Psychiatric Essentials 31 August 2012 Presented By

Psychiatric Essentials
31 August 2012
Presented by AMA Victoria Section of Psychiatry
AMA Victoria
Advancing the Medical Profession. Advancing the health of Victorians
www.amavic.com.au
GRAHAM D. BURROWS, AO, CJSJ
BSc, MB, ChB, DPM, MD, DipMHlthSc(Clinical
Hypnosis),DSc, FRANZCP, FRCPsych,
AFRACMA, FAChAM,
Professorial Fellow - Psychiatry
University of Melbourne
The Melbourne Clinic
Chairman, Mental Health Foundation of Australia
Chairman of Council AMA Victoria
Board Member AMA Victoria
Chairman Section of Psychiatry AMA Victoria
Chairman Mental Health Foundation
Australia (MHFA) 1982 - present
President Mental Health Foundation Victoria
(MHFV) 1970 - present
Member RANZCP Victoria 1970 - present
Editor/Author of 104 Books
Published over 743 scientific articles in refereed journals
Contributor to other books – 180 chapters
Editorial Board of 30 International and Australian Journals
1989 ‐Awarded the Officer of the Order of Australia (AO) – distinguished contributor to Medicine.
2010 ‐ Recipient of the Royal Australian & New Zealand College of Psychiatrists “College Medal of Honour”
MENTAL HEALTH WEEK
7 – 13 OCTOBER 2012
MENTAL HEALTH – WHAT DO YOU KNOW?
www.mentalhealthvic.org.au
www.health.vic.gov.au/mentalhealth/mhweek.htm
Dr Ajit Selvendra
Chairperson 1
Premenstrual Disorders
Professor Lorraine Dennerstein
AO MBBS PHD DPM FRANZCP
The University of Melbourne
Introduction
Clinical significance: premenstrual symptoms are
frequent, up to 30% have PMS and 1-5%
experience PMDD
Burden of illness: women with moderate to severe
premenstrual symptoms have increased work
absenteism, decreased productivity, decreased
activities of daily life and increased health care
costs. HRQoL for PMDD similar to that of
rheumatoid arthitis
Impacts: woman, studies/occupation, family life,
social relationships
Objectives: Premenstrual Disorders
Types of Premenstrual Disorders
Prevalence
Aetiology
Role of Psychiatrist
Diagnosis
Treatments
Premenstrual Disorders Timeline
- 370 BC Hippocrates
”Women are subject to intermittent agitations which make
their way from the head to the uterus whence they are
expelled”
- 1931 : Frank (New York) - Premenstrual Tension
(PMT)
- 1953 : Premenstrual Syndrome (PMS) (Dalton UK)
- 1980s: Severe PMS / physiological symptoms
- 1987 : LLPDD included in DSM III-R- appendix
- 1994 : PMDD included in DSM-IV - appendix
- 2000 : PMS ACOG Practice Bulletin
- 2011 : Premenstrual Disorders, ISPMD
- 2012 : PMDD included in DSM V under Mood
Disorders
Core / Typical PMD
O’Brien PMS, Rapkin A, Dennerstein L, Nevatte T.
Premenstrual Disorders: Diagnosis and Management. BMJ 2011;342:D2994.
1. Ovulation underlies Core PMD
2. Symptoms are not defined – there are typical symptoms
3. The number of symptoms is not proscribed
4. Physical and psychological symptoms are important
5. Symptoms must recur in the luteal phase
6. Symptoms must disappear by the end of menstruation
7. There is a symptom-free week between menstruation
and ovulation
8. Symptoms must be prospectively rated
9. Symptoms are not an exacerbation of an underlying
psychological or physical disorder
10. Symptoms must cause significant impairment
Variants of the Core Premenstrual Disord
(a)
premenstrual exacerbation of an underlying
physiological, somatic or medical condition
(b)
premenstrual symptoms with absent
menstruation (after hysterectomy with ovarian
conservation, endometrial ablation or with a
levonorgestrel intra-uterine system)
(c)
progestogen-induced PMS occurring during
progestogen therapy (cyclical menopausal
hormonal therapy (HT), hormonal
contraception)
Premenstrual Disorders
ICD-10- PMS- 1 symptom
PMS – ACOG
PMDD- DSM IV
►1
►5
mood & 1 physical
symptom premenstrually in
each of last 3 cycles
free phase
postmenstrually
►Woman must be negatively
affected in her daily life or
relationships
►Prospective daily ratings for
2 months to confirm
symptoms ( 1 mood) in the
week before menses,
alleviated during menses, in
most cycles in last 12
months
►Symptom
►Symptom
free phase
postmenstrually
►Woman must be negatively
affected in her daily life or
relationships
►Prospective daily ratings for
2 months to confirm
*PMDD Defining Symptoms
1*- Markedly depressed mood, feelings of
hopelessness, or self-depreciating thoughts
2*- Marked anxiety, tension, feelings 'keyed
up,' or 'on edge'
3*- Marked affective lability
4*- Persistent and marked anger, irritability, or
increased interpersonal conflicts
from DSM-IV, 1994
PMDD
+ ONE OR MORE OF FOLLOWING SYMPTOMS
Decreased interest in usual activities
Subjective sense of difficulty concentrating
Lethargy, fatigue, lack of energy
Marked change in appetite, overeating, speciifc
food cravings
Hypersomnia or insomnia
Feeling overwhelmed or out of control
Breast tenderness or swelling, headaches, joint or
muscle pain, bloating, weight gain
Objectives: Premenstrual Disorders
Types of Premenstrual Disorders
Prevalence
Aetiology
Role of Psychiatrist
Diagnosis
Treatment
Global Study of Premenstrual Symptoms
Dennerstein L, Lehert P and Heinemann K. Menopause International 2011;17:88-95
Study Design (n=7226)
Europe/Latin America:
► 4,085 women (500 women per country)
► subsampling used for age, region and education
► Women aged 15-49 years
► Europe: France, Germany, Italy, Spain, UK and Hungary
► Latin America: Brazil and Mexico
Asia Pacific:
► Hong Kong, Pakistan, Thailand, (n=1200)
► Australia (n=400), Korea (n = 1,000); Japan (n=1,039)
Methodology:
► CATI (Computer aided telephone interview) Europe/LAmerica
► Online (Australia, Japan, Korea), questionnaire- other Asian
► 23 different symptoms:
► Severity of the symptom (Mild, moderate, severe)
► Frequency of experiencing the symptom
 In the last 3 months
 In the last 12 months
• Effect of premenstrual symptoms on Activities of Daily Living
Premenstrual Symptom Prevalences.
(Prevalence of at least moderately perceived symptom
Dennerstein et al. A global study of women’s experiences of premenstrual
symptoms and their effects on daily life. Menopause Int. 2011: 17:88-95
Abdominal Pain
31%
Irritability
Bloating
30%
29%
Joint/back/muscle pain
25%
Breast pain
24%
Lack of Energy
23%
Headaches
22%
Mood swings
21%
Anger
21%
Appetite changes
19%
Prevalence of PMS and PMDD - Region
Asia
Pacific
PMDD
LatAm +
Europe
4%
3%
PMS-ACOG criteria
22%
37%
ICD 10 Definition
90%
93%
100%
100%
definition
Total female population (15-49)
Prevalence of PMS and PMDD – By Country
Australia
Japan
Hong
Kong
Pakistan
Thailand
PMDD
9%
0.7%
1%
5%
0.5%
PMS-ACOG
43%
34%
17%
13%
15%
ICD 10 Definition
94%
97%
94%
80%
94%
Total female population (15-49)
100%
100%
100%
100%
100%
Asia Duration X Severity Symptom Indexes by Age
1.4
1.2
1
Total DSI Score Mean
0.8
Mental Score DSM Mean
Physical Score DSP Mean
0.6
0.4
0.2
0
Less 20
years
20<25
years
25<30
years
30<35
years
35<40
years
40<45
years
45 and
more
Objectives: Premenstrual Disorders
Types of Premenstrual Disorders
Prevalence
Aetiology
Role of Psychiatrist
Diagnosis
Treatment
Aetiology
PMDs-Stages with no symptoms
Pre-puberty
Pregnancy
Menopause
Hormonal Fluctuations and PMDs
Triggers
Ovulation
Cyclical Progesterone (normal levels)
= Trigger
CNS Progesterone Sensitivity
Proposed Aetiology of Premenstrual
Disorders
Genetic
predisposition
Neurotransmitters and
neurohormonal systems*
interact
Vulnerability
Increased sensitivity to
changes in gonadal
hormones
with
gonadal hormones
and metabolites
Altered responses to changes in
gonadal hormone levels
Premenstrual Symptoms
* serotonin, renin-angiotensin-aldosterone system, -aminobutyric acid (GABA), cholecystokinin.
Halbreich U. Psychoneuroendocrinology. 2003;28(suppl 3):55–99.
Objectives: Premenstrual Disorders
Types of Premenstrual Disorders
Prevalence
Aetiology
Role of Psychiatrist
Diagnosis
Treatment
What psychiatrists have to offer in
treatment of PMDs
•
Diagnostic skills
• PMDD, MDD, Anxiety Disorder, Personality
Disorder
• Identifying aetiological factors both
psychosocial (eg marital conflict, stressors)
and biological
•
Patience in evaluation
•
Experience in using rating scales
•
Ability to evaluate complex cases
Objectives: Premenstrual Disorders
Types of Premenstrual Disorders
Prevalence
Aetiology
Diagnosis
Treatments
Achieving Accurate Diagnosis
