Volume 34 - Número 4 - Sociedade Brasileira de Neurocirurgia

Transcription

Volume 34 | Number 4 | 2015
ISSN 0103-5355
BRAZILIAN
NEUROSURGERY
ARQUIVOS BRASILEIROS DE NEUROCIRURGIA
OFFICIAL JOURNAL OF THE SOCIEDADE BRASILEIRA DE NEUROCIRURGIA AND SOCIEDADES DE NEUROCIRURGIA DE LÍNGUA PORTUGUESA
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ISSN 0103-5355
Brazilian Neurosurgery
Arquivos Brasileiros de Neurocirurgia
Editor-in-Chief | Editor-Chefe
Eberval Gadelha Figueiredo
Emeritus Editors | Editores Eméritos
Milton Shibata
Gilberto Machado de Almeida†
Editorial Board | Conselho Editorial
Chairman | Presidente
Manoel Jacobsen Teixeira
National Board | Conselho Nacional
Albedi Bastos
Belém, PA
Arnaldo Arruda
Fortaleza, CE
Benedicto Oscar Colli
Ribeirão Preto, SP
Carlos Telles
Rio de Janeiro, RJ
Carlos Umberto Pereira
Aracaju, SE
Eduardo Vellutini
São Paulo, SP
Ernesto Carvalho
Porto, Portugal
Evandro de Oliveira
São Paulo, SP
Fernando Menezes Braga
São Paulo, SP
Francisco Carlos de Andrade
Sorocaba, SP
Hélio Rubens Machado
Ribeirão Preto, SP
Hildo Azevedo
Recife, PE
João Cândido Araújo
Curitiba, PR
João Paulo Farias
Lisboa, Portugal
José Alberto Gonçalves†
João Pessoa, PB
José Alberto Landeiro
Rio de Janeiro, RJ
José Carlos Esteves Veiga
São Paulo, SP
José Carlos Lynch Araújo
Rio de Janeiro, RJ
José Marcus Rotta
São Paulo, SP
José Perez Rial
São Paulo, SP
Jose Weber V. de Faria
Uberlândia, MG
Luis Alencar Biurrum Borba
Curitiba, PR
São Paulo, SP
Marco Antonio Zanini
Botucatu, SP
Marcos Barbosa
Coimbra, Portugal
Marcos Masini
Brasília, DF
Mário Gilberto Siqueira
São Paulo, SP
Nelson Pires Ferreira
Porto Alegre, RS
Pedro Garcia Lopes
Londrina, PR
Ricardo Vieira Botelho
São Paulo, SP
Roberto Gabarra
Botucatu, SP
Sebastião Gusmão
Belo Horizonte, MG
Sérgio Cavalheiro
São Paulo, SP
Sergio Pinheiro Ottoni
Vitória, ES
Jorge Luiz Kraemer
Waldemar Marques
Porto Alegre, RS
Lisboa, Portugal
International Board | Conselho Internacional
André G. Machado
USA
Antonio de Salles
USA
Beatriz Lopes
USA
Clement Hamani
USA
Daniel Prevedello
USA
Felipe Albuquerque
USA
Jorge Mura
Chile
Kumar Kakarla
USA
Michael Lawton
USA
Nobuo Hashimoto
Japan
Oliver Bozinov
Switzerland
Pablo Rubino
Argentina
Paolo Cappabianca
Italy
Peter Black
USA
Peter Nakaji
USA
Ricardo Hanel
USA
Robert F. Spetzler
USA
Rungsak Siwanuwatn
Thailand
Volker Sonntag
USA
Yasunori Fujimoto
Japan
ISSN 0103-5355
Society Board | Diretoria (2014–2016)
Modesto Cerioni Junior
Vice-Chairman | Vice-Presidente
Clemente Augusto de Brito Pereira
General Secretary | Secretário-Geral
Marco Túlio França
Treasurer | Tesoureira
Protocols and Guidelines Director | Diretor de Diretrizes e
Protocolos
International Relations Director | Diretor de Relações
Internacionais
José Marcus Rotta
Institutional Relations Director | Diretor de Relações Institucionais
Cid Célio Jayme Carvalhaes
Marise Augusto Fernandes Audi
Regional Representatives Director | Diretor de Representantes
Regionais
First Secretary | Primeiro Secretário
Paulo Ronaldo Jubé Ribeiro
Roberto Sérgio Martins
Publications Director | Diretor de Publicações
Executive Secretary | Secretário Executivo
Ítalo Capraro Suriano
Former Chairman | Presidente Anterior
Sebastião Nataniel Silva Gusmão
Advisory Board | Conselho Deliberativo
Next Chairman 2016–2018 | Presidente Eleito 2016–2018
Ronald de Lucena Farias
Jorge Luiz Kraemer
Congress Chairman 2016 | Presidente do Congresso 2016
Secretary | Secretário
Marcio Vinhal de Carvalho
Benjamim Pessoa Vale
Congress Chairman 2018 | Presidente do Congresso 2018
Directors | Conselheiros
Marcelo Paglioli Ferreira
Aluízio Augusto Arantes Jr.
Jânio Nogueira
José Marcus Rotta
Luis Alencar B. Borba
Luis Renato G. de Oliveira Mello
José Carlos Saleme
Luiz Carlos de Alencastro
Marcos Masini
Osmar Moraes
Geraldo de Sá Carneiro
Jair Leopoldo Raso
José Fernando Guedes Correa
Orival Alves
Departments Director | Diretor de Departamentos
José Marcus Rotta
Policy Director | Diretor de Políticas
Clemente Augusto de Brito Pereira
Neurosurgery Director | Diretor de Formação Neurocirúrgica
Benedicto Oscar Colli
Honorary Director | Diretor de Honorários
José Carlos Esteves Veiga
Director of Parliamentary | Diretor de Parlamentário
Marcos Masini
Estate Director | Diretor de Patrimônio
Samuel Tau Zymberg
Volume 34, Number 4/2015
Homage | Homenagem
265
Homenagem ao professor Gilberto Machado de Almeida
Felix H. Pahl
Original Articles | Artigos Originais
267
Abusive Head Trauma: Epidemiological Aspects and Diagnosis
Trauma Craniano por abuso: aspectos epidemiológicos e diagnostico
José Roberto Tude Melo, Federico Di Rocco, Estelle Vergnaud, Juliette Montmayeur, Marie Bourgeois, Christian Sainte-Rose,
Michel Zerah, Philippe Meyer
274
Perfil clínico e sociodemográfico de vítimas de traumatismo cranioencefálico atendidas na área vermelha
da emergência de um hospital de referência em trauma em Sergipe
Clinical and Sociodemographic Profile of Traumatic Brain Injury Victims Attended on Emergency Red Area
from a Hospital Reference in Trauma of Sergipe
Mérilin Sampaio da Cruz Passos, Karem Emily Pina Gomes, Fernanda Gomes de Magalhães Soares Pinheiro,
Caio Lopes Pinheiro de Paula, Daniele Martins de Lima Oliveira, Airton Salviano de Sousa Júnior
280
The Role of the Intraoperative Auxiliary Methods in the Resection of Motor Area Lesions
O papel dos métodos auxiliares intraoperatórios na ressecção de lesões em área motora
Stênio Abrantes Sarmento, Emerson Magno de Andrade, Helder Tedeschi
291
Tratamento das hemorragias intracranianas espontâneas: o dilema continua
Treatment of Spontaneous Intracranial Hemorrhages: the Dilemma Continues
Iuri Santana Neville, Djalma Felipe da Silva Menéndez, Leonardo Moura Sousa Júnior, Eberval Gadelha Figueiredo,
295
Treatment of Giant Intracranial Aneurysms: a Review Based on Experience from 286 Cases
Tratamento dos aneurismas gigantes intracranianos: uma revisão baseada na experiência de 286 casos
Atos Alves de Sousa, José Lopes de Sousa Filho, Marcos Antônio Dellaretti Filho
Review Article | Artigo de Revisão
304
Seizure Outcome after Anterior versus Complete Corpus Callosotomy in Children: A Systematic
Review with Meta-Analysis
Controle das crises epilépticas após calosotomia anterior versus completa em crianças: uma revisão
sistemática com metanálise
Lucas Crociati Meguins, Rodrigo Antônio Rocha da Cruz Adry, Sebastião Carlos da Silva Júnior, Carlos Umberto Pereira,
Jean Gonçalves de Oliveira, Dionei Freitas de Morais, Gerardo Maria de Araújo Filho, Lúcia Helena Neves Marques
Case Reports | Relatos de Caso
309
Schwannoma como etiologia de síndrome do túnel do carpo – relato de caso
Schwannoma as a Cause of Carpal Tunnel Syndrome – a Case Report
Marcelo José da Silva de Magalhães, André Jin Fujioka, Raiana Barbosa Chaves
Thieme Publicações Ltda
online
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Brazilian Neurosurgery | Arquivos Brasileiros de Neurocirurgia
313
Volume 34, Number 4/2015
Epidural Capillary Hemangioma of the Thoracic Spine
Hemangioma capilar extradural da coluna torácica
Eberval Gadelha Figueiredo, Anderson Rodrigo Souza, Gabriel Reis Sakaya, Daniella Brito Rodrigues, Raul Marino Jr.
317
Atypical Presentation of Temporal Dermoid Cyst: Case Report
Apresentação atípica de cisto dermoide temporal: caso clínico
Sérgio Gonçalves da Silva Neto, Thiago Martins, Leonardo Moura, Clemar Correa, Wellingson Paiva, Hector Navarro,
321
Giant Pseudoaneurysm as a delayed Surgical Complication in a Patient Operated on a Giant Neuroma
of the Vagus Nerve: Case Report and Management Considerations
Pseudoaneurisma gigante como complicação cirúrgica em paciente operado com neuroma gigante do
nervo vago: relato de caso e considerações
Demian Manzano-Lopez, Pablo Rubino, Pablo Mendivil Teran, Jesús Lafuente Baraza, Gerardo Conesa Bertran
327
Síndrome do trefinado: relato de caso
Syndrome of Trephined: A Case Report
Augusto Santos, Diego Oliveira da Mata, Rayane Toledo Simas, Rodrigo Moreira Faleiro, Thiago Oliveira Lemos de Lima
331
Traumatic Cervical Artery Dissection and Ischemic Stroke: Anticoagulation or Antiplatelet Therapy?
The Controversies Remain
Dissecção traumática da artéria cervical e AVC isquêmico: anticoagulação ou terapia antiplaquetária?
A polêmica continua
Leonardo Christiaan Welling, Camila Mariana Fukuda, Edek Francisco de Mattos da Luz, Mariana Schumacher Welling,
335
Criptococoma cerebral e pulmonar em paciente imunocompetente: relato de caso
Cerebral and Pulmonary Cryptococcoma in an Immunocompetent Pacient: Case Report
Caio Sander Andrade Portella Júnior, Marcelle Rehem Machado, Lucas Chaves Lelis, Jefferson Fonseca Dias,
Luiz Eduardo Ribeiro Wanderley Filho, Carlos Antonio Guimarães Bastos
Technical Note | Nota Técnica
338
Cranioplastia externa para a síndrome do trefinado – nota técnica
External Cranioplasty for the Syndrome of Trephined – Technical Note
Rodrigo Moreira Faleiro, Luiz Alberto Otoni Garcia, Luanna Rocha Vieira Martins
Letter to the Editor | Carta ao Editor
342
Hospital do Câncer de Barretos
Carlos Afonso Clara, MD, PhD
Retraction Notice | Retratação
343
Remote Cerebellar Hemorrhage after Surgery for Spinal Column Tumor: An Unusual Cause of
Impaired Consciousness
Hemorragia cerebelar remota após cirurgia para tumor da coluna vertebral: causa não habitual
de rebaixamento de consciência
Juliano Nery Navarro, Telmo Augusto Barba Belsuzarri, João Flávio Mattos Araujo
Copyright © 2015 by Thieme Publicações Ltda Inc. Arquivos Brasileiros de
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ISSN 0103-5355
THIEME
Homage | Homenagem
Homenagem ao professor Gilberto Machado de
Almeida
Felix H. Pahl1
1 Hospital do Servidor Público Estadual - SP; Hospital Sírio Libanês,
São Paulo, SP, Brasil
Address for correspondence Felix H. Pahl., DFV neuro, SP, Brasil,
(e-mail: [email protected]).
Arq Bras Neurocir 2015;34:265–266.
Gostaria de agradecer imensamente a oportunidade de
prestar esta homenagem ao nosso querido professor Gilberto
Machado de Almeida (►Fig. 1).
Para quem não o conheceu, “O Professor”, como era
chamado, foi um dos maiores líderes da neurocirurgia brasileira no seu tempo.
Eu o conheci em 1981, quando iniciei a residência médica
no Hospital das Clínicas (HC) em São Paulo. Naquele momento, o HC representava uma das residências médicas de
maior prestígio no país.
O Professor era um líder incontestável na clínica. Tudo
passava por ele. A decisão final era sempre a dele, apesar de a
clínica contar com valiosos assistentes, como Newton Domingos Cabral, Luis Alcides Manreza, José Luzio, Manoel J.
Teixeira, entre outros.
O Professor adorava o que fazia, e transparecia isso em
cada atitude. Mantinha-se atualizado, lia todas as revistas
importantes de neurocirurgia do primeiro ao último artigo.
Operava todos os dias. Via os pacientes em visita e em
discussões de caso. Sofria junto com os pacientes e familiares
os maus resultados e festejava os bons. Era rígido, detestava
bajuladores. Ganhar a sua confiança demorava um pouco,
mas uma vez conquistada, era para sempre.
Sua área de atuação foi inicialmente a neurocirurgia
infantil. Foi um dos pioneiros no uso da válvula para controle
da hidrocefalia nas crianças. Posteriormente, dedicou-se a
neurocirurgia vascular e tumores da base do crânio. Foi um
dos pioneiros no uso do microscópio cirúrgico. Operou mais
de 300 MAV e um número muitíssimo maior de pacientes
com aneurismas cerebrais. Era a referência nacional em
neurocirurgia vascular.
Esta vasta experiência era transmitida diariamente. Ele próprio e os seus assistentes ensinavam os residentes a posicionar o
paciente, a fazer a craniotomia, e os guiavam durante a cirurgia
para que conseguissem finalizá-la com êxito.
Foi ideia dele a divisão da clínica em grupos de trauma,
vascular, base de crânio, tumores, infantil, funcional. Isto
fomentou uma expertise sem precedentes que foi copiada por
vários serviços no Brasil.
Sua conduta, isenta de interesses pessoais em relação aos
pacientes e familiares, colegas e fornecedores, era um exemplo a ser seguido pelos mais novos.
Muitos expoentes da neurocirurgia nacional foram formados por ele, como Manoel J. Teixeira, Mario Taricco,
Hamilton Matushita, Guilherme Carvalhal Ribas, Eduardo
Vellutini, Paulo Henrique Aguiar, entre outros.
Publicou quarenta artigos em revistas indexadas e vários
capítulos de livros. Entre os artigos, o mais importante foi
sobre cirurgia dos aneurismas de oftálmica, publicado na
Surgical Neurology em 1976, amplamente citado.
Do ponto de vista associativo, foi presidente do congresso
latino americano de neurocirurgia em 1983. Foi presidente
da Sociedade Brasileira de Neurocirurgia (SBN) entre 1990 e
1992, e do Congresso Brasileiro de Neurocirurgia (CBNC) em
published online
October 28, 2015
Copyright © 2015 by Thieme Publicações
Ltda, Rio de Janeiro, Brazil
DOI http://dx.doi.org/
10.1055/s-0035-1565006.
ISSN 0103-5355.
Fig. 1 Professor Gilberto Machado de Almeida.
265
266
Homenagem ao professor Gilberto Machado de Almeida
Pahl
1992. Foi amigo pessoal de lideranças neurocirúrgicas internacionais, como Charles Drake, Eugene Flamm, Bennet Stein,
Madjid Samii.
Foi casado com Elenice, eminente escritora de literatura
infantil com 28 livros publicados, com quem teve quatro filhos
(Eduardo, Otávio, Gil e Renato), dois deles se tornaram médicos.
Era um líder da família.
Gostava de esportes, criava cavalos.
Após longa tentativa de criar a disciplina de neurocirurgia
na Faculdade de Medicina da Universidade de São Paulo
(FM-USP), conseguiu a vaga e a abertura do concurso em abril
de 1990. Acabou sendo vencido; quem ficou com a cátedra foi
o professor Raul Marino Jr.
Um pouco antes do concurso, perdeu a sua esposa Elenice,
vitimada por um câncer, e logo após o seu filho Gil.
Como pessoa de personalidade forte, focado na profissão, O Professor recuperou-se, dedicando-se à SBN e ao
CBNC, à neurocirurgia do Hospital Nove de Julho, em SP –
junto com os doutores Milton Shibata e Eduardo Bianco –,
e ao cargo de professor convidado na Faculdade de Medicina de Botucatu.
Casou-se novamente com Maia e nos últimos anos viveu
em Florianópolis, dedicando-se à criação de pássaros.
Gilberto Machado de Almeida era um homem de princípios, justo, honesto e brilhante neurocirurgião. Faço minhas
as palavras de Mario Sergio Cortella: “Infeliz é o homem que
não ensina o que sabe e não pratica o que ensina. Virtuosos e
felizes são os homens que têm generosidade mental
(e portanto ensinam o que sabem) e honestidade moral
(e portanto praticam o que ensinam).”
Sem dúvida, O Professor Gilberto Machado de Almeida foi
um homem virtuoso e feliz em sua vida, e os que tiveram o
prazer da sua convivência só podem agradecer por este
privilégio.
Vol. 34
No. 4/2015
THIEME
Original Article | Artigo Original
Abusive Head Trauma: Epidemiological Aspects
and Diagnosis
Trauma Craniano por abuso: aspectos epidemiológicos e
diagnostico
José Roberto Tude Melo1,2 Federico Di Rocco1 Estelle Vergnaud3 Juliette Montmayeur3
Marie Bourgeois1 Christian Sainte-Rose1 Michel Zerah1 Philippe Meyer3
1 Department of Pediatric Neurosurgery, Hôpital Universitaire Necker-
Enfants Malades, Université Descartes Paris 5, Paris, France
2 Pediatric Neurosurgical Unit, Hospital São Rafael, Salvador, Bahia,
Brazil
3 Pediatric Surgical Critical Care Unit and Anesthesiology, Hôpital
Universitaire Necker-Enfants Malades, Université Descartes Paris 5,
Paris, France
Address for correspondence José Roberto Tude Melo, MD, Hospital
São Rafael, Avenida São Rafael 2152, São Marcus, Salvador, Bahia,
Brazil CEP: 41.253-190 (e-mail: [email protected]).
Abstract
Keywords
► brain injuries
► child abuse
► shaken baby
syndrome
► subdural hematoma
Resumo
Palavras-chave
► traumatismos
encefálicos
► maus-tratos infantis
► síndrome do bebê
sacudido
► hematoma subdural
received
May 9, 2013
accepted
August 7, 2015
published online
October 19, 2015
Objective Abusive head trauma (AHT) is defined as a severe, non-accidental traumatic
brain injury. Early recognition and treatment are instrumental in limiting the immediate complications and long-term disabilities. The goal of this study was to describe our
experience with traumatic head injuries in children younger than 2 years of age.
Methods We reviewed the medical records of 195 children aged under 2 years with
suspected AHT who presented with a head injury without witnessed accidental trauma,
between January 2008 and June 2013.
Results AHT was considered in 145 children. Familial problems (ρ ¼ 0.008), cutaneous hematoma/bruising (ρ < 0.001), retinal hemorrhages (ρ < 0.001), and bone
fractures (ρ ¼ 0.04), were significantly more frequent in the AHT group.
Conclusions The association between the subdural hematoma and retinal hemorrhage, resulting from an unwitnessed and incoherent history of trauma, is a strong
argument for AHT, particularly when associated lesions and socioeconomic risk factors
are evident.
Objetivo O traumatismo craniano por abuso (AHT) é definido como uma grave lesão
cerebral traumática não acidental. O reconhecimento e tratamento precoce são
fundamentais para limitar as complicações imediatas e sequelas tardias. O objetivo
deste estudo foi descrever a nossa experiência em crianças menores de 2 anos de idade,
vítimas de trauma craniano.
Métodos Foram revisados os prontuários de 195 crianças com idade inferior a 2 anos
com suspeita de AHT, sem trauma acidental testemunhado e com diagnostico de
hematoma subdural, entre janeiro de 2008 e junho de 2013.
10.1055/s-0035-1565914.
ISSN 0103-5355.
267
268
Abusive Head Trauma
Melo et al.
Resultados AHT foi considerado em 145 crianças. Problemas socioeconômicos
familiares (ρ ¼ 0,008), hematomas e lesões cutâneas (ρ <0,001), hemorragias
retinianas (ρ <0,001), e fraturas em ossos longos (ρ ¼ 0,04), foram significativamente
mais frequentes no grupo de crianças com suspeita de AHT.
Conclusões A associação entre hematomas subdurais e hemorragia retiniana, resultante de uma história incoerente de trauma sem testemunhas, é um forte argumento
para a AHT, particularmente quando lesões cutâneas e fatores de risco socioeconômicos forem identificados.
Introduction
Abusive head trauma (AHT), defined as a severe, non-accidental traumatic brain injury, was first described by the
French forensic expert August Ambroise Tardieu in 1860,1
and occurs particularly in the first year of life.2–8 Several
authors have highlighted the possibility of underestimating
the diagnosis, speculating that not every child is taken to
receive medical assistance and not all cases are recognized
and confirmed to be AHT by the health professionals treating
these children.2,4,5,7–12
In this study, we discuss the epidemiological profile of
AHT based on our experience in traumatic head injuries on
children aged under 2 years at a pediatric trauma center in
Paris, France. We compare the main characteristics of AHT
and non-AHT (nAHT), providing evidence to help clinicians
consider and confirm this diagnosis.
Materials and Methods
Study Design and Sample
We conducted a review of the medical records of 195
consecutive children aged under 2 years with suspected
AHT, treated between January 2008 and June 2013 in the
Île-de-France region. The inclusion criterion was the presence of a head injury, predominantly a subdural hematoma
(SDH) identified by a computed tomography (CT) scan,
without a clear history of witnessed accidental trauma or
evidence of a metabolic or infectious disease or
coagulopathy.
All children enrolled in this study were admitted to a Level
I pediatric trauma center (Hôpital Universitaire Necker–
Enfants Malades, Paris, France). The same protocol was
applied for all children. After in-hospital stabilization, seizure control or systematic prophylactic treatment, endotracheal intubation, mechanical ventilation, and invasive
monitoring probe insertion (central venous and arterial
line catheters) were undertaken as necessary, and all children underwent CT scanning. Complete biologic screening
eliminated associated metabolic and infectious diseases or
coagulopathies. Transcranial Doppler (TCD) examination,
electroencephalography (EEG), ophthalmologic examination, and whole-body bone radiography were performed as
soon as possible. Parents were systematically evaluated by a
specialized team of social workers and psychologists. Data
Vol. 34
No. 4/2015
about parents or caregivers were recorded for age and
familial, marital, educational, and socioeconomic status.
After the completion of exploration and social evaluation,
all cases of suspected AHT were discussed by a multidisciplinary panel consisting of neurosurgeons, intensive care
specialists, pediatricians, forensic specialists, psychologists,
nurses, and social workers. This multidisciplinary panel has
been described in other French studies.12 After careful data
analysis by the panel, children were classified into two
groups:
• Group 1 (nAHT Group): where a potential mechanism of
trauma (mainly falls and other direct impacts on the head)
could be identified through caregivers, parents, or witnessed reports and could be compatible with the observed
lesions.
• Group 2 (AHT Group): where the reported cause of trauma
was inconsistent with the severity of the clinical presentation, and the history was not clarified during hospitalization. All these cases were reported as required by law to
the state prosecutor and further investigated by a specialized police squad.
For the purpose of this analysis, the following characteristics of victims and potential perpetrators of AHT were
particularly recorded:
• In parents or caregivers:
• Young age, history of family violence, alcoholism, drug
abuse, unemployment, financial problems, or other
factors that may compromise the balance of the
family.9,12,13
• Parents seeking medical assistance with prior emergency department visits.14
• The child’s representation in the family.
