frequently used immunosuppressive medications, cyclosporine and
tacrolimus. Experience over the past 15 years, however, has established the fact that there are other neuropsychiatric side effects, varying
from seizures, stroke, and profound cognitive impairment to very subtle forms of neuropsychiatric difficulty. Here we present two cases
that underwent uncomplicated renal transplantation and after the immunosuppressive therapy, developed psychiatric symptoms. The
first case was a 29 year old woman with psychotic mania, and the second was a 25 year old male with severe depression that followed a
hypomanic episode (1-3).
Case No 1: A 29 year-old female patient, with a history of kidney transplantation 9 months ago, developed
insomnia, nervousness, mobility, speaking too much, aggressive behavior towards her mother at home, destruction of items, thinking
people were trying to poison her, self-talk in the office, increased skepticism, left her workplace without permission, angry and rowdy
behavior.
History: No previous psychiatric treatment. No family history of substance abuse and psychiatric illness. Surgery for kidney transplantation
9 months ago. Twenty mg/day oral olanzapine treatment was started.
Mycophenolate Mofetil 1000 mg tb 2*1 07:30 and 19:30, prednisolone 5 mg tb 1*2 07:30, cyclosporine 100 mg tb 1*1 19.30 cyclosporine
100 mg tb 1*1 21:30 therapy was continued.
Blood samples for monitoring of cyclosporine levels were sent outside the center. MPPI, Rorschach, and psychometric examinations were
performed and she was evaluated in the direction of psychotic process. PMA is returning to normal; irritability and the patient’s insight
improved on olanzapine 20 mg/day treatment and she was discharged.
Case No 2: A 25 year-old, male patient, with a history of kidney transplantation 4 years ago. The symptoms included unhappiness,
reluctance, discomfort, passive thoughts of death, and insomnia.
Hisstory Kidney transplant in 2007. Approximately 1.5 years ago he had increased speech and movement and affective elation observed
indicated a hypomanic episode in the hospital outpatient clinic as the patient was evaluated. Risperidone 2 mg/day treatment was
started. Two months ago the patient presented with depressive symptoms and started sertraline 50 mg/day, quetiapine 25 mg/day, 500
mg 2 * 2, Mycophenolate mofetil, prednisolone 5 mg, 1 * 1, tacrolimus 1 mg tb 2 * 2, a month after inpatient treatment, the patient became
euthymic, anxiety resolved, and after the disappearance of suicidal ideation the patient was discharged.
Key words: Renal transplantation, immunosuppresive treatment, depression, affective disorder
References:
1.
Trzepacz PT, Brenner R, Van Thiel DH. A psychiatric study of 247 liver transplantation candidates. Psychosomatics 1989;30: 147-153.
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[PP-068]
Varenicline induced psychotic disorders: A case report
Ref. No: 303
İkbal İnanlı, İbrahim Eren, Tahsin Etli
Konya Eğitim ve Araştırma Hastanesi Beyhekim Psikiyatri Kliniği, Konya, Turkey
Varenicline is a new agent, commonly used to assist individuals with smoking cessation. There is an increase in case reports of psychiatric
disorders induced or activated by using the agent. Due to the agent’s mechanism of actions, it is possible to make this correlation. Patients
who have a mental illness or high-risk persons should be careful about using this drug. In this report, the case of a psychotic disorder
induced by varenicline is presented.
Key words: Psychotic disorder, smoking cessation, varenicline
[PP-069]
Affective disorders and catatonia: Report of two cases
Ref. No: 309
Feride Büyükşahin, Jülide Güler, Başak Ünübol, Hüseyin Ünübol, Alper Ünal
Erenkoy Mental Health Education and Research Hospital, İstanbul, Turkey
Catatonia refers to a broad group of movement abnormalities usually associated with schizophrenia, but also found in other disorders
such as mania, depression, many neurological disorders (especially those involving the basal ganglia, limbic system, diencephalon, and
frontal lobes), systemic metabolic disorders, and toxic drug states. Catatonia is often neglected when screening and examining psychiatric
patients. Undiagnosed catatonia can increase morbidity and mortality, illustrating the need to effectively screen patients for presence
of catatonia, as well as their response to treatment. We describe the clinical presentation of catatonia in a 32 year-old woman with
schizoaffective disorder and in a 25 year-old woman with severe psychotic depression.
Key words: Catatonia, mood disorders, depression
[PP-070]
The relationship of incarceration, past suicide attempts, depression, anxiety and
attention deficit hyperactivity disorder in cases of anti-social personality disorder
Ref. No: 224
Hakan Balıbey1, Türker Türker2, Zülküf Perdeci1, Nalan Bayar1, Mehmet Boran Evren1
Department of Psychiatry Ankara Military Hospital, Ankara, Turkey
1
Department of Public Health Division of Epidemiology Gulhane Military Medical Faculty, Ankara, Turkey
2
Bacgrounds and Objective: Even though attention deficit/hyperactivity disorder (ADHD) has been considered as a childhood disorder
for a long time, currently it is widely accepted that this is a disorder that continues well into adulthood. Attention deficit hyperactivity
disorder (ADHD) is a chronic developmental psychiatric disorder, which starts in early childhood, although its primary symptoms can
still be observed in adulthood. The main symptoms are attention loss, impulsiveness, and hyperactivity which result in mental, social,
and educational/occupational problems in adulthood (1). The current study aimed to study the relationship of incarceration, suicide
attempts, depression, anxiety, and attention deficit hyperactivity disorder in men, who had been diagnosed with antisocial personality
disorder (APD). There are previous studies in the literature for equivalent diagnoses (2,3). METHODS: A total of 80 subjects, 44 of whom
were diagnosed with antisocial personality disorder according to the DSM-IV-TR diagnostic criteria in Ankara Military Hospital psychiatry
clinic and 36 controls, who did not have a psychiatric diagnosis were included in the study. The subjects had been administered a semistructured interview form for identifying their demographic properties, criminal history, and past suicide attempts. The subjects had also
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been given the Wender-Utah rating scale, Hamilton anxiety scale, and Hamilton depression scales. The diagnosis of anti-social personality
disorder has been corroborated by a second mental health professional for all such cases.
Results: There was a statistically significant difference between the Wender-Utah test scores of the APD group and the control group
(p<0.001). There were statistically significant differences between the WU scores of those subjects who had suicide attempts and those
who did not; those who were incarcerated and those who were not and those who were diagnosed with depression and anxiety and
those who were not (p<0.001).
Conclusions: The current study shows that there is a strong relationship between ADHD, anxiety, depression, incarceration, and past
suicide attempts among subjects with an APD diagnosis. Better understanding of related factors in APD cases which make up a significant
portion of those who have been incarcerated and have past suicide attempts may lead to more effective treatments. Overlooking
comorbidity may worsen symptoms and result in resistance to treatment and thus worsen prognosis.
It is important that patients with anti social personality disorder should be screened for comorbidities and that those patients should not
go untreated for ADHD, anxiety and depression.
Key words: Antisocial personality disorder, anxiety, adult attention deficit hyperactivity disorder, depression, Wender-Utah rating scale
[PP-071]
Relation between unintended pregnancy and post-partum blues
Ref. No: 096
Azar Aghamohammadi, Mandana Zafari
Islamic Azad University, Sari Branch
To assess the prevalence of post-partum blues in mothers with unintended pregnancy compared with other mothers.
Methods: One hundred normal primiparous women were studied and divided into two groups based on whether their pregnancy was
intended or unintended. The maternity blues were assessed in both groups.
Results: Three days after delivery, the blues were noted in 30 of 50 mothers, 20 of 30 women who had unintended pregnancies and 10
of 50 (20%) who had intended pregnancies. There was a significant difference ten days after delivery between the two groups (P<0.0001).
Conclusion: Unintended pregnancy may be a potential causal factor for maternity ‘blues’.
Key words: Unintended pregnancy, post-partum blues
[PP-072]
Comparison of antipsychotic prescribing in the treatment of schizophrenia
between the years of 2004-2009
Ref. No: 252
Tacettin Kuru1, Mehmet Emrah Karadere2, Sinem Çelenk1, Başak Demirel3, Kasım Fatih Yavuz4
Alanya Public Hospital, Clinic of Psychiatry, Antalya, Turkey
1
Dışkapı Yıldırım Beyazıt Education and Research Hospital, Clinic of Psychiatry, Ankara, Turkey
2
Isparta Public Hospital, Clinic of Psychiatry, Isparta, Turkey
3
Bakırköy Prof. Dr. Mazhar Osman Mental Healt and Disorders Education and Research Hospital, 5th Clinic of Psychiatry, Istanbul, Turkey
4
Antipsychotic treatment is a basic part of active schizophrenia treatment. Typical antipsychotics have been in use since the 1950s. In the
1990s the antipsychotics that are called atypical, with similar effectiveness and lower extrapyramidal side effects (EPS), were introduced
and they have taken the place of typical antipsychotics quickly. Although there are comprehensive practice guidelines and suggestions
about optimal antipsychotic prescribing, polypharmacy and the use of high doses (over a dose equivalent of 1000mg of chlorpromazine)
are prevalent in clinical practice. Some clinicians propounded that using more than one antipsychotic is more effective and prescribing
different antipsychotics is not wrong because of the different effects on different signs of psychosis.
The objective of this study was to review the practice of antipsychotic prescribing in schizophrenia patients, compare the variation
of antipsychotic prescribing over a number of years and to generate additional information for studies to understand the underlying
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motivations for the use of antipsychotic prescription by psychiatrists.
Five hundred and sixty patients, who applied to the psychiatry clinic of the SSK Ankara Education and Research Hospital in 2004 and
were diagnosed with schizophrenia and 423 patients who presented to the same clinic (name changed to the Psychiatry Clinic of Dışkapı
Yıldırım Beyazıd Education and Research Hospital) in 2009 and were diagnosed with schizophrenia were included in the study. The data
were recorded on the data gathering form that we prepared and included socio-demographic information and details of medication use.
We determined that 77.5 percent of the schizophrenic patients were prescribed atypical antipsychotics in single or combined (typicalatypical or atypical-atypical) form in 2004. Forty-five percent of patients were using typical antipschotics as monotheraphy or in
combination. In 2009, 91.7 percent of patients were using atypical antipschotics in single or combined form. Only 19.9 percent of patients
were taking typical antipschotics in single or combined form. Using atypical antipsychotics reduced the use of typical antipsychotics
by a significant amount ( χ2=246.26 and p<0.001) (2004), χ2=235.24 and p<0.001 (2009). While 62 percent of patients were using an
antipsychotic, 36.6 percent of them had used more than one antipsychotic and 1.4 percent of them weren’t take any drug in 2004. In 2009,
63.6 percent of patients were using an antipsychotic, 36.2 percent of patients were using more than one antipsychotic and 0.2 percent
of patients weren’t using any antypsychotics. Between the two index years there was no difference in the use of one or more than one
antipsychotic. We didn’t examine why some patients were not on any antipsychotics because it was out of the scope of our study.
The ratio of use of typical-atypical antipsychotics and polypharmacy was similar to the current literature in our study. We determined
that the ratio of using atypical antipsychotics increased distinctively in schizophrenia treatment. In 2004, atypical antipsychotics were
prescribed in single or combined form (typical-atypical or atypical-atypical) to 77.5 percent of patients, while in 2009 this ratio increased
to 91.7 percent. We determined that antipsychotic polypharmacy continued in a high ratio similar to previous studies, altough there is no
evidence of additional advantage, but rather an increased risk of adverse effects. More than one antipsychotics were prescribed to 36.6
percent of patients in 2004 and 36.17 percent in 2009. More large-scale studies are needed especially about the motivations that effect
the practice of pharmacotherapy in schizophrenia treatment.
Key words: Schizophrenia, atypical antipsychotics, typical antipsychotics, polypharmacy
[PP-073]
Valproate-induced hyperammonemic encephalopathy: A case report
Ref. No: 257
Yücel Yılmaz, Ömer Yanartaş, İshak Saygılı, Ümit Başar Semiz
Erenkoy Mental Health and Disorders Training and Research Hospital, Istanbul, Turkey
Valproate-induced hyperammonemic encephalopathy (VHE) is an unusual complication characterized by a decreasing level of
consciousness, focal neurological deficits, cognitive slowing, vomiting, drowsiness, and lethargy. VHE may occur in people with normal
liver function, despite normal doses and serum levels of valproic acid (VPA). We describe a case of valproic acid-induced hyperammonemic
encephalopathy in a bipolar disorder patient with therapeutic VPA levels.
We report a case of a 50 year-old woman with bipolar disorder who presented to the inpatient psychiatry clinic with a manic episode.
Sodium valproate was started at a dosage of 500 mg two times a day together with the extended release form of quetiapine 400 mg once
a day. After a week she was confused about the day of the week, but was oriented to month, year, person, and place. Her vital signs were
stable. The patient reported that she did not feel better and said that she felt slowed down and depressed. The next day she gradually
became lethargic, proceeding to stuporous, and she had vomiting and drowsiness. Her blood level of valproic acid was at 97.2 μg/ml.
Liver function tests were normal. The blood urea level was 33 mg/dL. Her blood ammonia level was 304 μmol/L, more than ten times the
upper limit of the normal range. All psychotropic medications were stopped. After three days her vital signs were stable, and she had no
obvious neurological deficits. She recovered fully. Clinical manifestations and hyperammonemia tend to normalize after VPA withdrawal.
VHE is a serious condition that can lead to coma and even death. It can, however, be reversed if a precocious diagnosis is made and VPA
treatment is discontinued (1). VHE is clinically characterized by an acute or subacute decreasing level of consciousness that goes from
drowsiness to lethargy and coma, ataxia, vomiting, and focal neurological deficits (1). Laboratory tests usually show normal liver functions
with hyperammonemia. Blood VPA levels are within therapeutic range in most VHE cases (2). The primary treatment for VHE is stopping
VPA. Complete recovery generally occurs over a period of one to a few days (3).
Etiopathogenesis is not completely understood, although hyperammonemia has been postulated as the main cause of the clinical syndrome (4).
Psychiatrists and the other staff may need to be informed about the potential for hyperammonemia when starting valproic acid, and
patients whose tolerance for valproic acid is unknown may need to be monitored for liver functions and blood levels of urea and ammonia.
Key words: Sodium valproate, hyperammonemic encephalopathy, neurological deficits
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References:
1.
Segura-Bruna N, Rodriguez-Campello A, Puente V, Roquer J. Valproate-induced hyperammonemic encephalopathy. Acta Neurol Scand 2006; 114(1):1-7.
2.
Chen WT, Yen DJ, Yu HY, Liao KK. Valproate-induced encephalopathy. Zhonghua Yi Xue Za Zhi (Taipei) 2001; 64(8):474-8.
3.
Wadzinski J, Franks R, Roane D, Bayard M. Valproate-associated hyperammonemic encephalopathy. J Am Board Fam Med 2007; 20(5):499-502.
4.
Gurjar M, Singhal S, Baronia AK, Azim A, Poddar B. Valproate-induced hyperammonemic encephalopathy: A reminder of rare complication of valproate. J Emerg
Trauma Shock 2011; 4(2):321-2.
[PP-074]
Two cases of tardive dyskinesia associated with the use of paliperidone ER and
their management
Ref. No: 274
Ömer Yanartaş, Yücel Yılmaz, İshak Saygılı, Selma Bozkurt Zincir, Ümit Başar Semiz
Erenkoy Mental Health and Disorders Training and Research Hospital, Istanbul, Turkey
Paliperidone is an extended-release (ER) medication used in the treatment of schizophrenia and the recommended dose range is 3-12
mg/day (1). Tardive dyskinesia (TD) associated with the use of antipsychotics is characterized by involuntary choreic-athetoid movements
occurring in the late stages of the treatment. Choreathetoid movements mostly occur around the mouth and face and athetoid
movements alone mostly occur on the head-neck and pelvis (2, 3). We hereby present two cases of perioral dyskinesia who were using
paliperidone, and discuss their response to the treatment.
Both patients were females in their 20s and had been diagnosed with paranoid schizophrenia according to the DSM-IV-TR diagnostic
criteria. Both patients had been using olanzapine before being switched to paliperidone ER. Olanzapine treatment had been discontinued
due to side effects and treatment failure. The durations of paliperidone ER use were 9 months and 1 year, respectively; the doses of
paliperidone ER were 9 and 12 mg/day that is consistent with the literature in terms of side effect risk (4). In one of the cases, the
occurrence of side effects in combination with a psychotic exacerbation led to a change in antipsychotic drug therapy. In the other case,
the drug was not discontinued due to the remission of initial psychotic symptoms and satisfaction of the patient with the treatment;
however, the drug dose was reduced. In the treatment of TD associated with the use of paliperidone ER, one case responded to vitamin
E 400 MU/day and omega 3 fatty acids while the other was administered propranolol 40 mg/day and clonazepam 1 mg/day. After one
month, the scores of both patients on the extrapyramidal symptoms assessment scale were markedly reduced. The patient who had the
psychotic exacerbation also had a history of childhood trauma, which we feel had negatively influenced the course of the treatment.
Young age and female sex, and drug use for more than 6 months may increase the risk of TD in patients taking paliperidone; the use of
vitamin E, omega 3 fatty acids, propranolol, and clonazepam may lead to a significant improvement in symptoms.
Key words: Extrapyramidal side effects, paliperidone, tardive dyskinesia
References:
1.
Janicak PG, Winans EA. Paliperidone ER: a review of the clinical trial data Neuropsychiatric Disease and Treatment 2007:3(6) 869–883.
2.
Kaplan HI, Sadock BJ Synopsis of Psychiatry: Eighth ed. Baltimore: Williams & Wilkins, 1998
3.
Bernstein JG. Drug Therapy in Psychiatry. Third ed. St.Louis: Mosby-Year Book, 1995
4.
Meltzer HY, Bobo WV, Nuamah IF, Lane R, Hough D, Kramer M, Eerdekens M. Efficacy and tolerability of oral paliperidone extended-release tablets in the treatment
of acute schizophrenia: pooled data from three 6-week, placebo-controlled studies. J Clin Psychiatry 2008 May;69(5):817-29.
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[PP-075]
Effects of agmatine in rats with chronic unpredictable mild stress
Ref. No: 301
Feyza Arıcıoğlu1, Tijen Utkan2
Department of Pharmacology and Psychopharmacology Research Unit, Marmara University, Faculty of Pharmacy, Istanbul, Turkey
1
Department of Pharmacology, Kocaeli University, Medical Faculty, Kocaeli, Turkey
2
Depression is one of the most common psychiatric disorders which is a leading cause of total disability and economic burden.
Although there are medications that alleviate depressive symptoms, they have serious limitations. Therefore better understanding of
the neurobiology of the disease is required. Agmatine (l-amino-4-guanidinobutane) is an endogenous amine synthesized from the
decarboxylation of arginine. Agmatine has been quantified in nearly all of the organs of the rat including brain and plasma. Agmatine
exerts a wide range of biological activities on several organ systems, including the central nervous system, where it has been proposed
to act as a neurotransmitter. Agmatine interacts with the imidazoline receptors, alpha-2-adrenoceptors, nicotinic cholinergic receptors,
and serotonergic 5-HT3 receptors. It selectively modulates the N-methyl-D-aspartate (NMDA) subclass of glutamate receptors in rat
hippocampal neurons via an interaction between the guanidino group of agmatine and the NMDA channel pore and is an endogenous
inhibitor of all isoforms of nitric oxide synthase. Agmatine is released from neurons and has neuroprotective properties. The present study
was designed to evaluate the effect of agmatine in a chronic unpredictable mild stress (CUMS)-induced depression model.
Animals were allocated to the following study groups: animals not exposed to CUMS (Control group, n=12), animals exposed to CUMS for
5 weeks (CUMS group, n=12), and animals exposed to CUMS and treated with agmatine (CUMS+Agmatine group, n=12). The control and
CUMS groups were injected with saline and the CUMS+Agmatine group was injected with agmatine 40 mg/kg, i.p. daily throughout the
experiment. CUMS was applied as previously described with a minor modification. Briefly, the CUMS and CUMS+Agmatine groups were
subjected to different types of stressors: restraint for 4 h, cage tilting for 24 h, wet bedding for 24 h, swimming in 40C cold water for 5
min, swimming in 45 C hot water for 5 min, pairing with another stressed animal for 48 h, level shaking for 10 min, nip tail for 1 min, and
inversion of the light/dark cycle for 24 h. These nine stressors were randomly applied for 5 weeks, during which each stressor was applied
for 4-5 times. The rats received one of these stressors per day and the same stressor was not applied continuously for 2 days so that
animals could not predict the occurence of stimulation. The control group not receiving stress treatment had free access to food and water
but all groups were food and water deprived 24 h before the sucrose consumption test only. After 5 weeks, the sucrose consumption,
sucrose preference and forced swimming tests were performed.
The results of this study showed that agmatine administration during CUMS suppressed CUMS-induced depression-like behavioral
changes, including a reduction in sucrose preference, body weight, locomotor activity, and a decrease in immobility time in the forced
swimming test. Our findings suggest that agmatine may have a protective effect either by inhibiting oxidative damage and/or by
modulating neuronal activity in CUMS. Based on these findings, agmatine, as an endogenous molecule, has a promising effect and further
studies are required to understand the underlying mechanism.
Key words: Agmatine, sucrose preference, forced swimming test, chronic unpredictable mild stress
[PP-076]
A case of obsessive compulsive disorder with psychotic features that suffered
from sexual trauma
Ref. No: 302
Fatma Fariha Cengiz, Esra Aydın Sünbül
Erenköy Psychiatric Training and Research Hospital, İstanbul, Turkey
Introduction: Although the relationship between obsessive compulsive disorder (OCD) and psychosis is a noteworthy phenomenon, the
limits of the two disorders have not been defined. Eisen and Rasmussen (1993) evaluated a total of 475 patients with OCD and 14% were
identified as having psychotic symptoms in addition to OCD. They classified the patients into 4 groups: 6% OCD without insight, OCD
and schizophrenia (4%), OCD and delusional disorder (2%), OCD and schizotypal personality disorder (3%) (1). In clinical observation it is
seen that, the shift from an obsession to a delusion is described when insight into obsessive signs is lost and resistance abandoned. These
delusions do not signify a schizophrenic diagnosis but represent reactive affective or paranoid psychoses (3).
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Case: A 32 year old single man, who has not been a soldier, presented with aggressive, contamination, sexual, need for symmetry, somatic
obsessions; checking, washing, counting, need for confession compulsions; thinking he was followed by the secret service, sense of anal
burning, and inability to sleep. His mood and affect were anxious, speech increased, and associations were dispersed. He had a history
of sexual abuse by his brother. Obsessive symptoms started at the age of 12, feeling some problems about his gender, anxiety about
his future, sleeplessness and not talking to people at 16. After 15 days he had talked about the sexual abuse with her mother, who died
because of a myocardial infarction and he started to blame himself. He lost 15 kg in 6 months and started to experience auditory and
visual hallucinations. He was treated with many antipsychotics, SRIs, TCAs, and benzodiazapines. He had a hypomanic attack under the
treatment of aripiprazole. In the Rorschach test he showed schizoid reactions and dissociation in 2003. He was hospitalized 2 times. At his
last visit his treatment was sertraline 200 mg/day and olanzapine 5 mg/day. The appearance of the psychotic symptoms occurred, when
the depressive symptoms started. Olanzapine was increased to 10 mg/day after sleeplessness and psychotic symptoms flared up. The last
Rorschach test assessed the patient as being in pregenital organization and requiring close control of affective and psychotic symptoms.
Discussion: The clinical observations emphasize the interest in OCD patients with psychosis, who are neglected often. The shift from
an obsession to delusion is triggered by stress and is generally transient (2). The strong association between psychotic features and
depressive features in OCD may also have important implications in the treatment strategies (3). OCD represents a psychopathological
spectrum varying along a continuum of insight and requires careful clinical observation and treatment.
Key words: Obsesive compulsive disorder, psychosis, sexual trauma
References:
1.
Eisen JL, Rasmussen SA. Obsessive-compulsive disorder with psychotic features. J Clin Psychiatry1993; 54(10):373-379.
2.
Özerdem A. Obsesif-Kompulsif Bozukluk ve Psikoz Üzerine Bir Gözden Geçirme. Klinik Psikiyatri 1998;2:98-102
3.
Khess CDJ, Das J, Parial A et. al. Obsesive Compulsive Disorder with psychotic features.Hong Kong J Psychiatry1999;9(1): 21-25
[PP-077]
Priapism associated with zuclopenthixol treatment: A case report
Ref. No: 304
Alparslan Asil Budaklı, Mehmet Alpay Ateş, Ayhan Algül
GATA Haydarpasa Education Hospital, İstanbul, Turkey
Background: Priapism is pathologically prolonged and painful penis erection, usually without sexual desire or stimulation. Priapism is
classified as veno occlusive low flow (ischemic) and arterial high flow (non ischemic). The low flow–ischemic type is the most common
type of priapism and if it is untreated, leads to irreversible ischemic cavernosal tissue changes. The causes include generally certain
medications, although the mechanism for drug-induced priapism is unknown (1-4).
Here we discuss, in light of the literature, a 62-year-old- male paranoid schizophrenic patient, who had been treated with oral
zuclopenthixol since 1995 and developed an acute and painful erection.
Case: It was revealed that the patient, who presented with priapism, that hadcontinued for a week, took zuclopenthixol 20 mg a day for
2 days prior to the veno occlusive priapism.
After emergency urological treatment, the psychiatric examination revealed paranoid psychosis. Zuclopenthixol was stopped and
risperidone 6 mg/day and biperiden 4 mg/day were prescribed. A week later he was discharged from hospital.