Obtain a careful history
Rule out other psychiatric or medical disorders or
psychosocial problems
• medical disorders
• major psychiatric disorders
• substance/alcohol/domestic violence
• premenstrual exacerbation of other disorders
Establish severity and luteal cyclicity prospectively to
clinch the diagnosis
History Taking
Menstrual History: pain, regularity, LMP, amenorrhoea
Premenstrual Symptom History: severity, type, absence or
presence following menstruation, symptom-free follicular
phase week,
Has there been any suicidal ideation.
Impairment: work, school, hobbies, social activities, family,
partner, work and colleagues. Distress ?
Is the patient receiving hormonal therapy – combined or
progestogen-only contraception, progestogen therapy, HT
What are the patient’s contraceptive needs, current
contraception, is family complete, is she trying to become
pregnant.
.
History
What treatment approaches would she find acceptable –
non-medical, behavioural therapy, psychotropics,
hormones, intrauterine hormones, surgical interventions
Is she prepared to receive therapy that will usually prevent
her getting pregnant during the treatment. Is she happy to
use barrier methods of contraception during treatment?
History of treatments experienced :self-administered or
prescribed and effects.
Examination
Daily charting - www.symptometrics.com
Daily Symptom Rating Chart
Adapted from Dennerstein L et al Psychoneuroendocrinology: 19:
293-304 1994
Which Patients are Referred to Psychiatrists
Those women with psychiatric disorders or
psychosocial comorbidities
PMDs or PMDD sufferers without adequate
response to treatment
Women at risk of suicide or violence
premenstrually
Objectives: Premenstrual Disorders
Types of Premenstrual Disorders
Prevalence
Aetiology
Role of Psychiatrist
Diagnosis
Treatment
What psychiatrists have to offer in
treatment of PMDs
•
Management
• Experience in using psychotropic drugs,
particularly SSRIs
• CBT and other techniques to reduce
stressors (internal and external)
PMDs treated by Psychiatrists
•PMDD
•Premenstrual
exacerbation of psychiatric
disorders
Whereas other PMDs- treated by gps or
referred to gynecologists
Therapies for Premenstrual Syndrome
Pharmacologic agents
• Antidepressants
• Diuretics
• Anti-Anxiety medications such as
benzodiazapines
• Induce pharmacologic menopause
• Oral contraceptives (OCs) such as YAZ®
Cognitive-behavioral therapy
Evidence-based Management of PMDs
[oestrogen meta-analysis awaited]
favours placebo
favours treatment
vitamin B6
SSRIs(overall)
SSRIs(continuous)
SSRIs(luteal phase)
progesterone(overall)
progesterone(oral)
progesterone(suppository)
progestagens
GnRHa
danazol(luteal phase)
danazol(continuous)
danazol(breast symptoms)
cognitive behavioural therapies
0.1
1
odds ratio
10
100
Anti-depressants
Selective serotonin reuptake inhibitors (SSRIs) and SNRI
Help lessen the impact of hormone changes on
serotonin.
May be used either daily or for the 14 days before
menstruation
Improve mood and physical symptoms within 48 hours
Three SSRIs (fluoxetine, sertraline, and controlledrelease paroxetine) have FDA indication for PMDD1
Fluoxetine, paroxetine, citalopram, sertraline all sign.
more effective than placebo
Serotonin/norepinephrine reuptake inhibitors (SNRIs)
(venlafaxine)
1.Brown C, Ling FW. In: Bieber EJ, Sanfilippo JS, Horowitz IR, eds. Clinical Gynecology.
Philadelphia, PA: Churchill Livingstone Elsevier, 2006: 19–35
Luteal-phase (intermittent) SSRI dosing
14 days before expected menses thru to menses
11 RCTS of luteal dosing SSRIs, SNRIs and other
serotonergic antidepressants show efficacy for
PMDD
Not as effective for physical symptoms
Advantages: limiting drug exposure, rare to have
serotonin withdrawal syndrome, potentially
increasing compliance and decreasing side
effects, less costly
Side effects of SSRIs
Fatigue, insomnia, nausea, gastrointestinal
disturbance, headache, sweating and tremor.
Continuous use - decreased libido and
anorgasmia.
Serotonin withdrawal- Dizziness, lethargy,
nausea, irritability, decreased mood and vivid
dreams (rare with intermittent therapy).
SSRIs can be given concurrently with OCs.
.
Ovarian Suppression
►
PMS not present in anovulatory cycles
PMS not present after surgical and natural menopause
(bilateral ovariectomy)
►
GNRH - improvement in physical and behavioural symptoms
►
LHRH agonist - successful versus placebo
►
GNRH + addback CEE+MPA – 60% improvement
►
GNRH + addback hormones may precipitate symptoms for some
women
►
(Muse et al 1984)
(Hammarback and Backstrom 1988)
(Mortola et al 1991)
(Schmidt et al 1998)
►
Danazol reduces severe PMS symptoms and cyclical menstrual
psychosis
(Dennerstein et al 1983; Sarno et al 1987; Halbreich et al 1991; O’Brien and Abukhalil 1999)
►
High dose estradiol can prevent ovulation and reduce PMS (protect
endometrium)
(Watson et al 1989)
►
Combined oral contraceptive (OC) use? Variable results!
Progestins in Oral Contraceptives
Progestins in OCs derived from 19-nortestosterone may
cause these adverse effects1,2
• Irritability/nervousness
• Headache
• Bleeding irregularities
• Weight gain
1. Mishell DR, Jr. In: Katz VL et al, eds. Comprehensive Gynecology, 5th edition.
St. Louis: Mosby, 2001: 275-325.
2. Moghissi KS. In: Ransom SB, ed. Practical Strategies in Obstetrics and
Gynecology. Philadelphia: W. B. Saunders Company, 2000: 3–14.
Oral contraceptive pill
YAZ®, the first oral contraceptive pill approved to
treat the emotional and physical symptoms of
PMDD
Contains 3 mg drospirenone and 20 mcg ethinyl
estradiol in a 24-day active hormone pill and 4day placebo pill (24/4) regimen
Drospirenone is derived from 17-spirolactone
30 hour half life
Causes less hormonal fluctuations than traditional
21-day active pill regimen
Safe and well-tolerated in majority of women in
clinical trials
Significant improvement in mood, physical
and behavioral symptoms
A greater proportion of women recorded a decrease in mood,
physical and behavioral symptoms with YAZ® vs. placebo
*p<0.005; change from baseline assessed in subscales from
Daily Record of Severity of Problems (DRSP)
Yonkers et al. Obstet Gynecol 2005;106:492–501
PMDD: Effect Size (standardized mean difference)
of a low dose COC (Drospirenone/EE20) vs SSRIs
Drospirenone/EE 20 parallel
study
Drospirenone/EE20 crossover
study
SSRI`s pool ed data from 13 RCT`s
844 patients
Yonkers et al. JAMA 1997
(Wyatt et al. Cochrane Library 2002)
Cohen et al. ACOG 2002 *
Pooled data from SSRI studie s *
(incl. 774 parti cipants) using
DRSP scale as outcome
Halbreich et al. ACOG 2002
-2
-1,5
-1
-0,5
Favours treatment
Large medium small
0
favours placebo
(by convention, Cohen 1969)
Treatments for PMDs with evidence from at least 1 RCT
Femal (Swedish herbal) – for premenstrual insomnia
St John’s wort and Vitex agnus-castus (Chasteberry) for
PMS
Alprazolam (GABAergic): 6 RCTS : 4 showed efficacy,0.25
to 0.5 mg bd to tds luteal phase only
Buspirone : 2 small RCTs at up to 60 mg divided dose/day
Spironolactone: 100mg daily for 8 days premenstrually
Calcium: 1200 mg/day
Complex carbohydrate suppl. for affective PMS symptoms
Soy supplementation for physical but not mood symptoms
Vit B6 – 80 mg/day,
Saffron
CBT for mental symptoms
Massage, biofeedback, hand acupuncture
Conclusions
►
Physical symptoms are the most prevalent
premenstrual symptoms experienced
►
Psychiatrists treat predominantly exacerbations
of underlying psychiatric disorders (with better
control of those disorders or increase or
addition of SSRI in second part of cycle)
►
Some psychiatrists treat PMDD, usually with
SSRI
►
Psychiatrists also use CBT and stress
reduction techniques for PMDs
►
Need for evaluation of combined therapies, eg
Yaz + SSRIs
Acknowledgements
Data was made available by Bayer Schering
pharma for independent analysis.
Statistical analysis by Prof. Philippe Lehert
Profs Dennerstein and Lehert received a research
grant to fund analysis
Co-investigators Drs. K. Heinemann, T.
Backstrom, Lam Siu Keung ,Sadiah Ahsan Pal,
Dooseok Choi
Questions?
Dr Jane Hendtlass
Risk Assessment
Psychiatric Essentials for
International Medical
Graduates
RISK ASSESSMENT
Dr Jane Hendtlass B.Sc.(Hons.), LL.B.(Hons.), Ph.D,
A.R.A.C.I., F.A.I.C.D., A.I.M.M.
31 August 2012
Outline