• Parental reactions after the announcement of
diagnosis.
• In children:
• Age, sex, prematurity, prior hospitalization, and comorbidities such as neurologic disabilities or other
diseases described as risk factors.12,15
• Recent medical history and initial clinical presentation.
• The presence of initial seizures and/or status
epilepticus.16
• Clinical evolution, ophthalmologic exams, skeletal radiographs, and EEG findings.16
Abusive Head Trauma
• CT scan results: the estimated thickness of SDH, its
localization, scan density, and/or associated
lesions.11,16,17
After a complete radiologic examination, AHT was classified into three predefined categories6:
• Battered child syndrome: head injury associated with an
extracranial lesion.
• Shaken baby syndrome: SDH and/or subarachnoid hemorrhage with no focal lesion or skull fracture.
• Shaking-impact baby syndrome: fractures of the skull or
subgaleal hematomas in a shaken baby.
Follow up was ensured in all children for at least 6 months,
and cognitive and/or motor neurologic deficits, epilepsy,
developmental and behavioral disorders, and visual disturbances were evaluated by a multidisciplinary team.16,18
Statistical Analysis and Ethical Aspects
Some results were presented in a descriptive manner, without
statistical analyses. When necessary, proportions were compared with ρ < 0.05 considered statistically significant. Fisher’s
exact test or the chi-squared (χ2) test were applied when
appropriate, with one degree of freedom. For elaboration and
analysis of the database, we used EpiInfo Version 7, publicdomain statistical software for epidemiology developed by the
Centers for Disease Control and Prevention (Atlanta, GA, USA).
This research adhered to legal guidelines regarding research on
human beings and respected and ensured the confidentiality of
participants. This single-center study was conducted in agreement with French law (institutional review board approval was
granted, no informed consent was deemed necessary, and databank information was anonymized).
Results
We examined the medical records of 195 consecutive children aged under 2 years, with head injuries initially consid-
Melo et al.
ered AHT, reviewed by our institutional multidisciplinary
panel between January 2008 and June 2013. In 50 cases
(26%), after further investigation of the reported details of
the accident, coherence was found between the accounts of
parents or caregivers and medical findings. None of these
children presented evidence of inflicted extracranial trauma
(unexplained bruising, hematoma, or burns), and all were
considered nAHT. The remaining 145 children (74%) were
considered potential victims of AHT.
An examination of family characteristics revealed that the
median parent age did not differ significantly between the
nAHT (Group 1) and AHT (Group 2) groups (Group 1 Fathers:
median age, 35 years; range, 26–60 years versus Group 2
Fathers: median age, 32 years; range, 17–53 years and Group
1 Mothers: median age, 31 years; range, 21–41 years versus
Group 2 Mothers: median age, 30 years; range, 17–49 years).
A history of conjugal or familial violence, unemployment,
alcoholism, or drug abuse was evident in 20% of the parents
in the group 1 versus 42% of those in group 2 (ρ ¼ 0.008;
χ2 ¼ 6.89; ►Table 1). ►Table 2 details the main complaints
that led parents or caregivers to seek medical assistance and
the presentation upon hospital admission.
An examination of children’s characteristics revealed a
median age and male predominance common to both
groups (Group 1: median age: 5.7 months; range, 5 days
to 19 months versus Group 2: median age, 5.9 months;
range, 1–23 months and male, 76%, female 68%). In the
group 1, 36% of the children had been recently evaluated by
a physician prior to admission compared with 44% in the
group 2 (ρ ¼ 0.4; χ2 ¼ 0.70). Other intercurrent diseases or
comorbidities were recorded in 46% of the group 1 and 37%
of the group 2. The main comorbidity described was previously noted as macrocephaly (25% in each group), defined
as two points over the standard for age and qualified as
external hydrocephaly (benign childhood hydrocephalus)
before the occurrence of head trauma. Prematurity was
noted in 4% of the nAHT children and 7% of the AHT children
(ρ ¼ 0.7) and did not significantly differ from the nationally
reported rate.
Table 1 Epidemiological profile of 195 families researched because of suspected abuse, between January 2008 and June 2013
(Paris, France)
Epidemiological characteristics
nAHT (n ¼ 50)
AHT (n ¼ 145)
35 (ranging from 26 to 60 years)
48 (96)
125 (86)
2 (4)
20 (14)
10 (20)
61 (42)
Father’s age (years)
Median age (variation)
Mother’s age (years)
Median age (variation)
Origin
Ile de France n (%)†
Other regions n (%)
Social economical or familiar problems†† n (%)
Abbreviations: AHT, abusive head trauma; nAHT, nonabusive head trauma.
†Region of Ile de France (including Paris, Essonne, Hauts-de-Seine, Seine-Saint-Denis, Seine-et-Marne, Val-de-Marne, Val-d’Oise, Yvelines).
††Considering according to social worker evaluation: family violence, alcoholism or others drug use, unemployment, and other factors that may
compromise the balance of the family.
ρ¼ 0.008; x2¼ 6.89; 1 degree of freedom.
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Melo et al.
Table 2 Main complaints referred that led parents or caregivers to seek medical care, and the findings on hospital admission for
195 children admitted with suspicion of abusive head trauma, between January 2008 and June 2013 (Paris, France)
Main symptoms and clinical features
Regarding parents or caregivers
n (%)
Findings on hospital admission
n (%)
Unspecific complainsa
40 (20)
8 (4)
64 (33)
151 (78)
Other or not related
91 (47)
36 (18)
Total
195 (100)
195 (100)
Neurological abnormalities
a
b
Irritability, vomiting, poor feeding, malaise.
Considering if children had bulging fontanels, sunset eyes, or Cushing triad (bradycardia, arterial hypertension and respiratory disorders), was
unresponsiveness or hypotonic or a history of epileptic seizures.
b
CT examination identified SDH in 90% of the children in
Group 1 and 97% of the children in Group 2. Of the children in
the AHT group (n ¼ 145), only one child could be classified as
a potential victim of battered child syndrome, whereas 132
(91%) were determined to have shaken baby syndrome, and
12 (8%) were determined to have shaking-impact baby
syndrome. According to clinical evaluations, no children in
Group 1 and 33 (23%) children in Group 2 (ρ < 0.001)
exhibited signs of potential abuse or impact (such as cutaneous bruises in various stages of absorption or burns).
Children in Group 2 exhibited retinal hemorrhage (RH)
more frequently (79% versus 10%; ρ < 0.001; χ2 ¼ 72.5),
with bilateral and diffuse hemorrhage in 77% of cases,
whereas RH was only focal in Group 1. Associated extracranial skeletal fractures were noted in 18% of participants in
Group 2 and 6% of Group 1 (ρ ¼ 0.04). The main characteristics of children with AHT and nAHT are presented
in ►Table 3.
Children with AHT tended to have a more severe initial
presentation and worse outcome than their nAHT counterparts. Long-lasting or recurrent seizures consistent with
status epilepticus were more frequently observed in cases
of AHT compared with cases of nAHT (66% versus 20%;
ρ < 0.001). Motor, behavioral, cognitive, or visual disabilities
persisting for at least 6 months after trauma were identified
in 10% of the nAHT children and in 36% of the AHT children
(ρ ¼ 0.001; χ2 ¼ 10.6). Death occurred in six children in
Group 2 (4%) and none in Group 1.
Discussion
Abuse against children may include physical aggression,
negligence, and emotional or sexual abuse.11,19 Different
qualifications are used for AHT, making the evaluation of
its real incidence more difficult. Non-accidental head injury
or inflicted traumatic brain injury are commonly used to
define AHT.3,6,7 The incidence varies according to the region
studied and is influenced by socioeconomic and cultural
factors.2,4,5,7–9,11,20,21 In the United States, it is estimated to
occur in 17:100,000 people/year, and in the United Kingdom this figure is 21:100,000 people/year.4 In our hospitalbased series from 2008, 26 new cases were observed each
Table 3 Profile of 195 children examined by a multidisciplinary group, with initial suspicious of abuse, between January 2008 and
June 2013 (Paris, France)
Characteristic
nAHT
(n ¼ 50)
n (%)
AHT
(n ¼ 145)
n (%)
ρ
External signs of abusea
0
33 (23)
< 0.001
Presence of retinal hemorrhage
5 (10)
115 (79)
< 0.001
5 (100)
27 (23)
0
88 (77)
3 (6)
26 (18)
10 (20)
96 (66)
< 0.001
5 (10)
50 (36%)†
0.001
Unilateral
Bilateral
Bone fractures other then skull
b
Abnormalities at Electroencephalogram
c
Long term neurological and/or ophthalmological disabilitiesd
Abbreviations: AHT, abusive head trauma; nAHT, nonabusive head trauma.
a
Cutaneous bruises in various stages of absorption, abrasions and burns.
b
Fractures in other regions of the body such as ribs and limbs detected in skeletal radiographs.
c
We considered any kind of abnormalities described at the first Electroencephalogram.
d
Considering motor, behavioral, cognitive or visual disabilities that persist for at least three months after trauma.
†
Considered 139 survivals (50/139).
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Abusive Head Trauma
year. This represents a slightly reduced incidence compared
to a previously reported series.16 This could be due to the
results of effective national prevention programs and a more
precise analysis of the cases by the multidisciplinary panel.
Previously described risk factors for the perpetrators of
AHT are young parental age, low educational and low socioeconomic–cultural level, family instability,4,7–9 alcoholism,
and drug abuse.3,11 We were unable to verify in these series
the influence of young parental age, although there were
some very young parents (<19 years) in the AHT group.
However, unbalanced families with socioeconomic problems
and low cultural level were clearly more numerous in the
AHT group. This underlines the need for efficient and specific
preventive measures in families identified as at risk, as
highlighted by other authors.22–25 As in other reports, boys
represented more than 65% of the population, and most
children were aged under one year.2,4–8,11,12,16,17
The absence of reported trauma or an informed clinical
history that does not match the severity of injuries has been
cited as 92% predictive for abuse/aggression.4 Often in the
cases of AHT, the perpetrator is their own witness, the victim
is usually aged under one year, and the most frequent brain
injury is SDH.12,26 Severe nAHT remains very unusual in
children aged under 12 months and mainly results from
witnessed traumas such as traffic accidents or falls from
heights; isolated SDH, however, is found in these cases only
exceptionally.27,28 For these reasons, all head injuries occurring in children aged under two years without a clear
witnessed history of an accident must be considered as a
potential victim of AHT at first glance, requiring further
investigations, including an ophthalmologic exam, complete
skeletal bone radiographs, and EEG.7,16,19,21,29 In some cases,
nAHT occurs at home as the result of falls, but this mostly
occurs in older children and is immediately described by
parents and caregivers. In our nAHT group, careful further
inquiries led to the identification of possible accidental
mechanisms compatible with the brain injuries observed
in all cases. These home accidents were frequently only
witnessed by other children or underestimated by caregivers
and could therefore be initially overlooked as potential
severe head trauma by adult caregivers.12,28
In AHT, a scenario of aggression is described that begins
with a child who “cries a lot.” Typically, young and stressed
parents or caregivers fail to stop a baby from crying, get
angrier, lose self-control, and begin shaking the child in an
aggressive way or attacking them physically in other
ways.11,30 The mechanism usually underlying this type of
trauma is rapid acceleration, deceleration, and rotation of the
child’s skull during repeated and forceful shaking by an
aggressor holding and lifting the child by the chest or
arms.5,11 The high prevalence of intracranial hypertension,
epilepsy, and status epilepticus,16,31 that, together, are responsible for 78% of the clinical manifestations diagnosed in
hospital admissions in this study, demonstrate the severity of
this trauma mechanism. Compared with a previous study,32
we observed that children aged under 1 year who experience
an “accidental fall” or “home-related injury” seldom present
with the symptoms described here upon hospital admission.
Melo et al.
Although falls are extremely common in the same age group
as the victims of AHT, the biomechanics of these injuries are
different in terms of the acceleration, rotation, deceleration,
and final impact.28
Recurrent aggression was identifiable in up to 20% of
cases, frequently leading to repeated visits to the emergency
department for medical assistance.7,11 Prompt recognition of
the problem and adequate explorations leading to the early
diagnosis of AHT could be life-saving, preventing further
aggression.14 In our sample, 44% of children with suspected
AHT had a history of medical care before diagnosis. Impaired
or delayed neurodevelopment and other disabilities,15 low
birth weight, previous hospitalization, or prematurity are
commonly reported in victims of AHT.2,4–8,11,12,16,17 Comorbidities were recorded in 46% (nAHT) and 37% (AHT) of our
population. Macrocephaly, with a previous diagnosis of
external hydrocephalus, was the most common. The presence of enlarged subdural spaces, relatively tensed bridge
veins, cranial disproportion, an immature brain, and open
sutures and fontanels potentially put these children at
increased risk of vascular and parenchymal lesions, resulting
from acceleration and deceleration movements.33
External signs of violence should be systematically ruled
out.12,19,21 When no external signs of violence/impact are
evident, doubt can persist regarding the trauma mechanism.4,7,20,21,34 Although more frequent in Group 2 (AHT),
burns (from cigarette butts or other agents), skin abrasions,
bruises, hematoma, subcutaneous cranial impact, and bite
marks were noted in fewer than 50% of our cases. The
presence of external signs are valuable for predicting AHT,
but their absence must not eliminate the possibility of
abuse.4,7,20,29
The most common CT findings of AHT include isolated
SDH, which is present in more than 70%,6,16,20,29,34,35 commonly bilateral, and sometimes associated with interhemispheric and/or convexity hyperdensity.20,33,35 As we
examined children aged under 2 years presenting with at
least one traumatic intracranial injury on initial CT scan and
without a clear history of trauma, excluding all traffic- and
fall-related injuries, SDH was an almost constant finding in
both groups. A potential mechanism of shaking with an
isolated SDH was the most frequent situation (91%), and a
shaking-impact mechanism has occurred in 8% of cases. In
our previously described population of children with severe
nAHT,27,28 we observed that the most frequently identified
injuries were brain swelling, skull fractures, and multiple
brain contusions, with isolated SDH present in fewer than 2%
of cases. Isolated SDH is rare in victims of home accidents
aged under one year; however, skull fractures (linear or
depressed) are the most frequently reported lesions.32,35
An ophthalmologic evaluation for RH is a prerequisite in
all infants and toddlers presenting with a severe head injury.
In AHT, RH is usually diffuse and bilateral,19,29,36–38
highlighting the violence of acceleration and deceleration,11,35,39,40 and present in over 50% of cases.6,11,17,19–21,34
In our sample, 79% of children in the AHT group had RH, and
of those, it was bilateral in 77%. RH cannot be considered
specific to AHT because it is rarely observed in nAHT
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Melo et al.
involving acceleration, deceleration, and impact, such as falls
from heights or traffic accidents. However, in these cases, RH
is generally smaller and unilateral,7,11,19,31,37 as we verified.
Associated skeletal lesions are frequently metaphyseal in
the tibia, femur, humerus, and posterior aspect of the
ribs.4,7,19–21,39,40 Extracranial fractures were more frequent
in children with suspected AHT (18%) compared with those
with nAHT (6%; ρ ¼ 0.04), highlighting the importance of
skeletal radiography in all children with suspected AHT.
However, the absence of bone fractures in skeletal radiographs cannot exclude the possibility of AHT.
AHT should be considered a severe traumatic brain injury,
with a high risk of evolutive complications, long-term disabilities, and mortality, requiring early aggressive specialized
management.39–42 Although isolated inaugural seizures are a
common finding in infants and toddlers in both groups, AHT
carries a major risk of status epilepticus development that
must be taken into account as soon as possible. Uncontrolled
epilepsy is present in a large proportion of survivors of
AHT.11,16 A bad outcome with severe disabilities, visual deficits, and epilepsy occurs in 36% of the survivors, contrasting
with a bad outcome in 10% of the children with nAHT.
Monitoring these children, particularly for the identification
of disabilities, should be undertaken by a multidisciplinary
team comprising a pediatric neurosurgeon, neurologist, ophthalmologist, pediatricians, and specialists in developmental
behavioral disorders.16,41,42 It is also worth noting that neurologic disabilities resulting from AHT or nAHT sometimes
manifest after the first 6 months, the scope of this study did
not include their identification after this period.
The mortality rates of AHT vary from 15–35%.6,7,10,11
Therefore, our 4% mortality rate seems to be underestimated.
One possible explanation could be the selection bias, because
the most severely injured children who died early could not
be referred to our center. Another possible explanation could
be that battered infants, representing less than 10% of our
population, could have been dispatched to other pediatric
intensive care units, with the neurosurgical problem being
considered as non-dominant in these children. However, this
bias highlights the possibility of underestimating the incidence of AHT and the fact that some health providers do not
consider it a primary neurosurgical emergency.7,10
early recognition, adequate exploration, and aggressive
management are warranted and are the keys to limiting
the immediate complications and long-term disabilities
arising from AHT.
Acknowledgment
Mireille Amona and Christelle Custos (social workers of
the Necker Hospital) for their help in searches of social
histories of families.
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THIEME
274
Perfil clínico e sociodemográfico de vítimas de
traumatismo cranioencefálico atendidas na área
vermelha da emergência de um hospital de
referência em trauma em Sergipe
Clinical and Sociodemographic Profile of Traumatic
Brain Injury Victims Attended on Emergency Red Area
from a Hospital Reference in Trauma of Sergipe
Mérilin Sampaio da Cruz Passos1 Karem Emily Pina Gomes1
Fernanda Gomes de Magalhães Soares Pinheiro2 Caio Lopes Pinheiro de Paula3
Daniele Martins de Lima Oliveira2 Airton Salviano de Sousa Júnior4
1 Enfermeira, Universidade Tiradentes, Aracaju, SE, Brasil
2 Mestrado; Enfermeira; Professora Assistente, Universidade
Tiradentes, Aracaju, SE, Brasil
3 Médico, Hospital de Urgências de Sergipe; Residente em
Neurocirurgia, Fundação Beneficência Hospital de Cirurgia Aracaju,
SE, Brasil
4 Acadêmico de Medicina, Universidade Tiradentes, Aracaju, SE, Brasil
Address for correspondence Mérilin Sampaio da Cruz Passos, MD,
Universidade Tiradentes e Hospital de Urgências de Sergipe, Rua
Monsenhor Constantino, 1017, Centro, Itabaiana, SE, Brasil CEP:
49.500-000 (e-mail: [email protected];
[email protected]).
Resumo
Palavras-Chave
► traumatismos
cranioencefálicos
► causas externas
► mortalidade
► atendimento de
emergência
► neurocirurgia
received
March 17, 2015
accepted
August 7, 2015
published online
October 13, 2015
Objetivo Traçar o perfil clínico e sociodemográfico das vítimas de TCE atendidas na
área vermelha da emergência de um hospital de referência em trauma em Sergipe.
Método A amostra foi composta por 96 vítimas de TCE, para coleta de dados foram
usados instrumento estruturado, prontuário e ficha de atendimento.
Resultados A faixa etária mais acometida foi de 18 a 30 anos; a grande maioria do
sexo masculino, natural de Sergipe. Quanto ao estado civil, escolaridade e profissão, foi
notado o não preenchimento destes campos na totalidade das fichas de atendimento.
A grande maioria dos acidentes ocorreu em via pública com motocicletas procedentes
de outros municípios de Sergipe, domingo; a maioria dos TCEs foi classificada em grave.
Para a grande maioria foi adotado o tratamento conservador. A maioria das vítimas
utilizou analgesia. O suporte ventilatório que prevaleceu foi o TOT. A totalidade usava
monitorização não invasiva; 81,3% fizeram uso de nutrição enteral, sendo 51,0% por via
nasal; 60,4% com balanço hídrico e 77,1% com sonda vesical de demora; 64,6% das
vítimas foram transferidos para outras áreas do hospital e 21,9% evoluíram para óbito.
Conclusão O TCE grave prevaleceu no adulto jovem do sexo masculino; o trauma por
moto foi representativo com número de óbitos significativo. Estima-se que o tratamento conservador e as terapias de suporte sejam padrão na condução clínica das
10.1055/s-0035-1564886.
ISSN 0103-5355.
Perfil de vítimas de traumatismo cranioencefálico em Sergipe
Passos et al.
vítimas de TCE, o que exige dos profissionais de saúde intervenções a fim de minimizar
danos físicos e psicológicos.
Abstract
Keywords
► traumatic brain
injury
► external causes
► mortality
► emergency care
► neurosurgery
Objective Draw a clinical, social and demographic profile of TBI victims attended on
emergency red area from a hospital reference in trauma of Sergipe.
Methods The sample was composed for 96 TBI victims; for the search of data was
used structured instrument and clinical and service records.
Results The age group more affected was from 18 to 30 years old; the great majority
male, born in Sergipe. It was noted that the fields of marital status, education and
profession were not filled in the total of the service records. The great majority of
accidents occurred in public way originated in others cities of Sergipe; the trauma
mechanism was motorcycle accident on Sunday; the majority of the TBI was classified
as serious. For the most of victims it was chosen the conservatory treatment. The
majority of them used analgesics. The ventilatory support most used was the
endotracheal tube. The totality used non-invasive motorization; (81.3%) were in enteral
nutrition, being (51.0%) nasally; (60.4%) with hydric balance and (77.1%) with urinary
catheter; (64.6%) of the victims were transferred to other hospital areas and (21.9%)
evolved to death.
Conclusion The serious TBI, in the male young adult was prevalent; the motorcycle
trauma was representative with significant number of deaths. It is estimated that the
conservatory treatment and the support therapies be a pattern on the clinical
management of TBI victims, what requires interventions from the health professionals
to minimize the physical and physiologic damages.
Introdução
No Brasil, o traumatismo cranioencefálico (TCE) é um grave
problema de saúde pública, por acometer mais o sexo
masculino em idade produtiva, gerando custos diretos –
como despesas médicas, diagnóstico, tratamento, recuperação e reabilitação – e indiretos – como afastamento do
trabalho e limitações físicas, que resultam em perda de
produtividade. Grande parte dos sobreviventes consegue
readquirir parte significativa de suas funções, como deambular; porém, a maioria apresenta déficits físicos e
cognitivos.1,2
No cenário atual o TCE é uma das causas mais comuns
de morbimortalidade em todo o mundo, afetando de
forma direta a qualidade de vida, tanto do traumatizado
quanto da família. No ano de 2010 a estimativa anual de
TCE nos Estados Unidos foi de 1,7 milhão de casos; destes,
52 mil resultam em morte, 275 mil em hospitalizações,
1,365 milhão em atendimentos em caráter de urgência e
emergência. No Brasil, em 2011, foram realizadas 547.468
internações devido a causas externas variadas, e destas
resultaram 12.800 óbitos. No estado de Sergipe, em 2008,
ocorreram 7.000 internações por causas externas e 150
óbitos.3,4
O TCE é descrito como todo tipo de patologia oriunda de
traumas externos, com consequentes alterações ósseas no
crânio, lacerações no couro cabeludo, podendo comprometer
as meninges, o encéfalo e vasos sanguíneos. As lesões podem
ser temporárias ou permanentes, e afetar a função motora,
emocional ou cognitiva, podendo ainda evoluir para óbito.5,6
As lesões cerebrais são classificadas em primárias e secundárias. As primárias ocorrem no momento do trauma
direto do parênquima encefálico, ou ainda dos traumatismos
fechados, decorrentes das forças de aceleração e desaceleração, não necessariamente havendo impacto do crânio contra
estruturas externas. O encéfalo e a caixa craniana possuem
densidades diferentes, respondendo de forma desigual
quando submetidos às mesmas forças, podendo ocasionar
ruptura de veias, laceração do parênquima, estiramento de
axônios e de vasos sanguíneos cerebrais.7
As lesões secundárias ocorrem após o momento do
trauma, devido a fatores intracerebrais e extracerebrais –
como hipotensão arterial, hipoglicemia, hipercarbia, hipóxia
respiratória, hemorragia intensa, distúrbios hidroeletrolíticos, substâncias neurotóxicas, hidrocefalia, alterações hemodinâmicas intracranianas, morte celular, neuronal,
endotelial – que podem estar associados a lesão primária
e/ou a algum dos próprios fatores secundários.7
O uso de escalas de avaliação neurológica é muito importante para indicar o comprometimento neurológico, realizar
a monitoração do estado de saúde do paciente e o prognóstico. O TCE pode ser classificado em leve, moderado e grave,
segundo a escala de coma de Glasgow (ECG), através da
seguinte pontuação: 14 a 15, leve; 9 a 13, moderado; e 3 a
8, grave (estado de coma). A ECG foi criada por Teasdale e
Jennett em 1974, com o intuito de avaliar o nível de
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consciência e duração de alterações motoras, visuais e verbais, esta é a escala mais utilizada para indicar a gravidade
dessas condições, pois permite uma avaliação neurológica
confiável e rápida de maneira padronizada.