Discussion: In many cases it has been reported that psychotropic drugs may cause priapism. Some of them are trazadone, chlorpromazine,
haloperidol, zuclopenthixol, olanzapine, ziprasidone, and clozapine (3). Although the mechanism of priapism associated with antipsychotics is not
clear, it is thought to be related to blockage that is mediated by the alpha receptors in the corpora cavernosa of the penis (3). Similarly, the capacity
of zuclopenthixol to induce priapism is thought to be due to its antagonist activity on alpha-1 adrenergic receptors (1,3).
Therefore it is important that clinicians must take notice of side effects of antipsychotics, including rarely seen ones.
Key words: Zuclopenthixol, priapism, side effect, drug induced, antipsychotics
References:
1.
J Salado, A Blazquez, R Diaz-Simon, F Lopez-Munoz, C Alamo and GG Rubio Priapism associated with zuclopenthixol: Ann Pharmacother June 1, 2002 vol. 36 no. 6 1016-1018
2.
Brichart N, DElavierre D, Peneau M, İbrauhim H, Mallek A. Priapism induced with antipsychotic medications: a series of four patients. Prog.Urol. 2008 Nov; 18 (10):
699-73.Epub 2008 Jun 10.
3.
Sood S, James W and Bailon MJ. Priapism associated with atypical antipsychotic medications. a review. Int Clin Psychopharmacol 2008; 23: 9-17
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4. Şükrü Kartalcı, Işıl Göğceğöz Gül, Rıfat Karlıdağ, Birgül Elbozan Cumurcu Recurrent priapism during quetiapine treatment case report; Bulletin of Clinical
Psychopharmacology, Vol: 20, N.: 4, 2010 327-328
[PP-078]
Prescribing patterns and inappropriate use of medications in patients referred to
doctors in Ardabil City of Iran
Ref. No: 113
Firouz Amani, Amin Shaker
Iran- Ardabil University of Medical Sciences, Iran
Objective: To determine the drug use patterns and descriptive analysis of prescriptions among patients who visited doctors in Ardabil City.
Methods: A retrospective study was carried out on 2000 randomly selected prescriptions from all registered prescriptions in Ardabil City
using data from two insurance organizations. Data were obtained on demographics, prescribing indicators and potentially inappropriate
medications. The collected data were analyzed by descriptive statistical methods using SPSS software.
Results: From all prescriptions, 822 (41 %) were for men and 1178 (59%) were for women. The mean age of the subjects was 31.6 ± 21.3
years ranging from 1 to 91. On thousand three hundred and six (65.3%) of all prescriptions were from general practitioners and others from
specialists. The mean number of drugs per prescription was 3.58±1.3 ranging from 1 to 9. Dexamethasone, with 219 (24.7 %) prescriptions,
was the most commonly prescribed medication. The total number of medications prescribed in all the prescriptions was 7158 while the
mean number of medications per encounter was 3.6. Antibiotics, with 52.8% of the prescriptions, were the most prescribed drug group.
Conclusion: The results showed that the mean of prescription drugs per encounter and the rate of prescription injection drugs were more
than the global standards. Also, the pattern of prescription drugs was inappropriate. It is necessary to reduce irrational prescription of
drugs to patients by monitoring and control indicators of medical doctors who prescribe higher numbers of prescriptions.
Key words: Pattern, drug utilization, inappropriate medications
[PP-079]
Bipolar affective disorder and normal pressure hydrocephaly: A case report
Ref. No: 305
Kader Semra Karataş1, Jülide Güler1, Özgür Bilgin Topçuoğlu2, Ebru Damla Bostancı1, Beliz Soyer1
Erenkoy Mental and Nervous Diseases Training and Research Hospital, Department of Psychiatry, İstanbul, Turkey
1
Erenkoy Mental and Nervous Diseases Training and Research Hospital, Department of Neurology, İstanbul, Turkey
2
Background: The subject of this study was how affective disorders are related to structural changes in the brain. The use of lithium in
affective disorders can cause pseudotumor cerebri, which has been reported in the literature, although there is no information about the
occurrence of normal pressure hydrocephalus. We detected normal pressure hydrocephalus in a patient diagnosed with bipolar affective
disorder 10 years ago and treated with lithium.
Case: A 55 year-old woman, housewife, not working, lives in Istanbul with her husband and children. She was diagnosed with bipolar
affective disorder 10 years ago and treated with lithium. She had hand tremors, weakness and dizziness and was admitted to hospital.
The patient was dehydrated, walking with small steps, showed balance difficulty and urinary incontinence. The patient was admitted
to the psychiatric unit. A neurology consultation and cranial MRI were requested. The patient was thought to have normal pressure
hydrocephalus. Lumbar puncture was performed twice. The patient was diagnosed with arrested hydrocephalus; CSF flow could not be
identified. A CSF dynamic MRI was requested and the patient was transferred to neurosurgery.
Discussion: There are publications about the relationship between structural brain abnormalities and affective disorders. Hydrocephalus,
by definition, is the accumulation of CSF in the ventricular system due to an imbalance between production and absorption of CSF.
Presenting symptoms include memory impairment, urinary incontinence symptoms, and ventriculomegaly (2,3). The etiology of
normal pressure hydrocephalus can include head trauma, metabolic problems, endocrinopathies, infectious and immunological
conditions; danazol, tamoxifen, oxytocin, tetracycline, indomethacin, lithium, drugs such as retinol are mentioned (2.4). Normal pressure
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hydrocephalus is not known to be associated with lithium in the literature. Lithium is known for its relationship with pseudotumor cerebri.
Taking into account the patient saw benefits from lithium, it was decided to postpone to a change to the mood stabilizer.
Key words: Bipolar affective disorder, lithium, normal pressure hydrocephalus, structural brain abnormalities
References:
1.
Arnone D, Cavanagh J, Gerber D, Lawrie SM, Ebmeier KP, Mclntosch AM. Magnetic resonance imaging studies in bipolar disorder and schizophrenia: meta-analysis.
BJPsych 2009; 195:194-201.
2.
Görgülü O, Yurt A, Özer FD, Turan Y. Normal basınçlı hidrosefali ön tanılı 26 hastanın analizi. Demans Dergisi 2003; 3:117-120.
3.
Kempton MJ, Geddes JR, Ettinger U, Williams SCR, Grasby PM. Meta-analysis, Database, and Meta-regression of 98 Structural Imaging Studies in Bipolar Disorder.
Arch Gen Psychiatry. 2008;65:1017-32.
4.
Levine SH, Puchalski C. Pseudotumor cerebri associated with lithium therapy in two patients. J Clin Psychiatry. 1990; 51:251-3.
[PP-080]
Agmatine attenuats cognitive impairment and oxidative damage following chronic
unpredictable mild stress: A behavioral, biochemical, and histological study
Ref. No: 307
Salih Gümrü1, Emre Yarcı1, Özer Şehirli1, Yusufhan Yazır2, Tijen Utkan3, Feyza Arıcıoğlu1
Department of Pharmacology and Psychopharmacology Research Unit, Marmara University, Faculty of Pharmacy, Istanbul, Turkey
1
Department of Histology and Embryology, Kocaeli University, Medical Faculty, Kocaeli, Turkey
2
Department of Pharmacology, Kocaeli University, Medical Faculty, Kocaeli, Turkey
3
Agmatine (l-amino-4-guanidinobutane) is an endogenous polycationic amine synthesized by the decarboxylation of arginine by the
enzyme arginine decarboxylase and hydrolysed by agmatinase. Agmatine has been quantified in nearly all organs including brain. It
has been proposed to act as a novel neuromodulator in the mammalian brain. Previous studies have shown that endogenous agmatine
interacts with a number of receptor subtypes such as, imidazoline, 2-adrenergic and N-methyl-D-aspartate. It also blocks other ligandgated cationic channels, including nicotinic receptors, and inhibits all three isoforms of nitric oxide synthase. Although there are papers
showing that agmatine may have a modulator role in learning and memory, the question of whether it is able to reverse impaired learning
and memory still remains. This study was planned to investigate the effect of agmatine on cognitive functions and oxidative damage
following chronic unpredictable mild stress (CUMS).
Rats were allocated to the following study groups: animals not exposed to CUMS (control group, n=12), animals exposed to CUMS for
5 weeks (CUMS group, n=12), animals exposed to CUMS and treated with agmatine (CUMS+Agmatine Group, n=12). The control and
CUMS groups were injected with saline and the CUMS+Agmatine group was injected with agmatine 40 mg/kg, i.p. daily throughout the
experiment. CUMS was applied according a previous study with a minor modification. Briefly, the CUMS and CUMS+Agmatine groups
were subjected to different types of stressors: restraints for 4 h, cage tilting for 24 h, wet bedding for 24 h, swimming in 40C cold water for
5 min, swimming in 45 C hot water for 5 min, pairing with another stressed animal for 48 h, level shaking for 10 min, nip tail for 1 min, and
inversion of the light/dark cycle for 24 h. These nine stressors were randomly applied for 5 weeks. The rats received one of these stressors
per day and the same stressor was not applied continuously for 2 days so that animals could not predict the occurence of stimulation.
After 5 weeks, animals were tested in the passive avoidance (PA) and Morris’s water maze (MWM) tasks to evaluate learning and memory
functions. At the end of the experiment, the brains of the rats were either removed freshly for malondialdehyde (MDA), glutathione (GSH)
levels and myeloperoxidase (MPO) activity or removed with 4% paraformaldehyde perfusion for c-fos, glial fibrillary acidic protein (GFAP)
and brain-derived neurotrophic factor (BDNF) determination immunohistochemically in cortex and hippocampus.
There was a significant defect in cognitive functions of the CUMS group whereas agmatine treatment significantly reversed this effect
both in the PA and MWM tests. A decrease in GSH and an increase in MDA and MPO levels in the CUMS group were significantly inhibited
with agmatine treatment, which were considered markers of oxidative damage. In the immunohistochemical experiments, it was found
that c-fos and GFAP were overexpressed and BDNF was decreased in the CUMS group whereas data for the agmatine treatment group
were similar to those of the control group. The findings of the current study clearly showed beneficial effects of agmatine on cognitive
impairment and oxidative damage in CUMS.
Key words: Agmatine, BDNF, c-fos, chronic unpredictable mild stress, GFAP, malondialdehyde, glutathione, myeloperoxidase
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[PP-081]
Ceruloplasmin levels before and after treatment in patients with depression:
A case-control study
Ref. No: 308
Mehmet Cemal Kaya1, Yasin Bez1, Salih Selek2, Haluk Asuman Savaş3, Hakim Çelik2, Hasan Herken4
1
Harran University School of Medicine, Department of Psychiatry, Sanliurfa, Turkey
2
Gaziantep University School of Medicine, Department of Psychiatry, Gaziantep, Turkey
3
Pamukkale University School of Medicine, Department of Psychiatry, Denizli, Turkey
4
Objective: Ceruloplasmin is a serum protein synthesized by hepatocytes and involved in both copper and iron metabolism. It is an
acute phase reactant and has antioxidant capacity (1). Deficiency of ceruloplasmin is thought to cause neural cell damage secondary to
decreased mitochondrial energy production and increased lipid peroxidation, and iron associated free radicals (2,3). Ceruloplasmin, an
antioxidant agent, has previously been investigated in some psychiatric disorders like schizophrenia and obsessive compulsive disorder
(4). Studies about ceruloplasmin in depression are relatively scarce (5). In this prospective study, we aimed to determine the serum
ceruloplasmin levels of depressive patients before and after treatment, to compare them those of healthy control subjects and to assess
any possible association of ceruloplasmin levels to treatment response.
Methods: Among the admissions to the Psychiatry Outpatients Clinic of Gaziantep University Medical Faculty Hospital 19 (8 males, 11
females) patients who were diagnosed with major depressive disorder according to the DSM-IV criteria and 40 (17 males, 23 females)
healthy control subjects have been included in the study. The patients received naturalistic antidepressant treatment during the 8 weeks
period after the diagnosis. The serum ceruloplasmin levels and the Hamilton Depression Rating Scale (HAM-D) scores of the patients
were measured before and after the 8 week period of antidepressant treatment. Blood collection for ceruloplasmin measurement was
done only once for the healthy control subjects. The measurement of ceruloplasmin levels was conducted according to the standard
procedures.
Results: The ceruloplasmin levels of patients both before and after antidepressant treatment were significantly higher than those of
control subjects (t=7.569, p<0.001 and t=6.764, p<0.001, respectively). Despite clinical improvement, ceruloplasmin levels did not show
any statistically significant change after antidepressant treatment in the patient group (t= -1.163, p=0.260).
Conclusion: Compared to healthy control subjects, serum ceruloplasmin levels seemed to be higher in patients with depression. There
was no significant change in its level with antidepressant treatment. High levels of serum ceruloplasmin, an antioxidant agent, may be a
consequence of some mechanisms that try to balance increased oxidative stress which was previously shown in patients with depression.
The persistance of high levels of serum ceruloplasmin after antidepressant treatment may show some ongoing possible underlying
pathophysiological mechanisms in depression despite its acute treatment.
Key words: Antioxidant, depression, oxidative stress, ceruloplasmin
References:
1.
Floris G, Medda R, Padiglia A, Musci G. The physiopathological significance of ceruloplasmin. A possible therapeutic approach. Biochem Pharmocol 2000; 60: 1735-1741
2.
Yoshida K, Kaneko K, Miyajima H, Tokuda T, Nakamura A, Kato M, Ikeda S. Increased lipid peroxidation in the brains of aceruloplasminemia patients. J Neurol Sci
2000; 175: 91–95
3.
Vassiliev V, Harris ZL, Zatta P. Ceruloplasmin in neurodegenerative diseases. Brain Res Brain Res Rev 2005; 49: 633-640
4. Vırıt O, Altındağ A, Selek S, Yumru M, Bulut M, Erel O, Savaş HA, Herken H. Increased plasma ceruloplasmin levels in schizophrenia. Bulletin Of Clinical
Psychopharmacology 2008; 18: 282-287
5.
Bekaroğlu M, Bilici M, Değer O, Karaman SC, Örem A, Soylu C. Effect of Antidepressant Treatment on Acute Phase Protein Levels in Patients with Depression. Turkish
Journal of Psychiatry 1997; 8: 260-265
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[PP-082]
Foetality in schizophrenia
Ref. No: 159
Elif Mutlu, Mehmet Emin Ceylan, Agah Aydın
Objective: The aim of this study was to evaluate common morphological and neurological features of schizophrenia from an ontogenetic
perspective and to propose a new conceptual approach to schizophrenia, in which early foetal marks persist without diminishing in
comparison to other people.
Material and Methods: Fifty patients diagnosed with schizophrenia from the Bakırköy Research and Training Hospital for Psychiatry,
Neurology and Neurosurgery were chosen for the study group. The control group consists of fifty healthy male subjects. The ages of
all subjects varied between 18 and 65. All of the subjects were informed about the study and their written consents were obtained.
Sociodemographic data of all subjects were recorded and the Waldrop Minor Physical Anomalies Scale, the NES ( neurological evaluation
scale), and the Edinburgh Handedness Inventory were applied.
Results: We found significantly higher scores among schizophrenic patients in comparison to healthy subjects both in the NES total and
all four sub-categories of the scale. The minor physical anomalies scores, head circumference, and hypertelorism were significantly higher
in the schizophrenic group. In addition, for hand-eye dominancy, we observed more tendency to be crosswise.
Conclusion: Some characteristics of schizophrenia such as hypertelorism, large head circumference, high palate, thin muscle and
bone structure, primitive reflexes, mental and behavioral characteristics could be evaluated as a separate ontogenetic entity.Evaluating
schizophrenia within the context of a neurodevelopmental hypothesis, as an evolutionary process, in which foetal traits persist, would
contribute to our understanding of the disorder’s ambigous nature and phenomenology.
Key words: Schizophrenia, foetality, ontogenesis
[PP-083]
Metabolic changes in the acute phase with olanzapine treatment
Ref. No: 182
Mehmet Ak1, Abdullah Bolu1, Süleyman Akarsu1, Deniz Sezlev2, Tülin Yanık2, Özcan Uzun1, Fuat Özgen1, Aytekin Özşahin1
Department of Psychiatry, Gulhane Military Medical Faculty, Ankara, Turkey
1
METU, Faculty of Science, Biology department, Ankara, Turkey
2
Introduction: Atypical antipsychotics are used in treatment of psychotic disorders and severe behavior disorders. Despite the lack of extra
pyramidal side effects, they cause metabolic disorders (such as hyperlipidemia, weight gain, glucose intolerance), which are important
causes of mortality (1). The exact mechanisms of these side-effects of atypical antipsychotics have not been identified so far and therefore
and protective measures could not be established (2). In this study we aimed to examine the acute phase changes in blood lipid profile
and body mass index while using olanzapine.
Materials and Methods: Twenty four patients, who were diagnosed with first-episode psychotic disorder and received olanzapine
treatment in the Department of Psychiatry, Gulhane Military Medical Faculty, were enrolled in the study. The serum lipid levels and fasting
blood sugars were measured before the treatment and four weeks after the treatment; body mass index was calculated and the data
obtained were compared.
Results: The comparison of pre- and post-treatment data showed significant increases in the weight gain, measurement of waist
circumference, body mass index, total cholesterol, and VLDL levels (p <0.05). There were statistically no significant changes in fasting
blood glucose, HDL, LDL, and TG levels.
Discussion: It is reported that the reason of differences in severity of metabolic changes occurring due to the use of atypical antipsychotics
is variation of the genes that encode metabolizing enzymes, transporters, and receptors (3,4). In this study, the changes occurred within
four weeks may be predictors of developing long-term metabolic disorders and so that protective measures can be initiated. Identifying
the individual differences will contribute to the treatment regimens when weight gain can be detected early in the treatment.
Key words: Atypical antipsychotic, metabolic, olanzapine
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References:
1.
Jin H., Meyer J.M., Mudaliar S., Jeste D.V., 2008. Impact of atypical antipsychotic therapy on leptin, ghrelin, and adiponectin. Schizophrenia Research 100 (2008)
70–85.
2.
Yazıcı K. Yazıcı A., 2008. Weight Increase Induced by Antipsychotic drugs:What is the role of genes? Bulletin of Clinical Psychopharmacology 2008;18:59-70.
3.
Chagnon YC. Susceptibility genes for the side effect of antipsychotics on body weight and obesity.Curr Drug Targets 2006; 12: 1681-1695
4.
Evans WE, Johnson JA. Pharmacogenomics: the inherited basis for interindividual differences in drug response. Annu Rev Genomics Hum Genet 2001; 2: 9-39
[PP-084]
Do cultural factors effect clinical manifestations of OCD? Clinical features of
a Turkish sample
Ref. No: 183
Ramazan Konkan1, Ömer Şenormancı1, Oya Güçlü1, Erkan Aydın1, Mehmet Z. Sungur2
1
Marmara University School of Medicine, İstanbul, Turkey
2
Objective: In the present study we evaluated the clinical characteristics of OCD patients monitored in an outpatient program and
compared them with other cultures.
Method: The study included 116 OCD patients who presented to the clinics at the Bakirköy Research and Training Hospital for Psychiatry,
Neurology and Neurosurgery, met the inclusion criteria, volunteered to participate in the study after being diagnosed and were referred
by two psychiatrists. The diagnosis was confirmed using the Structured Clinical Interview Form for the DSM-IV Axis I Disorders (SCID-I). An
inquiry form was developed for obsessive compulsive symptoms based on the obsessions and compulsions included in the Yale-Brown
Obsession Compulsion Scale (Y-BOCS) according to their incidence and a sociodemographic form from the SCID-I clinical interview guide.
Results: Our sample consisted of 30 male (25.9%) and 86 female (74.1%) patients. The mean age was 34.96±10.23 years. The most
common obsessions were impurity-contamination (49.1%), followed by doubt (20.7%) and religious (11.2%) obsessions. Secondary
obsessions included doubt (53.4%), impurity-contamination (14.7%) and sexual obsessions (9.5%), respectively. In tertiary obsessions,
21 patients reported presence of symmetry-exactness (18.1%), 13 patients reported doubt (11.2%), 10 patients reported sexual (8.6%)
obsessions, and 43 patients (37.1%) had no tertiary obsessions (Table 1). Ninety-six percent of patients had accompanying compulsions.
The most common compulsions were cleaning and washing (53.4%), checking (26.7%) and repetitive ritual behavior (7.8%).DISCUSSION:
The most common obsession in the present study was impurity/contamination with a rate of 49.1% in line with the literature, followed by
doubt obsessions of 20.7%. The most common compulsion reported in literature is washing accompanied by obsession of contamination,
and it is followed by checking. Similarly, in our study, the primary compulsion was cleaning and washing with a rate of 53.4%, followed by
checking (26.7%) and repetitive ritual behaviors (7.8%). Although the first two obsessions and compulsions are in line with the literature,
the tertiary obsessions reported as aggressive or sexual obsessions in the literature were replaced by religious obsessions (11.2%) in our
sample. An intercultural study showed that religious obsessions were the most common obsessions with 60% in the Egyptian sample,
and 50% in the Saudi sample. However, the rate of religious obsessions was 6% in the U.S., 5% in the United Kingdom, and 11% in India.
Studies on Jewish populations showed similar results with the Muslim populations, with a religious obsession rate of 50%. We believe that
the rate of religious obsession is associated with our country’s position, being at the junction of Western and Eastern cultures. Relatively
lower rate of sexual obsessions compared to the literature may result from the fact that obsessions related with sexuality may be more
difficult to report than other obsessions in our population.
Key words: Clinical manifestation, cultural differences, OCD
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[PP-085]
Reliability and validity of Turkish version the Brief Fear of Negative Evaluation
Scale II (BFNE-II) among male patients with alcohol dependency
Ref. No: 196
Cüneyt Evren, Selime Çelik, Reşide Aksoy, Turan Çetin, Müge Ülkü, Sera Yiğiter, Elif Mutlu
Bakırköy Training and Research Hospital for Psychiatry, Neurology and Neurosurgery, Alcohol and Drug Research, Treatment and Training Center (AMATEM), İstanbul, Turkey
Background and Objective: The construct of fear of negative evaluation consists of feelings of apprehension about others’ evaluations,
distress over these negative evaluations, and the expectation that others will evaluate one negatively (1). The Brief Fear of Negative
Evaluation Scale (BFNE) is a measure of a person’s tolerance for the possibility they might be judged disparagingly or hostilely by others
(2). The aim of this study was to determine the reliability, validity and factorial structure of the Turkish translation of the BFNE-II in male
alcohol dependent inpatients.
Methods: Participants were 155 consecutively admitted male alcohol dependents. Patients were investigated with the BFNE-II, the Social
Phobia Scale (SPS), the Social Interaction Anxiety Scale (SIAS) and the Liebowitz Social Anxiety Scale (LSAS). The BFNE-II was repeated in
136 of these 155 patients after 2 weeks.
The BFNE is composed of 12 items describing fearful or worrying cognition. Eight of the twelve items describe the presence of fear or
worrying, while the remaining four items describe the absence of fear or worrying (3). In the BFNE-II (4) reversed items are corrected.
Results: The Turkish version of the BFNE-II was found to be compatible with the original scale. In alcohol dependents the internal
consistency coefficient (Cronbach’s alpha) was 0.91 for the BFNE-II. For each of the items, the corrected item-total correlation values were
between 0.57 and 0.84 (p<0.001). Test–retest correlations were between 0.28 and 0.53 for items and 0.54 for the total score. The BFNE-II
scores were correlated with three measures of social anxiety (the SPS, SIAS, and LSAS) providing evidence of convergent validity.
Conclusions: In the present study the Turkish version of the BFNE-II with 12 items and 2 factor solutions was found to be compatible
with the original scale among substance dependent inpatients. Each subscale and the BFNE-II had adequate reliability in terms of internal
consistency. The item-subscale and the corrected item-total correlation coefficient values were significant at moderate to high degrees
and were stable over two weeks of testing. Finding the BFNE-II factors and total score correlated with related constructs such as the LSA,
SPS and SIAS showed concurrent validity. This finding is consistent with previous research demonstrating a positive relationship between
the BFNE and other measures of social anxiety (4). Also in support of the discriminant validity of the BFNE-II, individuals with social phobia
scored significantly higher on the scale than non-anxious alcohol dependents. The differences in scores on the BFNE-II highlight the
discriminant ability of the measure for detecting clinically significant levels of social anxiety. In general, the findings showed promising
results and were comparable with most research findings throughout the world (1,2).
Key words: Alcohol abuse, fear of negative evaluation scale, social anxiety
References:
1.
Watson D, Friend R. Measurement of social–evaluative anxiety. J Consult Clin Psychol 1969;33:448–457.
2.
Leary MR. A brief version of the Fear of Negative Evaluation Scale. Pers Soc Psychol 1983; 9:371-375.
3.
Carleton RN, McCreary DR, Norton PJ, Asmundson GG. Brief Fear of Negative Evaluation scale revised. Depress Anxiety 2006; 23:297-303.
4.
Carleton RN, Collimore KC, Asmundson GJ. Social anxiety and fear of negative evaluation: construct validity of the BFNE-II. J Anxiety Disord 2007;21:131-41.
[PP-086]
Reliability and validity of Turkish versions of the Social Phobia Scale and Social
Interaction Anxiety Scale among male patients with alcohol dependency
Ref. No: 197
Cüneyt Evren, Selime Çelik, Reşide Aksoy, Turan Çetin, Sera Yiğiter, Müge Ülkü, Elif Mutlu
Bakırköy Training and Research Hospital for Psychiatry, Neurology and Neurosurgery, Alcohol and Drug Research, Treatment and Training Center (AMATEM), Istanbul, Turkey
Objective: The Social Phobia Scale (SPS ) was designed to measure social phobia defined as “anxiety and fear at the prospect of being
observed or watched by other people, and in particular, where the individual expresses distress when undertaking certain activities in the
presence of others” (1). TheSocial Interaction Anxiety Scale (SIAS) was designed to measure social interaction anxiety defined as “distress
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when meeting and talking with other people”’ (1). Thus the two companion measures were designed to distinguish between scrutiny fears
and concerns about interaction. The scales correspond to the DSM-III-R descriptions of Social Phobia--Circumscribed and Generalised
types, respectively. In this study, the reliability and validity of the Turkish translation of the Social Phobia Scale (SPS) and Social Interaction
Anxiety Scale (SIAS) in male alcohol dependent inpatients were determined.