A Coroner’s Perspective
Risk Assessment including

Definition of risk

Risk assessment

Management of assessed risk

Evaluation of risk assessment and management

Summary

Role of a Coroner
The coronial system of Victoria plays an
important role in Victorian society. That
role involves the independent investigation
of deaths for the purpose of finding the
causes of those deaths and to contribute to
the reduction of the number of preventable
deaths and the promotion of public health
and safety and the administration of justice.
Coroners Act 2008
We are all trying to
LEARN
FROM
OUR
MISTAKES
Deaths Reportable to the
Coroner include


A death that appears to have been
unexpected, unnatural or violent or to have
resulted, directly or indirectly, from an
accident or injury; or
The death of a person who immediately
before death was a person placed in
custody or care;
Coroners Act 2008
A Person Placed in Custody
or Care
includes—



a patient in an approved mental health service
within the meaning of the Mental Health Act 1986;
a person under the control, care or custody of the
Secretary to the Department of Human Services or
the Secretary to the Department of Health;
a person under the control, care or custody of the
Secretary to the Department of Justice or a
member of the police force; … Coroners Act 2008
Reportable Deaths
In effect, reportable deaths include all deaths of:







Voluntary and involuntary inpatients in an approved
mental health service;
Involuntary patients of community mental health
services;
Patients subject to section 10 of the Mental Health
Act 1986 or otherwise in police custody;
Prisoners;
Homicides;
Motor vehicle incidents;
Suicides.
Coronial Investigation
A coroner investigating a reportable
death must find, if possible—
(a) the identity of the deceased; and
(b) the cause of death; and
(c) the circumstances in which the
death occurred… Coroners Act 2008
Powers to Obtain Information
A coroner may—




require a person to prepare a statement addressing
matters specified by the coroner and give the
statement to the coroner;
order a police officer to
take copies of any documents relevant to the investigation;
seize things (including documents) and take samples, which
may be relevant to the investigation;
 summon a person to attend as a witness or to
produce any document or other materials;

order a witness to answer questions.
Coroners Act 2008
Mandatory Inquest
A coroner must hold an inquest into a
death if the death or cause of death
occurred in Victoria and—
(a) the coroner suspects the death was
the result of homicide; or
(b) the deceased was, immediately
before death, a person placed in
custody or care;
Coroners Act 2008
Reports and
Recommendations
A coroner may make recommendations to any
Minister, public statutory authority or entity on any
matter connected with a death which the coroner
has investigated, including recommendations
relating to public health and safety or the
administration of justice.
If a public statutory authority or entity receives
recommendations made by the coroner, the public
statutory authority or entity must provide a written
response, not later than 3 months after the date of
receipt of the recommendations. Coroners Act 2008
Publication of findings
and reports


Unless otherwise ordered by a
coroner, the findings, comments and
recommendations made following an
inquest must be published on the
Internet.
The coroner must—
publish the response of a public
authority or entity on the Internet.
A Coroners’ Perspective
Summary


We only investigate circumstances where death has occurred.
We investigate deaths of people with mental illness who die in traumatic
circumstances or in hospital or custody of police or prison or are otherwise subject to
involuntary treatment.

We must hold an inquest if a person with a mental illness was in custody or care or it
is otherwise warranted.

We make comment and recommendations intended to help prevent further deaths
and promote public health.

Our comments and recommendations are public documents

We also learn from the formal responses from Ministers, government agencies or
entities.
We are all trying to
LEARN
FROM
OUR
MISTAKES
Risk
Risks for a person presenting with suspected
mental illness include:


Self harm and suicide and
Deliberate or unintentional harm to others
As well as risk of:



Absconding
Unintentional harm, such as the effects of physical
restraint, intolerance to medication, adverse effects
of treatment or assault by another
Effect of alcohol and/or other drugs alone and in
combination with prescribed medications
Risk Assessment and
Management


By definition, risk assessment and management are
important issues in the circumstances surrounding
deaths of people with a mental illness and in
exercising our prevention role.
Further, coroners rarely consider the circumstances
of people with a mental illness when their risk
assessment and management was effective in
preventing their death or their causing someone
else’s death.
Risk Assessment includes:








Mental state and diagnosis
History and circumstances of referral
Physical health
Prior admission history
Previous and recent risk assessments
Self reported immediate and long-term
intentions
Family, cultural and community
circumstances
Dual diagnosis and/or effects of alcohol and
other drugs
Risk Management includes










Management plan
Admission status
Medication
Security and opportunity of allocated bed: seclusion, high
dependency, low dependency
Observations and physical needs
Leave arrangements
Discharge plan
Referrals
Communications with family and community supports
Documentation in the medical record
Evaluation of Information
Assessment of risk requires evaluation of
information obtained from:
Communication
with referring agencies
Documentation
in medical record.
including:
oThe Patient, family members, general practitioner
oPolice and police medical officers
oECATT and emergency department medical officer
oCommunity treating team including case manager
Communication of
Information
Management of risk requires communication of
information through:
Communication with referral agencies including:
oThe Patient, family members, general practitioner
oInpatient treating team and case manager
oCATT and Community treating team including case
manager
oSpecialist medical and other professionals
oPolice, community and cultural supports
Documentation in medical record.
Evaluation
The Coroner will review your risk assessment
and management against:
 The patient’s subsequent history and death
and








Your communication with and consideration
of:
The Patient
The family
The treating teams
Community and cultural supports
General practitioner/local medical officer
Specialist medical and other professionals, and
Documentation in medical record
Summary




Risk includes self harm, harm to others, unintended
consequences of professional actions and decisions.
Risk assessment includes acute and chronic risk
factors and information provided by The Patient,
family members, the treating team and the
community including police.
Management of assessed risk includes
communication with The Patient, family members,
the treating team and the community including
police.
The patient’s subsequent history and the medical
record are the principal sources of information used
to evaluate the appropriateness of your risk
assessments.
We are all trying to
LEARN
FROM
OUR
MISTAKES
Questions?
Lunch
MOOD STABILIZERS,
ATYPICAL ANTIPSYCHOTICS
& BIPOLAR DISORDER
Professor Isaac Schweitzer
Medical Director, The Melbourne Clinic
Healthscope Chair of Psychiatry
Department of Psychiatry
University of Melbourne
Today’s Talk
1.
2.
3.
4.
Bipolar Disorder: Basic facts
Classification and Defining Bipolar Disorder
Psychotherapy for Bipolar Disorder
Pharmacotherapy of Bipolar Disorder
1. Mania
2. Depression
3. Maintenance
Some Basic Facts
Onset: 15 - 24 years old
 Lifetime prevalence:

◦
◦
Bipolar I – 1%
Bipolar II – 2%
Age of 1st treatment: 10 years later
 1/3 attempt suicide and 10% to 15%
succeed
 90% recurrence rate

Goodwin and Jamison. Manic-Depressive Illness 1990
Woods. J Clin Psychiatry 2000;61(suppl 13): 38-41
Bipolar Mood Disorders
 Bipolar I
 Bipolar II
 Cyclothymic disorder
 Bipolar Disorder NOS
Bipolar I Disorder
 Manic episodes and episodes
of Major Depression
 10% patients do not have
Major Depression but are
still classified as Bipolar I
Bipolar II Disorder
 Hypomanic episodes and
episodes of Major Depression
Cyclothymic Disorder
 Hypomanic episodes and
 episodes of “Minor”
Depression ie < 5/9 symptoms
 A diagnosis that is rarely made!
Bipolar Disorder is defined by
presence of episodes of elevated
mood ie hypomania or mania
DSM IV TR criteria for Hypomania


A distinct period of persistently
elevated, expansive or irritable
mood lasting throughout at least 4
days.
Three (or more) of the following
symptoms have persisted (four if the
mood is only irritable):
DSM IV TR criteria for Hypomania
◦ inflated self-esteem or grandiosity
◦ decreased need for sleep
◦ more talkative than usual or pressure
to keep talking
◦ flight of ideas or subjective experience
that thoughts are racing
DSM IV TR criteria for Hypomania



distractibility
increase in goal-directed activity (either
socially, at work or school, or sexually)
or psychomotor agitation.
excessive involvement in pleasurable
activities that have a high potential for
painful consequences
DSM IV TR criteria for Hypomania

The episode is associated with an
unequivocal change in functioning that is
uncharacteristic of the person when not
symptomatic.