Os exames de imagem – como tomografia computadorizada e ressonância magnética – também são muito importantes para a avaliação de vítimas de TCE, pois permitem
fazer o diagnóstico da lesão, fisiopatologia, terapêutica a ser
adotada e o prognóstico.8
Os traumatismos cranianos leves representam cerca de
50% dos casos; normalmente, possuem evolução satisfatória,
não ocasionam perda de consciência, apenas leve alteração
transitória das funções mentais superiores (memória, orientação etc.), podendo provocar cefaleia e vertigem, encontrando-se o paciente lúcido e orientado. O TCE moderado
ocorre no politraumatismos; geralmente, ocorre perda de
consciência e alterações neurológicas reversíveis, com presença de cefaleia progressiva, vômito, convulsão e perda de
memória. Já o TCE grave é caracterizado por inconsciência e
perda neurológica progressiva; geralmente, o paciente está
em coma; destes, 60% apresentam outros órgãos comprometidos e 25% apresentam lesões cirúrgicas.9
O tratamento do TCE é conduzido de forma conservadora ou cirúrgica. A primeira é realizada através de medicamentos,
suporte
respiratório,
hemodinâmico,
hidroeletrolítico, nutricional, e da avaliação do estado
neurológico, por meio de monitoração e controle da pressão intracraniana (PIC), da pressão de perfusão cerebral
(PPC), Doppler transcraniano, eletroencefalograma, oximetria venosa jugular, entre outros. Já a cirúrgica é adotada nos casos de hematomas extradurais, subdurais,
contusões cerebrais, intraparenquimatosos traumáticos e
laceração do lobo temporal ou frontal. Para que o tratamento cirúrgico seja escolhido, são levados em consideração a localização, o tamanho da lesão, aumento de volume,
desvio das estruturas, entre outros critérios.10,11
O presente trabalho tem como objetivo caracterizar as
vítimas de TCE atendidas na área vermelha da emergência de
um hospital de referência em trauma em Sergipe, quanto às
variáveis: idade; sexo; naturalidade; escolaridade; estado
civil; profissão; data da admissão; fonte de dados; local do
acidente; procedência; mecanismo do trauma; dia da semana em que o evento aconteceu; classificação do TCE de
acordo com a ECG; quantificação dos desfechos das vítimas
em relação à alta, transferência ou o óbito, sem preocupar-se
em explicar ou intervir na situação.
Materiais e Métodos
Estudo descritivo, documental, de corte transversal e natureza quantitativa, realizado por meio das fontes secundárias
como a ficha de atendimento e o prontuário de 96 vítimas de
TCE. O cenário da pesquisa foi o pronto-socorro adulto, na
área vermelha da emergência de um hospital de referência
em trauma no estado de Sergipe.
O universo da pesquisa envolveu todas as vítimas por TCE
admitidas nesta área, no período de 29 de agosto a 29 de
outubro de 2014 que contemplaram os respectivos critérios
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Passos et al.
de inclusão: adultos vítimas de TCE de ambos os sexos;
vítimas admitidas na área vermelha da emergência de um
hospital de referência em trauma em Sergipe. Foram excluídas as vítimas que não tinham diagnóstico de TCE, menores
de 18 anos de idade e com ficha de atendimento e prontuário
incompletos ou não localizados durante o período da coleta
de dados.
A coleta dos dados foi realizada de maneira aleatória, nos
turnos matutino, vespertino e noturno, em dias alternados,
sem que fosse comprometida a identificação das vítimas,
pois mesmo que não identificada naquele dia de coleta,
houve busca ativa dessa ficha e/ou prontuário da vítima.
Durante todo estudo os pesquisadores atenderam aos Critérios da Ética em Pesquisa com Seres Humanos, garantindo o
anonimato das vítimas, sendo iniciado após sua aprovação.
Os dados foram coletados por meio da aplicação de
instrumento estruturado, destinado à caracterização das
vítimas, e armazenados no programa SPSS, versão 20.0. As
variáveis categóricas foram descritas por meio de frequência
absoluta e relativa. O intervalo de confiança adotado foi de
95% e o erro máximo permitido de 5% (ou 0,05). Os resultados
foram discutidos à luz das bibliografias consultadas e apresentados no formato de tabelas, a fim de quantificar os
achados pertinentes às variáveis investigadas.
Resultados
De acordo com os dados coletados a faixa etária mais
vitimada por TCE é de 18 a 30 anos (45,8%), a grande maioria
das vítimas é do sexo masculino (89,6%), natural de Sergipe
(95,8%). Quanto às variáveis: escolaridade, estado civil e
profissão, não foi possível caracterizá-las, devido a não haver
informações no prontuário, em função de seu preenchimento ter sido negligenciado.
Quanto aos dados do acidente a grande maioria ocorreu
em via pública (96,9%), com maior número de vítimas
procedentes de outros municípios de Sergipe (79,2%), a
maioria por acidente de moto (62,5%), o domingo foi o dia
em que mais houve acidentes (33,3%), e o TCE grave prevaleceu (55,2%).
A partir da análise dos dados foi percebido que apesar de a
amostra ser composta de 96 vítimas, os exames foram
realizados 294 vezes. A tomografia computadorizada
(31,0%) e os raios X (21,4%) foram os exames mais realizados
entre as vítimas admitidas no setor estudado, seguidos dos
exames laboratoriais (18,7%).
Foram identificados 65 achados clínicos; os mesmos
repetiram-se 235 vezes, sendo o de maior visibilidade a
hipertensão arterial sistêmica, que esteve presente em 35
pacientes (14,9%), seguido de hematoma subdural (7,2%),
hipertermia (6,8%) e hipotensão (6,0%). A variável “outros”
corresponde a achados que ocorreram de maneira menos
expressiva, sendo eles otorragia / taquicardia (3,8% cada),
sangramento / taquipneia / perda de consciência (3,0% cada),
fratura de crânio (2,6%), hematoma subaracnóideo / cefaleia /
hematoma periorbital (2,1% cada), contusão em crânio /
bradicardia / fratura de base de crânio (1,7% cada), pneumoencéfalo / hemorragia subaracnóidea / equimose periorbital
278
de consciência, cefaleia, vômitos, otorragia e coma. Outras
pesquisas também apresentaram esses tipos de achados,
porém não foi possível realizar um comparativo devido a
diferença entre as linhas de pesquisa – uma visava identificar
todos os achados, enquanto as outras apenas os achados
obtidos por exames de imagem.6,8,15,19,20
Utilizar métodos diagnósticos adequados é fundamental
para tomar a decisão sobre o tratamento do TCE, além de
reduzir os custos. Ao buscar dados sobre os exames realizados, foi encontrado o seguinte: das 96 vítimas, 91 fizeram
tomografia computadorizada, 63 foram submetidas aos raios
X e 55 realizaram exames laboratoriais. Outros estudos
apresentaram a tomografia computadorizada como o exame
mais realizado na busca por lesões, seguido dos raios X,
corroborando os dados do presente estudo.15,18,21
De acordo com alguns estudos o tratamento conservador
foi adotado para a grande maioria das vítimas de
TCE;6,13,15,19 dados semelhantes foram encontrados na presente pesquisa, onde 87,5% da amostra foi tratada conservadoramente. Já segundo outros autores, o tratamento
cirúrgico prevaleceu uma vez que as suturas também foram
contabilizadas como intervenções cirúrgicas.12,22 Esse tipo
de tratamento acarreta grande ônus à saúde pública, uma vez
que necessita de cuidados especializados, e porque a recuperação do paciente é muito mais lenta, sem falar no
aumento das chances do paciente desenvolver infecções.
Segundo pesquisa realizada no ano de 2011, as condutas
adotadas no tratamento de vítimas de TCE visam manter a
perfusão cerebral, oxigenação e a prevenção de lesões secundárias ao trauma.23 No tocante ao manejo clínico, não
foram encontrados estudos que tivessem uma linha de
pesquisa parecida com a do presente estudo; as literaturas
consultadas preconizam o uso, mas não identificam os tipos
de sedação, de anticonvulsivantes, profilaxia de TVP, tipos de
nutrição, realização de balanço hídrico e controle glicêmico
no que se refere ao quantitativo de pacientes em uso destes.
O presente estudo identificou, em relação ao manejo das
vítimas de TCE admitidas na área vermelha, que é realizada
profilaxia com protetores gástricos; o omeprazol foi o medicamento mais usado pelas vítimas (26%), seguido da ranitidina (23,7%). O soro antitetânico também foi identificado
como profilaxia, porém em nenhum estudo consultado foi
relatado seu uso, embora as condutas de terapia intensiva
implementem a profilaxia para o tétano.
De acordo com as literaturas utilizadas a analgesia e a
sedação são essenciais para proporcionar conforto ao paciente, evitando o consumo de oxigênio do cérebro e a demora
na recuperação.23,24 A sedação mais utilizada nas vítimas foi
o fentanila (32,9%), seguida do midazolam (31,9%). A terapia
hiperosmolar foi o ringer-lactato (37,9%) e o manitol (15,5%).
A grande maioria estava em uso de analgesia (90,6%); destes,
65,6% faziam uso de dipirona (não opioide); 25,0% de tramadol (opioide); e 1,6% de morfina (opioide).
Segundo pesquisa realizada em 2011, foi identificado que
de 504 vítimas, apenas 8 estavam em uso de tubo orotraqueal
(TOT), 4 de máscara de Venturi, 3 de sonda orogástrica e 9 de
sonda vesical de demora14 dados estes discordantes dos que
foram encontrados no presente estudo, pois os números
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Passos et al.
foram mais significativos: das 96 vítimas, 67 estavam em
uso de TOT; 78, em nutrição enteral, sendo 49 por via nasal;
74 estavam com sonda vesical de demora, e o balanço hídrico
foi realizado em 58 pacientes.
Foi evidenciado que a totalidade das vítimas estava em
monitoração não invasiva. O controle glicêmico foi realizado
em 69,8% delas; 65,6% faziam uso de anticonvulsivantes, sendo a
droga mais utilizada a fenitoína (64,3%). A profilaxia de TVP
esteve presente em apenas 12 vítimas, todas com heparina.
Apesar de não ter sido possível realizar um comparativo
de algumas condutas identificadas no presente estudo com
outros devido a diferenças de linhas de pesquisa, algumas
literaturas consultadas preconizam o uso de suporte ventilatório através do TOT, sedação e analgesia com midazolam,
fentanila, morfina, tramadol, lorazepam, propofol e etomidato; terapia hiperosmolar com manitol, soluções hipertônicas e ringer-lactato; como anticonvulsivantes, a fenitoína,
fenobarbital, primidona e carbamazepina. Menciona-se que
o controle glicêmico com insulina é de grande importância
interferindo diretamente na redução na mortalidade e que o
suporte nutricional deve ser iniciado após estabilização
hemodinâmica, sendo a via nasal a mais indicada; ressaltase ainda a importância da profilaxia de TVP.23–27
Estudos mostram que a mortalidade por causas externas
vem crescendo em todo o Brasil, com maior visibilidade nas
regiões Sudeste e Nordeste. No que diz respeito ao desfecho
clínico o presente estudo evidenciou que 64,6% das vítimas
foram transferidas da área vermelha do pronto-socorro para
outras áreas do hospital, como centro cirúrgico, unidade de
terapia intensiva e enfermarias; 21,9% evoluíram para óbito e
apenas 13,5% tiveram alta hospitalar. Em outros estudos
realizados foram encontrados resultados diferentes, sendo
que a maioria das vítimas recebeu alta, seguida das transferências para outras áreas do hospital e pelos óbitos, que
aparecerem em menor proporção. O longo tempo de internação é um fator negativo, uma vez que gera altos custos,
atrapalha a rotatividade dos leitos, aumenta as chances de
infecção e afasta o paciente do convívio familiar.13–15,22,28,29
Conclusão
O presente estudo reforça que oTCE por causa motociclística, em
via pública, nos dias de domingo, acomete vítimas que são
formadas em sua maioria por homens na faixa etária entre 18
e 30 anos. E ainda que o registro sobre os pacientes é uma
ferramenta indispensável para a prestação da assistência. Pôdese observar que a dinâmica do serviço de urgência e emergência
dificulta o preenchimento de algumas informações importantes
para o conhecimento do perfil dos pacientes admitidos na área
vermelha, dados estes que são de grande utilidade para os
profissionais envolvidos diretamente na assistência e também
para os gestores, porque possibilitariam a adoção de medidas de
forma mais rápida e objetiva.
Conflito de Interesses
Os autores declaram a inexistência de conflito de interesse
na realização deste trabalho.
/ hematoma extradural / hipotermia / rinorragia / afundamento de crânio (1,3% cada), hipóxia / escoriação / hemiplegia /
hiperglicemia / hemotórax / epistaxe / edema periorbitário /
sinais de hemorragia tronco-cerebral / lesão axonal difusa /
edema facial / hematoma / vômitos / síncope / crise convulsiva
(0,9% cada), equimose palpebral / anisocoria / hemiparesia /
hemopneumotórax / dispneia / tosse / edema cerebral / acidose
respiratória / hipercarbia / hematúria / oligúria / amnésia /
dificuldade para falar / exposição de massa encefálica / hematoma epidural / fratura facial / paresia / bléfaro-hematoma /
perda de massa encefálica / hemorragia frontal e temporal /
rebaixamento de nível de consciência / hemorragia intraventricular / hemorragia subdural / contusão em crânio e face /
concussão cerebral / contusão subcortical / hemorragia parenquimatosa (0,4% cada). Quanto ao tratamento escolhido a
maioria foi conservador (87,5%).
No tocante ao tratamento medicamentoso a droga mais
utilizada para a realização de profilaxia foi o omeprazol
(26,0%) dos casos, para sedação foi o fentanila (32,9%) e
como terapia hiperosmolar a maior parte não encontravase em uso de medicação (46,6%).
Com relação ao manejo e as medidas gerais adotadas,
pode-se notar que a grande maioria estava em uso de
analgesia (90,6%), e a Dipirona foi utilizada na maioria dos
pacientes (65,6%). O tubo orotraqueal foi encontrado em
69,8% dos pacientes. A totalidade das vítimas estava sob
monitoração não invasiva (100%). No que diz respeito à
nutrição, 81,3% estavam com nutrição enteral, e 51,0% por
via nasal. O controle glicêmico se fez presente em 69,8% dos
pacientes. Os anticonvulsivantes profiláticos foram utilizados na maioria 65,6% das vítimas, e a droga, foi a fenitoína
(64,3%). A profilaxia para trombose venosa profunda (TVP)
fez-se presente em apenas 12,5% dos pacientes; destes, todos
estavam em uso de heparina. O balanço hídrico rigoroso foi
realizado na maioria (60,4%). Quanto à sonda vesical de
demora, a grande maioria das vítimas estava fazendo uso
dela (77,1%).
Ao correlacionar o mecanismo do trauma com a gravidade
do TCE, segundo a escala de coma de Glasgow, foi identificado
que o TCE grave esteve mais presente nas vítimas de acidente
de moto (31), seguido das agressões físicas (7).
O presente estudo identificou ao correlacionar os dados,
que o dia mais frequente dos acidentes de moto é o
domingo (24 casos), seguido da segunda-feira (13 casos).
As agressões físicas foram mais frequentes nos sábados (4
casos), sendo este o segundo mecanismo de trauma mais
visível.
Ao analisar o desfecho clínico dos casos, foi possível
visualizar que a transferência dos pacientes para outras áreas
do hospital prevaleceu (64,6%), seguido dos óbitos (21,9%)
dos internos na área vermelha.
Discussão
A pesquisa possibilitou identificar dados referentes ao perfil
sociodemográfico das vítimas de TCE e o manejo clínico
adotado durante a admissão e permanência no setor
estudado.
Passos et al.
Os dados do presente estudo evidenciaram que o TCE
acomete mais o adulto jovem, do sexo masculino (89,6%), na
faixa etária de 18 a 30 anos (45,8%), com naturalidade de
Sergipe (95,8%). Outros estudos realizados também apresentaram informações semelhantes quanto ao sexo e faixa etária.
Essa maior vitimização de homens em idade produtiva por
causas externas é atribuída a uma maior exposição a situações perigosas, como a ingestão de álcool e outras drogas, alta
velocidade, a não utilização de equipamentos de proteção
individual, entre outras, o que permite supor não haver fator
biológico associado a essa maior predisposição.4,12,13
De acordo com estudo sobre caracterização das vítimas de
violência e acidentes realizado em Sergipe, no ano de 2011,
no mesmo hospital do estado, quanto ao estado civil, escolaridade e profissão, foi identificado que eram solteiras, com
baixa escolaridade e atividade remunerada. A baixa escolaridade pode proporcionar maior vulnerabilidade ao indivíduo, por não proporcionar-lhe o entendimento da
importância da prevenção; da mesma forma, o estado civil
solteiro faz supor a ausência de comprometimento com a
família, o que desencadeia a exposição mais frequente a
situações de risco. Ao pesquisar essas mesmas variáveis, não
foi possível realizar um comparativo em virtude de não haver
essas informações na ficha de admissão e no prontuário da
amostra estudada.6,14
Com relação aos dados do mecanismo do trauma, os
acidentes de moto tiveram maior incidência (62,5%); quase
que a totalidade dos episódios traumáticos ocorreu em via
pública (96,9%) e nos finais de semana – domingo (33,3%) e
sábado (17,7%) – vindo em seguida a segunda-feira (15,6%); a
grande maioria das vítimas é procedente do interior do
estado. Evidências semelhantes foram encontradas em outros estudos realizados na região Nordeste.4,5,15–17
No tocante à escala de coma de Glasgow, ao analisar os
prontuários foi possível identificar que 9,4% não continham
essa informação, sendo um ponto negativo para a tomada de
decisão quanto ao tratamento e manejo da vítima. O TCE
grave foi mais prevalente na amostra estudada, seguido do
TCE leve. Em um estudo realizado na região Sul do país,
também foi evidenciada a falta de informação sobre a
gravidade do TCE, porém em uma menor proporção (3%);
quanto à classificação, o TCE grave também prevaleceu,
seguido do leve.18
Ao relacionar o mecanismo do trauma com a gravidade do
TCE, evidenciou-se que o TCE grave teve destaque nos acidentes de moto, seguido das agressões físicas, diferentemente dos resultados encontrados em estudo realizado no
Rio Grande do Sul, onde ocorreu uma maior incidência de
TCE relacionado à queda com classificação leve; em outro
estudo, realizado em Pernambuco, o TCE leve prevaleceu
tanto nos acidentes de moto, quanto nas quedas; já em outro
trabalho, também em Pernambuco, os achados destacaram a
queda como principal causa de TCE grave.1,6,15
No que se refere à variável “achados clínicos”, foram
identificados 65 achados, de maior ocorrência a hipertensão
arterial sistêmica (14,9%), o hematoma subdural (7,2%), a
hipertermia (6,8%), seguidos da hipotensão (6,0%); em outro
estudo os achados mais frequentes foram a alteração do nível
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279
THIEME
280
The Role of the Intraoperative Auxiliary Methods
in the Resection of Motor Area Lesions
O papel dos métodos auxiliares intraoperatórios na
ressecção de lesões em área motora
Stênio Abrantes Sarmento1,2
Emerson Magno de Andrade1
1 Instituto Paraibano do Cérebro, João Pessoa, PB, Brazil
2 Universidade Federal da Paraíba (UFPB) and Faculdade de Medicina
Nova Esperança (FAMENE), João Pessoa, PB, Brazil
Helder Tedeschi3
Address for correspondence Stênio Abrantes Sarmento, MD, PhD,
Instituto Paraibano do Cérebro. Av. São Paulo 854, João Pessoa, PB.,
CEP 58030-040 (e-mail: [email protected]).
3 Department of Neurosurgery, Universidade Estadual de Campinas
(UNICAMP), Campinas, SP, Brazil
Abstract
Keywords
► motor cortex
► brain neoplasms
► stereotaxic
techniques
► neuronavigation
Resumo
Palavras-chave
► córtex motor
► neoplasia cerebral
► técnicas
estereotáxicas
► neuronavegação
received
March 30, 2015
accepted
August 7, 2015
published online
October 28, 2015
Objective In recent years, technologies have advanced considerably in improving
surgical outcome following treatment of lesions in eloquent brain areas. The aim of this
study is to explore which method is best in the resection of motor area lesions.
Methods Prospective, non-randomized study Evaluate on 74 patients who underwent
surgery to remove lesions around the motor area.
Results Total lesion removal was achieved in 68 patients (93.1%). Fifty-four patients
(73.9%) presented normal motor function in the preoperative period; of these, 20
(37.3%) developed transitory deficits. Nevertheless, 85% of these patients later
experienced a complete recovery. Nineteen patients presented with motor deficits
preoperatively; of these, five presented deteriorating motor abilities. Intraoperative
stimulation methods were used in 65% of the patients, primarily in cases of glioma.
Conclusions The morbidity in patients submitted to resections of motor area lesions is
acceptable and justify the surgical indication with the purpose of maximal resection.
Intraoperative stimulation is an important tool that guides glioma resection in many cases.
Objetivo Nos últimos anos, consideráveis avanços tecnológicos têm surgido no
sentido de melhorar os resultados cirúrgicos no tratamento de lesões em áreas
eloquentes do cérebro. O objetivo deste estudo é investigar qual o melhor método
para ressecção de lesões em área motora.
Método Estudo prospectivo não aleatório que avaliou os resultados pós-operatórios
em 74 pacientes submetidos à ressecção de lesões em área motora ou adjacente.
Resultados A ressecção cirúrgica foi considerada total em 68 (93,1%) pacientes. 54
pacientes (73,9%) apresentavam força muscular normal no pré-operatório. Destes, 20
(37,3%) apresentaram déficit no pós-operatório imediato, sendo que 17 (85%)
recuperaram completamente o déficit. 19 pacientes apresentavam déficit no préoperatório, sendo que 05 apresentaram piora do déficit no pós-operatório imediato.
10.1055/s-0035-1564422.
ISSN 0103-5355.
Ltda, Rio de Janeiro, Brazil.
Intraoperative Auxiliary Methods for Motor Area Lesions
Sarmento et al.
A estimulação intraoperatória foi utilizada em 65% dos casos, principalmente nos
gliomas.
Conclusão A morbidade em pacientes operados de lesões em área motora é bastante
aceitável e justifica a indicação cirúrgica com objetivo de ressecção máxima. A
estimulação intraoperatória é uma ferramenta importante para guiar a resseção dos
gliomas em muitos casos.
Introduction
The resection of brain lesions situated in or adjacent to the
motor cortex is still a challenge in modern neurosurgery.
Technological advances have allowed for a more precise
localization of eloquent brain areas, including the motor
and language cortex, minimizing the risk of neurological
deficits in the postoperative period.
There are a large number of reports supporting the use,
isolated or not, of cortical stimulation, functional magnetic
resonance (fMRI), motor evoked potentials, neuronavigation
systems, and other techniques of defining the precise functional resection of lesions located in eloquent motor
areas.1–8 In addition to the preservation of cerebral function
during surgery, these techniques also offer optimization of
resection limits, which helps in achieving removal of lesion
or epileptic focus to a greater extent and with increased
safety.9–11 Despite increased use of such techniques, the
anatomical knowledge and the use of precise neurosurgical
techniques still play a decisive role in the attempt to preserve
the full integrity of vascular structures and decrease the risk
of functional deficits.12–15
The aim of this study was to explore which of the abovementioned methods is best in the resection of motor area
lesions. We also investigated the relationship between methods used and the development of postoperative motor
deficits. Furthermore, we attempted to identify cases that
only required knowledge of microanatomy and neuroimaging analyses for safe resection of lesions in the motor cortex.