Method: The study was conducted with hospitalized patients between August 2008 and March 2009 in the Bakirkoy State Hospital
for Mental Health and Neurological Disorders, AMATEM (Alcohol and Drug Research, Treatment and Education Center) in Istanbul.
Participants were 155 consecutively admitted male alcohol dependents. Diagnoses of alcohol dependence and social anxiety disorder
were made with the SCID-I modules of these disorders. Patients were investigated with the SPS, the SIAS (2), the Brief Fear of Negative
Evaluation II (BFNE-II) and the Liebowitz Social Anxiety Scale (LSAS).
Results: The Turkish versions of both the SPS and the SIAS were found to be compatible with the original scales. In alcohol dependents,
the internal consistency coefficient (Cronbach’s alpha) was 0.92 for the SPS and 0.93 for the SIAS. For each of the items, the corrected
item-total correlation values were between 0.21 and 0.68 (p<0.001) for the SPS and were between 0.48 and 0.80 (p<0.001) for the SIAS.
Test–retest correlations were between 0.19 and 0.72 for items and 0.79 for the total score for the SPS and were between 0.26 and 0.73
for items and 0.85 for the total score for the SIAS. The SPS and SIAS scores were correlated with each other and with two measures of
social anxiety, the BFNE-II and LSAS, providing evidence of convergent validity. According to the ROC analysis a cut-off point of 24 was
appropriate for the SPS and 30 was appropriate for the SIAS.
Conclusions: The Turkish versions of these scales were found to be compatible with the original ones among male alcohol dependent
inpatients. The results suggest that each scale had an adequate reliability in terms of internal consistency. The corrected item-total
correlation coefficient values were significant at moderate to high degrees and were stable over two weeks of testing. Also the finding
that the SPS and SIAS correlated with related constructs such as the BFNE-II and LSAS showed concurrent validity. The Turkish versions of
the SPS and SIAS have been proven to be acceptable, reliable and valid measures of social phobia in male alcohol dependent inpatients.
Key words: Alcohol abuse, social anxiety, Social Phobia Scale, Social Interaction Anxiety Scale
References:
1.
Mattick RP, Clarke JC. Development and validation of measures of social phobia scrutiny fear and social interaction anxiety. Behav Res Ther 1998;36:455–470.
2.
Heimberg RG, Mueller GP, Holt CS, Hope DA, Liebowitz MR. Assessment of anxiety in social interaction and being observed by others: the social interaction anxiety
scale and the social phobia scale. Behav Ther 1992;23:53–75.
[PP-087]
ECT in treatment of pathological gambling: A case report
Ref. No: 117
Mehmet Ak, Cihat Yükselir, Ali Bozkurt, Murat Erdem, Aytekin Özşahin
Gulhane School of Medicine, Ankara, Turkey
[email protected]
Pathological gambling is a disorder, the prevalence of which has been increasing continuously and it cannot be diagnosed easily. It can
also be treatment resistant and restricts the individual’s life increasingly. In studies related to pharmacological treatment of pathological
gambling, SSRIs, mood stabilizers, antipsychotics and naltrexone have been used. In all these alternatives the response rate is below
expectations. In the literature, there is no discussion about the use and results of ECT treatment of pathological gambling. Here, a case
that has been diagnosed with pathological gambling and that received ECT treatment will be presented.
Key words: Pathological gambling, treatment, electroconvulsive therapy
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[PP-088]
Venlafaxine-mirtazapine combination in the treatment of post traumatic stress disorder
Ref. No: 217
Abdullah Bolu, Süleyman Akarsu, Cemil Çelik, Barbaros Özdemir, Kamil Nahit Özmenler
Department of Psychiatry, Gulhane Military Medical Faculty, Ankara, Turkey
Introduction: Posttraumatic stress disorder (PTSD) is an incapacitating clinical syndrome characterized by intrusive recollections,
emotional numbing and withdrawal, cue-related responses, and psychological and physiological hyperarousal. In the treatment of PTSD
pharmacotherapy must be supported with psychotherapy to increase the success of treatment. In this study we aimed to evaluate the
effect of venlafaxine-mirtazapine combination in the PTSD patients, who did not respond to antidepressant treatment at
adequate dose for an adequate duration.
Material and Methods: The hospital records of the patients who were diagnosed with PTSD according to DSM-IV diagnostic criteria and
did not respond to adequate doses of an antidepressant treatment for adequate duration were examined retrospectively. Data of the
patients (n=28), whose treatment were venlafaxine- mirtazapine combination, were obtained. These data were IES-R, Hamilton Anxiety
scale and Hamilton Depression Scale scores.
Results: IES-R score, Hamilton Anxiety, Hamilton depression scores of 28 patients who were diagnosed with PTSD were evaluated. A
significant decrease in IES-R total, IES-R avoidance, Hamilton Anxiety and Hamilton depression scores (p> 0.05) with adequate dose and
duration of venlafaxine-mirtazapine treatment were detected. The same change was not accompanied in IES-R hyperarousal and IES-R
intrusive test scores.
Conclusion: Post-traumatic stress disorder treatment takes longer and sometimes becomes chronic. According to the results of this study,
venlafaxine- mirtazapine combination can be used in the treatment of PTSD patients who did not respond to antidepressant treatment
at adequate doses for an adequate duration.
Key words: Mirtazapine, posttraumatic stress disorder, PTSD, venlafaxine
References:
1.
McDougall SJ, Widdop RE, Lawrence AJ (2004) Medial prefrontal cortical integration of psychological stress in rats. Eur J Neurosci; 20: 2430-2440.
2.
Radley JJ, Rocher AB, Janssen WG, Hof PR, McEwen BS, Morrison JH (2005) Reversibility of apical dendritic retraction in the rat medial prefrontal cortex following
repeated stress. Exp Neurol; [Epub ahead of print].
3.
Kılıçoğlu A. Stress and effects of brain: A review. New Symposium Journal; July 2007, Volume 45, İssue 3
[PP-089]
Efficacy and 3-month follow-up of repetitive transcranial magnetic stimulation
(rTMS) in treatment resistant depression: Three cases
Ref. No: 221
Onur Durmaz, Mehmet Alpay Ateş, Mesut Çetin, Servet Ebrinç, Cengiz Başoğlu, Ayhan Algül
Introduction: rTMS(Repetitive Transcranial Magnetic Stimulation) is an effective non-invasive cortical stimulation method that is being used
in the treatment of drug resistant major depressive disorder. The underlying mechanism of effect of rTMS has not been fully understood
yet. Neuromodulation, neuroplasticity, and cortical excitability are the most accepted theories (1). Even though the post-treatment effect of
rTMS in depression is well known, little is known about its lasting effect (2).Therefore in this report we investigated the effect of add-on rTMS
treatment with 3 month follow-up after treatment in 3 outpatient cases diagnosed with drug resistant unipolar major depression.
Case 1: A 33 year-old female patient was diagnosed with major depressive disorder and received venlafaxine 300 mg/day for two years.
An add-on 15 sessions of DLPFC rTMS (20 Hz, 110% MT, 1000p/d) was applied due to insufficient medication response. The MADRS and
HAM-A scales were assessed before and the day following treatment and then 1 and 3 months after treatment. The MADRS scores were
found to be 37, 11, 2 and 4, while the HAM-A scores were found to be 35, 9, 5 and 6, respectively.
Case 2: A 35 year-old male patient was diagnosed with major depressive disorder since age 12 and received escitalopram 20 mg/day for
three months. An add-on 15 sessions of DLPFC rTMS (20 Hz,110% MT,1000p/d) was applied due to insufficient medication response. The
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MADRS and HAM-A scales were assessed before and the day following treatment and then 1 and 3 months after treatment. The MADRS
scores were found to be 28, 10, 5 and 5, while the HAM-A scores were found to be 33, 18, 7 and 6, respectively.
Case 3: A 44 year-old male patient was diagnosed with major depressive disorder since age 15 and received venlafaxine 375 mg/day and
ziprasidone 40 mg/day for five months. An add-on 15 sessions of DLPFC rTMS (20 Hz,110% MT,1000p/d) was applied due to insufficient
medication response. The MADRS and HAM-A scales were assessed before and the day following treatment and then 1 and 3 months after
treatment. The MADRS scores were found to be 29, 9, 6 and 7, while the HAM-A scores were found to be 28, 13, 10 and 8, respectively.
Conclusion: Maintenance of improvement in major depression treatment has been another concern apart from efficacy of current
interventions. rTMS is an effective method as monotherapy and also as add-on treatment of depression. In this study each of three
patients responded favorably to rTMS. In the post-treatment course, significiant improvement was maintained at the 3-month follow-up.
Given its relatively benign side effect profile, long lasting therapeutic effect, and more practical non-invasive application than ECT, we
conclude that rTMS can be considered as an optional treatment before ECT in treatment-resistant depression patients.
Key words: rTMS, resistant depression, treatment, follow-up, maintenance
References:
1. Pell GS, Roth Y, Zangen A.Modulation of cortical excitability induced by repetitive transcranial magnetic stimulation: Influence of timing and geometrical
parameters and underlying mechanisms. Prog Neurobiol. 2010 Nov 5.
2. Bortolomasi M, Minelli A, Fuggetta G, Perini M, Comencini S, Fiaschi A, Manganotti P.Long-lasting effects of high frequency repetitive transcranial magnetic
stimulation in major depressed patients. Psychiatry Res. 2007 Mar 30;150(2):181-6.
3.
Hadley D, Anderson BS, Borckardt JJ, Arana A, Li X, Nahas Z et all. Safety, tolerability, and effectiveness of high doses of adjunctive daily left prefrontal repetitive
transcranial magnetic stimulation for treatment-resistant depression in a clinical setting. J ECT. 2011 Mar;27(1):18-25.
[PP-090]
The effects of brain-derived neurotrophic factor Val66Met polymorphism on
executive functioning in patients with obsessive-compulsive disorder
Ref. No: 225
Raşit Tükel1, Hakan Gürvit2, Berna Özata1, Banu Aslantaş Ertekin1, Erhan Ertekin1, Bengi Baran2, Şükriye Akça Kalem2,
Nalan Öztürk1, Güher Saruhan Direskeneli3
Istanbul University, Istanbul Faculty of Medicine, Department of Psychiatry, İstanbul, Turkey
1
Istanbul University, Istanbul Faculty of Medicine, Department of Neurology, İstanbul, Turkey
2
Istanbul Faculty of Medicine, Department of Physiology, Istanbul University, İstanbul, Turkey
3
Objective: In the present study, we investigated the association between the brain-derived neurotrophic factor (BDNF) Val66Met
polymorphism and performance on tests measuring executive functions in a sample of patients with obsessive-compulsive disorder
(OCD).
Method: A total of 71 patients diagnosed with OCD by the DSM-IV criteria were included in the study. All patients were assessed using the
Yale-Brown Obsessive-Compulsive Scale and the Hamilton Depression Rating Scale. Patients also performed the Wisconsin Card Sorting
Test (WCST), the Trail Making Test part A (TMT A) and part B (TMT B), the Tower of London Test (ToL), the Verbal Fluency Test (semantic and
lexical fluency) and the Stroop Test. Genomic DNA was extracted from whole blood. The single nucleotide polymorphism (G/A) leading
to amino acid substitution at the 66 codon in the BDNF gene (dbSNP number rs6265) was screened by a polymerase chain reaction
and restriction digestion analysis in the DNA samples. The performance of the patients on the neuropsychological tests of executive
functioning was compared between the patients with Val/Val genotype and Met carriers.
Results: Subjects with Val/Val genotype and Met carriers (Met/Met or Val/Met genotypes) did not differ on socio-demographic and clinical
factors, except for the age of onset of the illness, which was earlier in subjects with Val/Val genotype than Met carriers. The performances on the
TMT B and TMT B-A, the Stroop Test, and the two measures of the ToL were found to be significantly lower in the Met-allele carriers, compared
to the Val/Val group. There were no significant differences in the WCST and the Verbal Fluency Test performances between the two groups.
Conclusions: These findings suggest that the BDNF Met allele may be associated with poorer performance on neuropsychological tests
of executive functions in OCD patiens.
Key words: Brain-derived neurotrophic factor, executive functions, obsessive-compulsive disorder, polymorphism
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[PP-091]
Diagnostic confusion about OCD and schizophrenia: A case report
Ref. No: 228
Sevgi Gül Kabak, Mustafa Burak Baykaran, Selma Bozkurt Zincir
Erenköy Mental Health Training and Research Hospital, İstanbul, Turkey
Introduction: Both obsessions and delusions are based on wrong, absurd and extreme ideas and it is thought that they could be
separated on the basis of the presence of insight. Between obsessions and delusions there is the protection of insight and the ability to
resist compulsive thoughts and/or behaviors. The insight of obsessive patients against obsessions may be protected or completely lost
(1). In this paper, the diagnostic process in a patient with OCD, who also had delusions, is discussed.
Case: A 30 year-old, married, female patient applied to the hospital with complaints of unhappiness, suspiciousness, self-reproach, thoughts
of death, hearing noises and insomnia. The patient had a four year medical history. She considered her 6 year-old son as her “love.” Four
years ago she had sexual feelings towards her female collegues and she thought that her feelings were mutual and her thoughts could be
read by them. During psychiatric examination, her thought content had Schneiderian symptoms such as paranoia, thought withdrawal,
thought insertion, and reference delusion. Just after the hospitalization and evaluation, the patient was medicated with 6 mg/day risperidone
and 2 mg/day biperiden for a preliminary diagnosis of schizophrenia. Later the preliminary diagnosis was changed to atypical obsessivecompulsive disorder and her treatment was changed to sertraline 200 mg/day, quetiapine 300 mg/day and clonazepam 2 mg/day. Due to the
fact that after a 10-day period of improvement, her reference delusion and fear of death had restarted, and inappropriate affect was detected,
a treatment regimen of pimozide 2mg/day, sertraline 200mg/day, clomipramine 75mg/day, clonazepam 2mg/day had been prescribed.
The difference between the facts and the idea had been discussed through a cognitive approach. After 12 days, her affect recovered and
obsessive thoughts decreased, therefore the patient was discharged from hospital on the previously mentioned treatment. After 2 months,
there had been no psychotic symptoms, she had been able to cope with distress better and her psycho-social functioning had been fine.
Discussion: The frequency of psychotic symptoms in OCD was detected at the ratio of 0.7-12.3% in a former study and 14% psychotic
symptoms and 4% schizophrenia was reported in another study. Thomsen and Jensen demonstrated that 5% of 135 OCD patients, who
applied to the hospital for the first time, were later diagnosed as schizophrenic (3). Despite the psychotic nature of OCD that has been
noticed for a long time, modern classification systems still refer to OCD as an anxiety disorder. Although the DSM-IV mentions poor
insight in OCD, there has been no objective description for what degree of insight should be accepted as poor. The diagnostic criteria and
treatment of schizo-obsessions and whether the patients who have schizophrenia and OCD comorbidity should be considered as schizoobsessive disorder are still under discussion(2).
Key words: Comorbidity, differential diagnosis, obsessive compulsive disorder, schizophrenia
References:
1.
Aydın A. Ceylan ME. Türkcan A. Şizofrenide Obsesif Kompulsif Fenomenler: Bir Gözden Geçirme. Klinik Psikofarmakoloji Bülteni 2008;18:222-234
2.
Demir EY. Aslan S. Şizo-Obsesif Bozukluk: Tanı, Sınıflandırma ve Tedavi. Türkiye’ de Psikiyatri 2005;7(1):38-43
3.
Güleç G. Güneş E. Yenilmez Ç. Obsesif Kompulsif Belirtileri Olan Şizofreni Hastalarının Şizofreni ve Obsesif Kompulsif Bozukluk Hastaları İle Karşılaştırılması. Türk
Psikiyatri Dergisi 2008;19(3):247-256
[PP-092]
Is vaginismus a specific phobia?
Ref. No: 232
Ramazan Konkan1, Meltem Bayrak1, Oya Güçlü1, Ömer Şenormancı1, Mehmet Z. Sungur2
1
Marmara University School of Medicine, İstanbul, Turkey
2
Objective: Although vaginismus is classified under the title of “sexual pain disorders”, its etiological roots are still controversial. It has been
suggested that vaginismus should be considered as a phobic reaction resulting in an avoidance behavior due to a dominant fear of pain. It
has also been argued that, in patients with vaginismus, other fears usually accompany the fear of pain during coitus. Excessive sensitivity
particularly in the genital area is said to prevail in vaginismus. In our study, patients with vaginismus were compared to a healthy group
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in terms of commonly seen phobias, amplified perception of somatic sensations and sensitivity to pain
Method: As a part of a different aspect of a vaginismus trial 40 subjects with vaginismus, who was referred to the Sexual Functioning
Disorders outpatient clinic and agreed to take part in the study and 50 women of the control group who described penile penetration
difficulty and pain during coitus, were evaluated. The participiants were evaluated using a sociodemographic form developed by the
researchers, the SCL-90-R (Symptom Checklist-90-Revised), and the Somatosensory Amplification Scale Halam and Hafner (1977) fear
checklist. The data were analysed using the SPSS for Windows 10.0 statistical packet program and P<0.05 was considered to be significant.
Results: The subjective pain endurance and total SSAS scores were not statistically significant. In reported fear of pain, dryness, narrowness and
pain during coituswas highly significantly different between the two groups. A statistically significant difference was found in the vaginismic group
as compared to the control group when items in the Fear Questionnaire for Phobia 11 (Closed Small Rooms), Phobia 15 (Being in High Places),
Phobia 37 (Seeing Others’ Nausea or Vomiting), Phobia 41 (Seeing Blood ) and Phobia 46 (Going to a Dentist) were assessed one by one. When the
subscale scores were evaluated, a statistically significant difference was found only in the F subscale (Diseases and Injuries).
Discussion: It seemed from these results that the fear of feeling pain during coitus and the sensations of narrowness, dryness and pain
during coitus are important variables contributing to the etiology of vaginismus. It was thought that the fear of pain during coitus and the
fear of somatic injury might trigger a perception of threat and this could explain the muscle spasm used in the definition of vaginismus.
The statistical significance of the high level of the fear of bleeding and the fear of a dentist, which might symbolize the fear of pain, was
thought to indicate this relationship. Again, it was considered that the thoughts of bleeding during coitus and pain and the somatic injury
following it might have a relationship with the high scores in the fear of disease and injury scale. As in all of the sexual function disorders,
a diagnosis of vaginismus should also rely on evidence-based criteria rather than on a consensus of specialist views. We think that largescale studies integrated with clinics are needed to obtain such evidence-based criteria
Key words: Vaginismus, phobias, pain threshold, amplified perception of somatic sensations
[PP-093]
Ref. No: 244
Are personality traits helpful to predict psychosis?
Agah Aydın, Mehmet Emin Ceylan, Elif Mutlu, Ayşe Fulya Maner
Bakırköy Research and Training Hospital for Psychiatry, Neurology, and Neurosurgery, İstanbul, Turkey
Objective: The aim of this study was to investigate the incidence and specificity of personality traits and personality disorders among
patients with psychotic disorders. Making a comparison (regarding to personality traits) between patients with acute transient psychosis
and patients with unipolar major depressive disorder with psychotic features was another aim of the study. The relationship between the
variety of delusions and personality disorder clusters was also evaluated.
Methods: Fifty-one patients with Acute Transient Psychosis (ATP) (brief psychotic disorder n=25, schizophreniform disorder n=2,
psychotic disorder NOS n=24), 41 patients with Major Depressive Disorder with Psychotic Features (MDDPF) and 47 healthy controls were
evaluated with a structured interview form based onthe DSM IV (Structured Clinical Interview for the DSM IV, SCID-I, SCID-II). Also the
PANSS (Positive and Negative Symptom Scale) and the HDS ( Hamilton Depression Scale) were applied to the patients.
Results: Thirty patients with ATP (58.8%) showed at least one personality disorder comorbidity. The frequency of observed personality
disorder clusters was cluster B (39.2%), cluster A, (31.4%), and cluster C (21.6%). The most common personality disorders among the patients
with ATP were borderline (27.5%) and paranoid (27.5%). Twenty-two patients with MDDPF (48,9%) had at least one personality disorder
comorbidity. The most frequent personality disorder cluster was cluster C (40%); followed by cluster B (20%) and cluster A (17.8%). When the
two diagnostic groups were compared, cluster B, narcissistic, schizotypal and antisocial personality disorders were observed more frequently
in the ATP group and the cluster C and avoidant personality disorders were more frequently observed in the MDDPF group. Paranoid
delusions had higher rates in cluster A and other delusions (like jealousy, erotomanic, and mystic delusions) had higher rates in cluster B.
Conclusion: In spite of the high rates of personality disorders in both diagnostic groups, the same disorders were also observed in people
with no personality disorders. ATP and MDDPF did not seem to have a relationship with any personality disorder. Nevertheless, some
personality disorders (narcissistic, schizotypal, and avoidant) can contribute to ATP and MDDPF by different mechanisms. Performing a
personality assessment after the first year of improvement of the post psychotic symptoms might have given more accurate results. On
the other hand, it could be said that, personality traits may have an effect on delusions.
Key words: Psychosis, personality disorder, depression
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[PP-094]
Switching to fluoxetine due to sertraline-induced urinary incontinence: A case report
Ref. No: 291
Pınar Güzel Özdemir1, Adem Aydın1, Mustafa Güleç2, Emine Füsün Akyüz Çim1
Yuzuncu Yil University, Medical Faculty, Department of Pyschiatry, Van, Turkey
1
Ataturk University, Medical Faculty, Department of Pyschiatry, Erzurum, Turkey
2
Urinary incontinence is involuntary leakage of urine. It is not life-threatening but adversely affects the quality of life (1). The patient usually
complains about frequent or periodic urinary incontinence in small amount or just leakage.
Here we report a case of urinary incontinence induced with sertraline and resolved after sertraline was discontinued.
Case: A 38 year-old married female patient presented to our clinic with complaints such as boredom, avolution, and depression. In
her history, there was no psychiatric treatment or treatment with any other medications. On her psychological examination, she was
cooperative, oriented, replying to questions briefly and properly. Her affect was depressive. The patient was diagnosed with depressive
disorder and prescribed sertraline 50mg/day. She was suggested to come to the clinic for follow up after 3 weeks, however she came back
a week later complaining of urinary incontinence. Without any pressure feeling, she developed urinary incontinence which negatively
affected her daily activities. Her medication was changed to fluoxetine 20mg/day from sertraline 50mg/day. Her urinary incontinence
complaint disappeared 2 days after. On the follow-up the patient did not have any urinary incontinence.
We presented a case report of urinary incontinence, which developed after starting sertraline. In the literature, there are case reports
about sertraline induced urinary incontinence and switching to fluoxetine (1,2).
Despite extensive research, the mechanism of enuresis has not been clarified in detail. Continence is maintained by alpha-adrenergically
mediated constriction of the bladder sphincter (3). Sertraline has alpha-adrenergic blockage, which may partially explain urinary incontinence
in our case.
Enuresis is usually underdiagnosed because of clinicians do not ascertain about it or the masking of this side effect by multiple drugs such
as antimuscarinic or noradrenergic agents (3).
Fluoxetine may be a choice in sertraline induced urinary incontinence cases in the treatment of depression and anxiety disorders. Larger
case series are needed on this issue.
Key words: Urinary incontinence, sertraline, fluoxetine
References:
1.
Votolato NA, Stern S, Caputo RM: Serotonergic antidepressants and urinary incontinence Int Urogynecol J Pelvic Floor Dysfunct 2000;11:p 386–8.
2. Maalouf Fadi T, Gilbert Andrew R. Sertraline-Induced Enuresis in a Prepubertal Child Resolves after Switching to Fluoxetine. J Child Adolesc Psychopharmacol
2010;20:161
3.
Andersson KE: Advances in the pharmacological control of the bladder. Exp Physiol 1999;84:195–213
[PP-095]
The relationship between the serum bilirubin levels and metabolic syndrome
in schizophrenia patients
Ref. No: 292
Filiz Karadağ1, Hasan Herken1, Bünyamin Kaptanoğlu2, Yaşar Enli2, Özgür Kalkancı1, Ceyhan Balcı Şengül3, Hüseyin Alaçam1
Pamukkale University Medical Faculty Psychiatry Department, Denizli, Turkey
1
Pamukkale University Medical Faculty Biochemisry Department, Denizli, Turkey
2
*Denizli State Hospital, Denizli, Turkey
Objective: Especially with the use of atypical antipsychotics, the increase of the metabolic side effects constitutes a major problem
in schizophrenia patients. Serum bilirubin levels have been reported to be associated with insulin resistance, abdominal obesity, and
metabolic syndrome (MS) (1,2). However, the relationship between MS parameters and bilirubin levels has not been investigated in
schizophrenia patients. It has been reported that antipsychotic drugs do not cause significant changes in serum bilirubin levels (3).
The objective of this study was to investigate the association between bilirubin levels and the parameters associated with MS in
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schizophrenia patients.
Methods: Ninety one schizophrenic patients (38 female, 53 male) receiving antipsychotics for at least one year were included in the study.
The parameters associated with MS were as follows: Body mass index, body weight, waist circumference, systolic and diastolic blood
pressure, fasting blood glucose, insulin, serum triglycerides, HDL cholesterol levels, and the insulin resistance as calculated by using the
value HOMA (homeostasis model assessment). The criteria were based on ATP-III criteria for metabolic syndrome (Adult Treatment Panel
III). Statistical analysis was performed by using SPSS 17.0 (for Windows).
Results: Serum triglyceride levels were inversely correlated with serum direct bilirubin (p=.006) and positively correlated with indirect/
direct bilirubin ratio (p =. 002). Serum HDL levels (p=.018) showed a significant positive correlation with indirect/direct bilirubin ratio.