The disturbance in mood and the change
in functioning are observable by others.
DSM IV TR criteria for Hypomania
The episode is not severe enough

◦
◦
◦
to cause marked impairment in social or
occupational functioning, or
to necessitate hospitalization, and
there are no psychotic features.
DSM IV TR criteria for Mania
Descriptively the same features
except:

◦
◦
◦
The episode is at least seven days
duration unless hospitalization occurs
There is marked impairment in social or
occupational functioning, ie more
severe, and
there may be psychotic features.
Burden of bipolar depression
Time spent in phases of illness: dominated by depression
Bipolar Depression
The diagnosis of Bipolar Disorder is often
missed
 Patients typically present with depression
and neglect to mention their elevated
mood states - use appropriate probes.
 The index episode for Bipolar Disorder is
often Major Depression

When is Depression More
Likely to be Bipolar?
Reversed vegetative symptoms
 Psychomotor retardation
 Psychotic features
 Affective lability
 Family history of Bipolar Disorder

Mitchell et al, 2008 Diagnostic
guidelines for bipolar depression: a
probabilistic approach

“There are no pathognomonic
characteristics of bipolar I depression
compared to unipolar depressive
disorder.”

“There are………clinical characteristics
that are more common in both bipolar I
depression and unipolar depressive
disorder, respectively,”
Bipolar Depression:
Not a Unitary Condition

Biological reaction to elevated mood
state – rebound neurochemical changes.

Psychological response to
manic/hypomanic episode

Co-morbid depressive disorder eg
associated with current psychosocial
circumstances;
Bipolar Depression:
Not a Unitary Condition

Co-morbid substance abuse disorder

Co-morbid personality disorder

Demoralization due to effects of
chronic illness;
Bipolar Depression:
Not a Unitary Condition

Medication side-effect – substance
induced mood disorder (mood
stabiliser or neuroleptic).

Combination of factors
Bipolar Disorder & Co-morbid
Anxiety Disorder
Otto et al 2006
 1000 outpatients with BPD were followed
for 12months
 31.9% co-morbid anxiety disorder
 Anxiety associated with fewer days well,
less likely to recover from depression,
poorer quality of life and diminished role
function
Psychotherapy for the
Bipolar Disorders
MAPS program

Combines Psycho-educational, CBT and
Social Rhythms approaches including:
◦
◦
◦
◦
M - monitoring mood and activities
A - assessing prodromes
P - preventing relapse and
S - SMART goal setting ie MAPS.
Method

84 participants randomised to receive:
◦ MAPS (12 week intervention plus 3 booster
sessions), or
◦ Treatment as usual (TAU).

follow up:
◦ face to face interviews (at baseline, 3 and 12
months) and
◦ monthly telephone interviews (for 9 months
post-intervention).
Results
 Participants
who received MAPS
programme were significantly less
likely to have a relapse of any type
and spent less time unwell.
Results

There was reduced rate of relapse in
the treatment group compared to
control, for pooled relapses of
◦ any type (hazard ratio 0.44; 95%CI 0.20 to 0.96, z=2.06, p= 0.04),
◦ depressive episodes (hazard ratio 0.28; 95% CI
0.09 to 0.84, z = -2.27, p = 0.02) and
◦ manic/mixed episodes (hazard ratio 0.15; 95%
CI 0.02 to 1.24, z = -1.76, p = 0.08).
0.00
Estimated survivor function
0.25
0.50
0.75
1.00
1st relapse of any type
0
100
200
Time (post treatment, days)
Treatment
Control
300
Pharmacotherapy of Bipolar
Disorders
Note – most RCT trials have been
performed on Bipolar I subjects.
 Most evidence for the treatment of
Bipolar II is based on the above studies or
small studies or open label studies.

Patient Adherence
in Bipolar Disorder



6 year longitudinal study of 1594
lithium users in HMO.
Lithium use mostly sporadic – median
use was 76 days.
Discontinuation associated with
hospitalization.
Johnson & McFarland 1996
Pharmacological Treatment of Acute
Mania: First Line

Monotherapy
◦
◦
◦
◦
◦
◦
◦
Lithium,
Valproate,
Olanzapine,
Risperidone,
Quetiapine,
Ziprasidone &
Aripiprazole
Monotherapy versus Combination
Therapy for Acute Mania
Response rates sig higher with combination
therapy (RR 1.53) compared with lithium ⁄
divalproex alone.
 A meta-analysis of 24 studies (n = 6,187),
found that adding atypical antipsychotic
agents to lithium ⁄divalproex was
significantly more effective than treatment
with lithium ⁄ divalproex alone for the
treatment of acute mania (Scherk etal, 2007).

Pharmacological Treatment of Acute
Mania: First Line

Combined Therapy –
◦ Lithium or Valproate plus




Risperidone or
Olanzapine or
Quetiapine or
Aripiprazole
Pharmacological Treatment of Acute
Mania: Second Line
Carbamazepine,
 ECT
 Lithium + Valproate
 Asenapine
 Asenapine + Lithium or Valproate
 Paliperidone

Pharmacological Treatment of Acute
Bipolar I Depression: First Line
Lithium
 Lamotrigine
 Quetiapine
 Lithium or Valproate + SSRI
 Olanzapine + SSRI
 Lithium + Valproate

Pharmacological Treatment of Acute
Bipolar I Depression: Second Line
Quetiapine + SSRI
 Valproate
 Lithium or Valproate + Lamotrigine
 Adjunctive Modafinil

Maintenance Pharmacotherapy for
Bipolar: First Line
Lithium
 Valproate
 Olanzapine
 Quetiapine

Maintenance Pharmacotherapy for
Bipolar: First Line
Lithium or Valproate + Quetiapine
 Risperidone LAI – alone or adjunctive
 Aripiprazole (mania only?)
 Lithium or Valproate + Ziprasidone

Maintenance Pharmacotherapy for
Bipolar: Second Line
Carbamazepine,
 Lithium & Valproate
 Lithium & Carbamazepine
 Lithium or Valproate & Olanzapine
 Lithium + Risperidone
 Lithium + Lamotrigine
 Olanzapine + Fluoxetine

Conclusions
The
Bipolar Disorders are a group of
mood disorders characterized by
episodes of elevated mood and
depression.
The diagnosis of Bipolar disorder is often
missed and delayed.
Though elevated mood states define the
disorder, patients spend more of their
lives depressed.
Conclusions
The
management of Bipolar Disorder
requires a biopsychosocial approach ie a
combination of psychotherapy and
pharmacotherapy.
Mood stabilizers are drugs which are
used in bipolar disorder to ameliorate
symptoms of mania, hypomania, bipolar
depression and to prevent episodic
relapse.
Conclusions
Lithium
remains the gold standard mood
stabilizer
Valproate and Carbamzepine are classic
mood stabilizers
Increasingly atypical anti-psychotics are
being used in bipolar patients and are
showing effective mood stabilizing
properties.
Conclusions
Choice
of agent requires careful
consideration and a weighing of the
pros and cons.
Most agents have potentially
significant side effects, particularly
over the long term.
Combination of medications is often
needed for effective treatment.
Questions?
Professor Graham Burrows
Chairperson 2
Dr Angelo Ferraro FRANZCP
Old Age Psychiatrist
North West Aged Persons Mental Health
Disclosure Statement
I, or an immediate family member including
spouse/partner, have at present and/or
have had within the last 12 months, or
anticipate NO financial
interest/arrangement or affiliation with one
or more organisations that could be
perceived as a real or apparent conflict of
interest in context to the design,
implementation, presentation, evaluation,
etc, of CPD activities – Angelo Ferraro,
FRANZCP
What is Cognition?
Cognition: The process of knowing (which
includes) being aware, thinking, learning, and
judging…from the Latin root “cognoscere”
meaning “to be acquainted with” 1
Memory: Is one important component of
cognition, which includes other faculties such
as attention, language (expression and
comprehension), executive function,
reasoning, visuospatial functioning
1 Adapted from Webster’s New World Medical Dictionary
Memory Deficits

Retrieval deficits versus Storage deficit

Diagnostic significance

Use of cues during recall
Ultra Brief Cognitive Screening
MINI-COG (Borson S, 2000,
International Journal of Geriatric
Psychiatry)
 1. Remember 3 words
 2. Draw a clock (11:10)
 3. Recall 3 words, with cues if required

Mini Mental Status Examination




Not to be confused with the MSE
MMSE, Folstein & Folstein. Maximum
score 30
Orientation, Memory and Recall,
Concentration, Language
Weaknesses:
 Best for English speaking Anglo-Americans
 Excessive focus on language; no assessment of
executive function
 Confusion re scoring – do standardised MMSE
Montreal Cognitive Assessment
(MOCA)
www.mocatest.org
 Maximum score 30
 Translated into several languages
 Incorporates testing of executive
function
 Memory test and naming more difficult
than the MMSE

Rowland Universal Dementia
Assessment Scale (RUDAS)
http://www.rudas.com.au
 On line video training
 minimises the effects of cultural learning
and language diversity on the
assessment of cognition
 Maximum score 30

Factors influencing results
Education
 Culture
 Normal aging
 IQ
 Ability and willingness to attend to task
 Distraction
 Cut off scores

Is it normal ageing?