Material and Methods
Patient Population
We conducted a prospective, non-randomized study on 74
patients who underwent surgery to remove lesions
around the motor cortex and in the insular lobe that
presented a close relationship with subcortical motor
structures. All surgeries occurred between January 2002
and 2009 by the same neurosurgeon, after obtaining
written informed consent from each patient. We excluded
from this study patients with a Karnofsky score lower
than 70 and subject to reoperation. We preoperatively
evaluated the topographic relationship between the lesion
and the motor area in all patients by computerized
tomography (CT) and magnetic resonance imaging
(MRI). MRI was performed, and the anatomical relation
between the brain lesion and the central lobe was identified using images of coronal, axial, and sagittal planes.
Following intravenous administration of gadolin, the
T1-weighted sequence permitted the identification of
the relationship between the lesion location and the
central sulcus and cortical vessels. We investigated demographic, clinical, CT, or MRI images, and treatment data,
which included the following: operative intervention,
lesion location and depth, histological diagnosis, extent
of lesion excision, the presence or absence of a motor
deficit either preoperatively, or early/late postoperatively.
We obtained approval from the Ethics Committee and
informed consent from patients or their closest relative.
Operative Techniques
We planned craniotomy based on the topographic relationship and neuroimaging information obtained from the sutures and craniometric points. The identification of the
coronal suture plays an essential role in the localization of
the central sulcus and motor lobe and can be projected
perfectly onto the scalp based on MRI data (►Fig. 1). In brief,
we stabilized a patient’s head by a three-point fixation device
(Mayfield head holder), and performed trichotomy prior to
the surgical procedure only on the planned incision. For
patients that required cortical stimulation, we left exposed
the side of the body including the face where we expected the
response. After localization of the coronal suture, we could
infer the location of the central gyrus and sulcus on the skull.
We used a high-speed drill to perform an initial burr hole,
which we extended with a footplate to turn the craniotomy
flap and expose the dura mater. We tailored the opening of
the dura for each patient; however, we typically opened the
dura and turned it medially to prevent damaging the sagittal
sinus and/or draining the veins. Cortical stimulation was
performed using a bipolar stimulator with a constant current, and a biphasic square wave (60 Hz) (Ojemann stimulator, Radionic, Burlington, MA; 5 mm between electrodes).
The electrode was put in contact with the cortical surface
corresponding to the anatomical location of the motor area.
The current used to elicit movement ranged from 2 to 10 mA.
Postoperative Course
The same neurosurgery team conducted follow-up evaluations
with all patients. They assessed and classified motor strength
by using the modified Dejong Scale: no contraction (grade 1),
active movement with gravity eliminated (grade 2), active
movement against gravity (grade 3), active movement against
resistance (grade 4), and normal strength (grade 5).
Statistical Analysis
We analyzed factors that correlated histological diagnosis
and motor strength during early and late postoperative
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Sarmento et al.
Fig. 1 (a) Axial and sagittal MRI of a 42-year-old patient presenting with metastasis in the pre-central gyrus. (b) Craniotomy planning based on
the relationship of the coronal suture with the central lobe and surgical aspect after surgical resection. In this case, the lesion was located 3cm
posterior to the coronal suture and 3cm lateral to the midline. The use of auxiliary methods was not necessary. (c) Postoperative MRI showing
total removal of the tumor. The patient recovered without manifestations of any motor deficits.
periods. We used the Friedman test and Student’s t-test; p
values < 0.05 were statistically significant. Due to the limited number of patients, the data available was insufficient;
therefore, multivariate analysis was not possible.
Results
This is a prospective study to evaluate the postoperative
surgical outcome in patients who underwent surgery to
remove lesions around the motor area. The study included
a total of 74 patients analyzed between January 2002 and
2009. All patients presented with lesions around the motor
area or immediately adjacent to it, and were underwent a
surgical procedure in accordance with a previously defined
Vol. 34
No. 4/2015
protocol. Morbidity and the presence or absence of a preoperative and early and/or later postoperative motor deficit
was also evaluated. Because of the limited number of patients, the wide-range of histological variation, and the
multiple variables analyzed, the overall survival rate was
not a goal of this study.
►Table 1 summarizes clinical and surgical characteristics
of the 74 patients. This group was composed of 31 (48.1%)
male patients and 43 (56.7%) female patients with an age
range of 3 to 80 years (mean 44 years). Thirty-two patients
(43.2%) were diagnosed with glioma, followed by 19 patients
(25.6%) with meningioma, 11 patients (14.8%) with metastasis, five patients (6.8%) with cavernoma, two patients each
with primary lymphoma, cisticercus, and cortical dysplasia
Sarmento et al.
Table 1 Summary of clinical and surgical characteristics in the 74 patients who underwent surgery
Case no.
1
Age(yrs)/Sex
44/M
Muscular strength
Pre op
Early post op
Late post op
5
4
5
Pathology
Degree of
resection
Lesion location/Side
Auxiliary method
astrocytoma IV
Total
fronto-pariet rt
cortic stimul
cortic stimul
2
34/M
5
4
5
astrocytoma IV
Total
frontal lt
3
70/F
5
3
4
astrocytoma IV
Total
insular rt
4
51/F
5
5
5
astrocytoma IV
Total
fronto-pariet rt
5
27/M
5
5
5
astrocytoma IV
Subtotal
fronto-insul rt
6
54/M
5
5
5
astrocytoma IV
Subtotal
fronto-insul rt
cortic stimul
7
47/F
5
1
5
astrocytoma IV
Total
frontal lt
cortic stimul
8
78/F
5
5
5
astrocytoma III
Total
frontal rt
9
41/M
4
3
5
astrocytoma III
Total
frontal rt
cortic stimul
10
68/F
4
3
5
astrocytoma III
Total
parietal lt
cortic stimul
11
77/F
3
3
4
astrocytoma III
Total
frontal rt
12
49/F
3
3
3
astrocytoma III
Total
fronto-pariet rt
cortic stimul
13
29/F
5
5
5
astrocytoma III
Total
frontal rt
14
69/M
3
3
5
astrocytoma III
Total
frontal lt
15
44/M
5
1
5
astrocytoma III
Total
frontal lt
cortic stimul
16
34/M
5
1
5
astrocytoma II
Total
frontal rt
cortic stimul
17
25/F
5
5
5
oligoastrocyt II
Total
fronto-insul rt
cortic stimul
18
46/M
5
5
5
astrocytoma II
Total
frontal lt
19
48/F
5
5
5
oligodendro II
Total
fronto-insul rt
20
29/M
5
5
5
astrocytoma II
Subtotal
fronto-insul rt
cortic stimul
21
57/M
5
5
5
astrocytoma II
Total
frontal lt
cortic stimul
22
39/F
5
5
5
astrocytoma II
Total
frontal lt
cortic stimul
23
42/M
5
5
5
astrocytoma II
Total
fronto-insul rt
neuronav þ cs
24
36/M
5
5
5
astrocytoma II
Total
fronto-insul lt
25
34/F
5
5
5
oligoastrocyII
Total
fronto-insul lt
cortic stimul
26
55/M
5
2
3
astrocytoma II
Total
fronto-insul rt
27
42/M
5
4
5
astrocytoma II
Total
parietal lt
cortic stimul
28
32/F
5
5
5
oligodendro II
Subtotal
frontal lt
29
18/F
5
5
5
astrocytoma II
Total
parietal rt
cortic stimul
30
28/F
4
3
5
astrocytoma II
Subtotal
fronto-insul lt
cortic stimul
31
11/F
5
5
5
astrocytoma II
Total
fronto-insul lt
32
50/F
5
4
5
astrocytoma II
Total
fronto-insul lt
cortic stimul
33
27/M
5
4
5
lymphoma
Total
parietal rt
cortic stimul
34
40/M
3
1
3
lymphoma
Total
frontal rt
cortic stimul
35
50/M
5
5
5
metastasis
Total
parietal rt
36
64/M
4
4
5
metastasis
Total
frontal rt
37
44/F
5
5
5
metastasis
Total
fronto-insul lt
38
48/M
5
5
5
metastasis
Total
frontal rt
39
58/M
3
3
5
metastasis
Total
fronto-pariet rt
40
66/F
5
5
5
metastasis
Total
frontal lt
41
59/M
5
5
5
metastasis
Total
frontal lt
42
42/F
4
4
4
metastasis
Total
frontal rt
43
57/F
4
1
3
metastasis
Total
frontal lt
cortic stimul
44
42/M
4
4
5
metastasis
Total
frontal lt
45
51/F
5
5
5
metastasis
Total
frontal lt
46
80/F
5
4
5
meningioma
Total
frontal rt
47
49/F
5
5
5
meningioma
Total
parietal lt
(Continued)
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Sarmento et al.
Table 1 (Continued)
Case no.
48
Age(yrs)/Sex
Muscular strength
Pathology
Degree of
resection
Lesion location/Side
Auxiliary method
5
meningioma
Total
frontal lt
Pre op
Early post op
Late post op
60/F
5
3
49
68/M
5
5
5
meningioma
Total
bifrontal
50
57/F
5
3
5
meningioma
Total
frontal lt
51
60/F
5
4
5
meningioma
Total
frontal lt
52
38/F
5
5
5
meningioma
Total
fronto-pariet rt
53
57/M
5
5
5
meningioma
Total
frontal rt
54
46/M
4
5
5
meningioma
Total
frontal rt
55
60/F
5
5
5
meningioma
Total
frontal lt
56
35/F
5
4
5
meningioma
Total
frontal rt
57
65/M
5
5
5
meningioma
Total
frontal rt
58
42/F
5
1
4
meningioma
Total
frontal lt
59
25/F
5
4
5
meningioma
Total
fronto-pariet lt
60
48/M
4
4
5
meningioma
Total
frontal rt
61
44/F
5
5
5
meningioma
Total
parietal rt
62
35/F
1
1
1
meningioma
Total
fronto-pariet rt
63
40/F
4
5
5
meningioma
Total
fronto-pariet lt
64
37/F
5
4
5
meningioma
Total
frontal lt
65
26/F
5
5
5
cavernoma
Total
parietal rt
stereotax
66
21/F
5
5
5
cavernoma
Total
frontal rt
stereotax
67
32/M
4
4
5
cavernoma
Total
fronto-insul lt
stereotax
68
44/M
5
5
5
cavernoma
Total
fronto-insul lt
69
54/F
4
4
5
cavernoma
Total
frontal lt
70
29/F
5
3
5
cysticercus
Total
parieta lt
71
38/F
5
5
5
cysticercus
Total
frontal rt
stereotax
72
54/F
4
4
5
abscess
Total
frontal lt
73
3/F
5
4
5
cort dysplasia
Total
insular rt
neuronav þ cs
74
14/M
5
5
5
cort dysplasia
Total
frontal lt
cortic stimul
Abbreviations: cort dysplasia, cortical dysplasia; lt, left; neuronav, neuronavigation system; oligodendro, oligodendroglioma; post op, postoperative; pre op, preoperative; rt, right; cortic stimu/cs, cortical stimulation; stereotax, stereotaxia.
(2.7% in each case), and one patient with an inflammatory
lesion (1.4%). Among patients with glioma, a grade IV astrocytoma was present in seven (21.8%), grade III astrocytoma
was present in eight (25%), and grade II astrocytoma was
present in 17 patients (53%) (►Fig. 2).
Thirty-eight (51.3%) lesions were located on the left
hemisphere
and
35
(47.2%)
on
the
right
hemisphere. ►Fig. 3 demonstrates the distribution of the
lesions according to the central lobe and insula (whether the
lesions were anterior, central, posterior, or paracentral in
location). Thirty-eight patients harbored lesions in the anterior region of the central lobe, 17 patients in the insula, eight
in the posterior part of the central lobe, seven patients in the
central part of the central lobe, and in four patients in the
paracentral gyrus. Compared with the lesions located in the
posterior region, lesions in the anterior region presented
greater impairment in motor strength (p < 0.05). Gross total
lesion removal was achieved in 68 (93.1%) patients and a
subtotal removal in five (6.84%).
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Fifty-four patients (73.9%) presented normal motor functioning in the preoperative period. Of these, 20 (36.3%)
developed transient deficits. Nevertheless, 85% of them
subsequently presented a complete recovery, while three
improved only partially. Nineteen patients presented preoperative motor deficits. Of these, five patients deteriorated;
however, four patients subsequently improved and two
recovered early in the postoperative period (►Fig. 4). The
improvement of motor strength in the late postoperative
period was significant (p < 0.05).
Because of histological variation and difference in
prognosis, we analyzed the data according to the category
of the lesion. ►Table 2 presents data describing the
evaluation of motor strength according to the histological
type of lesion. While comparing the evolution of motor
strength in the early postoperative period between highand low-grade gliomas, we observed a more evident
deterioration in the former (p < 0.05). Muscular strength
deteriorated more often in patients who had lesions in
Sarmento et al.
Fig. 2 Distribution of the 74 patients according to pathology of the lesions.
the left hemisphere than in patients with lesions in the
right hemisphere (p < 0.05); however, recovery was similar between groups.
Cortical stimulation was necessary in 8 patients harboring
high-grade tumors and in 13 patients who presented lowgrade lesions (65% of the patients). We also used this tool in
one patient with brain metastasis and in two patients with
cortical dysplasia. The neuronavigation system was employed in only two patients. Finally, we performed stereotaxic surgeries in three patients with cavernomas and in one
patient with neurocysticercosis (►Fig. 5).
There were no cases of mortality among the 74 participants. Complications unrelated to motor strength occurred
in four patients: one patient with a high-grade tumor had a
large hematoma in the tumor bed, which we treated through
surgery; two patients with cerebrospinal fistulas were
treated clinically; and one patient developed a cystic formation in the tumor bed and required surgical intervention.
Discussion
The central lobe is an eloquent area of the central nervous
system (CNS), surrounded anteriorly by the pre-central
sulcus and posteriorly by the post-central sulcus. The central
sulcus, which separates the pre- from the post-central gyrus,
is one of the most important anatomical landmarks of the
cerebral cortex.16,17
In various situations, a neurosurgeon must take a direct
approach to access cortical or subcortical lesions at the
convexity or at the midline hemisphere. Although technology already offers modern intraoperative localization tools
such as MRI and neuronavigation, anatomical knowledge
remains an important part of surgical planning.12–15
Craniotomy planning is an essential step in approaching
motor area lesions. Paul Broca (1824–1880) was the first
neurosurgeon to perform a craniotomy based on anatomical
localization.18 MRI, especially with contrast-enhanced T1
imaging, allows good visualization of the relationship between cerebral veins and lesions to be removed.19 Radiological data and anatomical landmarks can provide a projected
image of the lesion on the scalp, which influences patient
position, the size and conformation of the surgical incision,
and the location and extent of the craniotomy.12,20,21
Exposure of brain surface is necessary to identify the
relationship between the lesion and the motor gyrus, veins,
and arteries (►Fig. 6a). The motor and sensory cortices are
separated by the central sulcus, which begins at the superior
border of the lateral surface and extends to the medial
surface of the brain, running in an anterior-oblique direction
up to around the sylvian fissure.16 In previous anatomical
studies, we verified that the distance between the coronal
suture and the central sulcus ranged from 5.6 to 6.6cm in the
midline, and that the coronal suture on the pterion region to
the central sulcus ranged from 1.5 to 4.0cm.13 Additionally,
the coronal suture was 11.5 to 13.5cm behind the nasium. It
is possible to measure these distances by using radiological
images, which can then be transferred to the scalp or determined by palpation of the skull.14 This anatomical information is useful in localizing the central lobe and craniotomy
planning and dispenses non-essential use of neuronavigation. However, the use of this information during the surgical
procedure can be difficult in the presence of perilesional
brain edemas or in subcortical lesions. In such cases, it is
important to perform functional MRI or electrophysiology.3
The functional localization of the motor cortex during
surgery has been performed for some time and is a valuable
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Sarmento et al.
Fig. 3 (a) Anatomical specimen showing topographic distribution of the lesions: 38 patients harbored lesions in the anterior region of the
central lobe, 7 in the central region, and 8 in the posterior region. (b) Coronal view of the insula and internal capsule: 17 patients had harbored
lesions in the insular region and 4 in the paracentral region of the midline. (c) Topographic distribution of the lesions based on its relationship
with the central lobe: 61.4% were located in the superior ⅓, 29.8% were in the medial ⅓, and 8.7% were located in the lateral ⅓ of the central lobe.
instrument in operations performed within eloquent
areas.22 In the current study, cortical stimulation was the
preferred method. This surgical approach is an easy-to-use
method, which is effective and involves low cost. Cortical
stimulation is available for surgical removal of tumors as well
as epileptic and arteriovenous malformations, which reduces
the rate of postoperative deficits and increases the degree of
resection in the surgery of eloquent areas.
To obtain satisfactory cortical stimulation during surgery,
a patient needs to remain awake; however, somatosensory
and motor mapping can be performed while the patient is
under general anesthesia.1,2,23,24 Intraoperative seizures are
always a concern when using repeated stimulation of the
same cortical field or using a high-stimulus setting. In our
study, despite the prophylactic use of antiepileptic drugs, we
had five patients that suffered partial motor seizures during
cortical stimulation; however, four of these cases had a
previous history of epilepsy. Therefore, we realized that
the use of cortical stimulation is a safe and helpful technique
for treatment of lesions involving the motor cortex because it
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allows the surgeon to enlarge the resection, especially in
cases of gliomas.5,6,25
According to Duffau et al.,26 Forster first used cortical
stimulation in 1930, in a neurosurgery procedure. Soon
after, in 1937, Penfield, who described the famous homunculus, used the technique. The operating principle of
cortical stimulation is based on local neuron depolarization that induces excitation or inhibition.26 Although
cortical stimulation is technically feasible, elicitation of
responses is frequently difficult in children, in patients
under general anesthesia, or when stimulation is executed
through the dura mater. 4,27 In these cases, a higher current
setting could possibly be required. This technique can also
be used to identify descending subcortical motor fibers
when resection extends below the cortical surface, such as
during supplementary motor area and insular resections.3,28 Numerous published literature report the use
of cortical stimulation alone or combined with others
methods, which allows functional identification and
guides surgical resection.19,29
Sarmento et al.
Fig. 4 Distribution of the patients according to evolution of motor strength in the preoperative, early, and late postoperative periods. MS
1 ¼ contraction, MS 2 ¼ active movement with gravity eliminated, MS 3 ¼ active movement against gravity, MS 4 ¼ active movement against
resistance, and MS 5 ¼ normal strength.
real time, thus, facilitating an aggressive resection of the
lesion with acceptable postoperative neurologic deficits
(►Fig. 6b). When performing subcortical motor mapping,
the current required to elicit movement was the same as or
lower than the current needed at the cortical surface. In
patients, where the resection was very close to the functional
cortex, periodic repetition of the stimulation mapping procedure helped verify that the cortical and subcortical functional regions had not been damaged. In six patients, the
insular lesions were resected using an awake craniotomy. In
patients with subcortical or insular lesions, cortical stimulation can be used in combination with other methods such as
neuronavigation; however, this was not required in the
current study.
Intrinsic brain tumors may invade cortical and subcortical
structures with no impairment of function, and even the
grossly abnormal appearance of tissue is not an assurance
that such tissue can be safely removed without risking new
postoperative neurological deficits. Similar to MRI findings
of some studies, we could observe motor function existing
Among patients harboring high-grade gliomas, the use of
cortical stimulation was necessary to identify the motor area
in 65% of the patients. The criterion to use the cortical
stimulator was based on the ability to correctly distinguish
between normal brain tissue and tumor tissue. In other
words, in 34.4% of primary malign lesions, cortical stimulation was not required because the identification and dissection of the lesion was achieved based on knowledge of
anatomical parameters.
To treat subcortical lesions surrounding the motor area,
both the internal capsule and corona radiata, we used the
same techniques as before to avoid neurological deficits.
Although the insula is not considered a part of the motor
area, insular lesions close to descending motor fibers were
included in this study. Recently, several authors have
stressed the importance of the approach to treat lesions in
the insular lobe.17,25,30 Several patients in our study harbored lesions in the insular compartment and were treated
surgically. In some patients, an awake craniotomy was
performed, allowing us to evaluate the motor function in
Table 2 Presence of motor deficits according to operative period and pathology
Pathology
Astrocytoma III/IV
Astrocytoma I/II
Metastasis
Cavernoma
Motor deficit prior to surgery
Presence of motor deficit (number of patients)
Preoperative
Early postoperative
Late postoperative
Yes
10
5
1
No
5
2
0
Yes
16
4
1
No
1
1
0
Yes
6
0
0
No
5
1
0
Yes
3
0
0
No
2
0
0
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Fig. 5 Distribution of the lesions based on the use of auxiliary methods.
inside the tumor, generally low-grades gliomas, or on its
boundaries.31,32 This data facilitates and guides surgical
resection of the lesion. In our case, the preoperative demonstration of functional activity was not achievable, and we
used cortical stimulation only to improve the quality of our
surgical resection by determining the limits of the removal in
eloquent areas without producing a new permanent deficit.
However, it may not be possible to determine whether a new
postoperative deficit is related to damage in the motor area
because of surgical intervention, probable function presented in the tumor, or both.
The treatment of patients harboring a metastatic tumor
was easy because, despite the aggressiveness of these tumors, they behave as an extra-axial lesion. Therefore, although several authors use an intraoperative MRI approach
to these lesions, even small tumors can be thoroughly
resected using careful preoperative planning.6,8,33 In the
current study, we used cortical stimulation in one single
Fig. 6 (a) Surgery of a 50-year-old patient harboring a high-grade glioma in the posterior region of the central lobe. The anatomical localization
of the pre-central gyrus (dotted area) was achieved without the use of auxiliary methods, and the patient recovered with normal muscular
strength. (b) Pre- and postoperative axial MRI of a 34-year-old patient harboring a left fronto-insular glioma. The surgery was performed with
local anesthesia and the patient recovered without motor or speech deficits.
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patient who harbored a deep metastatic tumor with an
extensive brain edema. The reason why we used cortical
stimulation in this patient was to choose the best place for
the corticectomy.
In the patients harboring benign tumors, represented primarily by meningioma, cortical stimulation or other mapping
methods were not required to guide resection of brain tumors
near motor areas. Several studies in the literature describe the
use of auxiliary methods to perform safe resections of these
lesions5,25; however, in our opinion, they are not required and
increase both surgery time and surgical cost.
A neuronavigation system was used in only two patients. Its role was to verify the positioning of the craniotomy. To identify the margins of the lesion attached to
adjacent structures, the use of the neuronavigation system
was not of great significance, particularly because of the
shift of brain structures during the procedure. According to
Reithmeir et al., a more radical resection of tumors in the
motor cortex area via minimal craniotomies was achieved
by using neuronavigation combined with electrophysiological monitoring as compared when these methods were
not available.34 Although the literature indicates that the
use of neuronavigation combined with other methods can
optimize the quality of resection and decrease the risk of
postoperative deficits,35,36 in our study, the definition of
the size and craniotomy conformation was possible in all
patients solely based on the knowledge of topographic
anatomy of the skull.
The functional MRI is an important procedure to identify
the motor area and is capable of improving surgical planning
when associated to tractography. However, compared with
cortical stimulation, fMRI is not a real-time mapping method.37–39 Finally, the monitoring of motor-evoked potentials,
the introaperative MRI, magnetoencephalography, and the
intraoperative ultrasound imaging were not used in this
study because they were not available.