Waist circumference (p=.048) showed a significant negative correlation with serum total bilirubin. The levels of insulin (p =.038) and value
of HOMA (p =.015) were inversely correlated with serum direct bilirubin.
The rate of metabolic syndrome was significantly lower in the patients with highest quartile (75-100) of the serum direct bilirubin levels
than the other quartiles (p=.022).
In these patients, the ratio of the patients that meet criteria for metabolic syndrome according to levels of the fasting triglyceride (p=.013)
and HDL (p=.040) was significantly lower than others. Additionally, the means of body weight (p=.026), waist circumference (p=.022), and
serum triglyceride levels (p=.039) of these patients were found significantly lower.
Conclusions: In this study we found that bilirubin levels are associated with metabolic syndrome and its parameters and high levels of
serum direct bilirubin may be associated with the lower risk for MS in schizophrenia patients; similar to the healthy individuals (1,2,4).
Our study is the first study investigating this issue. Our results may be important for the following aspects: High serum direct bilirubin
levels may serve as an easily applicable, inexpensive marker indicating lower MS risk for schizophrenic patients. Additionally, it may be
possible to prevent antipsychotics induced metabolic side effects by avoiding the drugs with higher risk for MS, in the patients with low
levels of direct bilirubin. Due to the relatively limited number of patients and cross-sectional nature, our results required to be confirmed
by longitidunal studies with larger samples.
Key words: Schizophrenia, metabolic syndrome, bilirubin, antipsycotic drug
[PP-096]
Olanzapine abuse: A case report
Ref. No: 293
Introduction: Olanzapine is a thienobenzodiazepine which specifically blocks 5-HT2A and D2 receptors and additionally blocks
muscarinic (M1), H1, 5-HT2C, 5-HT3.5-HT6, a l, and D4 receptors. It has greater affinity for 5-HT2 receptors than for D2 receptors (Kelly,
Conley & Carpenter 2005). Olanzapine has consistently been found to be significantly superior to placebo and comparable with, or
superior to, haloperidol for the treatment of overall, positive, and negative symptoms of schizophrenia. In this case, we want to report a
case of olanzapine abuse.
Case Report: A 48-year old, primary school graduate, married, female patient was admitted to our psychiatry clinic with tachycardia,
insomnia, and anxiety. In psychiatric assessment, she mentioned that her symptoms have been similar for 15 years and in the last 3 years
she has used citalopram 40 mg/d and olanzapine 10 mg/d and after this treatment her symptoms decreased. During psychiatric treatment
when her consequent doctor wanted to stop the olanzapine treatment, she did not succeed and the patient had anxiety, insomnia, and
anger and reported decreased symptoms after using the drug again
Discussion: Besides medications with obvious abuse potential such as benzodiazepines and methyphenidate and other stimulants, abuse
of a number of commonly prescribed psychiatric medications has been reported. The abuse of anticholinergic drugs was first reported
in 1960 with the description of a patient, who increased her trihexyphenidyl to achieve antidepressant and euphoriant effects. Recently,
abuse of quetiapine for its sedative and anxiolytic effects has been reported. The abuse risk of quetiapine has been also reported in our
country and Kaya et al. studied the abuse risk of quetiapine with prisoners. In the literature there are only two cases of olanzapine abuse.
Key words: Abuse, olanzapine
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[PP-097]
Various reasons for self-destructive acts and objects used to commit them in 1991
Ref. No: 123
Elena Valzdorf
Irkutsk Regional Psychoneurologic Dispensary
Objective: The objective of the research was to study and assess the reasons for self-destructive acts committed by the individuals that
underwent outpatient forensic psychiatric examination in 1991 and to give a brief characteristic of the objects used to commit the selfdestructive acts.
Methods: The statistical method and comparative analysis were employed to study the historical data of 30 archive acts of outpatient
forensic psychiatric examinations covering the period of January-March, 1991.
Results: The analysis of the archive of acts revealed 30 males aged between 15 and 51 (the age range of 20 and 41 dominated). The
reasons for committing self-destructive acts by the examined individuals who underwent outpatient forensic psychiatric examination in
1991 included the following: Conflicts with people around them (in 12 patients), conflict situations with parents and other close relatives
(sister, brother, wife) (in 5), conflicts with inmates in place of imprisonment (in 4), conflict situations during military service (for example,
a self-destructive act was committed by a serviceman to be closer to his parents house) 9in 3), an effect of command hallucinations in 2,
ongoing investigation (in 1), conflict with loved ones (woman) (in 1), protest (investigator refused to allow relatives to visit the patient) (in
1), and severe headache in combination with high blood pressure (the suicide was attempted to ease the pain) (in 1). Also according to
the archive documents of forensic psychiatric examination 18 out of 30 individuals used sharp, cutting, or piercing objects (razor, kitchen
knife, or pen knife, glass, fragment of a broken mirror, wire, sharpened coin, cigar case, etc.), 3 individuals used washing line or belt, 3
patients used a medicine in tablet form, 1 individual used a medicine in liquid form, and 1 patient used the effect of low temperatures
(long deliberate stay in cold weather in winter).
Conclusion: The research findings demonstrated that the most common reasons for self-destructive acts committed by the examined
patients in 1991 were conflict situations with individuals, out of prison, and in the society rather than conflicts in place of imprisonment
or in place of military services. The objects used to commit self-destructive acts included: Sharp, cutting, or piercing objects (most often
razor and kitchen knife), washing line, and a medicine in tablet form (antibiotics, phenazepam, cyclodolum, etc.).
Key words: Self-destructive acts, outpatient forensic psychiatric examination, archive documents
[PP-098]
Topiramate induced acute psychotic disorder
Ref. No: 296
Serkan Barlak, Alpay Ateş, Cengiz Başoğlu, Servet Ebrinç
Introduction: The use of topiramate has increased in recent years. It is now used in several specialties to treat a wide range of medical
conditions. A small number of case reports describes psychosis as an adverse event of topiramate. While using topiramate as an option
for treatment-resistant epilepsy, clinicians need to be aware of the possibility of topiramate-induced psychosis in patients who have
not previously had a psychotic episode. Although there is a small literature in neurology journals regarding psychiatric adverse events
in epileptic patients, the psychiatric literature is silent about the topic. We report a patient without a previous history of psychosis, who
developed psychosis after use of topiramate.
Case: The patient on multiple antiepileptic drugs with refractory tonic-clonic epilepsy was prescribed topiramate. The patient developed
definite psychotic symptoms including auditory halucinations and paranoid-persecutory delusions and other behavioral symptoms
fifteen days after beginning topiramate. The psychotic and other psychiatric symptoms resolved quickly with discontinuation of
topiramate and by using a second-generation antpsychotic drug.
Discussion: Topiramate was originally discovered as an oral hypoglycaemic, afterwards was approved as an anticonvulsant agent and is
now used as an adjunct to various treatments. The several mechanisms of action include inhibition of sodium conductance, decreased
frequency of generated action potentials, activated gamma-aminobutyric acid activity, inhibition of AMPA receptor, and weak inhibition
of carbonic anhydrase (1). The mechanism underlying psychotic symptoms induced by topiramate is not clear, but overactivity of
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ascending dopaminergic pathways due to GABAergic inhibition of the substantia nigra has been proposed (3). The true prevalence of
topiramate-induced psychosis is not known. Although there have only been a few case reports of topiramate-induced psychosis, an
antiepileptic drug survey group found the incidence to be 1.5% in 596 patients (2). The risk of this side effect may be greater in the general
population as studies of topiramate exclude patients with past psychiatric history and past psychiatric history is the most important
predictor for psychiatric adverse events. As epilepsy could overlap with psychiatric conditions at a rate of 50-60% including mood, anxiety,
and psychotic disorders, clinicians should be cautious in diagnosing drug–induced psychosis.
Key words: Topiramate, antiepileptic, drug-induced psychosis
[PP-099]
Glass-aating behaviour with radiological findings: A pica case
Ref. No: 170
Pica is the persistent, compulsive ingestion of non-nutritive substances, which includes eating disorders with unusual cravings. Etiologies
of consumption of common and bizarre substances range from mineral deficiencies and helminthic infestations to cultural preferences.
Recently, pica has been linked to obsessive-compulsive (OCD) spectrum disorders.
Although there are few epidemiological studies and likely underreporting by embarrassed patients, pica exists in all ages, races, genders,
and geographical regions. Lower socioeconomic groups, young children, pregnant women, or nursing mothers with increased nutritional
demands are at higher risk, as well as those with brain damage, epilepsy, mental retardation, psychosis, or dementia.
Case Report: A 32-year-old, primary school graduate, unemployed, male patient referred to psychiatry clinic with glass eating behavior
for 10 years. There was not any history of psychiatry referral before the development of glass eating craving. He was referred to psychiatry
clinic with this craving and had difficulty to quit eating glass. In psychiatric examination we found cleaning and control obssessions.
The cranial MRI showed decrease in size of in corpus callosum, enlargement in Sylvian fissure and sulcus, asymmetry in III. and lateral
ventricules.
Discussion: In literature we did not a pica case like this one regarding glass eating. Even most pica cases are associated with element
deficiency in our case there was not any deficiency. Because of obsessive symptoms, it might be associated with obsessive spectrum
disorders with radiological findings. In OCD spectrum disorders, pica should also be considered and radiological investigation must
always be done.
Key words: Obsessive compulsive spectrum, pica, corpus callosum
[PP-100]
The use of bupropion in treatment Kleptomania’s: Two cases
Ref. No: 209
Özyıl Öztürk Sarıkaya1, Demet Güleç Öyekçin2
Bursa Devlet Hastanesi, AMATEM Birimi, Bursa, Turkey
1
On Sekiz Mart ÜTF Psikiyatri AD, Çanakkale, Turkey
2
Objective: Kleptomania is an impulse control disorder, which is characterized by one’s uninterrupted impulse of stealing objects
that needed neither for use nor for value, in a repetitive uncontrollable manner (1). Studies stated that those with kleptomania are
accompanied by other psychiatric conditions such as mood disorders, other impulse control disorders, or substance abuse and addiction
(2).
For the treatment, selective serotonin reuptake inhibitors, mood stabilizers, and opioid receptor antogonists have been shown to be
effective. In recent years, treatment for pathological gambling and trichotillomania as other impulse control disorders in which naltrexone
and bupropion were studied for effective treatment of pathological gambling and trichotillomania, bupropion has been found to be as
effective as naltrexone (3-4).
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The effectiveness of bupropion for treatment of kleptomania, which is classified as an impulse control disorder, is discussed on two cases
in this report.
Case 1: A 34 year-old married, women, graduated from high school presented with fatique, stress, lack of motivation, and complaints of
staying in house, which lasted for the last two months in March, 2011. She had been stealing objects which were not important for her
or she didn’t need for a year. She stated that she felt joy during kleptomanic behaviour and later felt guilty and depressed and she could
not leave the house.
She had substance abuse history and had been treated for major depression.
SCID-I revealed she had major depressive disorder recurring type and kleptomania.
For treatment, bupropion was given 150 mg/day initially, then increased to 300 mg/day. The depressive symptoms were apperently
reduced in 8th week of the treatment. In 12th week, psychiatric examination revealed that functionalty, stealing impulse, and behaviour
healed clearly.
Case 2: A 25 year-old single,women, graduated from high school presented with hypersomnia, eating too much, lying, suicide thoughts,
and stealing things that she didn’t need. Kleptomanic behaviour had begun one year ago.
She was told to be overweight when she was 8 year-old and tried to commit suicide when she was attending to secondary school. She
had been shopping compulsively for 3-4 years.
SCID-I revealed that she had major depressive disorder recurring type and kleptomania.
Bupropion 150 mg/day was started initially, then 300 mg/day was given for treatment. The depressive symptoms were reduced markedly
in the 10th week of the treatment. Desire and impulses to steal, hyperphagia, and suicide thoughts were found to be treated.
Discussion: There are studies (3-4) showed bupropion to be effective for treatment of pathological gambling and trichotillomania, both
of which are impulse control disorders. We investigated the effectiveness of bupropion treatment in two cases, who had kleptomania
and co-existing mood disorder. To our knowledge this is the first case report bupropion is used for kleptomania treatment. Larger and
controlled studies on kleptomania would make it possible to understand the pharmacotherapy and etiology of this disorder better.
References:
1.
Hocaoğlu Ç, Kandemir G. The use of SSRI (Selective Serotonin Reuptake Inhibitors) in kleptomania’s treatment: case reports. Bulletin of Clinical Psychopharmacology
2004;14:204-8.
2.
Bayle FJ, Caci H, Millet B, Richa S, Olie JP. Psychopathology and comorbidity of psychiatric disorders in patients with kleptomania. Am J Psychiatry 2003;160(8):1509-13.
3.
Bhanji NH, Margolese HC. Alternative pharmacotherapy for trichotillomania: a report of successful bupropion use. J Clin Psychiatry 2004;65(9):1283.
4. Dannon PN, Lowengrub K, Musin E, Gonopolski Y, Kotler M. Sustained-release bupropion versus naltrexone in the treatment of pathological gambling: a
preliminary blind-rater study. J Clin Psychopharmacol 2005; 25(6):593-6.
[PP-101]
A randomized, double-blind, placebo-controlled trial of celecoxib augmentation of
sertraline in the treatment of a drug-naïve women with major depression
Ref. No: 251
Farshad Hashemian1, Marzieh Majd1, Seyed Mohammad Hosseini2, Ali Sharifi1, Maryam Vahdat Shariat Panahi3, Ofogh Bigdeli1
Department of Clinical Pharmacy, Islamic Azad University, Pharmaceutical Sciences Branch, Tehran, Iran
1
Department of Psychiatry, Hamedan University of Medical Sciences, Hamedan, Iran
2
Islamic Azad University, Tehran Medical Branch, Iran
3
Objectives: A growing body of evidence strongly suggests that inflammatory process and immune responses are involved in the
pathophysiology of depression. While depression itself is considered a heterogeneous disorder, the involvement of immune system
further complicates the matter.
Meanwhile, several antidepressant medications (e.g. fluoxetine) have been reported to exert immunomodulatory properties, which may
affect human immune system and may partly contribute to their efficacy. Moreover, it must be noted that immune response/system
profoundly varies between the genders due to differences in sex hormones. However, there have been no controlled studies investigating
the benefits of celecoxib augmentation therapy in treatment-naïve women with depression.
To increase the homogeneity of the study population, the present study was designed to examine the antidepressant effects of celecoxib
augmentation of sertraline in the treatment of female drug-naïve patients with depression for 8 weeks.
Methods: Forty female patients diagnosed with first episode of major depression according to DSM-IV-TR criteria were recruited for this
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study. The inclusion criteria were: 1. First episode of major depression, 2. Female gender, 3. Antidepressant-naïve, 4. Age between 18 and
50 years, and 5. Hamilton depression rating scale (17 items) score ranging from 18 to 36. The patients with history of other psychiatric
disorders, significant suicidal ideation, liver and kidney dysfunction, and cardiovascular disorders were excluded. The patients were
randomly assigned into two equal groups receiving either sertraline 50-100 mg/day plus celecoxib 100 mg twice daily or sertraline 50-100
mg/day plus placebo twice daily. The participants were assessed by Hamilton depression and anxiety rating scale at baseline, and 4th and
8th weeks of the treatment. The data were analyzed by Mann-Whitney U test and Fisher’s exact test. The trial was registered in Iranian
Registry of Clinical Trials (IRCT registration number: IRCT201009043106N3). This study was approved by Azad University Pharmaceutical
Sciences Ethics Committee (No: 4114).
Results: No significant differences were observed between two groups regarding demographicals characteristics and the Hamilton
depression score at baseline. The mean Hamilton depression score decreased from 26.14 (SD=5.51) at baseline to 12.42 (SD=5) at 4th
week and from 26.22 (SD=5.38) at baseline to 17.33 (SD=5.24) at 4th week in the celecoxib and placebo groups, respectively. Celecoxib
group showed significantly greater decrease in Hamilton scores compared to placebo (P< 0.05) at the end of week 4. The mean decrease
in Hamilton score was greater in the treatment group compared to placebo over 8 weeks, although it was not statistically significant. In
addition, remission rate (HamD scores <= 7) was significantly higher in the celecoxib group compared to placebo group (57% and 11%
respectively, P<0.05).
Conclusion: It can be suggested that celecoxib augmentation therapy may accelerate the onset of therapeutic action of sertraline and
also result in higher remission rate at the endpoint of treatment. The results of present study substantiate the hypothesis that add-on
treatment with anti-inflammatory agents can be beneficial in the management of depression.
Key words: Inflammation, depression, COX-2 inhibitor, augmentation therapy
[PP-102]
To compare marital conflicts, between divorced and normal couples in Sirjan of Iran
Ref. No: 180
Sima Karimi1, Majid Kazemi2, Hadi Hasankhani3, Somayeh Kazemi4
Islamic Azad University- Sirjan Branch, Iran
1
Rafsanjan University of Medical science, Iran
2
Tabriz University of Medical sciences, Iran
3
Islamic Azad University- Mashhad Branch, Iran
4
Objectives: Marriage is supposed to be a holy agreement and union between couples. The healthy relationship between a couple is a
source of growth, maturity, and enlightenment. Unfortunately, some marriages are not only the source of peace and joy, but also can be
the origin of stress and conflict and at the end may lead to mental and physical disorders.
Comparing marital conflicts and emotional reactions between the couples exposed to divorce and normal ones in Sirjan.
Method: This research is causal-comparative and was conducted in Sirjan in 2010. Seventy couples who had applied for separation
and 70 normal couples in community health center were chosen at random and according to duration of marriage. A marital conflict
questionnaire including seven dimensions was completed by volunteers, the data were collected and analyzed by SPSS.
Results: The results showed that two groups, including the couples that applied for divorce and normal ones, were similar regarding
average of age, number of children, work time, and the duration of marriage. Comparing the average of marital conflict scores between two
groups illustrated the score was higher in couples who applied for divorce (100.97 ± 20.1) in comparison with the other group (76.48±18.67)
and a significant correlation was detected also between two groups, one of seven dimensions were different significantly (P<0.05).
Conclusion: The results showed that the marital conflicts and emotional reactions were higher in couples who applied for divorce and
these conflicts may increase divorce risk. We suggest more social support and family consulting in the community are needed and must
be expanded.
Key words: Mental disorder, marital conflict, divorce
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[PP-103]
Adult primary enuresis nocturna: A case report
Ref. No: 298
Yücel Yılmaz, Ömer Yanartaş, İshak Saygılı, Aytül Gürsü Hariri
Erenkoy Mental Health Training And Research Hospital, Istanbul, Turkey
Introduction: Nocturnal enuresis (bed-wetting) is a hereditary, medical condition, which effects both children and adults (1). Beside this
there is few studies on pevalance of enuresis nocturna (EN) among adults. EN cases are seldomly reported. Although most of the patients
recover spontaneusly from EN, in the resistant cases illness persist through adulthood (2). The patients who have frequent bed-wetting in
their childhood have greater risk for persistence of symptoms (3).
Case: A 29-year-old single, male patient does not work. The patient has been suffering from bed-wetting at nights, 2-3 times per week
since his early childhood. He reports that he never had a long period free from bed-wetting at nights. He was suffering from bedwetting
only at nights and never had daytime wetting. The patient reported that bedwetting becomes more frequent when he was under stress or
felt unhappy about something and decreased in frequency when he felt less stressed out. While his military service, for a short period his
symptoms had stopped when his millitary service was over his symptom has started again. In last six months, after he has suffered from
thoughts of worthlessness, relationship issues with his father, and some economic problems his bed-wetting frequency increased. After
his first application to the Erenkoy Mental Health Training And Research Hospital outpatient clinic, a consultation with a neurologist and a
urologist was planned. He had been examined separately by a urologist, a neurologist and a psychiatrist. Several investigations had been
performed in which they could not detect any organic disease. These investigations included urine analysis, abdominal USG, cranial MRI,
and EEG. According to the results of these investigations, organic etiology was ruled out and 25 mg/day imipramine had been commenced.
Later we increased imipramine dosage to 50 mg/day and added behavioral homework to the treatment. In his familiy history, there were
similar symptoms in his brother wich had persisted until age 15th, and in his cousin which had persisted until he turned to 19 years old. The
treatment response of the patient was good; his compliance with pharmacological treatment and behavioral therapy techniques was good.
Discussion: Our case, according to DSM-IV-TR diagnostic criteria, was fulfilling the criteria for enuresis nocturna and major depressive
disorder on axis I. His problems about his functionality and his relationship with his father have caused an increase in his depressive
symptoms and his bed-wetting. We think that patient’s good response to treatment is related to his high motivation in his first psychiatric
application and his compliance with behavioral threapy. It is compatible with literature data that the relatives of the patient have similar
symptoms.
Key words: Enuresis nocturna, imipramine, behavioral therapy
References:
1.
Yaluğ İ, Ünsalan N, Özten E, Öztep Kuruoğlu S, Tufan AE. Erişkinde ikincil enürezis nokturna: Bir olgu sunumu. Anadolu Psikiyatri Dergisi 2006; 7:185-190
2.
Burgu B, Gokce MI, Gucuk A, Soygur T. Prospective evaluation of factors affecting the response and relapse rates to desmopressin therapy in male monosymptomatic
enuretic adults. Urology 2009; 74: 915–919
3.
Yeung CK, Sihoe JD, Sit FK, Bower W, Sreedhar B, Lau J. Characteristics of primary nocturnal enuresis in adults: an epidemiological study. BJU Int 2004; 341-345
[PP-104]
Major depressive disorder and the 5-HTTLPR in Spanish and Mexican populations
Ref. No: 311
Pedro Dorado1, Hugo Trejo2, Elisa Alonso2, Eva Peñas Lledó1, Adrián Llerena1, Marisol López3
Clinical Research Centre (CICAB), Extremadura University Hospital and Medical School, Badajoz, Spain
1
National Institute of Neurology and Neurosurgery Manuel Velasco Suárez. Mexico City, Mexico
2
Metropolitan Autonomous University-Campus Xochimilco, Mexico City, Mexico
3
Co-Principal Investigators
4
Preliminary evidence of an increased risk of suffering from MDD for individuals carrying the 5HTTLPR S allele was described in 70 Spanish
patients [1].
The present study aimed to analyze the potential relevance of the 5-HTTLPR genotypes and the risk of suffering from MDD in Mexicans
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and Spaniards.
One hundred and twenty-two (70 previously analyzed) white Spanish and 101 Mexican Mestizo patients with a diagnosis of MDD (DSMIV) were studied. Additionally, 327 Spaniards and 153 Mexican Mestizo healthy volunteers were also studied by a previously reported PCR
method [1]. Genotypes and allele frequencies were compared between MDD patients and HVs by two-tailed Fisher’s test.
The frequencies of 5HTTLPR LL, LS and SS genotypes in the Spanish population (MDD vs. HV) were 19.7 vs. 28.8%, 54.9 vs. 50.5% and 25.4
vs. 19.9 %. In the Mexican Mestizo population the frequencies in the MDD vs. HV groups were 14.9 vs. 18.3%, 49.5 vs. 55.6%, and 35.6 vs.
26.1% for 5HTTLPR LL, LS, and SS genotypes, respectively. The frequencies of 5-HTTLPR genotypes of the four groups (MDD and HV from
Spain and Mexico) corresponded to those predicted by the Hardy–Weinberg law.
The odds ratio associated with the 5-HTTLPR-S allele were 1.72 (95% CI: 1.04-2.85) and 1.28 (95% CI: 0.64-2.55) for the MDD in comparison
with the HV group in Spaniards and Mexicans, respectively.
The frequency of S was higher than the frequency of L allele in both MDD groups. In the Spanish population, the S allele was significantly
higher (p<0.05) in MDD (52.9%) than in HV (45.1%). However, in the Mexican Mestizo population, the S allele was higher in the MDD group
(60.4%) compared to HV (53.9%), but this difference was not significant. Moreover, the frequency of 5-HTTLPR-S allele in the Spanish HV
(45.1%) was higher (p<0.05) than Mexican Mestizo HV (53.9%).
The S allele of 5HTTLPR is related to risk of MDD in both populations. In addition, we have found differences in the frequency of
5-HTTLPR-S allele between Spaniards and Mexican Mestizo populations.
Grants: Supported by grants from the Spanish Ministry of Health Instituto de Salud Carlos III and EU-FEDER PI10/02758, CP06/00030 (PD);
AEXCID (9IA006) Junta de Extremadura and EU-FEDER (BS10023) and Consejo Nacional de Ciencia y Tecnología de México (Nº 59366). This
work was coordinated by Network Red Iberoamericana de Farmacogenética y Farmacogenómica (CYTED206RT0290).
References:
1.
Dorado P, Penas-Lledo EM, Gonzalez AP, Caceres MC, Cobaleda J, Llerena A. Fundam Clin Pharmacol 2007;21:451-3.
[PP-105]
Phenytoin toxicity in a pediatric epileptic patient and CYP2C9, CYP2C19, and
ABCB1 genetic polymorphisms
Ref. No: 313
Pedro Dorado1, Enrique López Torres2, Eva M. Peñas Lledó1, Jacinto Martínez Antón2, Adrián Llerena3
Clinical Research Centre (CICAB), Extremadura University Hospital and Medical School, Badajoz, Spain
1
Neuropediatric Unit, Materno-Infantil Carlos Haya Hospital, Malaga, Spain
2
CICS-UBI-Health Sciences Research Centre, University of Beira Interior, Covilhã, Portugal
3
Pharmacogenetic studies have shown that genetic defects in drug-metabolizing enzymes encoded by CYP2C9 and CYP2C19 genes and
by the transporter ABCB1 gene can influence phenytoin plasma levels and toxicity. Present findings support the previously established
relationship between CYP2C9, CYP2C19, and ABCB1 genetic polymorphisms and the increased risk to develop phenytoin toxicity due to
high plasma concentrations. Nevertheless, while the association of these genes with phenytoin-induced adverse effects has been well
documented in adult populations, this is the first report examining the influence of these genetic polymorphisms on phenytoin plasma
levels and toxicity in a pediatric patient.