Brain is an organ, like heart and kidneys
When an older adult is interrupted while
completing a task, it is likely that the
original task at hand can be forgotten
“..now what was I doing when I was
interrupted..”
source information is also impaired Ie.
remembering the information but forgetting
where they obtained the information
Is it Mild Cognitive Impairment?





Have more memory problems than would be
accounted for by ageing
able to accomplish their usual daily tasks
Trouble remembering names, the flow of
conversation, and a greater tendency to
misplace things
It can be difficult to define how much
cognitive impairment is considered ‘more
than normal’
Increased risk of developing dementia
Depressive Pseudodementia











Depressed
Slow monotonous speech
Long time to respond
“I don’t know” responses
Quick to give up
Poor attention
Incomplete responses
Forgetfulness
Aware of cognitive problems
Believes they are going mad or losing their
memory…”do I have Alzheimer’s? See, I can’t
remember anything!”
No evidence of aphasia, apraxia or agnosia
Cognitive deficits of
schizophrenia
Memory, attention, executive function
 A subgroup of patients will worsen over
time
 Neuroimaging findings overlap

Disorders with cognitive
symptoms













active symptoms of mental illness: motivation, distraction.
Medication related effects (eg anticholinergic, sedatives, APs,
ADs, mood stabilisers)
Substance misuse
Visual and hearing deficits
Neurodegenerative disorders
Obstructive Sleep Apnoea
Delirium
Post surgery
Active medical illness
Normal Pressure Hydrocephalus
Head injury
Autoimmune/collagen vascular disorders
Neoplasms
Now what?
Obtain an accurate and corroborated
longitudinal history
 decline in activities of daily living?
 Exclude and treat reversible factors
 Driving
 Neuroimaging, organic screening,
neuropsychological assessment
 Repeat testing

Take home message

The presence of cognitive deficits does
not automatically signify the presence of
dementia