Roux Fe et al. described a cortical stimulation and fMRI
study involving five paretic patients with brain tumors in the
motor area6. The authors demonstrated that patients who
had motor impairment also had high activation of the
supplementary motor and prefrontal areas within the ipsilateral cortex as compared with that of intact patients. In
these patients, neuroplasticity may be involved in the dislocation of function; however, it is best to confirm this using
other methods.6
In the current study, although we applied the different
methods as described above in some patients, it was prudent
to leave a residual lesion to avoid producing a neurological
deficit that might occur due to a gross total resection.5,26,40–42 Previous studies have demonstrated that the
risk of new motor deficits is not greater in subsequent
operations compared to the first procedure.42 This may be
a factor of a particular type of reorganization involving the
motor cortex areas that render patients harboring large
lesions asymptomatic.5,26,43 The potential role of brain plasticity in these patients emphasizes the importance of future
studies with fMRI and others methods to predict the risk of
Sarmento et al.
new neurological deficits after surgery and to optimize
treatment planning.43–45
Conclusions
In this study, we demonstrated that the lack of morbidity in
the surgery of lesions involving the motor area justifies the
need for maximum tumor resection. The relationship between the coronal suture and the central sulcus was important in the planning of the craniotomy; however, when the
central sulcus or the motor lobe was displaced due to
pathological conditions, anatomical recognition was impaired. In these patients, it was important that the neurosurgeon used another tool for functional identification such
as fMRI, cortical stimulation, or an awake craniotomy.
We also demonstrated that extra axial lesions such as
meningioma and dural metastasis could be entirely removed
with low morbidity on the basis of anatomical knowledge
and appropriate microsurgical techniques, and that these
cases do not require additional auxiliary methods. Thus, we
can infer that cortical stimulation plays an important role in
the management of infiltrative lesions and in improving
quality and safety of surgical resections.
In some patients harboring subcortical lesions, an additional localization method was required to improve the
cortical approach, although this may be achieved by a careful
preoperative MRI analysis of the sulcus and cortical veins.
Finally, there was no difference between morbidity and
resection grade when we compared our results with those
using functional imaging methods, neuronavigation systems,
or other methods such as intraoperative MRI during surgery
around the motor area.
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THIEME
Tratamento das hemorragias intracranianas
espontâneas: o dilema continua
Treatment of Spontaneous Intracranial Hemorrhages:
the Dilemma Continues
Iuri Santana Neville1 Djalma Felipe da Silva Menéndez1 Leonardo Moura Sousa Júnior1
Eberval Gadelha Figueiredo2 Manoel Jacobsen Teixeira3
1 Médico Neurocirurgião do Serviço de Neurocirurgia do Hospital das
Clínicas da Faculdade de Medicina da Universidade de São Paulo
(HCFMUSP), São Paulo, SP, Brasil
2 Médico Neurocirurgião Chefe do Grupo de Neurocirurgia vascular da
Divisão de Clínica Neurocirúrgica; Supervisor da Divisão de Clínica
Neurocirúrgica do HCFMUSP, São Paulo, SP, Brasil
3 Professor Titular e Chefe da Divisão de Clínica Neurocirúrgica do
Departamento de Neurologia do HCFMUSP, São Paulo, SP, Brasil
Address for correspondence Iuri Santana Neville, MD, Divisão de
Clínica Neurocirúrgica do Departamento de Neurologia do HCFMUSP,
rua Dr. Ovídio Pires de Campos, 171, ap. 618, Cerqueira César, São
Paulo, SP, Brasil CEP 05403-010 (e-mail: [email protected]).
Resumo
Palavras-Chave
►
►
►
►
hemorragia
intracerebral
intracraniana
espontânea
received
November 10, 2013
accepted
August 7, 2015
published online
October 19, 2015
Introdução As doenças cerebrovasculares (DCV) são a principal causa de morte no
Brasil, sendo um grande problema de saúde pública em todo o mundo.
Métodos Revisão da literatura utilizando o banco de dados do MEDLINE. Buscados os
termos “intracerebral” e “hemorrhage” presentes no título e no resumo publicados em
qualquer data.
Resultados As hemorragias intracranianas (HIC) acometem, principalmente, os lobos
cerebrais, gânglios da base, tálamo, tronco cerebral (predominantemente a ponte) e
cerebelo como resultado da ruptura de vasos cerebrais afetados pelos efeitos degenerativos da hipertensão arterial sistêmica (HAS) ou da angiopatia amiloide. O
diagnóstico pode ser feito através da tomografia computadorizada de crânio (TCC),
sendo auxiliado pela ressonância nuclear magnética (RNM) do encéfalo e a angiografia
dos quatro vasos cerebrais na investigação etiológica. Tratamento: dividido em clínico
e cirúrgico. Atualmente, não há consenso sobre a seleção do tipo de tratamento para
pacientes com HIC, e esta decisão deve levar em consideração idade do paciente,
estado neurológico, tamanho e profundidade do hematoma, presença de hidrocefalia e
de efeito compressivo. Os estudos atuais mostram uma tendência de superioridade dos
procedimentos cirúrgicos minimamente invasivos, com menor risco de lesão encefálica
secundária decorrente do acesso cirúrgico ao hematoma.
Conclusão A escolha da melhor estratégia para o tratamento das HIC permanece um
desafio e ainda deve ser feita de forma individualizada.
10.1055/s-0035-1564888.
ISSN 0103-5355.
291
292
Tratamento de hemorragias intracranianas espontâneas
Abstract
Keywords
► intracranial
hemorrhages
► stroke
► brain injuries
► neurosurgical
procedures
Introduction Cerebrovascular Diseases are the major cause of death in Brazil and a
public health issue in the world.
Methods Review of the literature using the MEDLINE’s data bank. We have searched
the keywords “intracerebral” and “hemorrhages” in the title and abstract.
Results Intracranial hemorrhages (ICH) affect, mainly, the cerebral lobes, basal
ganglia, thalamus, brain stem and the cerebellum as a result of the rupture of diseased
cerebral vessels by the effects of hypertension or amyloid angiopathy. Diagnosis can be
done with the use of a non-contrast computed tomography (CT), magnetic resonance
imaging (MRI) and cerebral angiogram (useful in investigation of the etiology).
Treatment can be divided in clinical and surgical. This decision still should be taken
considering individual features, such as patient’s age and neurological status, hematoma’s size and deep, time between ictus and the procedure, presence of hydrocephalus and compressive effects. The studies has shown a preference for the minimally
invasive procedures, since the secondary brain lesions caused by the surgery tend to be
less.
Conclusion The choice of what would be the best strategy to treat the ICH is still a
challenge and this decision should be taken individually.
Introdução
Os dados oficiais de mortalidade no Brasil revelam que a
doença cerebrovascular (DCV) é a principal causa de morte,
sendo responsável por mais óbitos do que a doença coronária
nos últimos 40 anos, um fato que diferencia o nosso país dos
demais no hemisfério ocidental (DATASUS).1
As hemorragias intracranianas (HIC) espontâneas, um dos
subtipos de acidente vascular cerebral (AVC), são uma importante causa de morbidade e mortalidade no mundo, com
taxas superiores às notadas nos outros subtipos de AVC.2,3
Apesar da tendência declinante das taxas de mortalidade
por doença cerebrovascular no país, a magnitude da doença é
de grande importância, principalmente levando-se em consideração as outras consequências da doença cerebrovascular, como a invalidez, com alto custo social. Embora tenha
ocorrido um aumento no número de internações de pacientes com HIC nos últimos 10 anos, a mortalidade permaneceu
inalterada e ainda continua sendo uma condição catastrófica
para os pacientes e seus familiares.1
Métodos
Realizada revisão da literatura utilizando o banco de dados
do MEDLINE e a ferramenta de busca do PUBMED. Buscados
os termos “intracerebral” e “hemorrhage” presentes no título
e no resumo. Apenas os artigos escritos em inglês, realizados
em humanos e publicados em qualquer data foram incluídos
neste estudo.
Resultados
Fisiopatologia
As HIC podem ser classificadas em primárias ou secundárias
(induzidas pelo uso de anticoagulantes), mas apresentam
fisiopatologia semelhante.4 Acometem, principalmente, os
Neville et al.
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No. 4/2015
lobos cerebrais, gânglios da base, tálamo, tronco cerebral
(predominantemente a ponte) e cerebelo como resultado da
ruptura de vasos cerebrais afetados pelos efeitos degenerativos da hipertensão arterial sistêmica (HAS) ou da angiopatia amiloide. Boa parte dos sangramentos ocorre próximo
ou na bifurcação das artérias perfurantes que se originam
dos grandes vasos intracranianos.3,5 O sangramento que
sucede à ruptura dos vasos cerebrais leva a uma lesão
primária do tecido cerebral, decorrente da desconexão dos
neurônios e das células da glia causada pelo efeito expansivo
do hematoma, causando oligoemia, liberação de neurotransmissores (especialmente o glutamato), disfunção mitocondrial e despolarização da membrana neuronal.6–8 Uma
cascata se sucede ao evento inicial, gerando uma série de
lesões secundárias em decorrência do efeito tóxico dos
produtos de degradação da coagulação e da hemoglobina,
particularmente a trombina, que ativa a micróglia após 4
horas do íctus.9–12
Diagnóstico
Realizado através da tomografia computadorizada de crânio (TCC), que é capaz de mostrar a hemorragia como uma
lesão hiperdensa logo após a sua ocorrência.13,14 A ressonância nuclear magnética (RNM) de encéfalo pode ser útil
no sentido de identificar a etiologia da HIC. A arteriografia
dos quatro vasos cerebrais deve ser realizada quando a
suspeita de HIC secundária à ruptura de aneurisma cerebral ou de uma malformação arteriovenosa (MAV) é
levantada.15 A recomendação é de que seja feita em todos
os pacientes que não se enquadrem no perfil de HIC
devido a HAS. Portanto, não está indicada aos pacientes
com mais de 45 anos, previamente hipertensos e com HIC
talâmica, putaminal ou em fossa posterior. Caso o resultado seja negativo para aneurisma cerebral ou MAV, o
exame deve ser repetido após a absorção do hematoma,
por volta de 2 a 3 meses.2
Tratamento
O tratamento da HIC pode ser dividido em clínico e cirúrgico.
O primeiro envolve medidas de suporte ventilatório, controle
dos níveis pressóricos, da glicemia e de distúrbios metabólicos. O risco de deterioração neurológica e instabilidade
cardiovascular é máximo nas primeiras 24 horas após o início
dos sintomas, e portanto os pacientes devem ser mantidos
em uma unidade de cuidados intensivos ou de tratamento de
AVC.15 Diversos estudos já procuraram definir os níveis
tensionais ideais para o tratamento destes pacientes na
fase aguda, porque se por um lado os altos níveis tensionais
podem aumentar o risco de expansão do hematoma, por
outro, os baixos níveis pressóricos ocasionam a queda da
pressão de perfusão cerebral, levando à isquemia secundária
de regiões da chamada zona de penumbra.16–19
Já o tratamento cirúrgico consiste em: (1) monitoração da
pressão intracraniana (PIC), (2) tratamento da hemorragia
intraventricular (HIV), e (3) exérese do hematoma.
Atualmente, não há acordo sobre a seleção do tipo de
tratamento para os pacientes com HIC, e a decisão sobre quando
o tratamento cirúrgico seria o mais indicado permanece controversa.20 Nota-se uma grande variabilidade nas taxas de
cirurgias para o tratamento das HIC, sendo realizadas raramente
em países como a Holanda, porém alcançando até 50% dos
pacientes em alguns centros na Alemanha e Japão.21 Na literatura, encontramos estudos randomizados (o primeiro foi publicado em 1961, na era pré-microscópio e pré-tomografia de
crânio, e o mais recente, em 2006) comparando pacientes com
HIC tratados de forma clínica ou conservadora. Os resultados são
conflitantes, porém apresentam uma tendência a favorecer os
pacientes tratados de forma cirúrgica na atualidade, com técnicas mais adequadas de neuroanestesia, bem como melhoria dos
métodos diagnósticos e dos equipamentos utilizados na cirurgia.
Tratamento Conservador
Baseia-se nos achados de estudos prévios randomizados que não
mostraram benefício no tratamento cirúrgico, possivelmente
devido às lesões cerebrais adicionais advindas da manipulação
de parênquima cerebral íntegro no acesso ao hematoma.22
Tratamento Cirúrgico
Aparentemente, os pacientes com hematomas supratentoriais
de volume acima de 30 mL (porém menor do que 80 mL), de
localização lobar subcortical (< 1 cm do córtex) ou putaminal,
com compressão do tronco encefálico ou hidrocefalia obstrutiva,
não comatosos ou em vigência de deterioração neurológica, e
com delta tempo do íctus até a cirurgia inferior a 12 horas
parecem beneficiar-se da cirurgia, já que os estudos sugerem que
esta população apresenta resultados inferiores quando tratada
clinicamente.22–25 Já os pacientes com hematomas sem as
características supracitadas apresentam melhores resultados
quando tratados de forma conservadora.
Monitoração da Pressão Intracraniana (PIC)
Este recurso é útil em pacientes com o comprometimento do
nível de consciência. A monitoração da PIC é capaz de
identificar pacientes com risco de deterioração neurológica
devido ao aumento excessivo da PIC. Representa um papel
Neville et al.
importante dentro das unidades de cuidados intensivos,
orientando a terapêutica no sentido de manter uma pressão
de perfusão cerebral entre 50 e 70 mmHg.26
Técnicas de Drenagem do Hematoma
A exérese do hematoma pode ser realizada através de três
técnicas: (1) craniotomia clássica, (2) drenagem estereotática, e (3) drenagem através da neuroendoscopia.
Craniotomia: técnica clássica de exérese do hematoma
intracerebral através de cirurgia aberta. Associada a maior
risco de lesão encefálica secundária devido ao acesso cirúrgico ao hematoma. Atualmente existe uma tendência à
utilização de craniotomias menores, minimizando o dano
ao parênquima cerebral íntegro.21
Drenagem estereotática do hematoma: técnica minimamente invasiva, com grande utilidade para drenagem de
hematomas profundos (ex: HIC putaminal). A sua eficácia
foi comprovada em estudo randomizado.27 Pode ser realizada apenas com anestesia local, útil em pacientes com alto
risco cirúrgico.
Tratamento endoscópico das HIC: por muito tempo
considerada uma técnica investigacional, mas atualmente
com eficácia comprovada em estudos randomizados,
sendo o primeiro grande estudo publicado em 1989.23
Considerada uma técnica minimamente invasiva, realizada através de pequena incisão na pele seguida de uma
trepanação ou minicraniotomia. Permite a colocação de
derivação ventricular externa (DVE) sob visualização direta nos casos em que os ventrículos são acessados
durante a cirurgia para lavagem endoscópica e exérese
do hemoventrículo. Na maioria dos casos, a exérese do
hematoma é feita sem a identificação de um foco ativo de
sangramento (cerca de 70% dos casos).24
Discussão
As DCV ocasionam um grande impacto na saúde pública em
todo o mundo. Apesar do aumento do número de internações
nos últimos anos, e dos grandes estudos acerca do assunto, a
taxa de mortalidade ainda é muito alta, além do grande
problema decorrente dos pacientes com sequelas neurológicas graves.1,21 O tratamento permanence controverso,
principalmente com relação à seleção dos pacientes que
mais se beneficiariam do tratamento cirúrgico. Aparentemente, pacientes com as seguintes características teriam
melhores resultados quando tratados cirúrgicamente, através da drenagem do hematoma:
1. delta T do ictus > cirurgia: até 12 horas;
2. status neurológico: não comatosos ou em plena deterioração neurológica;
3. localização: subcortical (< 1 cm do córtex cerebral), lobar
e putaminal;
4. volume: maior do que 30 mL, porém menor do que 80 mL;
5. hidrocefalia obstrutiva;
6. compressão do tronco cerebral.
As técnicas utilizadas para a drenagem do hematoma
são basicamente três: (1) craniotomia, (2) drenagem
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294
estereotática, e (3) utilização da neuroendoscopia. Estudos randomizados já comprovaram a segurança e eficácia
dos três métodos, e atualmente tem-se dado preferência
para aqueles minimamente invasivos, com menor risco de
lesão encefálica secundária. Os pacientes com piora no
nível de consciência decorrente de hipertensão intracraniana podem beneficiar-se da monitoração da PIC.
Neville et al.
13 Fiebach JB, Schellinger PD, Gass A, et al; Kompetenznetzwerk
14
15
Conclusão
As HIC ainda são catastróficas para os pacientes, seus familiares e para a saúde pública. Apesar dos avanços na medicina, a mortalidade permaneceu inalterada na última década.
Vale ressaltar que a decisão sobre o melhor tratamento a ser
adotado deve ser individualizada, já que os pacientes com
HIC podem beneficiar-se do procedimento cirúrgico, desde
que bem selecionados. Ainda, os estudos atuais mostram
uma tendência da superioridade dos procedimentos minimamente invasivos, com menor risco de lesão encefálica
decorrente do acesso cirúrgico ao hematoma.
16
17
18
19
Referencias
20
1 Lotufo PA. Mortalidade pela Doença cerebrovascular no Brasil. Rev
Bras Hipertens 2000;4:387–391
2 Greenberg MS. Handbook of Neurosurgery, 6th edition. M-Login
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Graham DI, McIntosh TK, Maxwell WL, Nicoll JA. Recent advances
in neurotrauma. J Neuropathol Exp Neurol 2000;59(8):641–651
Lusardi TA, Wolf JA, Putt ME, Smith DH, Meaney DF. Effect of acute
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Qureshi AI, Ali Z, Suri MF, et al. Extracellular glutamate and other
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oxidative brain injury after experimental intracerebral hemorrhage. Acta Neurochir Suppl (Wien) 2006;96:194–198
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502–506
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detection of acute intracerebral hemorrhage. JAMA 2004;292(15):1823–1830
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Bacellar A. Detrimental effect of blood pressure reduction in
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56–66
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Orleans, LA.2008; 20–22
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THIEME
Treatment of Giant Intracranial Aneurysms: a
Review Based on Experience from 286 Cases
Tratamento dos aneurismas gigantes intracranianos:
uma revisão baseada na experiência de 286 casos
Atos Alves de Sousa1,2,3
José Lopes de Sousa Filho1
1 Department of Neurosurgery of the Santa Casa de Belo Horizonte,
Belo Horizonte, MG, Brazil
2 Faculdade de Ciências Médicas de Minas Gerais, Belo Horizonte,
MG, Brazil
3 Honorary President of the World Federation of Neurosurgical
Societies (WFNS), Rome, Italy
Marcos Antônio Dellaretti Filho1,2
Address for correspondence José Lopes de Sousa Filho, MD,
Department of Neurosurgery of the Santa Casa de Belo Horizonte, Av.
Francisco Sales, 1111, Sta Efigênia, Belo Horizonte, MG, Brazil CEP:
30150-221 (e-mail: [email protected]).
Abstract
Keywords
► giant aneurysm
► complex aneurysm
► microneurosurgery
Resumo
Palavras-chave
► aneurisma gigante
► aneurisma complexo
► microcirurgia
Aneurysms are classified as giant when their largest diameter is equal to or greater than
25 mm, which represents approximately 5–7% of intracranial aneurysms. Severe
disease with poor natural history presents with 68% mortality in two years and 85%
in five years for untreated cases. Thus, in the majority of cases, the patients require
treatment, despite the risks of therapeutic options. We discuss the epidemiology,
natural history, diagnosis, and treatment of giant aneurysms based on the experience
of 286 operations and literature data.
Os Aneurismas são classificados como gigantes quando seu maior diâmetro é igual ou
superior a 25 mm e representam aproximadamente de 5 a 7% dos aneurismas
intracranianos. Trata-se de patologia grave com história natural ruim apresentando
mortalidade de 68% em 2 anos e 85% em 5 anos para casos não tratados. Desta forma,
na maioria dos casos, estes pacientes devem ser tratados apesar do alto risco das
opções terapêuticas. Neste estudo, discutimos a epidemiologia, a história natural, o
diagnóstico e o tratamento desta grave patologia baseado na experiência de 286
pacientes tratados e dados da literatura.
Introduction
Morley and Barr classify cerebral aneurysms as giant when
their largest diameter is equal to or greater than 25 mm. The
arbitrary limit of 2.5 cm distinguishes an aneurysm group
with clinical and pathological characteristics, natural history, and treatment, which differ from those of small and
medium aneurysms.1–4
received
November 10, 2013
accepted
August 7, 2015
published online
October 22, 2015
10.1055/s-0035-1566156.
ISSN 0103-5355.
The most common location is in the internal carotid
artery (ICA), followed by the vertebrobasilar system (VBS),
middle cerebral artery (MCA), and most recently, the
anterior cerebral-anterior communicating artery (ACAACoA) complex.1,2,4,5
Manifestations include subarachnoid hemorrhage (SAH)
and/or intracerebral hemorrhage (ICH) and, particularly,
signs and symptoms related to mass effect on the adjacent
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Treatment of Giant Intracranial Aneurysms
Sousa et al.
neural structures. Seizures and cerebral ischemia occur with
less frequency. The natural history of giant cerebral aneurisms is very poor, since cases treated conservatively evolve to
death in a few years.1,5–8
The treatment of such aneurysms is one of the greatest
neurosurgical challenges. The difficulties involved are due to
the size of the aneurysm, the presence of calcification and
thrombus, the wide neck, and the incorporation of the artery
from which they originate. Despite the increased difficulties
in treatment and poor prognosis, they are potentially curable
lesions and some type of therapeutic intervention should
always be considered.9,10
Epidemiology
The literature reports that incidence of giant aneurysm
ranges from 2 to 7% of all intracranial aneurysms.2,4,5 In
the current series, incidence is 8.2%, thus, 286 giant aneurysms out of a total of 3,500 patients operated between 1977
and 2013. Of these, 163 patients (57.0%) were female and 123
(43.0%) were male.
Giant aneurysms predominate in the female population at
a frequency of 2:1 and affect all age groups, showing greater
prevalence among 40 to 70-year-olds. Several factors are
associated with the development and rupture of these
lesions, including being female, age, hypertension, smoking,
and connective tissue diseases.1,2,4,11
Natural History
The natural history of giant aneurysms is very poor, since
they are associated with high risk of bleeding, progressive
neurological defects, and death, mainly a result of bleeding,
but also of the mass effect and/or cerebral ischemia. The
condition presents increased risk of SAH and higher mortality than small and medium aneurysms. Location in the
posterior circulation is an isolated factor for poor
prognosis.1,6–8,12,13
Drake32 reported mortality of 68% at 2 years and 85% at 5
years for untreated giant aneurysms and the survivors showed
severe neurological sequelae. According to the International
Study of Unruptured Intracranial Aneurysms (ISUIA),11 the
cumulative risk of bleeding is 40 to 50% at 5 years. Meningeal
hemorrhage resulting from a giant aneurysm leads to higher
mortality and serious neurological sequelae compared with
smaller aneurysms (►Tables 1 and 2).
Table 1 Natural history of unruptured aneurysms11
Anterior circulation
aneurysms except ACoP
Annual risk of bleeding
7–12 mm
0.5%
13–24 mm
2.9%
25 mm
8.0%
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Table 2 Natural history of unruptured aneurysms11
Posterior circulation
aneurysms plus ACoP
Annual risk of bleeding
7–12 mm
2.9%
13–24 mm
3.7%
25 mm
10.0%
The exception to poor prognosis are giant aneurysms of
the extradural ICA (petrous and cavernous portion), which
usually have a benign natural history. These can manifest as
multiple cranial nerves paresis (III, IV, and VI), ischemia
secondary to migration of intrasaccular thrombus, carotid
cavernous fistula, and epistaxis.1,4,13
Imaging Diagnosis
Cranial computed tomography (CT) is the first examination
that the clinician should request, as in all cases of cerebral
aneurysms. This enables a diagnosis of SAH through the
visualization of the actual size of the lesion and presence
of thrombus and calcifications. The use of CT and/or magnetic resonance imaging (MRI) is essential for the determination of the thrombosed portion of the lesion, the exact size
of the aneurysm, the presence of cerebral ischemia, and its
relation with adjacent neural structures.10,15
Digital angiography with three-dimensional (3D) reconstruction remains the gold standard for the diagnosis and
treatment planning of giant aneurysms. It allows for a dynamic
study of the entire cerebral circulation as well as an evaluation
of the location and portions of the affected vessel and the
aneurysm neck for the balloon test occlusion (BTO).3,10,16
An intraoperative angiography is very useful as a quality
control method in giant aneurysm surgery. It allows the
surgeon to correct the clips in the reconstruction of the
aneurysm during surgery, avoiding stenosis at the artery
origin or persistence of part of the aneurysm not excluded
from circulation. All patients should undergo a study of
cerebral circulation with postoperative digital angiography.