The patient reported here is a 2-year-old girl with a medical history of cryptogenic or probably symptomatic epilepsy. At age 13 months,
she had a first focal seizure with secondary generalization. At age 20 months, she was admitted to the Emergency Department because
generalized convulsive Status Epilepticus (SE) needing rectal diazepam (0.5 mg/kg), intravenous diazepam (0.3 mg/kg), and intravenous
phenytoin with a loading dose of 15 mg/kg and a maintenance dose of 5 mg/kg/day. The convulsive SE with generalized tonic clonic
seizures lasted a total time of 30 minutes and stopped 15 minutes after the loading phenytoin dose was infused. Two hours after the first
intravenous phenytoin dosage was given, the patient was found to have dizziness, nystagmus (lateral and vertical), ataxia, and excessive
sedation. Phenytoin toxicity was suspected and phenytoin plasma levels were determined. The patient was back to treatment with
oxcarbazepin (30 mg/kg/day) and she has been seizure-free since then.
Pharmacogenetic analyses were conducted in order to examine whether CYP2C9, CYP2C19, and ABCB1 genetic polymorphisms might
explain the abovementioned phenytoin-induced neurological toxicity.
Pharmacogenetic analyses for the genes involved in phenytoin pharmacokinetics revealed that the patient was homozygous for the
CYP2C9*2 allele, heterozygous for the CYP2C19*4 allele, homozygous for the 3435C and 1236C ABCB1 alleles.
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Present data support CYP2C9 and CYP2C19 genotyping prior to phenytoin treatment in order to prevent adverse events. Consistently, for
patients carrying CYP2C9 and CYP2C19 defective alleles, valproate instead of phenytoin should be recommended to treat SE.
Grant: The study has been partly supported by the Institute of Health Carlos III-FIS and the European Union (FEDER) Grants, PI10/02010
and CP06/00030 (P Dorado) and from PRIS Extremadura, Consejería de Sanidad y Dependencia, FundeSalud PRIS10043. This study was
coordinated in the networks CIBERSAM and CAIBER, which are initiatives of ISCIII (Spain).
[PP-106]
Influence of CYP2D6 genetic polymorphism on fluoxetine and amitriptyline
clinical response
Ref. No: 314
M. López1, E. Peñas Lledó2, H. Trejo1, P. Dorado2, J. Guerrero2, M. E. Alonso3, A. Llerena2
1Metropolitan Autonomous University-Campus Xochimilco, Mexico City, Mexico.
2Clinical Research Centre (CICAB), Extremadura University Hospital and Medical School, Badajoz, Spain
3National Institute of Neurology and Neurosurgery Manuel Velasco Suárez. Mexico City, Mexico
Cytochrome P450 2D6 (CYP2D6) is involved in the metabolism of many antidepressants. It is characterized by a high individual variability
in catalytic activity mainly due to >75 CYP2D6 alleles that determine metabolizer status. The role of CYP2D6 genetic polymorphism in
the metabolism of amitriptyline and fluoxetine was previously demonstrated [LLerena et al, 2004]. Herein, we analyzed the relevance
of CYP2D6 genetic polymorphism for the clinical response to the antidepressant drugs fluoxetine and amitriptyline. Sixty-five patients
(DSM-IV) diagnosed with major depression and a score equal or greater than 17 on the Hamilton-Depression (HAM-D) were prospectively
studied. They were treated either with fluoxetine or amitriptyline under antidepressant monotherapy. The informed written consent was
obtained from all patients. Clinical Response was evaluated with HAM-D. The patients were evaluated every month. A two months period
evaluation is reported here. The patients with a 50% decrease on HAM-D were considered as “responders.” CYP2D6 genotyping was
assayed by PCR-RFLP and RT-PCR. The first month evaluation showed that 49 out of the initial 65 remained (16 dropped-out) in the study
and second month evaluation showed that 41 patients remained (8 more dropped-out). Among responders there were 56.6% and 60% to
fluoxetine, and 50% and 70% to amitriptyline, at first and second follow up evaluations, respectively. The responders were characterized
by presenting one or two CYP2D6 active genes. Furthermore, the number of active genes was related to better clinical response in both
drugs. The percentage of responders was higher for those with two active genes than for patients carrying just one: (a) fluoxetine, 81 %
vs.18 % at first month; 87% vs. 13% at second month; (b) amitriptyline, 60 % vs.40 % at first month; 83% vs. 17% at second month. All
ultrarapid metabolizers (n=3 UMs; those with more than two CYP2D6 active genes) were found to drop out during the first month. The
only poor metabolizer patient in the study (PM; with none CYP2D6 active genes) was found among “non-responders” in both follow-up
evaluations. The number of CYP2D6 active genes seems to be related to clinical response to the antidepressant drugs amitriptyline or
fluoxetine. Among responders, the frequency of patients carrying two CYP2D6 active genes is higher than those with one copy. Moreover,
UMs and PMs were not found in this group.
Grants: Supported by grants from the Spanish Ministry of Health Instituto de Salud Carlos III and EU-FEDER PI10/02758, CP06/00030 (PD);
AEXCID (9IA006) Junta de Extremadura and EU-FEDER (BS10023) and Consejo Nacional de Ciencia y Tecnología de México (Nº 59366). This
work was coordinated by Network Red Iberoamericana de Farmacogenética y Farmacogenómica (CYTED206RT0290).
[PP-107]
Evaluation of insight and functional recovery in patients with schizophrenia
Ref. No: 137
Aykut Karahan, Ahmet Tiryaki, Baykal İskender, Evrim Özkorumak
Karadeniz Teknik Üniversitesi, Tıp Fakültesi, Psikiyatri Ana Bilim Dalı, Trabzon, Turkey
Objective: Despite the fact that functional remission is the most important goal for the treatment of schizophrenia, standard definitions
have not yet been made due to differences in measurement methods, the variability in the course of the disease, cognitive levels of the
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patients, and psycho-social factors. Nevertheless, there exists an accumulation of knowledge regarding factors, which influence functional
remission. Insight levels of patients influence their level of functionality, while causing problems in treatment adherence and social
adaptation. The purpose of this study was to examine the factors which influence schizophrenia patients’ levels of insight and functional
remission.
Methods: In this cross-sectional descriptive study, 70 outpatients between the ages of 18-65, who applied to the Karadeniz Technical
University, Psychiatry Clinic and were diagnosed with schizophrenia according to DSM-IV, were evaluated. The patients who reported they
agree to take part in the study by signing the consent form were included in the study. The patients who had a history of traumatic brain
injury and/or any disease which affects the central nervous system, whose Clinical Global Impression (CGI) disease severity low score was
above four, who were taken as inpatients to the hospital in the last two months or whose treatment was changed were excluded from
the study. The patients were evaluated by using respectively socio-demographic data collection form, clinical interview structured for
DSM (SCID-I), the Positive and Negative Syndrome Scale (PANSS), Calgary Depression Scale (CDS), the Functional Remission of General
Schizophrenia Scale (FROGS), Schedule for Assessing the Three Components of Insight (SAI-E), and cognitive test battery.
Results: Insight levels of the patients determined through the SAI-E, were found to be highly correlated with the PANSS positive, negative,
and general psychopathology, Stroop Test, Controlled Word Association Test (FAS), and Trail Making Test A-B scores. In the regression
analysis, PANSS total score, Stroop Test, and FAS scores were the predictors of insight.The FROGS functional levels of patients were found
to be related with occupational status, sex, age of onset of illness, comorbid psychiatric illness, PANSS positive, negative, and general
psychopathology, CDS, SAI-E, FAS, Trail Making Test, Stroop Test, and Wisconsin Card Sorting Test. In the regression analysis, occupational
status, comorbid obsessive compulsive disorder, PANNS negative and general psychopathology, and FAS scores were the predictors of
patients functional status.
Conclusion: Although insight levels of patients are basically related to cognitive functions, it has been reported in previous studies that
clinical symptoms can cause changes in the levels of insight depending on the course of the disease. The relationship between insight
and depression can vary depending on the severity of the depression, patients’ defense mechanisms, and internalized stigma levels. The
effects of clinical symptoms of schizophrenia, levels of cognitive function, and levels of insight and employment status on the patients’
functionality levels are prominent.
Key words: Schizophrenia, functional remission, insight, cognitive functions
[PP-108]
Ref. No: 205
Comparison of superoxide dismutase, glutathione peroxidase, and adenosine
deaminase activities between respiratory and nocturnal subtypes of patients with panic disorder
Osman Özdemir1, Yavuz Selvi1, Halil Özkol2, Yasin Tülüce2, Lutfullah Beşiroğlu1
Department of Psychiatry,Yuzuncu Yil University, Van, Turkey
1
Department of Medical Biology, Yuzuncu Yil University, Van, Turkey
2
Background: Panic Disorder (PD) is a heterogeneous disease and panic attacks are divided according to the different symptom clusters as
respiratory, nocturnal, nonfearful, cognitive, and vestibular subtypes. Oxidative stress (OS) is produced by free radicals which are named as
reactive oxygen species (ROS). They can be evaluated indirectly by measurement of some antioxidant enzyme levels such as superoxide
dismutase (SOD), catalase (CAT), or glutathione peroxidase (GSH-Px). PD is known to be associated with a high frequency of comorbid
immunological and increased expression of T lymphocytes compared to controls. Adenosine deaminase (ADA) has been accepted as an
important enzyme in the maturation and function of T lymphocytes. The aetiology of panic disorder is yet to be fully understood. There
is mounting evidence indicating that ROS may have an important role in the pathogenesis of PD.
Objective: In the present study we aimed to compare SOD, GSH-Px, and ADA activities in panic disorder patients with/without nocturnal,
respiratory subytypes, and healthy subjects. Thus to evaluate the effects of OS and inflammatory process on pathogenesis of PD and to
determine biological parameters in the subtypes of PD.
Methods: The study comprised of 60 patients with PD and 30 healthy control subjects. Panic Attack Symptom Checklist (PASC), Panic and
Agoraphobia Scale (PAS), Hamilton Depression Rating Scale (HAM-D), and Hamilton Anxiety Rating Scale (HAM-A) were administered to the
patients. A nocturnal panic attack is defined as an abrupt waking from sleep in a state of panic attack. The respiratory subtype is four of the
following five symptom criteria during an individual’s most recent severe panic attack: Feeling of choking or smothering sensations; shortness
of breath; chest pain or discomfort; numbness or tingling sensations; and fear of dying. The nonrespiratory subtype is operationalized as that
which does not meet the mentioned symptom criteria. The biochemical analyses were made after all the blood samples were collected. The
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laboratory analyses of investigation were conducted in Department of Medical Biology, Faculty of Medicine, at the University of Yuzuncu Yil.
Results: We found that SOD and GSH-Px blood activities of patients were significantly lower, and ADA activities of patients were higher
than the healthy controls. All of the activities were not significantly different between respiratory and nocturnal subtypes. There were
no significant relationships between the duration of illness and Panic-Agoraphobia (PAS) scores of patients with nocturnal subtypes.
Hamilton Depression Rating Scale (HAM-D) and Hamilton Anxiety Rating Scale (HAM-A) scores of the patients with nocturnal subtype
were significantly higher than the patients without nocturnal subtype. When examining the correlations between these variables and
enzyme levels, there was only a positive correlation between duration of disease and serum activities of GSH-Px.
Conclusion: In conclusion, SOD and GSH-Px ADA activities of the patients with PD are different from healthy subjects. Our results suggest
that oxidative and inflammatory processes may play role in pathophysiology of PD. These findings may support the idea that both
nocturnal and respiratory subtypes of PD have different symptom clusters of the same disease.
Key words: Panic disorder, subtypes, oxidative stress
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):188-9
[PP-109]
The neural and cognitive effects of Bacopa Monniera: An fMRI study
Ref. No: 106
Chris Neale1, Andrew Scholey1, Matthew Hughes1, Patrick Johnston2
Brain and Psychological Sciences Research Centre (BPsyC), Swinburne University of Technology, Melbourne, Australia
1
Department of Psychology, University of York, York, England
2
Objectives: Bacopa Monniera is an ayurvedic herbal medicine used in Indian medicine as a memory tonic. Animal models have shown
that it is an antioxidant (1), a memory enhancer (2), and an antidepressant (3). Human trials have had variable results, but spatial memory,
attention, and information processing tasks seem to be affected by Bacopa.
Given the improvements shown the RVIP task as a result of a 12 week Bacopa intervention, an fMRI methodology was employed to see
how Bacopa affects the brain during this task. The improved performance in these tasks suggests Bacopa may modulate task specific brain
regions. This investigation looks at the effects of Bacopa on the BOLD signal in the RVIP task over a 90 day intervention.
Method: The study utilized a double blind, placebo controlled, crossover design where all participants completed a 90 day course of
both Bacopa (300mg daily) and placebo during the study. The participants were aged between 40 and 65 years and in good health.
Interventions were separated by a 120 day washout period. Scans were undertaken on a 3T Siemens TRIO magnet before and after each
90 day intervention where participants would complete two runs of the task per scan visit.
The RVIP task is a block design which requires participants to respond when they see three odd or even numbers in a stream of numbers
presented at 100/minute. The control block requires a response when a zero is seen in the stream of numbers. Blocks last for 1 minute and
are repeated 3 times per condition in each of two experimental runs per scan.
Results: Data collection is ongoing at present. Baseline data show a bilateral increase in BOLD activation in the precentral gyrus and
precuneus with activation extending to the left inferior frontal gyrus (n=7, p=.005) when compared with control using a task greater than
baseline mask. Behavioural data suggest fewer ‘hits’ in the active task compared to control task.
Conclusions: The methodology of the study sets a gold standard for clinical trials using nutraceuticals and fMRI. Given the ongoing nature
of the study, conclusions are merely speculative at this point. However, the task looks to be a sensitive reflection of sustained attention.
We anticipate that the 90 day intervention of Bacopa will affect the BOLD signal in these particular regions of interest.
Key words: Bacopa monniera, fMRI, nutraceuticals, human cognition
References:
1.
Bhattacharya et al (2000) Antioxidant Activity of Bacopa Monniera in Rat Frontal Cortex, Striatum and Hippocampus. Phytotherapy Research, 14, 174 – 179
2.
Hota et al (2009) Bacopa monniera leaf extract ameliorates hypobaric hypoxia induced spatial memory impairment. Neurobiology of Disease, 34 (1) 23-39
3.
Sairam et al (2001) Prophylactic and curative effects of Bacopa monniera in gastric ulcer models. Phytomedicine, 8 (6) 423-430
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[PP-110]
Methlyphenidate induced thrombocytopenia in a pediatric patient with
ADHD and stuttering
Ref. No: 98
Serdal Özdemir, Fatma Ayık Özdemir
İnönü Üniversitesi Tıp Fakültesi Turgut Özal Tıp Merkezi Psikiyatri AD, Malatya, Turkey
Stuttering and attention deficit hyperactivity disorder (ADHD) can be seen together. Anemia or thrombocytopenia, rarely even pancytopenia
may occur as a side effect of medications used to treat both disorders. Thrombocytopenia, although it may be seen in some cases using
methylphenidate, occurs rarely. An 8 year-old boy was brought to our outpatient clinic by his family with the complaints of stuttering, attention
deficit, and hyperactivity. After the psychiatric evaluation and history were conducted and psychometric tests were applied. One month later
methylphenidate 18mg/day was started for the treatment of ADHD. Soon after initiation of medication, petechia developed on both lower
extremities of the patient. CBC showed isolated thrombocytopenia and te patient was followed by hematology clinic. On the 6th day upon
stopping mehtlyphenidate, the thrombocyte count returned to normal. We also discussed possible mechanisms of thrombocytopenia.
Key words: Isolated thrombocytopenia, petechia, methylphenidate
[PP-111]
Use of mirtazapine and olanzapine in treatment of major depressive disorder with
psychotic features developed during pregnancy: A case report
Ref. No: 245
Mustafa Güleç1, Yavuz Selvi2, Ünsal Aydınoğlu1
Atatürk Üniversitesi Tıp Fakültesi, Psikiyatri Anabilim Dalı, Erzurum, Turkey
1
Yüzüncü Yıl Üniversitesi Tıp Fakültesi, Psikiyatri Anabilim Dalı, Van, Turkey
2
Objctive: To contribute to the of treatment of major depressive disorder with psychotic features developing during pregnancy
Case: A 25 year-old, married, female patient was 13 weeks pregnant and diagnosed with major depressive disorder (MDD) with psychotic
features. She was a housewife with primary school degree and was admitted to inpatient unit. The obstetrician did not find any fetal
anomalies. The patient was put on mirtazapine and olanzapine, doses of which ranged between 15-30mg/day and 5-10 mg/day,
respectively during her two months hospitalization. In her follow up, 15 days after discharge, olanzapine dose was decreased to 5 mg/day,
but mirtazapine was continued at 30mg/day until delivery. To decrease neural tube defect risk folic acid 5mg/day was prescribed during
the treatment, as well. She gave birth to a live and healthy baby on the expected due date during her outpatient treatment.
The information regarding the safety of use of mirtazapine and olanzapine during pregnancy primarily rely on case reports. While
there were no fetal abnormalities in majority of cases regarding olanzapine use (1,2), there are some reports including hip dysplesia (3),
meningocele ve ankyloblepharon (4), atrioventricular channel defect and unilateral pes equinovarus (5). However, more cases and studies
are needed to explore, whether these cases were coincidental or due to teratogenic effects of olanzapine. Currently available publications
(6,7,8,9) report that major malformation risk in general population does not increase with the use of mirtazapine during pregnancy. The
reports from our country are parallel to the reports in the literature (10,11).
Results: Even in majority of cases no fetal abnormalities were reported regarding olanzapine use during pregnancy, large case series are
needed to have more evidence for stronger judgments. Also even mirtazapine does not look like a teratogenic agent, is should be used
with caution during pregnancy and babies that are exposed to mirtazapine should be followed closely.
Key words: Depression, pregnancy, safety, mirtazapine, olanzapine, teratogenicity
References:
1.
Littrell KH, Johnson CG, Peabody CD, Hilligoss N. Antipsychotics during pregnancy. Am J Psychiatry 2000; 157(8):1342
2.
Mendhekar DN, War L, Sharma JB, Jiloha RC. Olanzapine and pregnancy. Pharmacopsychiatry 2002; 35(3):122-123
3.
Spyropoulou AC, Zervas IM, Soldatos CR. Hip dysplasia following a case of olanzapine exposed pregnancy: a questionable association. Arch Womens Ment Health
2006; 9(4):219-222
4.
Arora M, Praharaj SK. Meningocele and ankyloblepharon following in utero exposure to olanzapine. Eur Psychiatr 2006; 21(5):345-356
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5.
Yeshayahu Y. The use of olanzapine in pregnancy and congenital cardiac and musculoskeletal abnormalities. Am J Psychiatry 2007; 164(11):1759-1760
6.
Lennestål R, Källén B. Delivery outcome in relation to maternal use of some recently introduced antidepressants. J Clin Psychopharmacol 2007; 27(6):607-613
7.
Way CM. Safety of newer antidepressants in pregnancy. Pharmacotherapy 2007; 27(4):546-552
8. Djulus J, Koren G, Einarson TR, Wilton L, Shakir S, Diav-Citrin O, et al. Exposure to mirtazapine during pregnancy: a prospective, comparative study of birth
outcomes. J Clin Psychiatry 2006; 67(8):1280-1284
9. Einarson TR, Einarson A. Newer antidepressants in pregnancy and rates of major malformations: a meta-analysis of prospective comparative studies.
Pharmacoepidemiol Drug Saf 2005; 14(12):823-827
10. Yaris F, Kadioglu M, Kesim M, Ulku C, Yaris E, Kalyoncu NI, et al. Newer antidepressants in pregnancy: prospective outcome of a case series. Reprod Toxicol 2004;
19(2):235-328
11. Guclu S, Gol M, Dogan E, Saygili U. Mirtazapine use in resistant hyperemesis gravidarum: report of three cases and review of the literature. Arch Gynecol Obstet
2005; 272(4):298-300
[PP-112]
Effects of group musical therapy on inpatients with schizophrenia: A preliminary study
Ref. No: 253
Selma Bozkurt Zincir1, Ümit Başar Semiz1, Aynil Yenel1, Emel Başoğlu1, Mustafa Bilici1, Cumhur Tulay2
Erenköy Mental Health Training and Research Hospital, İstanbul, Turkey
1
Science, Culture, and Art Society (BIKSAD)
2
Background: Since ancient times, music has been used as a therapy method and has been considered to have some good effects on
the human body and mental health (1, 2, 5). Music might have beneficial effects on human life such as physiological functions, quality of
life, and psychosocial functioning. There is a wide acceptance about musical therapy practices for various disorders. This generalization
may mean that schizophrenia patients could have some benefits from musical therapy, too (1- 3). There is not enough scientific evidence
emphasizing the efficacy of musical therapy which is applied to severe mental disorders and has recovery potential for some deficits (2, 4).
Objectives: The first aim of this study was to examine the feasibility of music therapy for inpatients with schizophrenia, who need acute
care and also to explore its effects on mental health, general psychosocial functioning, and satisfaction with patient care.
Method: Forty-five patients with schizophrenia were randomly assigned to a study group (n=15) and a control (n=30) group in a ward for female
schizophrenia inpatients. Both groups received medication and standard care for their disorder. Additionally, the study group underwent group
music therapy with classical Turkish music tones for twelve sessions over four weeks. The assessment included measures of psychotic symptoms
using the Positive and Negative Syndrome Scale (PANSS), the Brief Psychiatric Rating Scale (BPRS), and quality of life and subjective satisfaction
with musical experiences. All of the measurement tools were applied before the randomization and weekly until the study was completed.
Results: This study demonstrated that music therapy for schizophrenia inpatients, who need acute care because of psychotic excitation,
is feasible. The comparison of the groups also showed that music therapy has significant advantages on improvement of interpersonal
relationships and general psychosocial functioning.
Conclusions: This study is the first musical group therapy trial with classical Turkish music tones in schizophrenic patients. Musical activity
diminishes negative symptoms, reduces social isolation, and improves patients’ abilities to adapt to the social environment in the community after
discharge from the hospital. Therefore, music therapy may increase the therapeutic alliance of schizophrenic patients in the long term.
Key words: Music therapy, schizophrenia, inpatient, quality of life
References:
1.
Altınölçek H. Türklerde psikiyatrik hastaların rehabilitasyonunda müziğin terapötik etkileri. Popüler Psikiyatri Dergisi 2006; 34: 16- 19.
2.
Talwar N, Crawford MJ, Maratos A, Nur U, McDermott O, Procter S. Music therapy for inpatients with schizophrenia: Exploratory randomised controlled trial. British
Journal of Psychiatry 2006; 189: 405- 409.
3. Ulrich G, Houtmans T, Gold C. The additional therapeutic effect of group music therapy for schizophrenia patients: A randomised study. Acta Psychiatrica
Scandinavica 2007; 116: 362- 370.
4. Hayashi N, Tanabe Y, Nakagawa S,et al. Effects of group musical therapy on inpatients with chronic psychosis: A controlled study. Psychiatry and Clinical
Neurosciences 2002; 56: 187- 193.
5.
Gold C, Heldal TO, Dahle T, Wigram T. Music therapy for schizophrenia or schizophrenia-like illnesses (Review). Cochrane Database of System Reviews. 2005, 2: 1- 20.
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[PP-113]
Clinical correlations of childhood trauma and dissociation in a sample of female
inpatients diagnosed with schizophrenia spectrum disorders and severe
nonpsychotic disorders: the preliminary data
Ref. No: 255
Selma Bozkurt Zincir, Ümit Başar Semiz, Aysun Demir, Yücel Yılmaz, Sevgi Gül Kabak
Erenköy Mental Health Training and Research Hospital, Istanbul, Turkey
Background: There is recent increasing interest in the relationship between early childhood trauma and the risk of developing psychotic
experiences later in life (2,3). Although a large number of studies of psychiatric patients, a majority of whom have a psychotic disorder,
indicate that the prevalence of childhood trauma in this group is high, whether childhood trauma is of etiological importance in psychosis
remains controversial (1, 2, 4).
Objectives: In the present study, we aimed to investigate the possibility of a link between psychotic disorders and childhood traumatic
experiences by comparing trauma exposure in a group of female patients with a diagnosis of psychotic disorders to a group diagnosed
with severe non-psychotic disorders. The secondary purpose of this study was to examine the clinical correlations between trauma
exposure, dissociative phenomena, and psychiatric symptomatology and psychosocial functioning for these two groups.
Methods: Patients with psychotic disorders, mostly schizophrenic (n=54), and with a non-psychotic diagnosis (n=24), were recruited
at the Women’s Clinic of the Istanbul Erenköy Mental Health Hospital. The data were collected through a semi-structured interview for
demographic, psychiatric, and trauma histories. Psychotic symptoms were measured by using the Positive and Negative Symptom Scale
(PANSS). At the main interview, the Childhood Traumatic Questionnaire (CTQ), Dissociative Experiences Scale (DES), Traumatic Experiences
Checklist (TEC), and SCL-90-R were administered to all participants by psychiatrists, who were blind to trauma history.
Results: In this preliminary study, high prevalence rates of childhood traumatic experiences and dissociative phenomenon were found in
a sample of consecutively admitted moderately ill psychotic inpatients. Another finding of the present study was that emotional abuse
during childhood was most strongly correlated with the experience of dissociative symptoms in adult schizophrenia patients. Additionally,
in this group a history of trauma was significantly related to somatization, poor communication skills, and depressive symptoms.
Conclusions: The results of this study are consistent with previous studies raising the possibility that such trauma is of etiological
importance in schizophrenia and other related disorders (4-6).