Assessment of cognition is the easy part
– Interpretation of your findings is hard
Questions?
Afternoon Tea
Update on
Psychopharmacology Professor Nicholas Keks
Monash University, Delmont Private Hospital
Competing interests statement
•
During my career I have received research support, and/or acted as consultant to, and/or received travel support and/or received honoraria from Astra Zeneca, Eli Lilly, Novartis, Wyeth, Bristol Myer Squibb, Janssen, Sanofi Aventis, Organon, Lundbeck, Servier and Pfizer
• During my career I have been employed by Government services and
acted as consultant to Governments
• I am affiliated with Monash University, the Mental Health Research Institute of Victoria, Epworth Healthcare & Delmont Private Hospital
Issues
•
•
•
•
•
Antidepressants: Agomelatine
Antipsychotics: asenapine
Diagnostic assessment of psychoses
Mortality and antipsychotic treatment
Polypharmacy in management of psychoses
Antidepressants 1
• tricyclics : imipramine (Tofranil)
amitriptyline (Tryptanol)
dothiepin (Prothiaden)
clomipramine (Anafranil)
• MAOIs : phenelzine (Nardil)
tranylcypromine (Parnate)
• moclobemide (Aurorix)
• reboxetine (Edronax)
• mianserin (Tolvon)
• mirtazepine (Avanza)
Antidepressants 2
• SSRIs : fluoxetine (Prozac, Lovan)
sertraline (Zoloft)
fluvoxamine (Luvox)
paroxetine (Aropax)
citalopram (Cipramil)
escitalopram (Lexapro)
• SNRIs: venlafaxine (Efexor)
duloxetine (Cymbalta)
desvenlafaxine (Pristiq)
Melatonin
(McCord & Allen, 1917)
O
NH
CH3
H3C O
N
H
N-acetyl 5-methoxy tryptamine
(Lerner, 1958)
Melatonin
• So called because bovine pineal extract made tadpoles pigmented (McCord & Allen 1917)
• Chemically characterised by Lerner, 1958
• Not till 1980s discovered melatonin is a non‐
photic messenger for circadian and diurnal rhythms
• Melatonin is the primary circadian synchronising hormone in brain
• With motor and mood implications Melatonin
• A key synthesizer of biological rhythms and sleep
• Secretion from pineal gland
• is tightly coupled to light‐dark and seasonal cycles
• Controlled by suprachiasmatic nucleus (SCN) located above hypothalamus
• SCN has input from retina and feedback from melatonin Melatonin, 5‐HT and the SCN
•
•
•
•
SCN is the neuronal master clock
Input from light at retina via GLU path
Outputs include pineal gland Melatonin is a potent agonist at MT1 & MT2
receptors in SCN
• SCN also gets input from 5‐HT pathway originating in brainstem Raphe nuclei through 5‐HT2c receptor (as well as other 5‐HT receptors)
Melatonin receptors
•
•
•
•
Cloned in 1990s
MT1 & MT2
High density in suprachiasmatic nucleus
Also in hippocampus, hypothalamus, frontal cortex, cerebellum, thalamus
• Possibly much more extensive physiological role than currently known
Chronorhythms in depression
•
•
•
•
•
•
Alterations in mood: diurnal variation
Changes in sleep e.g. EMW, delay in REM onset
Cortisol secretion peak earlier
Core body temperature alterations
Mostly phase advances
But seasonal affective disorder associated with phase delay • Atypical/bipolar depression
Melatonin in depression
• Nocturnal melatonin pulse blunted
• Less melatonin is released in depression
• Melatonin levels rise as antidepressants improve depression
• Melatonin improves sleep in depression
• But melatonin is not an effective antidepressant Chemical structures of agomelatine and melatonin
O
Melatonin
NH
Agomelatine
NH CH3
CH3
H3C O
H3C
N
H
O
O
Agomelatine
•
•
•
•
•
•
Naphthalene derivative of melatonin
Potently binds MT1 & MT2 receptors
Mimics action of melatonin
Inhibits firing of SCN α dose
Alters protein synthesis within SCN neurones
Normalizes disturbance of circadian rhythms (resynchronization)
• Antagonises 5‐HT2c receptor
Resynchronising effect of agomelatine
• In animals and humans, agomelatine reinstates normal circadian rhythms
• effect is via SCN, not pineal • Works for both phase delay and phase advance
• Needs only 1 hour of effect daily, maximal at light‐dark transition
• Effect by initiating intraneuronal protein synthesis to alter SCN neuronal function
Agomelatine and 5‐HT2c receptors
• Modest but effective antagonist
• SCN 5‐HT2c receptors mediate input to ‐VTA: Dopamine pathways ‐locus coeruleus: Noradrenergic pathway
• 5‐HT2c receptors are overactive in depression and anxiety • Antagonism of SCN 5‐HT2c receptors enhances frontal NA and DA
Noradrenergic and serotonergic pathways
Dopaminergic pathways
Agomelatine: mechanism of antidepressant activity
• Neither agonism at MT1 & MT2 receptors nor antagonism at 5HT2C receptors can individually explain MOA
• synergistic action at melatonin and 5HT2C receptors needed to explain antidepressant activity in models
• Antidepressant properties of agomelatine result from actions at MT1, MT2 and 5HT2C receptors Antidepressant efficacy of agomelatine versus SSRIs and SNRI after 6/8 weeks
HAM-D17 total score
0.92
CGI-I total score
NS
1.49
P=0.024
NS
1.46
-1
0
Favours
comparator
1
2
Favours
Agomelatine
0.29
vs sertraline
vs escitalopram
1.37 P<0.001
3
NS
0.18
vs fluoxetine
P=0.031
1.68
0.19
-0.2
P=0.023
NS
0.24 P<0.001
META
META ANALYSIS
ANALYSIS
4
P=0.016
0.32
vs venlafaxine
-0.1
Favours
comparator
0.0
0.1
0.2
0.3
0.4
0.5
0.6
Favours
Agomelatine
Agomelatine 25-50 mg (N=630)
sertraline 50 -100 mg, fluoxetine 20-40 mg, venlafaxine 75 -150 mg, escitalopram 10 -20 mg (N=642)
(Kasper et al. Europ Neuropsychopharmacol 2010 Volume 20, Supplement 3, Page S348)
Comments: agomelatine
• not hypnotic, sleep benefit takes days/weeks
• dose 25 to 50mg but tested to 100mg nocte
• contraindicated in active liver disease/cirrhosis;
hepatic metabolism therefore probably need wide
dose range
• do LFT at baseline, 6, 12, 24 weeks and as
needed (1% elevation, higher at high doses eg
1.5% at 100mg)
• nausea, dizziness and headache at same rate as
placebo, no weight gain, sexual dysfunction, or
cardiac issues
Classification of psychoses
Psychoses
Medical cause
• Drug intoxication
• Drug withdrawal
• Metabolic
• Endocrine
• Brain disease
• Epilepsy
• Infective, eg AIDS
No identifiable medical cause
Bipolar mood
disorder
Schizophrenia (including
schizophreniform and
schizoaffective) and other
disorders, (delusional
disorder/paranoid psychosis,
psychotic depression, etc)
Symptom dimensions in psychoses
• Positive (delusions, hallucinations, positive formal thought disorder)
• Negative (flat affect, poverty of thought, amotivation, withdrawal)
• Cognitive (executive function, concentration, working memory)
• Affective (elevated, depressed, mixed)
• Anxiety/obsessive compulsive
Typical antipsychotics
• Low potency: – chlorpromazine (Largactil)
• High potency: –
–
–
–
–
–
–
–
–
–
haloperidol (Serenace)
haloperidol decanoate (Haldol)
trifluoperazine (Stelazine)
pericyazine (Neulactil)
pimozide (Orap)
droperidol
fluphenazine decanoate (Modecate)
zuclopenthixol acetate (Acuphase)
zuclopenthixol dec (Clopixol)
flupenthixol dec (Fluanxol)
Novel/atypical antipsychotics
•
•
•
•
•
•
•
•
•
•
risperidone (oral & injectable)
olanzapine (oral & injectable)
quetiapine (IR & XR)
clozapine amisulpride aripiprazole ziprasidone paliperidone (oral & injectable)
sertindole
asenapine
Asenapine
Mirtazepine
Asenapine
• Asenapine belongs to dibenzo‐oxepino pyrrole family
• The structure of asenapine is unlike other antipsychotics • still effectively a serotonin dopamine antagonist with noradrenergic and antihistaminic properties
• non‐anticholinergic
Clinical implications
•
•
•
•
•
Serotonin blockade: nausea, headache
Noradrenergic: postural hypotension, dizziness
Antihistaminic: sedation, weight gain
Antidopaminergic: EPS, prolactin
No anticholinergic effect (dry moth, blurred vision, urine difficulties, constipation, tachycardia, memory, delirium)
Asenapine pharmacokinetics
• Poor bioavailability unless taken sublingually and nil orally for 10 minutes afterwards
• Biphasic elimination; terminal half life about 24 hours
• Steady state in 3 days
• Hepatic metabolism CYP1A2 (fluvoxamine) & CYP2D6
• Recommended to be taken BD (? to minimise EPS) but mostly used nocte in USA Asenapine: clinical effectiveness
• RCTs in acute schizophrenia and relapse prevention indicate effectiveness of comparable level to risperidone
• RCTs in bipolar disorder indicate effectiveness for mania and for manic and depressive symptoms in mixed states
• Also effective long‐term in bipolar, equivalent to olanzapine Asenapine: clinical effectiveness
• Real‐life clinical experience indicates asenapine is an effective antipsychotic
• Useful in mood disorders
• May have benefit for depression • Probably milligram equivalent to olanzapine.
Asenapine: tolerability
•
•
•
•
•
•
•
Sedation (< olanzapine)
Oral hypoaesthesia & bitter taste
Akathisia and EPS (low but > nil risk)
Dizziness and postural hypotension
About half weight gain of risperidone
Prolactin effect minor (similar to olanzapine)
NO anticholinergic effects (very important if changing from cholinergic drug eg olanzapine or quetiapine)
Cautions (all appear to be equivalent to class effects)
•
•
•
•
•
•
CVA in elderly; use smaller dose
Neuroleptic malignant syndrome
Seizures
Diabetes
QTc prolongation
Pregnancy and lactation
Using asenapine
•
•
•
•
Start 5mg nocte or 5mg BD
Increase as needed to 10mg BD
Most patients tolerate nocte dose eventually
Instruct not to touch tablet but to remove cover and keep tablet in foil to apply to bottom of tongue
• Always warn about 10 minute eat/drink rule, numbing of tongue and bitter taste
Tiihonen et al, Lancet, 2009
• Long‐term antipsychotic use associated with lower mortality than no AP use
• Clozapine associated with much lower mortality than other APs
• Combination APs caused lower mortality than risperidone and quetiapine monotherapies (Tiihonen et al, 2009)
Antipsychotic risk benefit evaluation
• Enormous emphasis on risk e.g. metabolic syndrome
• De‐emphasis of benefits, mixed up with dispute about whether SGAs are more effective than FGAs
• Tiihonen study strongly suggests that undertreatment can, with adverse effects taken into account, increase mortality
• Clear support for the benefit of treatment.
Antipsychotic polypharmacy
• Clinically, the use of two or more antipsychotics at the same time is very common
• Meta‐analyses have suggested that antipsychotic combinations may be more effective than monotherapy
• Tiihonen suggests polypharmacy causes less mortality than monotherapy
• CPGs still advocate antipsychotic monotherapy
(Correll et al, Schiz Bull, 2009)
Polypharmacy: Tiihonen et al, 2012