Another intraoperative control option is video angiography
with intravenous indocyanine using a microscope equipped
with this technology.13,16,17
Treatment
The treatment should be performed in a neurosurgical center
with experience in treating patients with cerebral aneurysms, which can perform both microsurgery and endovascular techniques. The treatment modalities are conservative,
surgical, endovascular and combined. Treatment management of giant aneurysms should take into account the risks
and benefits of each treatment option.7,11
There have not yet been any randomized clinical trials
conducted on the topic. Current literature data refer to large
series in select centers. The decision process for treating
these lesions has been individualized; however, this should
be discussed within a multidisciplinary team.
Conservative Treatment (►Fig. 1)
It is mainly indicated for asymptomatic patients with an
extradural giant aneurysm of the intracavernous or petrous
ICA. Patients with minor symptoms with a precarious health
status or of advanced age may also undergo monitoring.
Patients with symptoms of cerebral ischemia secondary to
migration of an intrasaccular thrombus of a cavernous
aneurysm that are not candidates for other treatments
may be administered an antiplatelet agent.11,18,19
Surgical Treatment
Surgical treatment of giant aneurysms remains the optimal therapeutic choice in most cases. The aim is to exclude
the aneurysm from circulation, maintaining the patency of
the artery involved, eliminating the mass effects and
conserving neurological functions.4,18,20 Factors that can
complicate surgery include: a wide neck, afferent and
efferent vessels encompassed by the aneurysm, the presence of intrasaccular thrombus, and calcifications in the
aneurysm neck and the source artery. Paraclinoid aneurysms and those located in the posterior circulation represent a greater challenge.9,17,18
Sousa et al.
The patient’s age and the morbidity of the treatment
options factor into the decision over treatment. In contrast
to poor natural history, several surgical series have reported
good clinical outcomes in 58 to 84% of patients, with mortality rates ranging from 14 to 22%.13,17,18,20
In the current series of 286 giant aneurysms, we
observe a good clinical outcome (Glasgow Outcome Scale;
GOS 4 and 5) in 81.1% of cases and poor clinical outcome
(GOS 1, 2, and 3) in 18.9%. The results of the main surgical
series (clipping, reconstruction and bypass) are presented
in ►Table 3.
Elderly patients with multiple comorbidities and aneurysms located in the posterior circulation tend to present a
worse clinical outcome. The use of adjuvant therapies, such
as temporary clipping, arresting the heart, deep hypothermia, and bypass, all present increased specific risks that must
be considered.13,18,20,23
Lawton et al22 evaluated the results of surgical management in 141 intracranial giant aneurysms operated between
1997 and 2010, on patients with a mean age of 54 years old.
The majority of patients presented symptoms of compression of the cranial nerves, while 23 patients presented
cerebral hemorrhage. One hundred aneurysms were located
in the anterior circulation, mainly in the ICA and the MCA,
and 41 in the posterior circulation.
Fig. 1 Conservative treatment. Patient, 65 years old, presenting hypertension and diabetes with paresis of the III right cranial nerve. CT scan
without (A) and with (B) contrast show nodular lesion right temporal. Cerebral angiography in lateral (C) and 3D reconstruction (D and E)
confirmed giant aneurysm of the cavernous internal carotid artery. Patient did not tolerate the balloon occlusion test (F).
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298
Sousa et al.
Table 3 Surgical morbidity and mortality of giant aneurysms in
literature4,17,18,21,22
Literature results
Percentage
Good or excellent clinical outcome
58–84%
Mortality
14–22%
Rebleeding
0–3%
Retreatment
0–1%
A direct approach with aneurysm neck clipping was the
preferred primary treatment strategy, comprising 66 (46.8%) of
the cases. Alternatively, 72 (51.1%) patients underwent an
indirect approach. Bypass formed part of the treatment strategy
in 54 (38.3%) aneurysms, with the following distribution: highflow bypass in 14 patients (25.9%); low-flow bypass in 11
patients (20.4%); and 15 (27.8%) intracranial bypasses in situ
and other forms of bypass (reimplantation/reanastomosis) in 14
patients (25.9%). During follow-up with control tests, 108
(76.6%) aneurysms were completely occluded, 14 (9.9%) had
minimal residual aneurysm neck, and 16 (11.3%) were incompletely occluded with aneurysm reversal or flow reduction.22
We observed good clinical outcomes (GOS 4 and 5) in 114
(80.9%) patients. The mortality rate was 12.8 and the neurological morbidity rate related to treatment was 9.2%. Factors
identified for poor prognosis were location in the posterior
circulation, clinical presentation with hemorrhage, and calcified aneurysms.22
Proximal and Distal Ligation of the Feeding Artery
(Hunterian Ligation and Surgical Trapping)
Dandy first proposed trapping, which consists of ligation of
the feeding artery proximally and distally to the aneurysm
neck. This can be achieved using a surgical or endovascular
approach, the latter involves using detachable balloons or
coils.3,10,16
The BTO should precede the applicaiton of such techniques. As described by Matas10 in 1911, temporary occlusion
of the internal carotid artery provides valuable information
for preoperative planning in cases of giant aneurysm. The
parameters used are early arterial filling difference, simultaneous capillary venous time, and collateral circulation
through the anterior communicating artery.10,16,24 Induced
hypotension is used to increase assay sensitivity, with reduction in blood pressure (BP) to 20% of the baseline value or
20 mm Hg for 30 minutes, with serial neurological examination assessment.10,16,18,24
When the patient shows tolerance for BTO, this means
that they present good cerebrovascular reserve and, therefore, should endure occlusion of the internal carotid artery
with low morbimortality. Surgical or endovascular occlusion of the internal carotid can be performed without prior
revascularization.10,18,24
According to Linskey et al,25 ligation of the internal carotid
without prior collateral flow studies results in 25% morbidity
and 12% mortality; whereas, when ligation is performed
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after collateral flow studies, morbidity is 4.7% and mortality
is 0%. Therefore, when the patient shows intolerance for BTO,
a high-flow bypass is required prior to occlusion of the
internal carotid to guarantee cerebral perfusion.
Direct Clipping of the Aneurysm Neck or Reconstruction
with Clips
According to some authors, the ideal treatment for giant
aneurysms remains the direct approach to the aneurysm
using microsurgery. This is possible in 50–60% of
cases.4,18,26 Occlusion of the aneurysm neck using clips
has several peculiarities. The success of clipping a giant
aneurysm depends on its morphology and anatomical complexity. The aneurysm must have a well-defined neck (►Figs.
2, 3, and 4). When direct neck clipping is inviable, the use of
reconstruction techniques is required to exclude the aneurysm from circulation (►Figs. 5 and 6).17,18,27
The presence of arterial branches incorporated into the
aneurysm body, a wide neck, calcifications in the arterial
wall, and/or aneurysm neck, all complicate the surgical
treatment. Calcifications can expel clips or prevent their
closure. Due to these characteristics, temporary clipping is
used in most cases of giant aneurysm, allowing for dissection
of the neural structures and manipulation of the bottom of
the aneurysm, thus, also facilitating the application of clips.
In giant partially thrombosed aneurysms, opening of the
aneurysm sac to empty the clots (thrombectomy) is required
for a definitive clipping of the neck.4,17,18
To minimize complications, neurosurgeons have relied on
numerous “checking methods” during the intraoperative
period to ensure aneurysm exclusion and prevent vessel
stenosis. The most commonly used methods are intraoperative Doppler ultrasound and digital angiography.
More recently, the advent of video angiography with intravenous indocyanine green has offered the neurosurgeon the
same parameters albeit in a less invasive manner.12,17,22,28
Spagnuolo et al13 reviewed 145 cases of giant aneurysm treated with direct surgical approach to the aneurysm neck. Twenty-six patients presented cerebral
hemorrhage. Patients with ruptured aneurysms presented
15% mortality and 10% morbidity; in contrast, patients
with unruptured aneurysms presented 6.5% mortality and
15% morbidity. Complications mainly related to occlusion/
thrombosis of the affected vessel, with consequent cerebral ischemia, hemorrhagic phenomena, and clinical
complications.
Bypass with Proximal and Distal Occlusion
Yasargil,11 in 1969, developed and introduced cerebral revascularization techniques into neurosurgery practice. A bypass
can be one of two types, according to the resulting blood
flow: high-flow or low-flow. The most commonly used type
of revascularization in giant aneurysm surgeries is a highflow bypass between the cervical external carotid artery and
one of the M2 branches of the middle cerebral artery, with
the interposition of a radial artery or saphenous vein graft
(►Fig. 7). It is indicated when the patient shows intolerance
for BTO and no other options are viable.26,29
Sousa et al.
Fig. 2 Direct approach to neck of the brain aneurysm. Patient with subarachnoid hemorrhage diagnosed by CT scan without contrast (A).
Cerebral angiography in lateral (B) and anteroposterior (C) shows a giant aneurysm at the apex of the basilar artery narrow neck. Performed
microsurgical clipping with direct approach to the neck of the aneurysm through fronto-orbitozygomatic craniotomy. Cerebral angiography
control (D) showing complete exclusion of the aneurysm with preservation of the posterior cerebral arteries.
Jafar et al21 analyzed the results of surgical treatment in
29 patients with giant aneurysms submitted to extracranialintracranial high-flow bypass with saphenous vein graft and
immediate occlusion of the vessel with the aneurysm.
Follow-up at 62 months showed 6% neurological morbidity
and 3% mortality with 100% occlusion of the aneurysm from
circulation. The graft occlusion rate was 7% early and 0% late.
The main complications related to ischemic phenomena,
such as choroidal artery infarction and perforating arteries.
The authors concluded that the use of extracranial-intracranial high-flow bypass with saphenous vein graft followed by
occlusion of the affected vessel is a safe, effective treatment
for giant aneurysms.21
Endovascular Treatment
The endovascular approach is a good treatment option for
giant aneurysms, particularly for unruptured aneurysms,
spindle aneurysms, located in the posterior circulation,
and for elderly patients with multiple comorbidities. Despite
the development of endovascular technologies in recent
years, they still present certain limitations, including incomplete occlusion with high rates of recanalization, the need for
retreatment, and occasional post-treatment bleeding. This
approach does not solve pseudo-tumor compressive effects
on the adjacent neural structures.19,27
Some factors intrinsic to giant aneurysms make them
pathologies of difficult endovascular treatment, such as a
wide neck, with incorporation of the feeding artery, intraluminal thrombosis, and the involvement of perforating.
Parkinson et al19 analyzed the clinical results of the largest
endovascular series for treatment of giant aneurysms published
since 1994, following the development of coils. They identified
316 patients submitted to endovascular treatment, in which 19%
of cases manifested cerebral hemorrhage. The average of complete aneurysm occlusion was 57% of cases, with 7.7% mortality
and 17.2% neurological morbidity during a mean clinical followup of 17.6 months. The recanalization rate was 27% in 238
aneurysms followed for 12.4 months.19
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Sousa et al.
Fig. 3 Direct approach to neck of the brain aneurysm. Giant aneurysm intracranial of the internal carotid artery left evidenced by cerebral
angiography AP (A) and lateral (B). Intraoperative findings revealed compression of optic pathways (D) and early proximal vascular control (E).
Performed clipping of the aneurysmatic neck without vascular stenosis (F). Control angiography (C) with complete exclusion of the aneurysm
from the circulation.
Fig. 4 Direct approach to neck brain aneurysm. Aneurysm of the middle cerebral artery (MCA) left with lower projection evidenced by cerebral
angiography AP (A) and lateral (B). Intraoperative findings showing wide neck aneurysm of the MCA (C). Performed clipping of the aneurysm
without stenosis confirmed by angiography control in AP (D) and lateral (E).
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Sousa et al.
Fig. 5 Vascular reconstruction with multiple clips. CT scan (A) shows nodular lesion in the right parasellar region. Cerebral angiography in AP (B)
and lateral (C) show a giant aneurysm of the intracranial internal carotid artery. Performed vascular reconstruction with multiple fenestrated
clips and control angiography (D) shows preservation of vascular flow.
Fig. 6 Vascular reconstruction with multiple Clips. Intraoperative findings of vascular reconstruction with multiple fenestrated clips show
compression of the optic pathways for aneurysm (A) and final aspect of the reconstruction of the internal carotid artery (B).
When analyzing the exclusive use of coils as a treatment
strategy, only 43% of cases presented complete aneurysm
occlusion, with 9% mortality and 24% major neurological
morbidity. The recanalization rate was 55% in 164 giant
aneurysms followed. The exclusive use of onyx, coil, and/or
onyx stents showed similar results, making these viable
strategies for the safe, definitive treatment of giant
aneurysms.19
Endovascular occlusion of the affected vessel with coil
following BTO proved to be safe and effective. In a review of
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301
302
Sousa et al.
Fig. 7 Bypass and surgical trapping of the aneurysm. CT scan (A) with hemorrhage and mass effect. Cerebral angiography in AP (B) and threedimensional reconstruction (C) show the internal carotid artery giant aneurysm (ICA) left with involvement of afferent and efferent vessels.
Performed bypass from the cervical external carotid artery to M2 branch of the middle cerebral artery (D and E). Control angiography showing
excluded the aneurysm with good cerebral perfusion by shunt (F).
72 cases, Parkinson et al. verified 81% initial occlusion and 1%
recanalization.19 Mortality rate was 7% of neurological morbidity followed for 14 months.19
Jahromi et al15 retrospectively analyzed the clinical and
angiographic outcomes following endovascular treatment of
39 giant aneurysms. Ten patients presented ruptured aneurysms. Treatment with stents and coils was used in 25
aneurysms. An average of 1.9 sessions was required to treat
each aneurysm, with 95% angiographic occlusion of aneurysms and 75% patency of the affected vessel. The 30-day
mortality was 8%, with 20% permanent neurological
morbidity.
Flow diverter stents are designed to induce redirection of
blood flow near the aneurysm neck, preserving it in the
affected vessel and its branches. They can be a good treatment option for basilar, petro-cavernous, and paraclinoid
aneurysms, for which surgical options present particularly
high morbimortality. Given the need for dual-antiplatelet
therapy, the use of flow diverters is not recommended when
the aneurysm is ruptured due to the higher incidence of
hemorrhage and worse clinical outcome.23,30
The Pipeline for Uncoilable or Failed Aneurysms (PUFs)
trial20 evaluated the safety and efficacy of the pipeline
embolization device (PED) in the treatment of large and
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giant aneurysms with a wide neck. The primary outcome
was death or ipsilateral stroke within 180 days. The PED
was used prospectively in 108 patients in 10 centers on 22
(20.4%) giant aneurysms and 85 (78.7%) large aneurysms.
The complete occlusion rate was 73.6% at 180 days and
86.8% at one year. The primary outcome for six (5.6%)
patients was death or ischemic stroke, while 44 patients
presented serious adverse effects, including cerebral
hemorrhage (4.7%), amaurosis fugax (4.7%), headache
(4.7%), non-neurological bleeding (4%), ischemic stroke
(3.7%), carotid cavernous fistula (1.9%), cardiac arrhythmia
(2.8%), and carotid occlusion (0.9%). 20
Prognostic Factors
Darsaut et al31 analyzed the clinical and angiographic predictors of clinical and neurological outcomes following the
treatment of very large (20–24mm) or giant cerebral aneurysms (>25mm). They analyzed 184 aneurysms, 99 of which
were giant, submitted to treatment and follow-up at Stanford
University.
After multivariate analysis, the main prognostic factors
for poor clinical outcome were a modified Rankim Scale
score greater than 2, aneurysms larger than 25 mm, and
aneurysms located in the posterior circulation. Risk factors
for incomplete angiographic occlusion were fusiform morphology, aneurysms located in the posterior circulation,
and aneurysms submitted to endovascular treatment.
Patients who presented incomplete occlusion in the angiographic follow-up showed high levels of SAH and increased mortality during follow-up, compared with
completely occluded aneurysms.31
13 Jaume A, Salle F, Fernandez M, Cobrera V, Aramburu I, Spagnuolo
14
15
16
Conclusions
Despite important advances in diagnostic imaging methods
and the development of microsurgical and endovascular techniques, the treatment of giant aneurysms remains a challenge
for neurosurgery. Treatment should be individualized and
discussed among a multidisciplinary team. The advent of
new endovascular technologies, such as flow-diverting stents
is a promising advance in the treatment of this pathology, with
good short and medium term results. The surgical treatment of
these lesions remains the principal therapeutic modality in
selected centers, due to the durability, costs, low rates of
recanalization, and good clinical outcomes obtained.
17
18
19
20
21
References
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Battaglia R, Pasqualin A, Da Pian R. Italian cooperative study on
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Morley TP, Barr HW. Giant intracranial aneurysms: diagnosis,
course, and management. Clin Neurosurg 1969;16:73–94
Peerless SJ, Wallace MC, Drake CG. Giant intracranial aneurysms.
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Rosta L, Battaglia R, Pasqualin A, Beltramello A. Italian cooperative
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Christiano LD, Gupta G, Prestigiacomo CJ, Gandhi CD. Giant
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Molyneux AJ, Kerr RS, Yu LM, et al; International Subarachnoid
Aneurysm Trial (ISAT) Collaborative Group. International
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intracranial aneurysms: a randomised comparison of effects on
survival, dependency, seizures, rebleeding, subgroups, and
aneurysm occlusion. Lancet 2005;366(9488):809–817
Piepgras DG, Khurana VG, Whisnant JP. Ruptured giant intracranial aneurysms. Part II. A retrospective analysis of timing and
outcome of surgical treatment. J Neurosurg 1998;88(3):430–435
Lawton MT, Spetzler RF. Surgical strategies for giant intracranial
aneurysms. Neurosurg Clin N Am 1998;9(4):725–742
Matas R. I. Testing the Efficiency of the Collateral Circulation as a
Preliminary to the Occlusion of the Great Surgical Arteries. Ann
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Wiebers DO, Whisnant JP, Huston J III, et al; International Study of
Unruptured Intracranial Aneurysms Investigators. Unruptured
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risks of surgical and endovascular treatment. Lancet 2003;362(9378):103–110
Ferguson GG. Physical factors in the initiation, growth, and
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E. Surgical Treatment of Giant Intracranial Aneurysms: Series of
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Drake CG, Peerless SJ. Giant fusiform intracranial aneurysms:
review of 120 patients treated surgically from 1965 to 1992. J
Neurosurg 1997;87(2):141–162
Jahromi BS, Mocco J, Bang JA, et al. Clinical and angiographic
outcome after endovascular management of giant intracranial
aneurysms. Neurosurgery 2008;63(4):662–674, discussion 674–
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Lawton MT, Sanai N. Microsurgical management of giant intracranial aneurysms. In: Youmans JR (Ed). Neurological Surgery.
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Jafar JJ, Russell SM, Woo HH. Treatment of giant intracranial
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bypass grafting: indications, operative technique, and results in
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THIEME
304
Review Article | Artigo de Revisão
Seizure Outcome after Anterior versus
Complete Corpus Callosotomy in Children: A
Systematic Review with Meta-Analysis
Controle das crises epilépticas após calosotomia anterior
versus completa em crianças: uma revisão sistemática
com metanálise
Lucas Crociati Meguins1 Rodrigo Antônio Rocha da Cruz Adry1 Sebastião Carlos da Silva Júnior1
Carlos Umberto Pereira2 Jean Gonçalves de Oliveira3 Dionei Freitas de Morais1
Gerardo Maria de Araújo Filho4 Lúcia Helena Neves Marques5
1 Neurosurgery Division, Hospital de Base, Department of Neurologic
Sciences, Faculdade de Medicina de São José do Rio Preto (FAMERP),
SP, Brazil
2 Department of Medicine, Universidade Federal de Sergipe (UFS),
Aracaju, SE, Brazil
3 Division of Neurosurgery, Department of Medical Sciences, School
of Medicine, Universidade Nove de Julho; Department of
Cerebrovascular and Skull Base surgery, Center of Neurology and
Neurosurgery Associates, Hospital Beneficência Portuguesa de São
Paulo, São Paulo, SP, Brazil
4 Department of Psychiatry and Medical Psychology, FAMERP, SP, Brazil
5 Neurologic Division, Hospital de Base, Department of Neurologic
Sciences, FAMERP, SP, Brazil
Address for correspondence Lucas Crociati Meguins, MD, MSc, Rua
Pedro Palotta, 101/31B, Jardim Maracanã, São José do Rio Preto, SP,
Brazil CEP: 15092-205 (e-mail: [email protected]).
Abstract
Keywords
► corpus callosotomy
► anterior versus
complete corpus
callosotomy
► refractory epilepsy
► meta-analysis
received
November 10, 2013
accepted
August 7, 2015
published online
October 20, 2015
Introduction Refractory epilepsy is a debilitating and challenging condition to
manage. Corpus callosotomy (CC) seems to be an effective treatment option for
patients with seizures not amenable to focal resection. The aim of the present study is
to compare seizure outcome of pediatric patients following anterior CC, compared with
complete CC.
Method The authors performed a systematic review and meta-analysis of the English
literature involving comparative studies.
Results The present investigation includes four retrospective case-controlled studies
and authors perform a pooled analysis of the surgical results. Seizure outcome
presented favorable results in patients who underwent complete CC (Odds Ratio,
M-H, Fixed, 95% CI: 3.02 [1.43, 6.387], p-value: 0.005). Clinical and neurological
complications occurred independently when a complete or anterior CC was performed.
Conclusion Complete CC seems to be the most effective treatment option to control
intractable seizure in children not amenable to focal resection.
10.1055/s-0035-1564581.
ISSN 0103-5355.
Seizure Outcome after Anterior versus Complete Corpus Callosotomy in Children
Resumo
Palavras-chave
► calosotomia
► calosotomia anterior
versus completa
► epilepsia refratária
► metanálise
Meguins et al.
Introdução Epilepsia refratária é uma condição debilitante e desafiadora para lidar.
Calosotomia parece ser uma opção de tratamento eficaz para pacientes com convulsões não passíveis de ressecção focal. O objetivo do presente estudo é comparar o
resultado de convulsões em pacientes pediátricos de acordo com calosotomia anterior
e completa.
Métodos Uma revisão sistemática e metanálise da literatura médica em inglês
envolvendo estudos comparativos.
Resultados Quatro casos retrospectivos foram incluídos na presente investigação e
uma análise dos resultados cirúrgicos foi realizada. Convulsões decorrentes tiveram
resultados favoráveis em pacientes submetidos a calosotomia complete (odds ratio,
M-H, fixo, 95% IC: 3,02 [1,43; 6,387], valor de p: 0,005). Complicações clínicas
e neurológicas ocorreram independentemente de se calosotomia complete ou
anterior.
Conclusão Calosotomia completa parece ser a opção de tratamento mais eficaz para
controlar convulsões não rastreáveis e não passíveis de ressecção focal em crianças.
Introduction
Refractory epilepsy is a debilitating and challenging condition to manage. Corpus callosotomy (CC) seems to be an
effective treatment option for patients with seizures not
amenable to focal resection. The most common indication
for corpus callosotomy (CC) is drop attacks (tonic or
atonic), which often lead to severe physical injuries.1–3
Other possible indications for CC include West Syndrome,
Lennox-Gastaut syndrome, and intractable episodes of
status epilepticus or complex partial seizures with secondary generalization without any obvious foci.4–6 CC may
be performed in both children and adults;7,8 however,
children seem to have fewer postsurgical complications
than adults, apparently because of the neuronal plasticity
of pediatric patients’ brains.3
A well-known adverse effect of CC is the “disconnection
syndrome”.9,10 Additionally, other adverse effects have
been described, including language impairments and memory deficits. The complications are often transient; however, in some cases, they become permanent affecting the
patient’s quality of life.3,6,11 Therefore, the use of CC is
restricted mainly to patients with intractable seizure.6 To
spare neurological functions, some authors advocate anterior or partial CC, leaving the splenium,12–14 whereas,
others consider complete or total CC to be more effective,
especially in children.14–17 The present study performs a
systematic review with meta-analysis of the literature that
involves direct comparisons of seizure outcome among
pediatric patients after anterior or complete CC. Our
hypothesis is that complete CC is superior to anterior CC
in producing favorable seizure outcomes, although the most
relevant surgical series are likely too small to reach a strong
statistical significance. A meta-analysis study improves
accuracy through a pooled estimate of treatment effects.