Key words: Childhood trauma, dissociation, psychosis, schizophrenia
References:
1.
Schafer I, Harfst T, Aderhold V, Briken P, Lehmann M, Moritz S, Read J, Naber D. Childhood trauma and dissociation in female patients with schizophrenia spectrum
disorders an exploratory study. J Nerv Ment Dis 2006; 194: 135- 138.
2.
Spence W, Mulholland C, Lynch G, Mchugh S, Dempster M, Shannon C. Rates of childhood trauma in a sample of patients with schizophrenia as compared with a
sample of patients with non-psychotic diagnosis. Journal of Trauma & Dissociation 2006; 7(3): 7- 22.
3.
Lysaker PH, LaRocco VA. The prevalence and correlates of trauma-related symptoms in schizophrenia spectrum disorder. Comprehensive Psychiatry 2008; 49: 330- 334.
4.
Larkin W, Read J. Childhood trauma and psychosis: Evidence, pathways, and implications. J Postgrad Med 2008; 54(4): 287- 293.
5.
Bendall S, Jackson HJ, Hulbert CA, McGorry PD. Childhood trauma and psychotic disorders: a systematic, critical review of the evidence. Schizophrenia Bulletin 2008; 34(3): 568- 579.
6.
Morgan C, Fisher H. Environmental factors in schizophrenia: childhood trauma- a critical review. Schizophrenia Bulletin 2007; 33(1): 3- 10.
[PP-114]
Comparison of neurocognitive skills between generalized anxiety disorder
and premenstrual dysphoric disorder patients: A controlled study
Ref. No: 256
Selma Bozkurt Zincir, Aynil Yenel, Selvinaz Çınar Parlak, Gülnihal Şimşek, Arzu Bayrak, Dicle Bilge, Ümit Başar Semiz, Mustafa Bilici
Erenköy Mental Health Training and Research Hospital, Istanbul, Turkey
Background: Recently, there has been increased interest in the ability of female reproductive hormones to impact psychoneurological
processes involving the interplay of several body systems. This lends reliability to the view of premenstrual dysphoric disorder (PMDD)
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as a disorder founded in real biochemical disturbances (1,2). Although the effects of the menstrual cycle on emotional state and
cognitive function have been only recently systematically studied, they have long been recognized. Previously published studies yielded
inconsistent data in terms of cognitive tests throughout the cycle phases (1, 3, 4).
Objective: This study aimed to compare the effects of cyclic reproductive hormonal changes on cognitive, emotional, and behavioral function
in childbearing age female patients with generalized anxiety disorder (GAD) and those with premenstrual dysphoric disorder (PMDD).
Method: One of psychiatric samples was a group of PMDD (n = 42), and the other was a group of GAD patients (n = 36), who had 20 and
higher on the Hamilton Anxiety Scale (HAM-A) score. An age matched healthy control group (n = 40) was also included in the study. The
psychiatric rating scales were applied twice according to the menstrual phases. The frontal assessment battery, Stroop test, and Weschler
verbal memory tests were applied for the evaluation of neurocognitive changes with respect to follicular and late luteal phases.
Results: There was a significant increase in dysphoric mood during the luteal phase in women with PMDD compared to their follicular phase
and compared to the GAD women and the control group. Taken together with the repeated measures and the data analysis, the GAD group
had significantly worse performance regarding overall neurocognitive functions in their luteal phase (particularly memory skills, attention,
and psychomotor function) as compared to the PMDD group, whereas the control group had significantly better performance overall.
Conclusions: Even though neurocognitive impairments seen in the women with PMDD were partly due to the dysphoric mood during
the late luteal phase, it seems to be related to the physiological and psychoneurological processes in which female reproductive
hormones may have a central role.
Key words: Neurocognitive functions, premenstrual dysphoric disorder, generalized anxiety disorder, female reproductive hormones
References:
1.
Farage MA, Osborn Thomas W, MacLean AB. Cognitive, sensory, and emotional changes associated with menstrual cycle: a review. Arch Gynecol Obstet. 2008; 278: 299- 307.
2.
Reed SC, Levin FR, Evans SM. Changes in mood, cognitive performance and appetite in the late luteal and follicular phases of the menstrual cycle in women with
and without PMDD (Premenstrual Dysphoric Disorder). Horm Behav. 2008; 54: 185- 193.
3.
Morgan M, Rapkin A. Cognitive flexibility, reaction time, and attention in women with premenstrual dysphoric disorder. J Gend Specif Med. 2002; 5: 28- 36.
4.
Morgan M, Rapkin AJ, D’Elia L, Reading A, Goldman L. Cognitive functioning in premenstrual syndrome. Obstet Gynecol. 1996; 88: 961- 966.
5.
Resnick A, Perry W, Parry B, Mostofi N, Udell C. Neuropsychological performance across the menstrual cycle in women with and without premenstrual dysphoric
disorder. Psychiatry Research 1998; 77:147- 158.
[PP-115]
Evaluation of olfactory function and olfactory bulb volume in major depressive disorder
Ref. No: 259
Meral Akbıyık, Oğuz Karamustafalıoğlu
Şişli Etfal Research and Teaching Hospital, Department of Psychiatry, İstanbul, Turkey
[email protected]
Objective: The purpose of this study was to assess olfactory function and olfactory bulb volume in patients with major depressive
disorder (MDD) in comparison to normal subjects.
Method: Twenty treatment-free premenopausal, 25-45 year-old women diagnosed with long-term, severe MDD at the Şişli Etfal Research
and Teaching Hospital psychiatric outpatient clinics and 20 healthy women matched by age, education, smoking behavior, and frequency
of upper respiratory tract infection participated in this study.
Odor threshold, discrimination, and identification functions were assessed by Sniffin’ sticks. Olfactory bulb volumes were calculated by
manual segmentation of acquired T2-weighted coronal slices according to a standardized protocol.
Results: When OB volumes of patients and controls were analyzed with a two-way Analysis of Covariance, with age and education as the
covariate and group as a factor, the patients had significantly larger OBs than the controls (right p=0.011; left p<0.001; largest p=0.008).
Education has a significant effect as a covariate in the OB volume X group analysis. Significant correlations between OB volumes in relation to olfactory
function were observed in the control group; however, there was no correlation between OB volume and olfactory functions in the patient group.
Conclusion: Our results showed that OB volume gets larger in long-term MDD. According to our study and former knowledge it is
possible that during MDD, the hippocampus, amygdala, and OB differ in terms of activity and volume to compensate for each other and
stabilize the patient’s mood.
Key words: Depression, neurogenesis, olfaction, volumetry
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[PP-116]
Fluoxetine induced hypomanic shift in a bulimic patient: A case report
Ref. No: 261
Mustafa Özten, Atila Erol
Department of Psychiatry, Sakarya University, Faculty of Medicine, Sakarya, Turkey
In the psychopharmacological treatment of bulimia nervosa (BN), antidepressants have a positive effect on mood and reduce the related
preoccupation with body weight and the number of binge eating episodes. Research with antidepressants such as imipramine, desipramine,
trazodone, phenelzine, amitriptyline and mianserin has been conducted to investigate their efficacy in the treatment of bulimia. A higher dose
of the fluoxetine (60 mg/day) was shown to be effective in BN and has received FDA approval. Comorbidity of eating disorders with mood,
anxiety, and substance use disorders is common. The presence of additional psychiatric disorders impairs compliance with treatment and makes
treatment difficult by increasing severity and chronicity. The treatment of bulimia nervosa with fluoxetine is adversely affected by the presence
of a mood disorder. High dose fluoxetine should be used for BN to be effective, but these high doses may increase the risk of a manic shift.
When using fluoxetine in patients with a history of bipolar mood disorder (BiPMD) or a positive family history of BiPMD, clinicians need to be
careful because of the possibility of a manic shift. There is not any developed algorithm for psychopharmacological treatment with comorbidity
of BiPMD and BN; generally the use of agents that have a positive effect on both disorders is recommended, although such a medication is not
available. Negative effects on weight gain or other negative interactions of mood stabilizers in BN, makes it difficult to use them. Like other
antidepressants SSRIs may also cause a manic shift. The use of antidepressant doses of fluoxetine for mood and anxiety disorders are known to
carry a risk for a manic or hypomanic shift. Hence, detailed examination of cases, where there is history of mood disorder or family history of mood
disorder, is recommended. Using high dose fluoxetine in BN also increases the possibility of manic or hypomanic shifts. The use of fluoxetine 60
mg in a patient with BN caused a hypomanic shift, even though there was no history of bipolar disorder or a positive family history. A review of
the treatment demonstrated that 60 mg of fluoxetine did not result in a significant decrease in symptoms and adequate treatment response.
Retrospectively inadequate response to the treatment was associated with the presence of comorbid BiPMD.
Key words: Bulimia nervosa, fluoxetine, hypomania, mania
[PP-117]
Schizophrenia and Mega Cisterna Magna: A case report
Ref. No: 262
Semra Karayılan, Atila Erol
Department of Psychiatry, Sakarya University Faculty of Medicine, Sakarya, Turkey
The cerebellum, which is known in general as an organ to control coordination, balance, and fine motor movements, has been demonstrated
to have an important role in cognitive functions by using anatomical and functional imaging methods. The anomaly of mega cisterna magna
is one of the various lesions of the posterior fossa which can influence cerebellar functions like cerebellar hypoplasia/agenesis, vermis
hypoplasia/agenesis, Dandy-Walker malformation or variant, persistent Blake’s pouch, arachnoid cyst, Joubert syndrome, and tumors of the
posterior fossa. Mega cisterna magna (MCM) is a developmental malformation of the posterior fossa, where morphologically the vermis and
cerebellar hemispheres are intact. Associated structural brain anomalies are common with mega cisterna magna and especially, MCM may
be a component of the Dandy-Walker variant (with cerebellum hypoplasia) or Dandy-Walker syndrome (with cerebellum agenesia). Our
knowledge about the relationship between this anomaly and psychiatric disorders is limited to very few case reports available. In this article,
we report a case of schizophrenia associated with mega cisterna magna. A 35-year-old married patient (house wife, graduated from primary
school) was brought to our clinic by her relatives with complaints of disorganized and inappropriate speech, strange behavior, and fear of
people. She had auditory and visual hallucinations and delusions of reference and persecution. Up to five months ago she had no psychiatric
or neurological symptoms or history. Her symptoms began with social isolation, decrease of self-care, and positive psychotic symptoms.
Neurological examination and EEG examination were normal, but mega cisterna magna was discovered in her cranial magnetic resonance
imaging scan. The patient was treated with risperidone 6mg/day for four weeks and was discharged after remission of psychotic symptoms.
The prevalence and prognostic significance of MCM has not been defined completely yet. Memory and verbal fluency were found to be lower
in cases of mega cisterna magna than in controls. Schizophrenic patients are known to have problems of memory and verbal fluency, too.
The role of the cerebellum in schizophrenia has been highlighted by Andreasen’s hypothesis of ‘cognitive dysmetria’. This hypothesis suggests
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that the cerebellum has a role in the general dyscoordination of sensorimotor and mental processes which are seen in schizophrenic patients.
The following observations demonstrating the involvement of the cerebellum are determined in studies of schizophrenic patients: high
prevalence of neurological soft signs, dyscoordination, abnormal posture, balance problems, impaired eye blink conditioning and impaired
adaptation of the vestibular-ocular reflex. Abnormal cerebellar activations have been showed in functional imaging studies. In the context of
this case, the relationship of schizophrenia with cerebellar anomalies was reviewed.
Key words: Schizophrenia, mega cisterna magna, cerebellum, brain imaging methods
[PP-118]
Congenital hypogonadism and comorbid anorexia nervosa in a male patient:
A case report
Ref. No: 263
Mustafa Özten, Atila Erol
Department of Psychiatry, Sakarya University, Sakarya, Turkey
Male hypogonadism results from a failure of the testes to produce adequate androgen. Patients have low circulating testesterone in
combination with clinical symptoms such as osteopenia, increased adiposity, decreased muscle mass, decline in energy and stamina,
decreased cognitive function, decreased libido and erectile dysfunction. The cause may be primary (genetic anomaly) or secondary (defect in
hypothalamus or pituitary), but often presents with the same symptomatology. Hypogonadal patients who are both symptomatic and who
have clinically significant alterations in laboratory values are candidates for treatment. Testosterone replacement therapy is widely applied.
The prevalence of eating disorders in men as compared to women is less than ten times and also shows differences in the course of the
disease and the causes of its appearance. Social, genetic, psychological factors, personality traits and a history of trauma are considered to
play a role in the development of anorexia nervosa (AN). In addition, steroid hormones affect the development of eating disorders and eating
behavior. Homosexuality, asexuality and sexual role disorders are known to be more common in male patients with AN. AN is associated
with notable medical complications and affects many systems like a general medical disease. One of the systems that is affected by AN is
the genitourinary system; hypogonadism is one of the known complications of AN. Endocrine abnormalities such as hypogonadotropic
hypogonadism mediate some of the clinical manifestations. Most of the endocrine changes that occur in AN are physiological adaptations
to starvation and are usually reversible with weight gain. Prolonged AN or cachexia can cause hypogonadism. In this article we report a
man, who had suffered from hypogonadism since infancy with no treatment and developed AN at age 18. Congenital hypogonadism with
comorbid AN is a rare illness. As a result of the interaction of hypogonadism with anorexia nervosa the patient developed a sexual identity
crisis, which is important in its clinical and theoretical aspects, since he suffered from delayed puberty, no secondary sexual characteristics,
and no ejaculation or erection although he was 22 years old. Up to now only one case from Japan is reported in the literature with congenital
hypogonadism and anorexia nervosa. Hypogonadism with comorbid anorexia nervosa has not been listed as a case in the Turkish indices yet.
Key words: Anorexia nervosa, congenital hypogonadism, male patient
[PP-119]
Review of diagnosis and treatment of pregnant psychiatric patients in a state hospital
Ref. No: 275
Kader Semra Karataş, Jülide Güler, Aytül Hariri
Erenkoy Mental and Nervous Diseases Training and Research Hospital, Department of Psychiatry, İstanbul, Turkey
Background: Because of the physiological changes during pregnancy there are changes of pharmacokinetic and pharmacodynamic
characteristics, and there are differences in the treatment of psychiatric disorders in this period.
Objective: The aim of this study was to evaluate the sociodemographical features, diagnoses, and treatments of 20 pregnant psychiatric
inpatients that were hospitalized between August 2010 and August 2011.
Method: The sociodemographical features, diagnoses, and treatments of the patients were evaluated retrospectively.
Results: The percentages of diagnoses of the patients were as follows: schizophrenia 27.3%, bipolar affective disorder manic episode
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22.7%, bipolar affective disorder depressive episode 9.1%, unipolar depression 27.4%, and obsessive compulsive disorder, dissociative
disorder, and schizoaffective disorder, each 4.5%. When the treatments of the patients were evaluated according to their diagnosis
we found that 13.6% of schizophrenia patients were treated with ECT, 9.09% with haloperidol and 4.5% with atypical antipsychotics;
the patients with bipolar depression were treated with mood stabilizers and ECT plus mood stabilizers at the same rate of 4.5%; 18.1%
of the patients with mania were treated with ECT plus haloperidol; and of the unipolar depressed patients 13.6% were treated with
psychotherapy and 9.09% with ECT and haloperidol.
Conclusion: ECT was used commonly as a treatment option in our patient group. ECT treatment was added onto haloperidol treatment
in severe cases. This treatment is consistent with the recommendations of the APA and with those in the literature.
Key words: Pregnancy, mental illness, treatment, ECT, antipsychotic drugs
[PP-120]
Peripheral edema associated with mirtazapine: Presentation of a case
Ref. No: 278
Birmay Çam1, Hüseyin Kurt2
Gönen Devlet Hastanesi Psikiyatri Kliniği, Gönen, Balıkesir, Turkey
1
Gönen Devlet Hastanesi İç Hastalıkları Kliniği, Gönen, Balıkesir, Turkey
2
In the medical literature, occurrence of edema during treatment with mirtazapine is stated as the least frequently reported side effect. A
case of edema occurring during mirtazapine treatment is reported below.
Case: A 34 year-old female patient was admitted to the psychiatric ward with a diagnosis of recurrent depressive disorder. There were no specific
findings in the patient’s medical history other than high blood pressure and irregularly administered antihypertensive drugs. There was no use
of alcohol or illicit drugs. The treatment regimen of the patient included escitalopram 5 mg daily, alprazolam 0.5 mg daily, and hydroxyzine 12.5
mg daily. Mirtazapine 15 mg daily was added to the medical treatment, as the depression and insomnia continued. The day after beginning
the treatment with mirtazapine pretibial edema developed. The CBC, ALT, AST, GGT, ALP, bilirubin, albumin, urea, creatinine, Na, K, Cl, Ca, urine
analysis, thyroid function tests and chest X-ray were repeated and all were within normal limits, as before. Cardiac insufficiency, cirrhosis, nephrotic
syndrome, and venous insufficiency, all of which can cause edema, were ruled out by the internal medicine consult. The patient was not in the
premenstrual period and not pregnant. It was also reported that such a side effect was observed during the administration of escitalopram to the
patient. The edema was assessed as being due to mirtazapine. The edema decreased three days after the cessation of the mirtazapine treatment
and the administration of furosemide 40 mg/day at the recommendation of internal medicine. It disappeared ten days later. Escitalopram 10
mg daily and hydroxyzine 25 mg daily were continued. The patient, whose depressive symptoms decreased and anxiety disappeared, has
continued to be followed up as an outpatient after discharge. The patient’s depressive symptoms did not recur and her blood pressure remained
within normal limits although she did not receive any antihypertensive treatment. She had no edema at her two month follow up visit. Her CBC,
electrolytes, biochemical and thyroid function tests, and urine analysis all remained within normal limits.
Discussion: In our case, the occurrence of edema simultaneously with the administration of mirtazapine, the exclusion of systemic
diseases that can cause edema, the lack of continuation or recurrence of the edema even as the patient remained on escitalopram
between the previous and the current depressive episodes, and finally the disappearance of the edema right after the cessation of
mirtazapine treatment made us to think that the edema was caused by mirtazapine. In the medical literature, it is reported that MAOIs,
escitalopram, and sertraline can cause edema. Kutscher et al. reported that peripheral edema occurred in a male patient of 60 years of age
after the use of mirtazapine and disappeared right after the cessation of mirtazapine treatment (1,2,3,4). More detailed studies should be
conducted to explore and understand this issue better.
Key words: Edema, mirtazapine
References:
1.
Remick RA,Froeze C,Keller FD(1989)Common side effects associated with monoamine oxidase inhibitors.Prog Neuropsychopharmacol Biol Psychiatry 13:497-504.
2.
Masdrakis VG,Oulis P,Kouzoupis AV,Masdrakis GV,Soldatos CR(2009)Bilateral ankle oedema in a patient taking escitalopram.World J Biol Psychiatry 10:939-41.
3. Dadic-Hero E,Ružic K,Grahovac T,Graovac M,Palijan TZ,Sepic-Grahovac D(2011) Allergic reactions--outcome of sertraline and escitalopram treatments.Psychiatr
Danub. Mar;23(1):120-2.
4.
Kutscher EC,Lund BC,Hartman BA(2001)Peripheral edema associated with mirtazapine. Ann Pharmacother.35(11):1494-5.
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[PP-121]
Abuse of tianeptine: A case report
Ref. No: 280
Hüsameddin Özer, Atilla Erol
Sakarya Teaching and Research Hospital, Psychiatry Clinic, Sakarya, Turkey
Tianeptine is an atypical antidepressant, which modestly enhances the mezolimbic release of dopamine. Tianeptine is an antidepressant
that is accepted as not being abused by patients. However, there have been some case reports regarding abuse and/or addiction to it.
The abuse of tianeptine is rare and so far has only been reported in patients with pre-existing multi substance abuse disorders. A total of
141 cases of abuse were reported between 1989 and 2004. The patients usually sought and experienced a psychostimulant effect. The
stimulant effect of tianeptine has been specifically emphasized in some case reports of tianeptine abuse in the literature.
In this poster, a twenty year-old female patient, who received tianeptine treatment for depression and developed tianeptine dependence
is presented. In our case, the patient was taking sixty pills daily. Although she took sixty pills, her biological tolerance was excellent and
hepatic and hematological parameters were not affected, similar to the findings of other reports in the literature.
This case emphasizes that while prescribing tianeptine treatment clinicians should be careful using it in patients with substance abuse
problems, as reported by other case reports in the literature.
Key words: Tianeptine abuse, tianeptine dependence
[PP-122]
GWAS with AHP based SNP prioritization approach to identify SNP biomarkers
for Alzheimer’s disease
Ref. No: 282
Onat Kadıoğlu1, Gürkan Üstünkar2, Yeşim Aydın Son3
Middle East Technical University, Bioinformatics Graduate Program Ankara, Turkey
1
Middle East Technical University, Informatics Institute Department of Information Science, Ankara, Turkey
2
Middle East Technical University, Informatics Institute Department of Health Informatics, Ankara, Turkey
3
Genome wide association studies (GWAS) is defined as search for biological variance associated with certain phenotypes and diseases
among individuals in a population depending on statistical analysis. Combined p-value approach has been introduced recently and
is defined as the second-wave GWAS. It helps mapping of significant SNPs to genes and pathways to evaluate SNP-gene-disease
associations. Identification of enriched genes and pathways significantly associated with diseases can be performed via this approach.
The major bottleneck of current standard GWAS approaches is the prioritization of statistically significant results. Our group has recently
developed a novel Analytical Hierarchical Process (AHP) based on a structured SNP prioritization algorithm. SNPs are scored according
to their biological relevance in terms of their genomic location and functional consequence, evolutionary conservation, and genedisease association. The recently developed METU-SNP application integrates GWAS, combined p-value while utilizing AHP based SNP
prioritization algorithms. Combined p-value and AHP prioritization approach for GWAS of Alzheimer’s Disease (AD) has been utilized for
the SNP-disease association of AD for the first the time in this study with METU-SNP software.
The results from the analysis of two different sets of AD genotyping data with the newly proposed AHP based prioritization yield promising
results for both datasets. For the ADNI data, all the top 100 SNPs according to AHP scoring map to OMIM associated genes and 18 of
them map to AD linked genes. For the GenADA data, all the top 100 SNPs according to AHP scoring map to OMIM associated genes and
37 of them map to AD linked genes. Glycolysis and gluconeogenesis, leukocyte migration, axon guidance, actin filament polymerization,
cell adhesion, DNA fragmentation during apoptosis, fatty acid metabolism, and negative regulation of cell proliferation are common
pathways residing at top 100 pathways according to combined p-value for pathways that are observed in GWAS results of both data sets.
GWAS of both data with METU-SNP confirms the literature for AD associated genes; A2M, ABCA1, ACE, APOA1, APP, CHRNA7, IL1A,
LDLR, LPL, MPO, PTGS2, SORL1. rs3781835 at SORL1, rs4343, and rs4351 at ACE1 are SNPs with high AHP scores are also listed to be AD
associated at PharmGKB database. Moreover, CT and TT genotype of rs6313 at HTR2A gene indicates resistance to the treatment with
antipsychotic drugs for AD patients presenting delusional symptoms. As presented here METU-SNP is a powerful tool with a novel AHP
based prioritization algorithm implemented, which can lead to discovery of new associations at SNP, gene, and pathway level. In near
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future, we expect that these new associations described through GWAS here and in other studies will lead to development of personalized
medicine approaches with application in pharmacogenomics and psychopharmacology.
Key words: AHP, Alzheimer’s disease, biomarker, GWAS, personalized medicine, pharmacogenomics, SNP prioritization
[PP-123]
Ref. No: 287
A case report of a relapse in a major depression patient with valsartan/hydrochlorothiazide
Alev Büyükkınacı, Devrim Öztürk Can, Gökçe Silsüpür
Boylam Psychiatry Hospital, Ankara, Turkey
It is known that some drugs can cause depression. In particular, there is evidence that barbiturates, vigabatrine, topiramate, flunarizine,
corticosteroids, mefloquine, efavirenz, and interferon alpha have been shown to cause depression (1). Angiotensin II is a strong
vasopressor with various physiological effects especially regulating blood pressure. It regulates water retention and aldosterone secretion.
Angiotensin II has two known receptors, AT1 and AT2. Valsartan is a non-selective angiotensin AT selective blocker, which prevents
angiotensin binding to AT2 receptors and controls hypertension in this way (2). It has been shown that angiotensin converting enzyme
polymorphism is related to relapse in major depression patients after partial sleep deprivation and this was related to its effect on the
dopaminergic system (3). This finding shows that drugs targeting the angiotensin system may effect depression. Here we present a case
with recurrent depression who was in remission and relapsed after she was given an antihypertensive medication containing valsartan
and hydrochlorothiazide. She was a 56 year old single woman, living alone. She had a depressive episode in 1983 for the first time and had
other episodes in 1997, 2001, and the last one in 2003. After having used venlafaxine and paroxetine, she was given citalopram in 2003 at
40 mg/day, which she has been using until now. She did not have any depressive attacks after 2003. She was given an antihypertensive
containing valsartan and hydrochlorothiazide 3 months before she presented to our clinic. After taking the medication she had reluctance,
despondency, intense feelings of guilt with statements like “she will not be even accepted to hell.” There were no stressors that the patient
or her relatives defined. The patient was admitted to our clinic after her symptoms increased the month prior to her admission. Since there
were published articles on depression triggered by valsartan and similar antihypertensives and since the patient’s symptoms started after
taking the medication, we continued on her drug regimen with citalopram 40 mg/day and changed her antihypertensive medication to
a calcium channel blocker, amlodipine. After 2 weeks her symptoms started to decrease. We concluded that her depression was triggered
by valsartan. This case is important for showing that medications affecting the angiotensin system can trigger depression and there is a
need to study the role of the angiotensin system in the etiology of depression.