• 7 year study in 2588 Finnish registry patients hospitalised with first episode schizophrenia
• Use of antipsychotic combinations did not increase mortality
• Benzodiazepine use was dissociated with a marked increase in mortality
• Antidepressant use was dissociated with decrease in suicide
(Archives Gen Psychiatry 69:476, 2012)
Polypharmacy in psychoses
• Generalisions about polypharmacy are none‐
sense • Some combinations are useful and safe
• Dose optimisation is also essential for effective treatment
• Personalised medicine
Psychopharmacology masterclass
•
•
•
•
•
Saturday October 6 9.45am – 4pm
Delmont Private Hospital 300 Warrigal Rd Glen Iris [email protected]
Questions?
Diagnosis and Formulation
Dr. Ajit Selvendra
Consultant Psychiatrist
St. Vincent’s Mental Health
205
Topics Covered
– The process of diagnosing psychiatric conditions
– Review diagnostic classification systems and
approaches used in psychiatry (including
upcoming changes in DSM)
– Use of a Multi-Axial Diagnostic system
– Developing a Formulation of the person’s current
presentation and context
206
What is a Diagnosis?
Why Diagnose?
207
Diagnosis – definition
Medicine
a) The act or process of determining the nature
and cause of a disease or injury
– done through evaluation of patient history,
examination, and review of laboratory data
b) The opinion derived from such an evaluation
208
Why Diagnose?
– A means of communication between healthcare
staff, and between research and clinical practice
– to assist in understanding the underlying
aetiology of the patient’s clinical features
– gives an indication of future prognosis and
possible trajectory of a condition
– allows the development of specific treatments
– Allows research with inter-rater reliability and
replicable clinical trials
– (used by departments and government for
funding and legal purposes)
209
Current Diagnostic Classification
Systems
– DSM IV TR (American Psychiatric Association, 2000)
– Diagnostic and Statistical Manual of Mental
Disorders
(originally developed as DSM I in 1952)
– ICD-10 (World Health Organisation, 1990) –
International Classification of Diseases and related
Health problems
(ICD-6 first included Mental Health Disorders)
Historical:
– Some psychiatric terms and the criteria required to
diagnose conditions have changed over time
210
– New conditions have been added
Future
DSM 5.0
May 2013
ICD-11
2014
Similar psychiatry classifications to DSM
Australian hospitals use ICD coding systems
211
Commonly used DSM IV Adult
Psychiatric Diagnoses and
Groupings:
Psychotic Disorders
–Schizophrenia
–Schizoaffective Disorder
–Delusional Disorder
Substance Abuse Disorders
(Drug or alcohol-related)
Anxiety Disorders
–Generalised Anxiety Disorder
–Obsessive Compulsive Disorder
–Social Anxiety Disorder
–Specific Phobia
–Post-traumatic Stress Disorder
–Panic Disorder
Mood Disorders
– Major Depressive Disorder
– Bipolar Disorder - I and II
– Cyclothymic Disorder
– Dysthymic Disorder
– Substance-Induced Mood Disorder
– Mood Disorder due to a General
Medical Condition
– Substance-Induced Mood Disorder
– Mood Disorder NOS
Somatoform Disorders
(Physical disorders which have a
psychological component)
Personality Disorders
212
Additional DSM IV Diagnostic
Groupings
– Disorders Usually First Diagnosed in Infancy, Childhood
and Adolescence
– Delerium, Dementia, and Amnestic and Other Cognitive
Disorders
– Mental Disorders Due to a General Medical Condition
– Factitious Disorders
– Dissociative Disorders
– Sexual and Gender Identity Disorders
– Eating Disorders
– Sleep Disorders
– Impulse- Control Disorders Not Elsewhere Classified
– Adjustment Disorders
213
Definitions and Concepts
Syndrome – cluster of signs and symptoms that occur together and are
characteristic for a specific disorder
e.g. Major Depressive Episode – depressed mood, weight loss,
insomnia, feelings of worthlessness or excessive guilt, suicidal ideation
DSM-IV Approach
Categorical approach – each diagnosis is separate
Criteria-based diagnostic system
Uses standard prototypes as “best examples” with vague or fuzzy
boundaries
But:
–a) cases sometimes fit criteria for two disorders
– b) sometimes need to distinguish the boundary between normal
variants and pathology/illness
–c) atypical presentations - there are variable presentations that are
different from standard ‘prototype’ clinical case
214
DSM IV General Criteria and Concepts
The disorder causes clinically significant distress or impairment in
social, occupational or other important areas of functioning
Diagnosing multiple conditions is possible except within certain rules:
1. Disorder is not due to the direct effect of a substance or a general
medical condition (requires a substance or medical related diagnosis)
2. Precedence of Diagnoses:
eg. pervasive disorder is more important
(pervasive – how extensively symptoms permeate patient’s life in
terms of their type, duration and intensity)
–“has never met the criteria for…”
–“does not occur exclusively during the course of”
3.Clinical judgement is necessary “not better accounted for by”
eg. Specific phobia – “Not better accounted for by Panic Disorder with
215
agoraphobia”
What are the psychotic disorders?
What is Psychosis?
– A condition which affect the mind, where there has been
some loss of contact with reality.
Features:
– Hallucinations – Hallucinations involve sensing things
while awake that appear to be real, but instead have been
created by the mind. Can occur in any sensory modality
Eg. hearing voices which no-one else can hear, or seeing
things which aren’t there
– Delusions – a fixed false belief which is held with
absolute conviction, not amenable to reason, not
culturally appropriate. E.g. from the way cars are parked
outside my house the police are watching me.
– Disorganisation of speech, thought or behaviour.
Thought Disorder often includes deficits in higher
216
intellectual or executive functioning, eg, making plans
Common Subtypes of
Psychosis
–
–
–
–
–
–
–
–
–
Brief Psychotic Disorder /Schizophreniform Disorder
Schizophrenia
Schizoaffective Disorder
Delusional Disorder
Substance Induced Psychotic Disorder (specify
substance)
Psychotic Disorder due to General Medical
Condition(specify condition)
Psychotic Disorder Not Otherwise Specified
Bipolar Disorder with psychotic features (manicdepressive psychosis)
Major Depressive Disorder with Psychotic Features
217
Schizophrenia – DSM-IV
218
Schizophrenia
A. Characteristic
Symptoms: Two (or more) of the
following, each present for a significant portion
of time during a 1-month period (or less if
successfully treated):
-delusions
-hallucinations
-disorganised speech
-grossly disorganised or catatonic behaviour
-negative symptoms i.e. Affective flattening,
alogia or avolition
219
Schizophrenia ctd.
– B: Social/occupational dysfunction: For a
significant portion of the time since the onset of
the disturbance, one of major areas of
functioning such as work, interpersonal
relations, or self care are markedly below the
level achieved prior to the onset
– C Duration: Continuous signs of the disturbance
persist for at least 6 months including at least 1
month of active symptoms (or less if
successfully treated) and may include periods of
prodromal or residual features
220
Schizophrenia ctd.
– D Schizoaffective disorder and mood disorder
exclusion: Schizoaffective disorder and mood
disorder with psychotic features have been ruled out
– E Substance/general medical condition exclusion
The disturbance is not due to the direct physiological
effect of a substance (e.g. drug of abuse, a
medication) or a general medical condition
– F Relationship to a Pervasive Developmental
Disorder: If there is a history of pervasive
developmental disorder then diagnose only if
prominent delusions or hallucinations are also
present for at least a month
221
Process of Making a Diagnosis
Case Example - Psychosis
222
Changes in Presentation
and Diagnosis Over Time
Level of
Activity and
Functioning
Mr ZZ. 18 year old male and a first
year university student. Has a few
friends and doing reasonably at
university.
A
C
B
19 years
20 years
21 years
Age
223
SITUATION A
– Keeping to self the past few months, lot of time in his
room, does not see friends
– known to be smoking marijuana but not talking about
it
– Not going to university regularly, academic results
down
– Not very communicative, isolates himself,
– He appears worried, anxious and upset
– Some odd ideas which occur particularly after
smoking marijuana
224
SITUATION A DIAGNOSES:
– “At Risk Mental State” or Ultra-High Risk
(prodrome) group
– Major Depressive Disorder
– Anxiety Disorder
– Personality Disorder or personality traits
– Drug or alcohol issues
– No clear diagnosis but stressors such as social,
family, work or study pressures
– No specific condition
225
Case Example
Level of
Activity and
Functioning
A
C
B
19 years
20 years
21 years
Age
226
SITUATION B
– Deterioration over past 2-3 weeks
– Has lots of plans and ideas, some are odd
and not practical
– Believes that his room is being invaded by
groups of people, and there is surveillance
happening in the house. Mr. ZZ feels people
are communicating with him by special
means
– Mr. ZZ claims to have done things to protect
himself and defend his room but will not
reveal what they are. He stated once that he
has special abilities
– Very disorganised, sleep very poor, up at all
hours of the night
227
SITUATION B
DIAGNOSES:
– “1st Episode Psychosis”
– Substance Induced Psychosis(cannabis)
– Schizophreniform Psychosis
Schizoaffective Psychosis/ Manic phase
of Bipolar Disorder with Psychotic
Features
– Psychotic disorder due to general
medical condition (Organic Psychosis)
228
Case Example
Level of
Activity and
Functioning
A
C
B
19 years
20 years
21 years
Age
229
SITUATION C
– Increasing worry about surveillance over
the past few days
– Starting to keep to self again, states there
are probably other people out to do
something nasty. Not clear on details
– Increasingly awake at night, less
organised in activities, not getting things
finished
– Ongoing marijuana use
– Parents concerned, bring him in for help,
he is refusing help, stopped medications
230
Situation C
Clearer Diagnosis
– Schizophrenia
– (Possibly additional diagnosis of
Substance Abuse Disorder)
Differential Diagnoses:
– Bipolar Disorder with psychotic features
– Schizoaffective Disorder
231
Diagnosis at First Presentation –
164 cases Diagnosis at 3 Months
Considerations and Approach to
Diagnosis:
– Review Severity and Clinical Features
– Rule out disorder due to direct effect of a
general medical condition or substance
use
– Develop a Diagnosis and Differential
Diagnosis
– Determine specific primary disorder(s)
• Multiple diagnoses
• Some hierarchies in diagnoses (ie. not
better accounted for by….)
234
Considerations in Diagnosis:
– Establishing boundary with no mental disorder i.e. clinically significant/ culturally appropriate
behaviour
– Distinguish Adjustment Disorder (response to a
stressor) and Not Otherwise Specified (NOS)
– Add subtypes/specifiers :
 severity (mild moderate, severe – with or
without psychotic features)
 treatment relevant (psychosis – subytypes,
depression -melancholic, atypical, etc.)
 longitudinal course (with/without full inter235
episode recovery, depression -seasonal pattern)
Challenges in Diagnosis Diagnostic Uncertainty and Role
of Clinical Judgement
Natural variance – occurs normally in natural world, varies
individual to individual
Information variance – the amount and type of clinical
information collected varies, due to sources and patient’s
different reports
Observation and interpretation variance – different clinicians
focus on different parts, attach different significance to a
feature. Especially difference between normal/pathological –
behaviour, mood, thought
Criterion variance – different criteria systems
236
Initial Assessment Requirements
–
–
–
–
–
–
Complexity of initial presentation
Risk assessment
Location of treatment
Consider medium term treatment requirements
More comprehensive history
Initiation of treatment, review likelihood of
compliance/treatment
– Comorbidity - assessment
237
Approaches Depression in Medically ill
–Inclusive
–Exclusive
–Aetiological
–Substitutive
Investigations used in Psychiatry
238
Brain Changes in Schizophrenia,
Established by Systematic Reviews
–
–
–
–
–
–
Enlargement of lateral and third ventricles (+25-40%)
Smaller brain volumes (-3%)
Smaller cortical volume (-4%)
Smaller Grey matter volume (-6%)
Relatively smaller medial temporal lobe volume (*-5%)
Relatively smaller thalamic volume (-4%)
Other replicated findings:
– Decrease or loss of cerebral asymmetries
Adapted from Harrison PJ, 2000
239
Course of Schizophrenia
Inter-rater
reliability
(Francis, 2012)
241
DSM-III Changes
-
Descriptive
Non-etiologic focus
Diagnostic criteria
Multiaxial system
Multiple diagnoses
Splitting
Reliability
242
Diagnostic Systems
DSM 5 Challenges:
–Diagnoses reified
–Dimensional vs Categorical
–Inter-rater reliability
–Over-medicalisation and stigmatisation
243
Unintended consequences
– Financial and legal uses
– Media and public perception
– Diagnosis used as entry requirement into
accommodation, social security and other
benefits
Oversimplification
Eg. Brief consultations and less skilled clinicians
244
What is in DSM-IV
– Systematic framework for diagnosis
(including Multiaxial system)
– Diagnostic criteria
– Detailed explanatory text
– Names and codes (from ICD-9)
– Appendices to expand
educational/practical utility
245
Multi-Axial System of
Diagnosis
Axis I - Clinical Disorders
Axis II – Personality Disorders and Mental
Retardation
Axis III – General Medical Conditions
Axis IV – Psychosocial and Environmental
Problems
Axis V – Global Assessment of Functioning
(GAF)
246
Axis II – Disorders Arising in the
Developmental Period
Personality Disorders:
–An Enduring pattern of inner experience and behaviour that
deviate markedly from expectations of the individual’s
culture. Pattern is manifested in two(or more ) of the
following areas:
1. Cognition
2. Affectivity
3. Interpersonal Functioning
4. Impulse Control
–Enduring pattern is:
inflexible and pervasive
–leads to clinically significant distress or impairment in
functioning
–stable , long duration and onset traced to adolescence or
early adulthood
247
DSM IV Types of Personality
Disorders
Cluster A – “odd, eccentric, isolative or suspicious behaviour”
–* Paranoid Personality Disorder
–Schizoid Personality Disorder
–* Schizoptypal Personality Disorder
Cluster B - “dramatic, emotional, erratic or impulsive
behaviour or a reduced capacity for empathy”
–* Antisocial Personality Disorder
–* Borderline Personality Disorder
–Histrionic Personality Disorder
–Narcissistic Personality Disorder
Cluster C – “anxious, fearful or perfectionistic behaviour”
–Avoidant Personality Disorder
–Dependent Personality Disorder
–Obsessive Compulsive Personality Disorder
248
Axis V – Global Assessment
of Functioning
Numerical scale (0 through 100) to subjectively rate the social, occupational,
and psychological functioning of adults, e.g., how well or adaptively one is
meeting various problems-in-living:
–81 - 90 Absent or minimal symptoms (e.g., mild anxiety before an exam),
good functioning in all areas, interested and involved in a wide range of
activities, socially effective, generally satisfied with life, no more than
everyday problems or concerns (e.g., an occasional argument with family
members)
–51-60 Moderate symptoms (e.g., flat affect and circumstantial speech,
occasional panic attacks) OR moderate difficulty in social, occupational, or
school functioning (e.g., few friends, conflicts with peers or co-workers).
–41 - 50 Serious symptoms (e.g., suicidal ideation, severe obsessional
rituals, frequent shoplifting) OR any serious impairment in social,
occupational, or school functioning (e.g., no friends, unable to keep a job).
–11 - 20 Some danger of hurting self or others (e.g., suicide attempts without
clear expectation of death; frequently violent; manic excitement) OR
occasionally fails to maintain minimal personal hygiene (e.g., smears feces)
OR gross impairment in communication (e.g., largely incoherent or mute
249
Sample DSM Diagnosis
Case of ZZ , after treatment of Stage B:
Axis I
Schizophrenia – (Single Episode, in Partial Remission)
Cannabis Abuse Disorder
Axis II Diagnosis Deferred
Axis III Nil
Axis IV Problems with primary support group (disruption of
family)
Educational problems (difficulties at university)
Axis V GAF Score
During episode 25
Current 60
250
FORMULATION - Why does this patient
suffer from these problems at this
particular time?
– An integrated understanding of this unique individual,
describing his/her vulnerabilities and resources and how he/she
comes to be in the current predicament
– Highlight possible linkages between factors and this
presentation
– A hypothesis
– General types of Contributory Factors:
– Biological
– Psychological
– Social
– Also provide a broad description of the mechanism of
contribution:
Predisposing
Precipitating
Perpetuating
Protective
251
Formulation ctd.
– Identify key contributing factors for the presentation
– Attempt to suggest a clearer mechanism of contribution
i.e. how each factor may have contributed – this may
require knowledge of various theories and concepts:
 biological (genetic, physical illness etc.)
 psychological (psychodynamic and cognitive
behavioural)
 social (family systems theory etc.)
– Advanced: develop skills in various styles of formulation &
tailor approach to the type of case e.g. diagnostic dilemma,
predominant biological focus, or psychological focus
252
Grid of Contributing Factors
Biological
Psychological
Social
Predisposing
“vulnerable to
this condition
because of…..”
Underlying medical
conditions,
Genetics, childbirth
issues
Early attachment
& relationships,
personality traits
(eg. obsessional)
Social avoidance,
Social isolation,
Unemployment,
Family history of illness
Precipitating
“This Episode
was triggered
by….”
Cannabis use
Lack friendships,
Academic pressures
and trying to keep up
Perpetuating
“He remains
vulnerable to
this due to….”
Ongoing cannabis Poor insight and
use
acceptance of
condition
Decision to continue
at University
Difficult family
environment
Protective
“On the other
hand his
strengths are….”
Maturity of
personality
Supportive parents
Reasonable
engagement with
Mental Health Service
253
Variety of Trajectories
and phases
254
Genetics of Schizophrenia
– CNV's (Copy Number variants) - deletion or duplication of
nucleotide pairs
– Relatively rare, explain small amount of variance of
schizophrenia
– Usually also associated with other conditions - intellectual
disability, autistic spectrum disorders and epilepsy
(Levinson, AJP 2011)
– risk alleles
– Endophentypes
– Associated with disorder, present whether ill or active
– found in non-affected family members>general population
(Gottesman and Gould 2003)
255
Potential Mechanisms
(Stefanis, 2012)
Genes
Cells
Systems
Behaviour
multiple
susceptibility
alleles each
of small effect
subtle
molecular
abnormalities
abnormal
information
processing
complex
functional
interactions
and emergent
phenomena
Cognition
behavioural
phenotypes
temperament
256
The Stress Vulnerability Model
Genetic Vulnerability 
Early trauma  Substance use 
Death of a loved one  Work stress 
Relationship break-up  Psychosis
Protective Factors
Medication
Coping Skills
Social Network
257
Formulation Presentation
– Paragraph 1: Brief introduction of case and context – few
lines
–
Paragraph 2: Highlight important factors which explain this
case “Vulnerable to….because….”
– Exercise judgement in which factors to choose
– Paragraph 3: Make links between vulnerabilities and
current presentation: (suggest a mechanism in some
cases). Utilise theories if appropriate
Eg. his childhood conflict with parents  resulted in noncompliance and conflict with authority figures
Eg. Childhood abuse  resulted in guilt/lower selfesteem/poor self-image later contributed to depression
258
Summary
– DSM diagnosis is categorical and criteria based, but
it is important to understand the broader clinical
scenario
– Explored benefits and limitations of systems
– Explored skills required to make a clear diagnosis
and differential diagnosis, and to be able to discuss
pros and cons of each diagnosis
– Broader case presentation skills include:
 Multi-Axial Diagnosis
 Case Formulation
259
Comments ?
Additional Reading / References
–American Psychiatric Association, Diagnostic
and statistical manual of mental disorders (4th
ed.) ,1994, Washington, DC
–Fauman M, Study Guide to DSM-IV American
Psychiatric Press, 1994, Washington DC
–American Psychiatric Association - DSM V
website
–Royal Australian and New Zealand College of
Psychiatrists RANZCP Formulation Guidelines
for Candidates, Trainee Clinical Examination
01/11/2004
260
Questions?
Panel Discussion
Psychiatric Essentials
31 August 2012
Thank you