Methods
Search Strategy
Two authors (LCM, RARCA) independently performed a
comprehensive literature search of PubMed, The Cochrane
Library, and Embase using the following terms, alone or in
combination: “callosotomy,” “corpus callosotomy,” “children,” “childhood,” “pediatric,” “anterior,” “anterior twothirds,” “partial,” “complete,” “full”, and “total.” The investigators identified potentially relevant articles by reviewing
abstracts and then thoroughly reviewed references. Searches
were restricted to English-language articles published from
2000 to 2014.
Study Selection
Inclusion criteria for the present systematic review consisted
of the following: 1) articles comparing seizure outcome in
pediatric patients after anterior and complete CC, 2) studies
with a minimum follow-up of 3 months, 3) well-defined
measure of seizure frequency reduction, either in numbers
or ranges, after anterior or complete CC, 4) brief description
of surgical and clinical complications following either operative procedure under investigation. Studies were excluded if
seizure frequency data could not be extracted from the study
population’s data. Two authors (LCM, RARCA) independently
reviewed studies that met inclusion criteria to determine
their suitability and quality and unanimously agreed upon
the studies to be included in this meta-analysis.
Data Collection
Data were collected on the following: first author’s name,
year of publication, country and institution of investigation,
study design, sample size, type of treatment, number of
patients enrolled on each type of treatment (anterior vs.
complete CC), duration of follow-up, seizure-free rate,
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complication rate, and mortality. In studies where patients
were listed individually, means and sums were used to
represent the study in the final analysis. When possible,
the outcome data were gathered according to the last followup. Not all data were available for every study.
Ethical Statement
The Ethical Committee of our institution analyzed the project for the present study and approved the performance of
our investigations. The study complies with the Declaration
of Helsinki.
Statistical Analysis
The software used to aid in statistical analysis were Microsoft
Excel 2013 and Bio Stat 5.0 (Belém, Brazil, 2007). The authors
organized the data collected from all patients in tables
comparing with previous studies. Averages are expressed
as the means SD for parametric data and as median values
for nonparametric data. Forest plot and meta-analysis of
post-operative seizure outcomes were performed using the
Mantel-Haenszel test (fixed effect) and odds ratio. Heterogeneity evaluation was performed using the chi-square test for
contingency Tables (2 2). Studies were the unit of analysis.
Odds ratio with 95% CIs were used to compare pooled
proportion of clinical improvement in seizure frequency
between anterior and complete CC groups. A p-value < 0.01
was considered statistically significant.
Results
Eligible Articles
►Fig. 1 summarizes the strategy utilized during the literature search for this study. After excluding non-comparative
investigations, four case-controlled articles comparing seizure outcome of anterior and complete CC were included in
the present meta-analysis. All studies were retrospective
investigations performed in North America (►Table 1).
Fig. 1 Summary of the literature search strategy.
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Meguins et al.
Seizure Outcome
The pooled analysis of seizure outcome after anterior and
complete CC is presented in ►Table 2 and ►Fig. 2. A favorable
surgical outcome was considered when patients achieved
more than 50% of seizure reduction during follow-up or were
included in one of the three groups: Engel I, II, or III. A seizure
outcome was considered unfavorable when patients
achieved less than 50% of seizure reduction or were classified
as Engel IV during follow-up.
Complications
►Table 1 presents the rate of surgical and neurological
complications from studies included in the present metaanalysis. Significant complication rates did not achieve more
than 5% and disconnection syndrome was a transient neurological complication in most studies.
Discussion
Children with severe and refractory epilepsy usually suffer
significant morbidity and disability. Many of them suffer
cognitive decline due to the effects of frequent seizures and
chronic use of anti-epileptic drugs, as well as from physical
harm as a result of sudden loss of consciousness. CC is a
palliative procedure for patients with medically uncontrolled seizures not amenable to focal resection.18 Van
Wagenen and Herren19 first introduced it in 1940 as a
therapeutic option for refractory epilepsy. Since then,
many studies regarding the indication and outcome of
corpus callosotomy have been published.20–25 However,
there has yet to be universally accepted standard guidelines
for the selection of patients for anterior versus complete CC.
In the past, anterior CC was believed to prevent postsurgical neurological deficits, such as the disconnection
syndrome, marked by mutism, hemiataxia, and/or alexia.26
With these controversies in mind, we performed a systematic review with meta-analysis of studies directly comparing
seizure outcome and evaluating complications descriptions
of pediatric patients following anterior or complete CC. Our
hypothesis was that complete CC was superior to anterior CC
to produce favorable seizure outcomes, but most relevant
surgical series were likely too small to carry strong statistical
significance. Therefore, a meta-analysis study would improve precision through a pooled estimate of treatment
effect.
Four studies were included in the present meta-analysis
after review of the literature. The pooled analysis found
that complete CC is superior to anterior CC in improving
seizure outcome of pediatric patients (►Fig. 1
and ►Table 2). Rahimi et al. showed a significant benefit
when complete CC was used for secondary generalized
seizures compared with anterior CC.14 Additionally, Bower
et al. and Kasasbeh et al. also reported favorable outcomes
of complete CC in controlling drop attacks and astatic
seizures compared to anterior CC.16,17 Jalilian et al. reinforced that complete CC should be considered as the
initial procedure in lower-functioning children afflicted by
absence, atonic, or myoclonic seizures and that severely
Meguins et al.
Table 1 Characteristics of studies included in the meta-analysis
No. of Patients
Year
Design
AntCC
CompCC
Follow-up
Neurological Complications
14
2007
Retro
11
28
1.2
2%
15
2010
Retro
15
12
2
4%
16
2013
Retro
28
22
4.2
4%
2014
Retro
21
31
3.2
5%
Study
Rahimi et al.
Jalilian et al.
Bower et al.
Kasasbeh et al.17
Abbreviations: AntCC, Anterior corpus callosotomy; CompCC, Complete corpus callosotomy; , mean duration of follow-up in years; Retro,
Retrospective.
Table 2 Meta-analysis of seizure outcome after AntCC and CompCC
AntCC
Study
Rahimi et al.14
CompCC
Odds Ratio
Successβ
Total
Successβ
Total
Weight
M-H, Fixed, 95% CI
9
11
25
28
1.016
1.85 [0.26, 12.94]
15
10
15
11
12
0.719
5.50 [0.54, 55.49]
Bower et al.16
14
28
14
22
2.947
1.75 [0.55, 5.481]
12
21
28
31
1.775
7.00 [1.60, 30.48]
Subtotal (95% IC)
–
75
–
93
–
3.02 [1.43, 6.387]
Total (Event)
45
–
78
–
–
–
Jalilian et al.
Kasasbeh et al.
17
Abbreviations: AntCC, Anterior CC; CompCC: Complete CC; M-H, Mantel-Haenszel test.
Heterogeneity: Chi2 ¼ 2.29, p ¼ 0.51.
Test for overall fixed effect (M-H): p ¼ 0.005.
β: Success: Patients classified as Engel I/II/III or presenting >50% seizure frequency reduction.
affected higher-functioning children may also benefit
from complete CC, without significant neurological
complications.15
Statistical data from all four studies demonstrated that
neurological morbidity in patients receiving complete CC is
not greater than those receiving an anterior CC. Jalilian et al.
reported suspicion of disconnection syndrome in one patient
who received an anterior CC and transient mutism and
weakness in four other patients after complete CC.15 Rahimi
et al. also described one case of mild disconnection syndrome after complete CC, characterized by a change in the
dominant hand.14 Bower et al. and Kasasbeh et al. affirmed
that clinical and neurological complications were independent of whether the CC was complete or anterior. No
statistically significant difference was observed between
groups with regards to length of surgery, length of hospitalization, or estimated blood loss.16,17
There are several methodological aspects in the present
findings, which should be interpreted in the context of several
limitations. Although an extensive systematic literature review
was performed, we included only four retrospective non-randomized case-controlled studies for meta-analysis. Additionally,
most studies had a small number of patients and the follow-up
was relatively brief, with a mean time of 2.65 years for a pooled
analysis. Nevertheless, future prospective and randomized studies with a greater number of patients are certainly necessary to
confirm such observations.
Conclusion
Fig. 2 Forest Plot of seizure outcome after AntCC and CompCC (M-H,
Mantel-Haenszel test; AntCC, Anterior CC; CompCC, Complete CC).
To conclude, the management of medically refractory epilepsy is complex and challenging, and CC seems to be an
appropriate option when patients have failed maximal
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308
medical therapy. Additionally, complete CC is the most
effective treatment option to control intractable seizure in
children not amenable to focal resection with similar neurological complications, when compared with partial CC.
13 Ping Z, Ji-Wen X, Gui-Song W, Hong-Yu Z, Xin T. Evaluation of
14
15
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1 Tanriverdi T, Olivier A, Poulin N, Andermann F, Dubeau F. Long-
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term seizure outcome after corpus callosotomy: a retrospective
analysis of 95 patients. J Neurosurg 2009;110(2):332–342
Stigsdotter-Broman L, Olsson I, Flink R, Rydenhag B, Malmgren K.
Long-term follow-up after callosotomy—a prospective, population based, observational study. Epilepsia 2014;55(2):316–321
Maehara T, Shimizu H. Surgical outcome of corpus callosotomy in
patients with drop attacks. Epilepsia 2001;42(1):67–71
Suzuki Y, Baba H, Toda K, Ono T, Kawabe M, Fukuda M. Early total
corpus callosotomy in a patient with cryptogenic West syndrome.
Seizure 2013;22(4):320–323
Liang S, Zhang S, Hu X, et al. Anterior corpus callosotomy in
school-aged children with Lennox-Gastaut syndrome: a prospective study. Eur J Paediatr Neurol 2014;18(6):670–676
Asadi-Pooya AA, Sharan A, Nei M, Sperling MR. Corpus callosotomy. Epilepsy Behav 2008;13(2):271–278
Park MS, Nakagawa E, Schoenberg MR, Benbadis SR, Vale FL.
Outcome of corpus callosotomy in adults. Epilepsy Behav 2013;
28(2):181–184
Iwasaki M, Uematsu M, Nakayama T, et al. [Corpus callosotomy for
children with intractable generalized epilepsy: factors for longterm seizure remission]. No To Hattatsu 2013;45(3):195–198
Yang PF, Lin Q, Mei Z, et al. Outcome after anterior callosal section
that spares the splenium in pediatric patients with drop attacks.
Epilepsy Behav 2014;36:47–52
Jea A, Vachhrajani S, Widjaja E, et al. Corpus callosotomy in
children and the disconnection syndromes: a review. Childs
Nerv Syst 2008;24(6):685–692
Mamelak AN, Barbaro NM, Walker JA, Laxer KD. Corpus callosotomy: a quantitative study of the extent of resection, seizure
control, and neuropsychological outcome. J Neurosurg 1993;
79(5):688–695
Liang S, Li A, Jiang H, et al. Anterior corpus callosotomy in patients
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efficacy and safety of anterior corpus callosotomy with keyhole in
refractory seizures. Seizure 2009;18(6):417–419
Rahimi SY, Park YD, Witcher MR, Lee KH, Marrufo M, Lee MR.
Corpus callosotomy for treatment of pediatric epilepsy in the
modern era. Pediatr Neurosurg 2007;43(3):202–208
Jalilian L, Limbrick DD, Steger-May K, Johnston J, Powers AK,
Smyth MD. Complete versus anterior two-thirds corpus callosotomy in children: analysis of outcome. J Neurosurg Pediatr 2010;
6(3):257–266
Bower RS, Wirrell E, Nwojo M, Wetjen NM, Marsh WR, Meyer FB.
Seizure outcomes after corpus callosotomy for drop attacks.
Neurosurgery 2013;73(6):993–1000
Kasasbeh AS, Smyth MD, Steger-May K, Jalilian L, Bertrand M,
Limbrick DD. Outcomes after anterior or complete corpus callosotomy in children. Neurosurgery 2014;74(1):17–28, discussion
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VanStraten AF, Ng YT. Update on the management of LennoxGastaut syndrome. Pediatr Neurol 2012;47(3):153–161
Van Wagenen WP, Herren RY. Surgical division of commissural
pathways in the corpus callosum: relation to spread of an
epileptic attack. Arch Neurol Psychiatry 1940;44(4):
740–759
Gates JR, Leppik IE, Yap J, Gumnit RJ. Corpus callosotomy: clinical
and electroencephalographic effects. Epilepsia 1984;25(3):
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for control of intractable epilepsy in children. Neurology 1983;
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Purves SJ, Wada JA, Woodhurst WB, et al. Results of anterior
corpus callosum section in 24 patients with medically intractable
seizures. Neurology 1988;38(8):1194–1201
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Neurol 1991;48(4):364–372
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outcome following corpus callosotomy in children. Stereotact
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Rayport M, Ferguson SM, Corrie WS. Outcomes and indications of
corpus callosum section for intractable seizure control. Appl
Neurophysiol 1983;46(1–4):47–51
Harbaugh RE, Wilson DH, Reeves AG, Gazzaniga MS. Forebrain
commissurotomy for epilepsy. Review of 20 consecutive cases.
Acta Neurochir (Wien) 1983;68(3–4):263–275
THIEME
Case Report | Relato de Caso
Schwannoma como etiologia de síndrome do
túnel do carpo – relato de caso
Schwannoma as a Cause of Carpal Tunnel Syndrome – a
Case Report
Marcelo José da Silva de Magalhães1
André Jin Fujioka2
1 Professor de Medicina das Faculdades Unidas do Norte de Minas
(FUNORTE); Faculdades Integradas Pitágoras; Neurocirurgião do
Hospital Aroldo Tourinho, Montes Claros, MG, Brasil
2 Acadêmicos de Medicina das Faculdades Integradas Pitágoras de
Montes Claros – FIPMoc, Montes Claros, MG, Brasil
Raiana Barbosa Chaves2
Address for correspondence Marcelo J. S. Magalhães, MSc, Serviço de
Neurocirurgia do Hospital Aroldo Tourinho, rua Capelinha 375, Bairro
Antônio Pimenta, Montes Claros, Minas Gerais, Brasil CEP: 39402-315
Resumo
Palavras-Chave
► schwannoma
► neurilemoma
► síndrome do túnel do
carpo
Abstract
Keywords
► schwannoma
► neurilemoma
► carpal tunnel
syndrome
A síndrome do túnel do carpo (STC) é uma condição clínica resultante da compressão
do nervo mediano no túnel do carpo. É a neuropatia de maior incidência no membro
superior e apresenta diferentes etiologias, entre elas o distúrbio osteomuscular
relacionado ao trabalho (DORT) e, mais raramente, a tumores de nervo periférico. O
DORT é a etiologia mais comum da STC e vem aumentando sua incidência por causa de
sua associação com o trabalho. Eentre os tumores que envolvem o nervo mediano está
o schwannoma, ou neurilemoma, que também é o tumor benigno mais comum de
nervos periféricos. Este relato almeja descrever um caso de schwannoma como
etiologia da STC.
The carpal tunnel syndrome (CTS) is a clinical condition resulting from compression of
the median nerve in the carpal tunnel. It is the neuropathy of higher incidence in the
upper limb and as different etiologies, is related to work-related musculoskeletal
disorders (WMSDs) and rarely tumors of peripheral nerve. The WMSDs are the most
common, and its incidence is increasing more and more due to the intimate association
with type of work. Among the tumors involving median nerve is the Schwannoma, or
neurilemoma. The Schwannoma is the most common benign tumor of the peripheral
nerve. This report aims to describe a case of schwannoma as a cause of CTS.
Introdução
Os tumores que envolvem os nervos periféricos são incomuns, sendo o schwannoma o tumor benigno mais comum
destes.1 Também denominado neurilemoma tem origem nas
células de schwann que se localizam na bainha de mielina
dos nervos periféricos.2 Os nervos periféricos mais acome-
received
May 9, 2013
accepted
August 7, 2015
published online
October 7, 2015
10.1055/s-0035-1564828.
ISSN 0103-5355.
tidos pelo tumor são o ulnar e fibular, e apenas 7% destes
estão situados no mediano.3 Geralmente, acometem indivíduos entre 20 e 50 anos, sem predileção de raça e sexo.4
O schwannoma solitário é um tumor de crescimento lento
e, muito antes de apresentar a clínica de dor e os sintomas
neurológicos devidos à compressão, tem o quadro iniciado
apenas por um abaulamento local.5 Caso o crescimento do
309
310
Schwannoma como etiologia de síndrome do túnel do carpo
Magalhães et al.
tumor ocorra no interior do túnel do carpo, a sua progressão
possivelmente origina a síndrome do túnel do carpo pela
compressão local.6 A síndrome do túnel do carpo (STC) é a
neuropatia de maior incidência no membro superior que
apresenta como principal etiologia o distúrbio osteomuscular relacionado ao trabalho (DORT).6 No entanto, há etiologias diversas que podem gerar a STC. Apesar de a STC ser
relativamente frequente nos consultórios médicos, o
schwannoma como etiologia da síndrome é raro.5
Sendo assim, este relato clínico visa descrever um caso
raro sobre schwannoma como etiologia de síndrome de tú nel
do carpo além de fazer a revisão na literatura.
Relato de Caso
Paciente do sexo feminino, 43 anos, do lar, procurou atendimento no ambulatório de neurologia com a queixa de dor na
mão direita. A dor iniciou há cerca de 4 anos, com acentuação
da sintomatologia nos últimos 6 meses. A paciente afirmava
que a dor se apresentava com padrão de choque no polegar
direito. Os sintomas eram induzidos pelo toque leve sobre a
pele em determinado ponto da região palmar. Apesar de ter
procurado diversos médicos e realizado o uso de anti-inflamatório não esteroide (AINE) e fisioterapia, o quadro neurológico persistiu. A paciente era casada e mãe de duas filhas,
tabagista. Apresentava passado de salpingotripsia.
Na história familiar, tinha um irmão portador de epilepsia,
pai falecido por câncer de próstata e mãe asmática.
A paciente realizou eletroneuromiografia de membros
superiores em 2012 que revelou síndrome do túnel do carpo
na mão direita. O ultrassom de mão (►Fig. 1) mostrou
imagem sólida, nodular, hipoecoica e heterogênea com finas
traves, adjacente ao tendão flexor do primeiro dedo da mão
direita. Foi submetida à cirurgia para exérese da lesão com
acesso cirúrgico através de incisão clássica para tratamento
da STC (►Fig. 2).
Durante o peroperatório foi identificada a presença de
lesão nodular de consistência fibroelástica que foi ressecada
em bloco. Exame anatomopatológico mostrou como resultado schwannoma (►Fig. 3). A paciente, em controle 30 dias
Fig. 1 Ultrassonografia de mão direita em pré-operatório revelando a
presença de um nódulo sólido adjacente ao tendão flexor do primeiro
dedo da mão direita.
Vol. 34
No. 4/2015
Fig. 2 Fotografia intraoperatória para o tratamento da síndrome do
túnel do carpo. Note a presença do tumor após a abertura do
ligamento transverso do carpo.
após o procedimento cirúrgico, evoluiu com melhora dos
sintomas.
Discussão
Os tumores de nervos periféricos são raros, sendo o
schwannoma o mais comum destes.7 Na maior parte dos
casos, apresenta-se como tumor solitário e benigno, no
entanto pode ser múltiplo, sugerindo uma predisposição
primária e estar associado com a neurofibromatose tipo 1
e schwannomatose.7
Fig. 3 Schwannoma originado de fascículo do nervo mediano. Tumor
com aspecto fusiforme, coloração branco-amarelada, além de consistência fibroelástica.
O schwannoma caracteriza-se por crescimento lento e
inicialmente pode se apresentar assintomático ou gerar
apenas um abaulamento local, sem dor.5 O crescimento lento
favorece a adaptação do nervo aos efeitos pressóricos. Ainda
assim, com a progressão da lesão, o tumor pode produzir dor
e alterações sensoriais.6 Apesar de raramente provocar disfunção motora, este sinal, quando presente, representa indício de um tumor maligno.8 Clinicamente o schwannoma é
bem circunscrito, tem consistência de partes moles, móvel
transversalmente, no curso do nervo, e imóvel no plano
longitudinal.6 O schwannoma caso surja no túnel do carpo
pode gerar a STC, que se caracteriza inicialmente por queixas
sensitivas, como sensação de formigamento intermitente em
geral acompanhada de dor.5 A distribuição da dor e da
parestesia manifesta-se na região inervada pelo nervo mediano.9 Alguns sinais frequentemente utilizados para o diagnóstico são o teste de Phalen, teste de Tinel, compressão do
nervo mediano e sinal de fraqueza do músculo adutor curto
do polegar.5 Compressões crônicas podem causar hipotrofia
tenar, notada por redução das forças de preensão palmar e de
pinça polegar-indicador.9
Na análise patológica, o schwannoma tem uma cápsula
verdadeira composta de epineuro.3 A característica principal
deste tumor é a alternância entre áreas de Antoni A e Antoni
B.10 As áreas de Antoni A são áreas celulares, com células
fusiformes e núcleos em paliçada formando corpos de Verocay.8 Antoni B são áreas hipocelulares, microcísticas, ricas em
macrófagos e fibras de colágeno.3 Os tumores com mais
tempo de evolução podem apresentar alterações degenerativas atribuídas à insuficiência vascular, sendo esta necrose
cística, edema estromal, fibrose, hialinização perivascular,
alteração xantomatosa, calcificação e degeneração nucleica
com pleomorfismo e hipercromasia.10
Imuno-histoquimicamente, o tumor apresenta expressão
forte e difusa da proteína S100, útil para fazer diagnóstico
diferencial, já que o schwannoma apresenta maior quantidade desta que o neurofibroma.11 Outro marcador importante para a diferenciação é o CD34. Nota-se que o
neurofibroma apresenta tipicamente uma subpopulação
significativa de células estromais CD34 positivas, enquanto
o schwannoma mostra coloração CD34 mais acentuada
apenas nas áreas Antoni B e nos vasos sanguíneos.12 Além
disso, o antígeno Ki67 é um indicador de atividade mitótica
que possibilita mensurar o grau de malignidade do tumor.11
Os exames de imagem são fundamentais tanto para
identificar o tumor quanto para realizar diagnósticos diferenciais.13 Assim, a ressonância nuclear magnética consiste
no principal destes, fornecendo informações morfológicas da
lesão, com a limitação de mostrar alterações dinâmicas.14 As
áreas de Antoni A, por conter colágeno, exibem hipointensidade quando ponderadas em T1 e T2.14 Nas áreas de Antoni B,
a água produz uma matriz mixoide evidenciando hipointensidade em T1 e hiperintensidade em T2.15 Além disso, as
áreas císticas e necróticas apresentam baixo sinal em T1 e
não são evidenciadas com gadolínio, sendo facilmente interpretadas como achados agressivos.13 Para se obter informações da lesão de forma dinâmica, como flexão e extensão, o
melhor exame é a ultrassonografia (USG) que mostra a
Magalhães et al.
relação da lesão com estruturas anatômicas adjacentes.6 O
schwannoma aparece como estrutura homogênea, hipoecoica, bem delimitada e com sombra acústica posterior.15
Entre os principais diagnósticos diferenciais encontramse o neurofibroma, lipoma intraneural, cisto ganglionar,
neuroma traumático e as malformações vasculares.16 Os
neurofibromas, tais como os schwannomas são originados
em parte das células de Schwann, diferindo geralmente por
não serem solitários e crescerem dentro da substância
nervosa, o que impossibilita a dissecção dos fascículos durante o tratamento cirúrgico.17 Microscopicamente, o padrão
histológico varia consideravelmente, mas o mais comum é
encontrar células de Schwann fusiformes entremeadas com
matriz colágena.17 A diferenciação entre o neurilemoma e o
neurofibroma por métodos de imagem até pouco tempo era
limitada; no entanto, a literatura mais recente cita características ultrassonográficas que podem ajudar a diferenciar os
tumores de partes moles.9 O neurofibroma apresenta-se com
menos alterações degenerativas e uma hipervascularização
menos intensa quando comparado ao schwannoma.16
O tratamento pode ser tanto conservador quanto cirúrgico. Caso o tumor seja assintomático e permaneça inalterado durante o acompanhamento, opta-se por um
tratamento conservador.7 Em se tratando de uma lesão que
gere sintomas, o tratamento cirúrgico pode ser indicado.18
No entanto, este ainda apresenta divergências na literatura,
pois alguns autores citam que se faz necessário realizar uma
biópsia antes da retirada do tumor propriamente dita, diferindo da conduta que indica excisão cirúrgica como diagnóstico terapêutico.1
O schwannoma é bem localizado tal como encapsulado
em relação ao nervo de origem, fato que possibilita a dissecação dos fascículos neurais sem prejuízo funcional.3 Ainda
assim, o procedimento cirúrgico é passível de complicações,
sendo a principal delas a parestesia pós-cirúrgica, podendo
causar também disfunção motora e/ou sensitiva.19 A recorrência do tumor é rara, mesmo em ressecções incompletas.19
Conclusão
Apesar de ser uma doença comum, a síndrome do túnel do
carpo (STC) pode apresentar como etiologia tumores que se
originam no nervo mediano no interior do túnel do carpo.