Key words: Valsartan, antihypertensives, depression, relapse
References:
1. Celano CM, Freudenreich O, Fernandez-Robles C, Stern TA, Caro MA, Huffman JC. Depressogenic effects of medications: a review.Dialogues Clin Neurosci.
2011;13(1):109-25.
2.
Black HR, Bailey J, Zappe D, Samuel R.Valsartan: more than a decade of experience. Drugs. 2009;69(17):2393-414.
[PP-124]
Monosymptomatic hypochondriacal psychosis: A case report
Ref. No: 158
Yasemin Şimşek, Gökçe Elif Sarıdoğan, Ebru Şahan, Melike Nebioğlu, Cem Cerit, Mecit Çalışkan
Haydarpaşa Numune Hastanesi Psikiyatri Kliniği, İstanbul, Turkey
Introduction: The somatic type of delusional disorder is also recognized as monosymptomatic hypochondriacal psychosis. According
to the DSM-IV, the disorder is characterized by the presence of a somatic delusion in which the person has a false belief of having some
physical defect or a general medical condition (1). The most substantial characteristic of the aforementioned disorder is the demand of
the patient attributing the symptoms to a serious physical illness, and seeking medical advice continuously in an effort to find transient
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relief by being informed of the absence of a disease (2).
Case Presentation: A 26- year old, female patient was admitted to an outpatient psychiatric clinic with complaints of having a possible ocular
disease, which may cause blindness. Her symptoms included her irises deviating involuntarily, her eyes moving incoherently, and having a
feeling in her eyes as if they are being drawn away. A previous psychiatric admission of the patient was reported to be 3 years ago with the
complaints of dysmorphism and tremor in her hands and having a serious disorder relevant to her hands for which she was seen by several
specialists although she wasn’t convinced by their answers. Although, thereafter she was hospitalized and was treated with several mood
stabilizers and antipsychotic medications for the following three years in outpatient clinics, a full remission could not be achieved.
She was hospitalized again. Her physical and neurological examination didn’t reveal any biological anomalies. It was noticed that she was
touching her eyes constantly and her speech was focused on her bodily sensations so that she couldn’t maintain her attention on any
other topic. In the contents of her thoughts, she had somatic delusions as defined above. She was treated with pimozide, started with 2mg
and increased up to a dose of 6 mg/day gradually. Her condition was observed to improve with a decrease in intensity of her symptoms,
increased interest, improved self-care, decrease in the amount of her speech and becoming more functional.
Discussion: Because there was no increase in psychomotor activity and the content of speech was solely about the sensations in her eyes,
we did not diagnose her with an affective disorder. We arrived at the diagnosis of monosymptomatic hypochondriacal psychosis after
evaluating the cues such as the worry about having an eye disease, not being persuaded with the medical examinations and diagnosis,
lack of any other psychotic symptoms, delusions being only about bodily sensations, several admissions to non-psychiatric physicians,
and her resistance to treatment with multiple drugs. In the literature there are cases reporting surgery, which was not required, such as an
operation to treat a patient stating that he had a lumbar nerve root compression (3). In the present case the patient presented to internal
medicine and ophthalmology clinics at the beginning insisting that she needed an eye operation. In a study on 23 patients it has been
reported that these cases have responded well to pimozide (4).
[PP-125]
Amisulpride in the treatment of treatment resistant tic disorder: A case report
Ref. No: 288
Onat Yılmaz, Mehmet Alpay Ateş, Gülşah Meral, Cengiz Başoğlu, Ayhan Algül, Servet Ebrinç, Mesut Çetin
GATA Haydarpasa Training Hospital, Department of Psychiatry, Uskudar, Istanbul, Turkey
Introduction: Tics are sudden, recurrent, involuntary motor movements or vocalizations caused by involuntary contractions of motor
or vocal muscles. Typically these disorders are characterized by early childhood onset and are more common in the male population.
Genetic, neurobiological, neurochemical and environmental factors play a role in the pathogenesis, and malfunctioning of the basal
ganglia is thought to be responsible for the disease. The presence of abnormalities in the EEG of some patients, worsening of the tics with
administration of dopamine agonists, and improvement of tics with antidopaminergic agents are some of the known biological evidence.
Amisulpride, with a pure antidopaminergic activity, and thus being used effectively in the treatment of Tourette’s syndrome, makes it a
candidate to treat other tic disorders, as well. In this report, an adult patient diagnosed with “Tic Disorder Not Otherwise Specified,” who
was previously treated with several antidepressant and antipsychotic drugs, is cured with amisulpride.
Case presentation: A 21-year-old single male patient was admitted to the hospital complaining of impairment in interpersonal relations,
difficulties in social adaptation due to the involuntary repetition of certain movements. His complaints had started at the age of nine after
his uncles were killed. Though the patient was tried on different treatment regimens, but he had no benefits. Because of his tics, he hardly
finished his primary school education and was not able to work for a long time.
In history there were no perinatal or neonatal complications and he was born by spontaneous vaginal birth. As the sixth of eleven children,
his developmental history was normal. There was no family history of any mental illness, epilepsy, alcoholism, or movement disorder.
On his admission to the unit, he was given amisulpride 200mg/day and the dosage was increased to 400mg/day in three days. He had a
score of 15 in motor tics on admission and he had a score of 3 for motor score (80% decrease) at the third week of the treatment. No side
effects were observed and he was discharged at the end of the third week. All of the signs were in remission on the follow up after two
months.
Discussion: Contrary to the antipsychotics effecting both D1 and D2 receptors in the nigrostriatal pathway, antipsychotics of the
benzamide group, which work as selective D2 receptor antagonists, are effective in the treatment of tic disorders. As the most preferred
drug in this group, amisulpride causes less extrapyramidal side effects by selectively acting on the limbic regions rather than striatal
regions. In the literature, there are case reports of amisulpride’s effective use in tic disorders.
Clinicians should keep in mind that, with less side effect risk compared to conventional antipsychotics and the benefits of its mechanism
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of action, amisulpride might be the drug of choice in tic disorders. On the other hand, larger controlled clinical trials should be planned
on this issue.
Key words: Tic disorders, echopraxia, amisulpride, side effect
References:
1.
Turan M, Çilli AS. Tik bozuklukları. Genel Tıp Derg. 1999;9(3):117-21
2.
Fountoulakis KN, Lacovides A, Kaprinis GS. Successful treatment of Tourette’s disorder with amisulpride, Ann Pharmacother. 2004; 3: 901.
3.
Leysen JE, Janssen PMF, Heylen L, Gommeren W, Van Gompel P, Lesage As.Receptor interactions of new antipsychotics: relation to pharmacodynamic and clinical
effects. Int J Psychiatry Clin Pract; 1998; 2(Suppl.1): 3-17.
4.
Ates MA, Algül A, Semiz UB, Güneş C, Çetin M. Tedaviye dirençli Gilles de la Tourette sendromunda amisülpirid kullanımı: Bir olgu sunumu. Yeni Sempozyum Dergisi.
2009; 47:1: 16-18.
[PP-126]
Evaluation of patients with obstructive sleep apnea syndrome referred to the sleep
disorders unit of a university hospital
Ref. No: 290
Evrim Özkorumak1, Haluk Hıdıroğlu2, Ahmet Tiryaki1, İsmail Ak1
Karadeniz Technical University, Psychiatry Department, Trabzon, Turkey
1
Ataköy State Mental Health Hospital, Trabzon, Turkey
2
Introduction: Obstructive sleep apnea syndrome (OSAS) is characterized by repetitive episodes of apnea and hypopnea, and decrease in
oxygen saturation (1). The relationship of OSAS and other medical conditions has been explored in the research literature while the relationship
between OSAS and mental health has not been sufficiently investigated yet. The aim of this study was to determine the distribution of mental
disorders and the type of distribution of mental disorders within clinical features of OSAS from the point of view of psychiatry.
Method: The patients, who were referred to the sleep disorders unit of Karadeniz Technical University, Faculty of Medicine Hospital for
1 year were considered the population for this study. A total of 102 patients, with a diagnosis of OSAS according to polysomnography
and patients with no exclusion criteria composed the sample of the study. The patients were classified according to the ICSD-2 (The
International Classification of Sleep Disorders) with polysomnography. Sociodemographical and clinical features of the patients were
recorded. The Montgomery Asberg Depression Rating Scale, the Beck Depression Inventory and the Epworth Sleepiness Scale were
administered. Psychiatric diagnoses were made by interviews based on the DSM-IV Axis I Disorders (SCID-I).
Results: According to the ICDSD-2, 19.6% (n=20) of the patients had a mild, 29.4% (n=30) had a moderate and 51,0% (n=52) had a severe
form of OSAS. The distribution of sex, marital status, and occupation are shown in Table I. The means of weight and height of the whole
sample were 91.15±16.78kg and 168.23±8.76cm, respectively. Fifty-seven point nine percent of the patients (n=59) had had a psychiatric
referral previously, 42.2% of them (n=43) did not. According to the body mass index (BMI), 5.9% of patients (n=6) were within normal
limits, 30.4% were (n=31) overweight, 54.9% were obese (n=59) and 8.8% were morbidly obese (n=9). The Epworth Sleepiness Scale total
score was significantly higher in severe OSAS patients (p=0.002). The relationship of mild and moderate OSAS with BMI was significant
(p=0.010). The median age of severe OSAS patients was significantly higher than mild OSAS patients (p=0.0529).
Thirty-one point four percent (n=32) of patients had 1 diagnosis according to the SCID-I, 22.5% (n=23) had more than one diagnosis, and
46.1% (n=47) did not have any diagnosis. The total scores of the BDI and the MADRS were 5.49±9.05 and 5.82±9.40, respectively.
Discussion: There are many risk factors for OSAS. Male predominance is present for adult OSAS patients. The number of male patients was
higher than female patients in this study. One of the most important risk factor is obesity (2). Most of the patients were obese or morbidly
obese in our group. The detected depression rate was correlated with many studies which reported higher depression rates in OSAS (2-5).
In this study the rate of anxiety disorders was higher than in the healthy population while being similar or lower than the rate estimated
in previous studies with OSAS patients.
Conclusion: Mental disorders associated with medical diseases are important clinical syndromes effecting morbidity and mortality.
Recognizing the symptoms and signs of OSAS is important. Regarding this issue, further studies with larger samples comparing different
subgroups are needed.
Key words: Obstructive sleep apnea, mental diseases
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[PP-127]
Clozapine use in idiopathic tardive dystonia and paranoid schizophrenia comorbidity:
A case report
Ref. No: 286
Mustafa Güleç, Elif Oral, Esat Fahri Aydın
Department of Psychiatry, Medical Faculty, University of Atatürk, Erzurum, Turkey
Objective: To present brief idea about a suitable and safe antipsychotic usage in patient with schizophrenia and tardive dystonia.
Method: Results will be discussed.
Results:
Case: A 42-year-old woman with diagnose of first episode and drug naïve schizophrenia presented with involuntary movements in her
orobuccal region, including tongue and lips. At first administration, routine biochemical and hematological assessments were normal, and
patient had positive and negative features of schizophrenia. According to the information received her relatives, although she has not taken
any antipsychotic medication, her involuntary movements has been risen 18 month earlier her antipsychotic treatment. These movements
were consulted with neurology clinic. Her brain MRI, EEG, and further assessments including detailed neurological examination, jaw MRI was
normal, and specialist of neurology suggested that the clozapine usage may be helpful because of the possible idiopathic tardive dystonia.
Clozapine medication was started with gradually, although there was not enough proof about prior antipsychotic usage and anatomical
or functional deficit. During her hospitalization, all of the involuntary movements were recovered with 200 mg/day clozapine, and more
than 35% percent decrease was observed at her positive (SAPS) and negative (SANS) scale assessments with 600 mg /day clozapine. In this
period, there was no side effect except moderate sialorrhea. Etiology of the idiopathic tardive dystonia is still remaining unclear, and data
for treatments is receiving from the case reports. There is some evidence about efficacy of clozapine treatment (1,2). In addition, there is a
consensus about that clozapine can cause extrapyramidal side effects rarely and effective treatment option for schizophrenia as well (3). On
the other hand, tendency of the general psychiatry practice would prefer to this molecule in the resistant schizophrenia which is describe as
show no remission despite of two different kinds of antipsychotic usage for minimum six weeks (4). In this case, clozapine usage in the first
line seems to be necessary because of the idiopathic tardive dystonia. It may be clarified with further studies whether this case was remitted
incidentally or this remission was related with antagonistic effects of clozapine on the receptors of D1.
Conclusion: Clozapine may be a first line treatment option for the drug naïve patients with first episode schizophrenia and tardive
dystonia. However, we need further studies performed with wide case series to achieve this kind of opinion.
Key words: Tardive dystonia, neurological, schizophrenia, clozapine, safety, efficacy
References:
1.
Kwan Y, Sim K. Resolution of tardive dystonia in a patient with bipolar disorder treated with clozapine: a case report. Prog Neuropsychopharmacol Biol Psychiatry
2010; 34(1):238-239.
2.
Aukst-Margetic B, Margetic B. Treatment of generalized tardive dystonia with clozapine. Psychiatr Danub 2008; 20(3):329-331.
3.
Asenjo Lobos C, Komossa K, Rummel-Kluge C, Hunger H, Schmid F, Schwarz S, et al. Clozapine versus other atypical antipsychotics for schizophrenia. Cochrane
Database Syst Rev 2010; (11):CD006633.
4.
Kane J, Honigfeld G, Singer J, Meltzer H. Clozapine for the treatment-resistant schizophrenic. A double-blind comparison with chlorpromazine. Arch Gen Psychiatry
1988; 45(9):789-796.
[PP-128]
The clinical use of Buprenorphine-Naloxone in the opioid-dependent patient
with Hepatitis C
Ref. No: 306
Tuğba Kara, Arzu Çiftçi
Bakirkoy Research and Training Hospital for Psychiatry and Neurology, Istanbul
Introduction: Guidelines for the treatment of opioid dependence which developed by organizations such as American Society
of Interventional Pain Physicians (ASIPP) and the American Psychiatric Association (APA) recommend extensive treatment with
S201
pharmacological treatments such as methadone, buprenorphine, buprenorfine-naloxone as well as psychosocial therapy. BuprenorphineNaloxone therapy is being used effectively as an alternative treatment to entering patients into a methadone outpatient clinics (1). The
clinical relevant effect of buprenorphine depends on m-opioid receptor agonism (2).
Case: 16-years-old male patient with opioid dependence diagnosed according to DSM-IV criteria entered CEMATEM ( Child and
Adolescent Alchol and Substance Treatment Centre ) clinic for out-patients in Bakirkoy Research and Training Hospital for Psychiatry and
Neurology and a week later the patient has been hospitalized. Liver enzyme levels were normal and opiat value was found as positive in
sub-threshold in routine controls and after 6- 8 hours Buprenorfin-Naloksan combination (Suboxone) treatment was received the patient
experienced withdrawal symptoms.In patient’s routine blood tests, hepatitis C virus (HCV) was determined and the patient developed
significiantly elevated liver enzyme levels during buprenorphine-naloxone treatment.
Conclusions: Although Buprenorphine has been used clinically in the early 1970s, it’s metobolism has not been fully unterstood already
(3). Buprenorphine was mainly metobolized by N-dealkylation and glucuronidation of buprenorphine and norbuprenorphine by CYTP450
isoforms in liver ( 4). For non-hepatitis subjects, buprenorphine treatment showed no evidence of altered liver enzyme levels.
In contrast, AST and ALT levels increased significantly with buprenorphine treatment among patients with a history of hepatitis (5).
Liver enzym values significiantly elevated in this case with hepatitis C received Buprenorphine-Naloxone combination treatment.
[PP-129]
The use of z hypnotics in the management of insomnia in forensic psychiatric
units in Oxford, England
Ref. No: 105
Hasanen Ali Altaiar
Oxford Health NHS Trust, Littlemore Hospital, Oxford, ox4 4xn, UK
Objectives: Insomnia has an estimated prevalence of 30% in general population and its prevalence is higher among psychiatric patients. In 1987 a
survey showed around half of psychiatric patients received a hypnotic medication. Also people with mental health problems have an increased risk of
developing dependence on hypnotics. “Z-drugs” are benzodiazepine like medications and are used as primary pharmacological treatment for insomnia.
They include zolpidem, zaleplon, and zopiclone. Zopiclone is not available in the US, although its active stereoisomer, eszopiclone is available. NICE
guidelines recommend trying non-pharmacological interventions such as sleep hygiene prior to considering “z drugs.” The symptoms, findings of
evaluation, and the reasoning behind prescribing “z drugs” should be documented in medical and nursing notes. The maximum duration should not be
longer than 2 weeks when “z drugs” were used.
The aims of this study included: To review if ‘z-drugs’ were prescribed according to the NICE guidelines, whether “insomnia” was documented in patient
charts or not, if other measures were tried before prescribing a “z drug,” and if the reason for switch was documented, in case of switching from one “z
drug” to another.
Methods: We reviewed all the progress notes and medication charts for a 6-month duration between January 1-June 30, 2010 for all of the inpatients (n=
74) in the 6 forensic wards at the Littlemore Hospital. We identified the patients, who were prescribed “z drugs” for insomnia, and reviewed their records.
Results: We found out that only 3 patients were prescribed “z drugs,” which was zopiclone 7.5mg/day for all of three cases. All orders were for as needed
basis use. Insomnia was recorded in medication charts, but not in the notes section. Non-pharmacological measures were tried in only one of the patients
and documentation was found in one case, too. The maximum duration was not documented and there was no revision in original orders.
Conclusions: Based on our data the “z drugs” are rarely used in forensic units of Littlemore Hospital. The only prescribed one was zopiclone and it was
used only for a couple of days. The documentation regarding use of those medications was rare and no case of switch to another “z drug” was found.
Checking for the response to the treatment and conducting the study in general wards beside forensic units would have improved this study and
provided more patients, who were prescribed those medications.
The majority of forensic patients are on high doses of antipsychotics or rapid tranquilizers, which might help to cope with insomnia. We found that
other than documentation the standards were followed by the Trust. As forensic patients were supervised at all times on-call doctors should be able to
prescribe Z hypnotics, when needed. The use of sleep hygiene in treatment of insomnia should be encouraged for all patients.
Key words: Z hypnotics, forensic, psychiatric, z drugs, Oxford
S202
[PP-130]
Pathological gambling: A case report
Mehmet Fatih Tastan, Haluk A. Savas
Gaziantep University, Medical School, Department of Psychiatry, Gaziantep, Turkey
E-Mail: [email protected], [email protected]
Pathological gambling(PG), is a disorder which is growing everyday with the increasing prevalence of opportunities for play, usually properly diagnosed,
treatment can be difficult and increasingly restricting the individual’s living area. PG, for the first time in 1980, by The Union of American psychiatry has
been recognized as a disorder and the DSM-3 was unable to resist the urge to gamble as a continuous and progressive definition of a “Impulse Control
Disorders Not Elsewhere Classified” has been included under the heading. Physiological symptoms of DSM-3-R were included in the PG, “the excitement is
to be obtained to provide the desired amount of bets or the need to increase the frequency of hearing,” such as tolerance and “gambling oynayamayınca
hearing restlessness or irritability, such as” withdrawal symptoms participated in the diagnostic criteria. We present a case of PG, 28 year old male patient
who is treated with quetiapin and cognitive behavioral treatment (CBT). With CBT, we did daily psychotherapeutic interview and patient had discovered
his cognitive distortion. Also we saw that SSRIs, Naltrexone, Lithium and Carbamazepine could be used in PG treatment. Patient was externed after 11
days hospitalizing. At the controls we obtained that patient had not gamble again. As a result this was the effect of Cognitive Behavioral Treatment.
Key words: Pathological gambling, cognitive behavioral treatment, cognitive distortion
S203
Subject Index
(±)-3-4-methylenedioxymethamphetamineS36
1-benzylpiperazineS36
5-HT1B A-161T
S108
Absence convulsion
S118
AbsenteeismS150
AbuseS180
Academic achievement
S154
Academic performance
S58
AcceptanceS105
AccessS156
Access to health care
S156
Addiction
S54, S42, S83, S109, S151, S155
ADHD
S57, S66, S73, S96, S97, S136, S148
AdolescenceS96
Adolescents
S126, S153
ADRA2AS148
Adult ADHD
S159
Adult attention deficit hyperactivity disorder
S163
Affective disorder
S161
Agmatine
S166, S169
AgranulocytosisS46
AHPS198
AlcoholS155
Alcohol abuse
S173, S174
Alcohol dependence
S108
AlexithymiaS56
Alkaline phosphatase
S116
AlloxanS116
Alzheimer’s disease
S52, S198
AmenorrheaS135
Amisulprid
S160, S200
Amplified perception of somatic sensations
S178
Amygdala
S110, S133
AngerS138
Animal model of depression
S140
AnorexiaS92
Anorexia nervosa
S130, S195
Antidepressant
S38, S39, S43, S51, S81, S121, S136, S140
AntiepilepticS182
AntihypertensivesS198
AntioxidantS170
Antioxidant vitamins
S74
Antipsychotic
S63, S135, S144, S149, S167
Antipsychotic development
S50
Antipsychotic drug
S180, S196
Antisocial personality disorder
S163
Anxiety
S69, S163, S132, S133, S141, S155
Anxiety disorders
S40, S67, S68
Anxiety models
S69
Anxiety symptom levels
S153
Archive documents
S181
Aripiprazole
S135, S144, S152
Assessment
S150, S151, S155
AtherosclerosisS143
AtomoxetineS136
AttachmentS56
Attention deficit hyperactivity
S58
Attention deficit hyperactivity disorder
S95, S139
Atypical antipsychotics
S63, S144, S164, S171
AugmentationS126
AutismS72
Avoiding behavior
S122
Bacopa monniera
S108, S153, S189
Basal ganglia hemorrhage
S157
BDNF
S91, S169
Behavioral therapy
S185
BilirubinS180
Binge eating
S54
Biogenic amines
S51
Biological rhythm
S88, S89
Biomarker
S102, S198
Bipolar
S36, S57, S149
Bipolar affective disorder
S169
Bipolar disorder
S39, S59, S98, S100, S124, S126, S140, S142, S158
Blood level
S142
Blood sugar
S111
Body dysmorphic disorder
S143
Brain imaging methods
S195
Brain injury
S136
Brain microdialysis
S36
Brain-derived neurotrophic factor
S176
Bright light
S89
BulimiaS92
Bulimia nervosa
S95, S194
BuprenorphineS35
Bupropion
S113, S121, S143
C-fosS169
CabergolineS124
Calcium
S72, S123
Cannabis
S37, S83, S130
Cannabis dependency
S159
Caregiver burden
S141
CatatoniaS162
CBT
S105, S106, S111
Cerebellar cognitive affective syndrome
S138
Cerebellum
S138, S195
Cerebral ischemia
S112
CeruloplasminS170
Character
S34, S54
ChemotherapyS132
Chest pain without cardiac etiology
S138
Child
S36, S57
Childhood trauma
S79, S86, S192
Children
S74, S75, S97, S139
Cholinesterase inhibitors
S136
Choreoathetoid movement
S152
Chronic schizophrenia
S125
Chronic unpredictable mild stress
S166, S169
ChronotherapeuticsS89
CigaretteS156
Clinical characteristics
S82
Clinical manifestation
S172
Clozapine
S46, S126, S201
CNR1 1359 G/A
S108
Co-morbidity
S96, S97
Cognition
S34, S91, S153
Cognitive behavior therapy
S40, S41
Cognitive functions
S83, S136, S138, S158, S188
Cognitive processing of emotions
S56
Cognitive side effects
S149
Combination drug therapy
S40
Community care
S129
Comorbidity
S92, S95, S177
Complementary and alternative medicine
S65
Confidence interval
S104
Congenital hypogonadism
S195
Corpus callosum
S182
COX-2 inhibitor
S184
CravingS156
CRHS51
Crisis team
S129
Cultural differences
S172
Cytochrome P450 2C9
S132
CytokinesS70
D-serineS50
DeathS155
Deep brain stimulation
S61
Dementia
S62, S134
Depression
S36, S38, S39, S43, S57,S60, S60, S64, S65, S70,
S77, S78, S81, S82, S85, S87,S89, S130, S132, S139, S141, S145,
S155, S161, S162, S163, S170, S178, S184, S190, S193, S198
Depression treatment
S58
Depressive symmptom levels
S153
Descriptive statistics
S104
DevelopmentS74
Diabetic rats
S116
Differential diagnosis
S177
DiltiazemS119
DissociationS192
Dissociative disorder
S159
Dissociative symptoms
S146
Divorce
S144, S184
Don Juanism
S52
Dopamine
S49, S63
Dopamine agonists
S124
DRD2 TaqIA
S108
Drug
S100, S103
Drug discovery
S62
Drug induced
S167
Drug-induced psychosis
S182
Drug interactions
S97
Drug safety
S48
Drug utilization
S168
Dual diagnosis
S109
Duloxetine
S115, S139
E-selectinS143
Eating disorders
S54, S92, S93, S94, S130
Eating pattern
S125
EchopraxiaS200
EcstasyS36
ECT196
Ecuadorian population
S132
EdemaS196
EducationS65
Education factors
S128
EEG
S110, S133
EffectivenessS151
Efficacy
S38, S136, S201
Electroconvulsive therapy
S174
Electromagnetic induction
S117
EMDR
S106, S127
Emotion regulation
S40
EmotionalityS34
Enuresis nocturna
S185
Environmental risk S52
Erectile dysfunction
S137
EscitalopramS160
Essential fatty acids
S66
EstrogenS77
EuthymiaS158
Evidence based treatment
S41
Executive functions
S176
ExerciseS91
Extrapyramidal side effects
S144, S165
Eye movement desensitization and reprocessing
S123
Fear of negative evaluation scale
S173
Subject Index
Female adolescents
S125
Female reproductive hormones
S193
Fish oil
S135
Flight safety
S103
FluanxolS129
Fluoxetine
S113, S130, S147, S179, S194
FMRI
S62, S108, S189
FoetalityS171
Follow-upS176
Forced swimming test
S166
ForensicS202
Forensic psychiatric examination
S128
Functional outcomes
S136
Functional remission
S188
FunctioningS86
GABAS51
Galactorrhea
S147, S160
Ganser Syndrome
S159
GatingS49
GenderS140
Generalized anxiety disorder
S193
Generalized convulsion
S118
GenesS52
Genetic
S68S 100
Genetic association
S46
Genetic polymorphism
S131, S132
Genomic diagnostics
S157
GFAPS169
Ginseng augmentation therapy
S114
Glia
S50, S51
GlossodyniaS161
Glutamate
S40, S49, S50, S51, S69, S70
GlutathioneS169
GlycineS50
GOTS116
GPTS116
Guidelines
S98, S100
GWAS
S157, S198
HallucinationS121
HaloperidolS129
HappinessS34
Harm minimization
S42
HealthS34
HematologicalS130
HeroinS109
Hippocampal neurogenesis
S91
HIV/AIDSS42
HLA-systemS46
HoardingS134
Homework assignments
S41
HPA axis
S51
Human characteristics
S34
Human cognition
S108, S189
Huntington’s disease
S152
Hyperammonemic encephalopathy
S164
Hyperprolactinemia
S124, S135, S160
Hypersexual disorders
S52
HypersomniaS44
HypochondriasisS105
HypoglycemiaS78
HypomaniaS194
Hyponatremia
S139, S141
Hypothalamic-pituitary-thyroid axis
S77
ICAM-1S143
ImipramineS185
Immunosuppresive treatment
S161
Impulse control disorder
S53
ImpulsivityS94
In vitro analysis
S115
Inappropriate medications
S168
Individualized medicine
S101
InflammationS184
Information processing disorder
S49
InpatientS191
Insight188
InsomniaS139
InsulinS78
Insulin resistance
S78
Interethnic differences
S131
Iron deficiency
S74
Isolated thrombocytopenia
S190
Ketamine
S49, S69
Lack of self confidence
S111
Lactation
S48, S71, S71
LamotrigineS142
Lateral ventricle
S61
LearningS112
LeukopeniaS127
Lipid peroxidation
S140
LithiumS169
Lithium carbonate
S161
Locomotor activity
S141
Long QTc
S119
LosartanS132
Lung functions
141
Magnetic resonance imaging
S61
MaintenanceS176
Maintenance phase
S100
Major depressive disorder
S115
Male patient
S195
MalondialdehydeS169
ManagementS95
Mania
S157, S194
Manic episode
S124
Marital conflict
S144, S184
Mechanism of action
S63
Medical care
S156
Medical decision support systems
S157
Medical diseases
S67
Medical marijuana
S37
Medication
S40, S43
Mega cisterna magna
S195
MelatoninS75
Mental diseases
S200
Mental disorder
S144, S184
Mental health
S154
Mental illness
S196
Mental symptom
S123, S135
MentalizingS56
Metabolic syndrome
S180
MetabolicS171
Metabolic side effect
S140
Methadone
S35, S114
Methadone substitution therapy
S137
Methylphenidate
S139, S190
MetoprololS119
METU-SNP
S102, S157
MGLU receptors
S70
Middle-aged male
S139
Mindfulness
S40, S105
Mirtazapine
S139, S175, S190, S196
Mixed mania
S98
ModafinilS44
ModelsS49
Molecular diagnostics
S102
Mood
S89, S91, S153
Mood disorder
S77, S79, S134, S149, S162
Mood stabiliser
S149
MRIS62
Music therapy
S191
Myeloperoxidase
S46, S169
NADPH-oxidaseS46
Neuroactive steroids
S50, S51
Neurocognitive functions
S193
Neurodegeneration
S90, S91
NeurodevelopmentS49
Neurodevelopmental disorders
S75
NeurogenesisS193
Neuroimaging
S36, S62, S148
Neuroleptic malignant syndrome
S125
NeurologicalS201
Neurological co-morbidity, treatment
S97
Neurological deficits
S164
NeuromodulationS117
Neuropathic pain
S59
NeuroplasticityS90
NeuroprotectionS112
Neuroprotective effect
S90
NeuroregenerationS91
Neurotrophic factors
S70
NeutropeniaS127
NicotineS112
Nitric oxide
S50
NMDA
S40, S70
NMDA receptor
S49, S69
Non-seasonal affective disorder
S89
Normal pressure hydrocephalus
S169
Nutraceuticals
S108, S153, S189
NymphomaniaS52
ObesityS94
Obsessive beliefs
S137
Obsessive compulsive behavior
S126
Obsessive compulsive disorder
S71, S134, S176, S177
Obsessive compulsive spectrum
S182
Obstructive sleep apnea
S200
OccupationS58
OCD
S59, S137, S172
Olanzapine
S171, S180, S190
OlfactionS193
OmanS145
Omega fatty acids
S75
Omega-3 fatty acids
S64
OntogenesisS171
Opioid dependence
S35
Opioid withdrawal syndrome
S114
Orally disintegrating olanzapine
S115
Outpatient forensic psychiatric examination
S181
OxfordS202
Oxidative stress
S170, S189
Oxytocin
S76, S133, S118
P value
S104
Pain
S54, S55, S81, S82
Pain reflex
141
Pain threshold
S178
PaliperidoneS165
Panic disorder
S78, S106, S122, S137, S189, S71
Subject Index
Panic symptoms
S122
ParoxetineS156
Pathological gambling
S53, S174
PatternS168
Pentylenetetrazol (PTZ)
S118
Perinatal depression
S64
Persistent symptoms
S86
PersonalityS34
Personality disorder
S178
Personalized medicine
S102, S157, S198
PETS62
PetechiaS190
Pharmacogenetics
S63, S101
Pharmacogenomics
S102, S157, S198
Pharmacological treatment S93
PharmacologyS93
Pharmacotherapy
S53, S93
PhobiasS178
Physical activity
S91
Physical health monitoring
S149
Physical symptom
S123, S135
PicaS182
PilotsS103
PiracetamS146
Placebo
S38, S123, S135
Polymorphism
S63, S100, S108, S176
PolypharmacyS164
Post traumatic stress disorder
S141
Post-partum blues
S163
Post-traumatic stress disorder (PTSD)
S123, S175
Pregnancy
S35, S48, S71, S190, S196
Pregnant women
S149
Premenstrual dysphoric disorder
S193
Premenstrual syndrome
S123, S135
PriapismS167
ProgesteroneS77
Progressive muscle relaxation
S132
PsychiatricS202
Psychiatric disorders
S37, S48, S62, S74, S77
Psychiatry
S65, S74, S101, S109
PsychopathologyS125
PsychopharmacotherapyS71
Psychosis
S83, S167, S178, S192
Psychospiritual interventions
S42
PsychostimulantsS44
PsychosurgeryS61
Psychotherapy
S53, S95, S105, S106, S151
Psychotic disorder
S80, S162
Psychotropic drugs
S48, S88, S90, S103
PsychotropicsS140
PTSD
S59, S106, S175
Quality of life
S132, S191
Quantitative EEG
S58
QuestionnaireS151
Racine scale
S118
Radial-arm maze
S112
RapeS127
Rapid antidepressant efficacy
S69
RatS68
Rat behaviour
S36
Rational drug use
S102
RatsS141
Reaction time
S113
ReboxetineS130
Reference memory
S112
Referral pathways
S129
RehabilitationS86
Relapse
S149, S198
Religious beliefs
S155
Renal transplantation
S161
Repetitive transcranial magnetic stimulation (rTMS) therapy
S58
Resistant depression
S176
Risk factors
S137
Risky behavior
S153
RisperidoneS135
RTMSS176
Safety
S190, S201
Schizophrenia
S49, S50, S59, S61, S63, S77, S80, S86, S126,
S129, S134, S143, S157, S164, S171, S177, S180, S188,
S191, S192, S195, S201
Scientific basis
S63
SCL-90S144
Seasonal affective disorder
S89
Self-destructive acts
S181
Self-perceptionS138
Serotonin
S49, S63
Serotonin syndrome
S36
SertralineS179
Serum drug levels
S149
Sexual dysfunction
S80, S103
Sexual trauma
S167
Side effect
S63, S103, S127, S130, S161, S167, S200
Sigma receptor
S112
Single Nucleotide Polymorphisms (SNPs)
S102
SLC6A2S148
Sleep
S43, S89
Sleep deprivation
S87, S89
Smoking cessation
S162
SNP genotyping
S157
SNP prioritization
S198
SNRIS55
Social anxiety
S173, S174
Social behaviour
S76
Social Phobia Scale
S174
Social Interaction Anxiety Scale
S174
Sodium valproate
S164
Somatic symptoms
S139
Somatization
S56, S105
SomatoformS105
Soviet times
S128
SPECTS62
Spinal Cord Injury
141
SSRI
S55, S103
St. John’s Wort
S65
StressS111
Structural brain abnormalities
S169
Substance abuse
S83, S130
Substance P
S51
Substance use
S125, S159
SubtypesS189
Sucrose preference
S166
Sudden cardiac death
S119
Suicide rate
S145
SwitchingS130
Synaptic plasticity
S91
Tardive akathisia
S144
Tardive dyskinesia
S165
Tardive dystonia
S201
Tardive syndromes
S144
TemperamentS54
Ten year period
S145
TeratogenicityS190
TerlipressinS141
Testicular mutilation
S134
TestosteroneS77
Thalamic EEG
S118
The quran reciting
S145
Therapeutic relationship
S41
Therapy
S109, S123
ThinkingS34
ThrombocytopeniaS130
Thyroid hormones
S77
Tianeptine abuse
S197
Tianeptine dependence
S197
Tic disorders
S200
TMSS59
TopiramateS182
Tourette’s disorder
S160
Transcranial magnetic stimulation (TMS)
S60, S117
Transcultural psychiatry
S37
Transcultural psychiatry in USA
S37
TransgenicS68
Translational medicine
S157
Trauma
S56, S80, S123, S127
Treatment
S87, S89, S93, S96, S101, S105, S126, S151, S174, S176, S196
Treatment outcome
S41
Treatment principles and pitfalls
S41
Treatment resistance
S86
Treatment resistant depression
S85
Turkish American cases
S37
Typical and atypical antipsychotics
S110
Typical antipsychotics
S164
UGT1A4S131
Unintended pregnancy
S163
UnitsS202
Urinary incontinence
VaginismusS178
Vagus nerve stimulation
S60
Valproic acid
S126
ValsartanS198
VareniclineS162
VCAM-1S143
Venlafaxine
S127, S175
Ventricular arrhythmias
S119
Vigilance-promoting agents
S44
Visual and auditory tasks
S113
Vitamin D
S72, S116
VolumetryS193
VorbeiredenS159
Weight loss
S139
Well-beingS34
WellnessS34
Wender-Utah rating scale
S163
Z hypnotics
S202
Zinc deficiency S116
Zinc supplementation
S73
ZiprasidoneS119
ZuclopenthixolS167
Zuclopenthixol acetate
S125
γ –hydroxybutyrate
S44
Author Index
Abalı O.
Abnavi M. A.
Abolghasemi S.
Abtahi M. M.
Adler L. A.
Adzlin U. B.
Aghamohammadi A.
Ahl J.
Ak İ.
Ak M.
Akarsu S.
Akbıyık M.
Akça Ö. F.
Akdeniz F.
Akkaya C.
Aksoy A.
Aksoy R.
Aksoy Ş. G.
Aksoy U. M.
Alaçam H.
Alev L.
Algül A.
Allahtavakoli M.
Alnıak İ.
Alonso M. E.
Alowesie R. M.
Alpkan L. R.
Altaiar H. A.
Altın M.
Altındağ A.
Altınok Ü.
Altuğ A.
Altunkaynak Y.
Amani F.
Anderson I.
Annagür B. B.
Ansari A.
Antón J. M.
Arıcan H. A.
Arıcıoğlu F.
Arun K.
Ashna S. M.
Askari K.
Aslan S.
Asvadi I. T.
Atagün M. İ.
Atagün Z.
Ateş M. A.
Atila Erol
Atmaca M.
Ay M. E.
Ay Ö. İ.
Aydemir M. Ç.
Aydemir Ö.
Aydın A.
Aydın E.
Aydın E. F.
Aydın M. D.
Aydın S.
Aydınoglu U.
Ayhan Bilgiç
Ayhan M. G.
Aziz S. A.
Baharudin A.
Bahçeci B.
Bakar A. K. B. A.
Baker G. B.
Bakım B.
Balaban Ö. D.
Balıbey H.
Balikci A.
Baran B.
Barlak S.
Başabak A.
Başoğlu C.
Başoğlu E.
Bayar N.
Baykaran M. B.
Bayrak A.
Bayrak M.
S97
S155
S111
S111
S135
S42
S122, S134, S163
S115
S200
S54, S127, S171, S174
S171, S175
S193
S72
S142
S81
S150, S151
S173
S158
S158
S179
S114, S115, S135
S59, S167, S175, S199
S112
S152
S131, S185, S187
S136
S141
S202
S114, S115, S135
S55
S141
S149
S144
S168
S38
S94
S145
S186
S149
S70, S166, S169
S47
S117
S111
S85
S132
S141
S141
S167, S175, S181, S199
S194
S121
S108
S108
S101, S138
S90
S87, S130, S146, S171, S178, S179
S121, S136, S172
S201
S60
S58
S125, S143, S147, S190
S73
S135
S137
S137
S65, S126
S42
S35, S50, S68
S59
S141
S91, S123, S162
S123
S176
S181
S150, S151
S175, S181, S199
S191
S162
S140, S177
S192
S177
Beatson S.
Beltrán L.
Benson S.
Beşiroğlu L.
Bez Y.
Bigdeli O.
Bilge D.
Bilgin A. A.
Bilici M.
Boardman B. K.
Bolu A.
Bora S.
Bostancı E. D.
Bozkurt A.
Brueckl T.
Budaklı A. A.
Buturak Ş. V.
Büyükkınacı A.
Büyükşahin F.
Can D. Ö.
Canan F.
Cascorbi I.
Cengiz F. F.
Cerit C.
Cetin M.
Ceylan M. E.
Chichinadze K.
Cho S.
Choi J. S.
Cloninger C. R.
Cumhur Tulay
Cumurcu B. E.
Çalışkan M.
Çam B.
Çelenk S.
Çelik C.
Çelik H.
Çelik S.
Çetin T.
Çetingüç M.
Çiftçi A.
Çim E. F. A.
Çoban A. A.
Dalkilic A.
Deldar A.
Demir A.
Demir S.
Demirel B.
Demirgoren S.
Deveci E. Dilbaz N.
Diler R. S.
Direskeneli G. S.
Doğan S.
Doksat K. M.
Domac F. M.
Domianidze T.
Dorado P.
Döke M. A.
Döm H. A. Duran S.
Durell T. M.
Durmaz O.
Dursun S.
Durukan İ.
Ebrinç S.
Efe M.
Eker E.
Elbi H.
Elboğa G.
Enli Y.
Erbas O.
Erdal M. E.
Erdem M.
Eren İ.
Ermis A.
Erol A.
Ersoy M. A.
Ertekin B. A.
Ertekin E.
S128
S131
S152
S188
S98, S170
S113, S183
S192
S160
S142, S191, S192
S135
S171, S175
S109, S117, S133
S168
S127, S174
S44
S167
S60
S198
S162
S198
S125, S143, S147
S45
S138, S166
S198
S78, S175, S199
S133, S134, S171, S178
S140
S148
S139
S34
S191
S158
S198
S160, S196
S163
S175
S170
S173
S173
S102
S201
S179
S153
S37, S93
S135
S125, S142, S192
S158
S163
S133
S77
S124
S36, S57
S176
S52
S56
S125
S140
S131, S185, S186, S187
S156
S156
S138
S135
S175
S50, S68
S66
S71, S175, S181, S199
S108
S51
S67
S55
S179
S109, S117, S118, S133
S108
S80, S174
S99, S162
S133
S92, S129, S156, S180, S182, S194, S195, S197
S85
S176
S176
Author Index
Etli T.
Evren C.
Evren M. B.
Evren V.
Farjad S.
Felati N. M. A.
Girit O. C.
Glaser P. E.
Golchin M. T.
Göka Erol
Gönen M.
Guerrero J.
Gulec M.
Guveli H.
Güçlü O.
Güçlü O. G.
Gül I. G.
Güleç H.
Güleç M.
Güler J.
Gümrü S.
Günay H.
Güner S.
Gürol D. T.
Gürvit H.
Güven M.
Habil M. H.
Hamdikene M.
Hariri A. G.
Hasankhani H.
Hashemian F.
Hashmi S. S. A.
Hegazy R. R.
Hergüner A.
Hergüner S.
Herizchi S. E.
Herken H.
Hıdıroğlu H.
Hızlı G.
Hisim O.
Hnidek .
Hobbs D.
Hocaoglu C.
Hofmann S.
Horacek Jiri
Hosseini S. M.
Höschl C.
Hudson A. L.
Hughes M.
Ibrahim N.
Ismail I. E.
İnanlı İ.
İpekçioğlu D.
İskender B.
İşmen M.
Jaafar N. R. N.
Jan F.
Jarrott B.
Javadpour A. Johnston P.
Jung H. Y.
Kabak S. G.
Kadıoğlu O.
Kalem Ş. A.
Kalkancı Ö.
Kaptanoğlu B.
Kara T.
Karadağ F.
Karadayı G.
Karadere M. E.
Karagianis J.
Karahan A.
Karalar B.
Karaman U.
Karaman Z.
Karamustafalıoğlu O.
Karataş K. S.
Karayılan S.
Karimi S.
Karlıdağ R.
S208
S162
S80, S154, S173
S162
S117
S112
S145
S133, S134
S135
S132
S138
S157
S187
S130
S126
S121, S136, S172, S177
S144
S158
S55
S78, S89, S179, S190, S201
S161, S162, S168, S195
S169
S68
S106
S154
S176
S83
S42
S115
S142, S185, S195
S144, S184
S113, S183
S145
S141
S139
S139
S132
S108, S170, S179
S200
S58
S133
S48
S114
S64, S126
S40
S49
S183
S48, S49
S35
S108, S189
S137
S141
S162
S134
S187
S150
S137
S148
S112
S155
S108, S189
S139
S177, S193
S197
S176
S179
S179
S152, S201
S62, S154, S179
S149, S151
S163
S114
S187
S150
S149
S149
S193
S159, S168, S195
S129, S194
S144, S184
S158
Kartalcı Ş.
Kavzoğlu S. Ö.
Kaya M. C.
Kaya N.
Kaya Z. E.
Kazantzis N.
Kazemi M.
Kazemi S.
Kechrid Z.
Kenar J.
Kenawy S. A.
Kennedy V.
Kesebir S.
Khananashvili M.
Kheirabadi G. R.
Kılıç S.
Kılınç E.
Kırlı S.
Kim B.
Kim J.
Kim M. H.
Kirsch I.
Koca E. K.
Koç C.
Konkan R.
Korkmaz S.
Kuloglu M.
Kumsar N. A.
Kurt H.
Kuru T.
Kültür S. E. Ç.
Labadze I.
Lalies M.
Lazarashvili A.
Lee H. W.
Lee J. Y.
Lledó E. P.
Llerena A.
López M.
Machín E.
Mackay M.
Maden O.
Mahmodi G.
Majd M.
Maner F.
Maracy M. R.
Martin P. R.
Matitaishvili T.
Mazlum B.
Mcgough J. J.
Melledo J. M.
Meral G.
Meyers A.
Min S.
Mislan N.
Mitchell N. D.
Mohamadzadeh S.
Mohr P.
Mokri A.
Molavi H.
Monroy N.
Moshtaghian J.
Mutlu E.
Nachnani M.
Nasiripour A. A.
Neale C.
Nebioğlu M.
Negahban T.
Nuray Atasoy
Oakes T. M. M.
Oral E.
Ortega A.
Ozşahin A. A.
Ögel K.
Öneş K.
Öyekçin D. G.
Özata B.
Özbek K.
Özçelik N. B. V.
Özçetin A.
S158
S142
S66, S170
S127, S135, S149
S124
S41
S144, S184
S144, S184
S115
S159
S141
S148
S140, S142
S140
S116
S104
S134
S39, S81
S148
S148
S124
S38
S125
S150, S151
S121, S136, S144, S172, S177
S121
S121
S156, S180, S182
S196
S163
S73
S140
S35
S140
S139
S139
S131, S185, S186, S187
S45, S131, S185, S186, S187
S131, S187, S185
S131
S50
S127
S111, S155
S113, S183
S53, S133, S134, S158, S178
S116
S35
S140
S74
S135
S50
S199
S115
S124
S137
S50, S69
S154, S155
S48
S113
S111
S131
S111
S171, S173, S178
S128
S155
S108, S152, S189
S198
S145
S76
S115
S88, S201
S131
S125, S127
S105, S149, S150, S151, S153, S154
S141
S182
S176
S114, S115
S61
S103
Author Index
Özdemir B.
Özdemir F. A.
Özdemir O.
Özdemir P. G.
Özdemir S.
Özen N. E.
Özer H.
Özgen F.
Özkol H.
Özkorumak E.
Özmen M.
Özmenler K. N.
Özşahin A.
Özten M.
Öztürk M.
Öztürk N.
Palenicek T.
Panahi M. V. S.
Paparrigopoulos T.
Papavasiliou A.
Park K. C.
Parlak S. Ç.
Peker G. O.
Perdeci Z.
Perreault A.
Pieri M. C.
Pigott T. A.
Piri I. T.
Prakash A.
Ranjkesh M.
Rashid R. A.
Raskin J.
Rubin R. L.
Sabri A. A. A.
Sabri Hergüner
Saglam S.
Sahmelikoglu O.
Salehi M.
Sanaat Z. T.
Sarıdoğan G. E.
Sarıkaya Ö. Ö.
Sarkis E. S.
Sarp K.
Sarp N.
Savaş H. A.
Saygılı İ.
Sayyadi A. R.
Scholey A.
Seifertova D.
Selek S.
Selvi Y.
Semerci B.
Semiz Ü. B.
Sezlev D.
Shabanloui R. T.
Shafaie J.
Shaker A.
Sharaf O. A. Sharifi A.
Sheehan D.
Shin J.
Shin M.
Shohrati M.
Sidi H. Silsüpür G.
Sinani G.
Sinici E.
Soldatos C. R.
Son Y. A.
Sonmez E. O.
Sook A. J.
Soyer B.
Spaniel F.
Stough C.
Sundar A. S.
Sungur M. Z.
Sünbül E. A.
S175
S190
S188
S146, S179
S190
S68
S197
S171
S188
S64, S187, S200
S90
S175
S171, S174
S194, S195
S57
S176
S49
S183
S42, S43
S44
S124
S192
S117, S133
S162
S35
S109
S135
S132
S115
S116
S42
S114
S135
S145
S74
S121
S133
S116
S132
S198
S182
S135
S126
S153
S170
S164, S165, S185
S145
S108, S152, S189
S48
S170
S88, S146, S188, S190
S96
S164, S165, S191, S192
S171
S132
S112
S168
S141
S113, S183
S115
S124
S148
S113
S137
S198
S125, S143, S147
S127
S43
S101, S156, S197
S127
S124
S159, S168
S49
S152
S46
S41, S121, S136, S172, S177
S138, S166
Sünbül M.
Şahan E.
Şehirli Ö.
Şengül C. B.
Şenormancı G.
Şenormancı Ö.
Şimşek G.
Şimşek Y.
Tabatabayi M. S.
Taner E.
Taner H. A.
Taner Y.
Tarhan N.
Tellioglu T.
Terán E.
Tezcan A. E.
Thirunavukarasu M.
Tıkır Baise
Tiryaki A.
Toğul H.
Topçuoğlu Ö. B.
Toprak B.
Torres E. L.
Tosun M.
Trejo H.
Treuer T.
Tuncel Y. Y.
Turan T.
Tükel R.
Tülüce Y.
Türkbay T.
Türker T.
Uğur M.
Uguz F.
Uhr M.
Ulusoy S.
Utkan T.
Utkan T.
Uz Y.
Uzun Ö.
Ülkü M.
Ünal A.
Ünay D.
Ünübol B.
Ünübol H.
Üstünkar G.
Valesova V. B.
Valzdorf E.
Williams D. W.
Würz A.
Yaci H.
Yanartaş Ö.
Yang Y.
Yanık T.
Yarcı E.
Yavuz K. F.
Yazır Y.
Yeloglu Ç. H.
Yenel A.
Yeroham R.
Yeşil B.
Yılbaş B.
Yıldız M.
Yılmaz O.
Yılmaz Y.
Yiğiter S.
Yousefi F.
Yucel A.
Yuksel R. N.
Yüce M.
Yücel B.
Yükselir C.
Zafari M.
Zakaria H. B.
Zaki H. F.
Zepeda N.
Zincir S. B.
S138
S198
S169
S100, S108, S179
S144
S53, S121, S136, S144, S172
S192
S198
S113
S63
S160
S160
S58
S37
S131
S140
S46, S47
S138
S187, S200
S160
S168
S140
S186
S84
S185, S187
S114
S156
S76
S176
S188
S95
S162
S75
S70, S135, S146
S44
S152
S166, S169
S169
S125
S171
S173
S97, S161, S162
S62
S161, S162
S161, S162
S156, S197
S49
S128, S129, S181
S135
S104
S125
S164, S165, S185
S148
S171
S169
S152, S163
S169
S126
S191, S192
S150
S158
S157
S86
S199
S164, S165, S185, S192
S173
S154
S130
S124
S96
S94
S174
S111, S122, S134, S155, S163
S42
S141
S35
S79, S165, S177, S191, S192

Contents - (4. UPFK) 23-27 Kasım 2011

Transcription

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