Essa hipótese de diagnóstico deve ser aventada quando o
paciente apresenta abaulamento ou ponto de gatilho para
dor localizado na região palmar. Outros estudos ainda são
necessários para definir o resultado funcional destes pacientes a longo prazo.
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Bull N Y Acad Med 1985;61(7):611–620
Welker JA, Henshaw RM, Jelinek J, Shmookler BM, Malawer MM.
The percutaneous needle biopsy is safe and recommended in the
diagnosis of musculoskeletal masses. Cancer 2000;89(12):
2677–2686
Sawada T, Sano M, Ogihara H, Omura T, Miura K, Nagano A. The
relationship between pre-operative symptoms, operative findings and postoperative complications in schwannomas. J Hand
Surg [Br] 2006;31(6):629–634
THIEME
Epidural Capillary Hemangioma of the Thoracic
Spine
Hemangioma capilar extradural da coluna torácica
Eberval Gadelha Figueiredo1 Anderson Rodrigo Souza1
Daniella Brito Rodrigues2 Raul Marino Jr.3
1 Department of Neurological Surgery, Institute of Neurological
Diseases of São Paulo, São Paulo, SP, Brazil
2 School of Medicine, Universidade do Estado do Pará, Belém, PA, Brazil
3 Department of Neurological Surgery, Institute of Neurological
Diseases of São Paulo, Beneficencia Portuguesa Hospital, São Paulo,
SP, Brazil
Gabriel Reis Sakaya1
Address for correspondence Eberval G. Figueiredo, MD, PhD,
Maestro Cardim 808, São Paulo, SP, Brazil 01323-001
Abstract
Keywords
► hemangiomas
► spinal cord
► capillary
hemangioma
► neurilemmoma
received
August 9, 2014
accepted
August 7, 2015
published online
October 19, 2015
Background Hemangiomas are congenital vascular malformations pathologically
considered as harmatomas and classified as capillary, cavernous, arteriovenous or
venous, and usually located at soft tissue or bone, mainly in the spinal column. Pure
epidural capillary hemangiomas are extremely rare lesions that should be included in
the differential diagnosis of spinal epidural lesions; only three patients with epidural
capillary hemangiomas have been reported to date.
Case Report We report a case of a 57-year-old man that complained of dorsal and back pain.
The neurological examination revealed back tenderness and crural paraparesis. His reflexes
were exaggerated and Babinski sign was present on both sides. A magnetic resonance imaging
showed an epidural lesion at the level of T10–12 that demonstrated extension with intense
postgadolinium enhancement. These lesions were different from more common lesions,
mainly schwanommas, mainly due to the foraminal extension, which sets them apart from
cavernous hemangiomas. The surgical ressection was performed. After laminectomy, a
reddish epidural mass that extended into the right T11–12 foramina was revealed. The feeding
vessels had to be identified and divided. In such cases, the surgeon must carefully dissect the
lesion circumferentially away from the dura and employ judicious hemostasis. The patient́ s
histopathological examination revealed a vascular tumor composed of vessels of several
calibers. The imagery obtained from the exams led to the diagnosis of a capillary
hemangioma.
Conclusions Pure epidural capillary hemangiomas should be included in the differential diagnosis of spinal epidural lesions, mainly schwanommas, especially due to the
foraminal extension, which may differentiates them from cavernous hemangiomas.
Surgical excision is mandatory and intervertebral foraminal extension may preclude
gross total resection.
10.1055/s-0035-1564421.
ISSN 0103-5355.
313
314
Resumo
Palavras-chave
► hemangiomas
► medula espinhal
► hemangioma
capilar
► neurilemoma
Figueiredo et al.
Introdução Os hemangiomas são malformações vasculares congênitas patologicamente consideradas como hamartomas. Podem ser classificadas como capilar, cavernoso, arteriovenoso ou venoso, e são geralmente localizadas em tecidos moles ou
ossos, principalmente na coluna vertebral. Hemangioma capilar epidural puro é uma
lesão extremamente rara que deve ser incluída no diagnóstico diferencial das lesões
espinais epidurais, foram relatados casos de apenas três pacientes com hemangiomas
capilares epidurais.
Relato de Caso Relatamos o caso de um homem de 57 anos de idade com queixa de
dorsalgia. Ao exame neurológico, paraparesia crural, com hiperreflexia e sinal de
Babinski bilateral. A ressonância magnética mostrou uma lesão epidural no nível de
T10–12 com intenso realce pós-gadolíneo. Hemangioma capilar deve ser diferenciado
de lesões mais comuns, principalmente schwannomas, devido à extensão foraminal. A
ressecção cirúrgica foi realizada. Um processo expansivo epidural avermelhado, se
estendendo para o forâmen direito de T11–12, tornou-se evidente após a laminectomia. Os vasos que o irrigavam foram identificados e adequadamente separados. A lesão
foi cuidadosamente dissecada circunferencialmente e uma hemostasia criteriosa foi
realizada. O exame histopatológico revelou um tumor vascular composto por vasos de
vários calibres. Exames de imagem corroboraram com a hipótese de um hemangioma
capilar.
Conclusões Hemangiomas capilares epidurais puros devem ser incluídos no diagnóstico diferencial das lesões da coluna vertebral epidural, principalmente schwanommas, especialmente devido à extensão foraminal. A excisão cirúrgica é obrigatória e a
extensão para o forame intervertebral pode impossibilitar a ressecção total.
Introduction
Capillary hemangioma, also known as “Infantile hemangioma,” appears as a raised red lumpy lesion occurring
anywhere on the body, although 83% are located in the
head or neck area.1–6 Most of the epidural hemangiomas
described in the literature were cavernous hemangiomas.1,2,7 Epidural capillary hemangiomas are exceedingly
rare lesions. Thus far, only three cases have been
reported.4,7 We describe an additional case of a purely
epidural capillary hemangioma and discuss its clinical,
radiological, therapeutic, and prognostic features.
Case Report
A 57-year-old man complained of dorsal and back pain. Two
months prior, he had noticed progressive difficulty walking
and numbness in his legs. Neurological examination revealed
back tenderness and crural paraparesis. His reflexes were
exaggerated and Babinski sign was present on both sides.
Urine and stool incontinence were absent.
A magnetic resonance imaging (MRI) of the thoracolumbar spine showed an epidural lesion at the level of T7–8 that
extended into the right neuroforamina, as well as intense
postgadolinium enhancement (►Figs. 1 and 2). Signal flow
voids could be seen on T2, indicating that the lesion was
probably highly vascular (►Fig. 2). There was significant cord
compression; however, the cord signal was normal.
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Fig. 1 Magnetic resonance images. Axial view. An epidural mass with
foraminal extension is depicted compressing the spinal cord. Significant gadolinium enhancement can be seen.
Figueiredo et al.
the foraminal extension. The postoperative period was uneventful and the patient was discharged with no additional
neurological deficits.
Histopathological examination revealed a vascular tumor
composed of vessels of several calibers. Endothelium lined
the walls. We did not observe smooth muscles and saw
fibrous septa between the vessels. This image diagnosed a
capillary hemangioma (►Fig. 3).
DISCUSSION
Fig. 2 Magnetic resonance images. Sagital view. An epidural lesion at
the level of T7–8 presented intense postgadolinium enhancement.
Signal flow voids may be noticed, indicating that the lesion was
probably highly vascular.
He underwent a T6–8 laminectomy, bilaterally. Radioscopy was used to identify the level to be approached.
Electrophysiological monitoring was employed to minimize
the risks of neurological worsening. After laminectomy, a
reddish epidural mass that extended into the right T7–8
foramina was revealed. We noticed two feeding vessels in its
superolateral aspect, which we dissected and coagulated.
They were soft upon manipulation and we completely resected after circumferential dissection. Then, we removed
Fig. 3 Hematoxylin and eosin stain (x 32) shows a vascular tumor
composed of vessels with various calibers. The walls of the vessels are
lined with endothelium; there are no smooth muscles lining them.
Hemangiomas are congenital vascular malformations pathologically considered as hamartomas and classified as capillary, cavernous, arteriovenous or venous, and usually located
at soft tissue or bone, mainly in the spinal column.2,3,7–9
Vertebral hemangiomas are common, however purely epidural hemangiomas constitute rare findings.10,11 Although
cases of purely epidural cavernous hemangiomas have been
described, thus far, only three patients with epidural capillary hemangiomas have been reported.2,4,5
Differential diagnosis of epidural lesions includes nerve
sheath tumors, meningiomas, hemangiopericytomas, hemangioblastomas, cavernous hemangiomas, and lymphomas.7,11–13 A constant feature of the previously reported
cases is intervertebral foraminal extension, which is uncommon for a non-nerve sheath tumor.14,15 Therefore, schwannomas and capillary hemangiomas constitute the most
frequent differential diagnosis. There are reports of spinal
capillary hemangiomas in other locations, mainly the intradural and intramedullary spaces.7–9
The natural history of hemangiomas is poorly understood
due to the scarcity of cases.7 All four cases presented with
progressive myelopathy and pain.2,4 Myelopathy is thought
to be related to the direct compression of the spinal cord or
vascular steal phenomena. The cases of epidural capillary
hemangioma did not present any signs of hemorrhage.
In all cases, the lesion was located at the thoracic spine.
Radiological features were identical in every case reported
thus far. MRI findings include an isointense lesion in
T1–weighted images, with high signal in T2 and significant
enhancement after gadolinium injection. We observed low
density rim in two cases.2,4,5 Foraminal extension was
radiologically appreciated in all cases, as well it was during
surgical procedure. Such foraminal extension may be responsible for partial resection, even though no recurrence has
been described thus far.2,4,5
Surgical resection should always be indicated, regardless
of the clinical presentation, due to the risk of spinal cord
compression.5,15 Laminectomy or laminotomy are the most
used approaches. At surgery, the lesion presents as a reddish
epidural mass with arterial feeders surrounding it. The
surgeon must identify and divide the feeding vessels. It is
important to carefully dissect the lesion itself circumferentially away from the dura and exercise judicious hemostasis.
Total surgical resection is feasible, although intervertebral
foraminal extension may preclude it.
Most epidural hemangiomas are cavernous, constituting an important histological differential diagnosis.1,3,6
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315
316
Cavernous hemangiomas are comprised of a large number
of sinusoidal channels in collagenous tissue,6 whereas the
capillary hemangioma are composed of thin irregular
capillary-sized vessels in a fibrotic stroma, determining a
lobular architecture.3,14 Basal lamina is continuous and of
low mitotic activity presenting no atypia. Capillary hemangiomas stain positively for CD 31 and CD 34; 1,3,6,15
however, their reaction for S100 and epithelial membrane
antigen is negative.1
Figueiredo et al.
3 Caruso G, Galarza M, Borghesi I, Pozzati E, Vitale M. Acute
4
5
6
Conclusion
Pure epidural capillary hemangiomas are extremely rare lesions
that should be included in the differential diagnosis of spinal
epidural lesions. They differ from more common lesions, mainly
schwannomas, primarily due to their foraminal extension,
which also may differentiate them from cavernous hemangiomas. Surgical excision is mandatory and intervertebral foraminal extension may preclude gross total resection.
7
8
9
10
Conflicts of Interest
The authors received no funds in support of this work. No
benefits in any form have been or will be received from a
commercial entity with financial interests related directly
or indirectly to the subject of this manuscript.
11
12
13
References
1 Aoyagi N, Kojima K, Kasai H. Review of spinal epidural cavernous
hemangioma. Neurol Med Chir (Tokyo) 2003;43(10):471–475,
discussion 476
2 Badinand B, Morel C, Kopp N, Tran Min VA, Cotton F. Dumbbellshaped epidural capillary hemangioma. AJNR Am J Neuroradiol
2003;24(2):190–192
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14
15
presentation of spinal epidural cavernous angiomas: case
report. Neurosurgery 2007;60(3):E575–E576, discussion
E576
Gupta S, Kumar S, Banerji D, Pandey R, Gujral R. Magnetic
resonance imaging features of an epidural spinal haemangioma.
Australas Radiol 1996;40(3):342–344
Hasan A, Guiot MC, Torres C, Marcoux J. A case of a spinal epidural
capillary hemangioma: case report. Neurosurgery 2011;68(3):
E850–E853
Jo BJ, Lee SH, Chung SE, et al. Pure epidural cavernous hemangioma of the cervical spine that presented with an acute
sensory deficit caused by hemorrhage. Yonsei Med J 2006;
47(6):877–880
Alakandy LM, Hercules S, Balamurali G, Reid H, Herwadkar A,
Holland JP. Thoracic intradural extramedullary capillary haemangioma. Br J Neurosurg 2006;20(4):235–238
Bozkus H, Tanriverdi T, Kizilkiliç O, Türeci E, Oz B, Hanci M.
Capillary hemangiomas of the spinal cord: report of two cases.
Minim Invasive Neurosurg 2003;46(1):41–46
Hida K, Tada M, Iwasaki Y, Abe H. Intramedullary disseminated
capillary hemangioma with localized spinal cord swelling: case
report. Neurosurgery 1993;33(6):1099–1101
Roncaroli F, Scheithauer BW, Krauss WE. Hemangioma of spinal
nerve root. J Neurosurg 1999;91(2, Suppl)175–180
Shin JH, Lee HK, Jeon SR, Park SH. Spinal intradural capillary
hemangioma: MR findings. AJNR Am J Neuroradiol 2000;21(5):
954–956
Zander DR, Lander P, Just N, Albrecht S, Mohr G. Magnetic
resonance imaging features of a nerve root capillary hemangioma
of the spinal cord: case report. Can Assoc Radiol J 1998;49(6):
398–400
Kang JS, Lillehei KO, Kleinschmidt-Demasters BK. Proximal nerve
root capillary hemangioma presenting as a lung mass with bandlike chest pain: case report and review of literature. Surg Neurol
2006;65(6):584–589, discussion 589
Karikari IO, Selznick LA, Cummings TJ, George TM. Spinal capillary
hemangioma in infants: report of two cases and review of the
literature. Pediatr Neurosurg 2007;43(2):125–129
Nowak DA, Widenka DC. Spinal intradural capillary haemangioma: a review. Eur Spine J 2001;10(6):464–472
THIEME
Atypical Presentation of Temporal Dermoid
Cyst: Case Report
Apresentação atípica de cisto dermoide temporal: caso
clínico
Sérgio Gonçalves da Silva Neto1 Thiago Martins1 Leonardo Moura1
Wellingson Paiva2 Hector Navarro2 Manoel Jacobsen Teixeira3
1 Neurosurgery Resident Hospital das Clínicas, São Paulo Medical
School, Universidade de São Paulo (HC-FM-USP), São Paulo, SP, Brazil
2 Functional Neurosurgery Department, Psychiatry Institute, HC-FMUSP, São Paulo, SP, Brazil
3 Department of Neurosurgery, Universidade de São Paulo, São Paulo,
SP, Brazil
Clemar Correa2
Address for correspondence Sérgio Gonçalves da Silva Neto, MR, São
Paulo Medical School, Universidade de São Paulo (HC-FM-USP), São
Paulo, SP, Brazil (e-mail: [email protected]).
Abstract
Keywords
► dermoid cyst
► seizures
► brain tumor
Resumo
Palavras-chave
► cisto dermoide
► crise convulsiva
► tumor cerebral
Dermoid account for 0.04–0.06% of intracranial tumors. The rupture of these slowgrowing lesions are a rare event, generally taking place spontaneously. Their presentation are clinically variable according to cyst topography and integrity. Surgery remains
the first-line therapy and gross total resection should be attempted if feasible. We
report on a case of a 22-year-old male with a 2-year history of seizures and cognitive
impairment and a temporal mesial dermoid cyst successfully treated with gross total
resection microsurgery.
Os Cistos dermoides compreendem 0,04–0,06% dos tumores intracranianos. É uma
lesão de crescimento lento, e sua ruptura é um evento raro e espontâneo. A
variabilidade clínica vai de acordo com a topografia do cisto e sua integridade. A
cirurgia continua a ser a terapia de primeira linha, e a ressecção total é a opção sempre
que for possível. Os autores relatam um caso de paciente com 22 anos de idade com
histórico de 2 anos de convulsões e comprometimento cognitivo e diagnosticado com
um cisto dermoide mesial temporal, tratado com sucesso com ressecção
microcirúrgica.
Introduction
Dermoid and epidermoid cysts are benign that become
neurenteric cysts due to errors during gastrulation. In dermoid cysts, this occurs between the third and fifth week of
the embryonic period, with the inclusion of heterotopic
received
May 9, 2013
accepted
August 7, 2015
published online
October 13, 2015
10.1055/s-0035-1564693.
ISSN 0103-5355.
elements of the ectoderm during the closure of the neural
tube. Its contents include hair and hair follicles, sebaceous
glands and sweat.1,2 Dermoid cysts account for 0.04 to 0.06%
of intracranial tumors, with typical location in the midline of
the posterior fossa and predominance in females. These cysts
are sometimes associated to Klippel-Feil syndrome. In
317
318
Temporal Dermoid Cyst
Neto et al.
Fig. 1 BRAIN MRI, T1 weighted sequence with temporal lesion well
delineated, heterogeneous, predominance of increased signal.
Fig. 3 BRAIN MRI T1GD weighted sequence with low contrast
enhancement and evidence of a cystic content.
parallel with epidermoid cysts, dermoid cysts are more
frequently found as intracranial lesions than spinal lesions,
and usually as solid tumors, affecting adolescents and young
adults (mean age 15–16).1–3
the cyst causes the compression of surrounding structures,
when there is a rupture of the cyst (aseptic meningitis of
Mollaret), or when it is infected. Symptoms include headache, nausea, vomiting, cerebellar syndrome, cranial nerve
deficit, paresis, seizures, signs of meningism, and fever. These
vary with the topography of the lesion, presence of breakage
and/or infection of their contents.1,4,5
Upon physical examination, it is important to search for
dermal sinuses, which may be associated with underlying
dermoid cysts (e.g., dermal occipital sinus and cerebellar;
spinal dysraphism dermoid cyst and Spinalis dermoid cyst),
which, for being in contiguity, constitute a doorway for
infection and formation of abscesses in the cysts. Neuroimaging tests, especially the computed tomography (CT) scan
and magnetic resonance imaging (MRI) help in the diagnosis.
In a skull CT, dermoid cysts appear as very dense lesions
without iodized contrast uptake. In RNM, on the other hand,
they appear as heterogeneous lesions with hypersignal in
T1WI and T2WI. This is explained by their high cholesterol
content without contrast uptake in T1GD.1,5,6
When there is suspicion of rupture of the cyst and/or
meningism during physical examination, the specialist must
conduct the cerebrospinal fluid analysis. Mollaret’s aseptic
meningitis evolves with osteoblasts at 26% predominance of
lymphocytic and high protein concentration on CSF.1,5
Clinical Presentation and Diagnosis
The dermoid cyst is a slow-growing lesion, through the
exfoliation of epithelial cells and secretion of the sebaceous
glands. There seems to be a relationship between age and
growth and rupture, probably due to a hormonal mechanism
in adolescents.4 It is manifested clinically when the size of
Case Report
Fig. 2 BRAIN MRI RM T2 weighted sequence with temporal lesion well
delineated, heterogeneous, predominance of increased signal.
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No. 4/2015
C.A.P, male, 22 years old, previously healthy, from the state of
Bahia. Referred to Neurosurgery outpatients service/
HCFMUSP with a 2 years history of intermittent episodes
of partial seizures in the right upper limb and progressive
memory loss, culminating in December 2012 with generalized tonic-clonic seizures. General physical examination:
without notable changes neurological exam: alert and
Neto et al.
was submitted to surgery: left temporal craniotomy and
microscopic total tumor resections. During surgical planning,
the authors took into account the position of the left middle
cerebral artery (►Fig. 5). On the immediate post op the patient
evolved without any clinical or radiological complications (as
seen on ►Fig. 6). In the 4th post-operative, patient evolved
with symptoms of Meningitis, and after lumbar CSF analysis
was confirmed (pattern of aseptic meningitis), the patient
remained hospitalized for 14 days for antibiotic therapy. Discharged without complaints, during the 1st month follow-up
the patient denied new episodes of seizures.
The anatomical and pathological study of the surgical
piece confirmed dermoid cyst diagnosis.
Discussion
Fig. 4 BRAIN MRI DWI sequence with signs suggestive of rupture of
cystic content to the sub-arachnoid space.
oriented. No gait impairment, normal muscular strength,
sensitivity,
ocular
mobility,
normal
Funduscopic
examination.
Neuroimaging exams revealed a left temporal lesion suggestive of dermoid cyst (►Figs. 1–4). In June 2013, the patient
Until today, surgery aiming a total resection is still the most
appropriate conduct when facing a dermoid cyst, and should
always be attempted without rupturing the capsule to
reduce the chance of local recurrence or aseptic meningitis.
However, total resection is not always possible because these
lesions can be usually related with important neurovascular
structures.1,7
In the case in question, despite the atypical location,
characteristic neuroimaging examinations allowed bringing
the chance of dermoid cyst, corroborated by the anatomical
and pathological study. 1,7
Fig. 5 Surgical planning taking into account the displacement of the left middle cerebral artery and the surgical relation with the middle and
inferior temporal gyrus.
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320
Neto et al.
Fig. 6 Post operative brain CT.
References
4 Goyal N, Sharma MS, Gurjar H, Mahapatra AK. Multicentric
1 Hassaneen
W, Sawaya R. Epidermoid, dermoid and
neuro- enteric cysts.
In: Winn HR (ed). Youmans
neurological surgery. Philadelphia: Elsevier Saunders; 2011:
1523–1528
2 Xu XL, Li B, Sun XL, Li LQ, Ren RJ, Gao F. [Clinical and pathological
analysis of 2639 cases of eyelid tumors]. Zhonghua Yan Ke Za Zhi
2008;44(1):38–41
3 Miyagi Y, Suzuki SO, Iwaki T, Ishido K, Araki T, Kamikaseda K.
Magnetic resonance appearance of multiple intracranial epidermoid cysts: intrathecal seeding of the cysts? Case report. J Neurosurg 2000;92(4):711–714
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intracranial epidermoid or epi/dermoid cysts? Acta Neurochir
(Wien) 2012;154(7):1285–1286
5 Gumerlock MK. Epidermoid, dermoid, and neurenteric cysts in
youmans neurological surgery. 5th ed. Philadelphia: W.B.
Suanders; 2004:1223–30
6 Mehta MP, Chang SM, Vogelbaum MA, Guha A. Principles &
Practice of Neuro-Oncology: A Multidisciplinary Approach. Dermos Medical 2011:2880–2893
7 Park SK, Cho KG. Recurrent intracranial dermoid cyst after
subtotal removal of traumatic rupture. Clin Neurol Neurosurg
2012;114(4):421–424
THIEME
Giant Pseudoaneurysm as a delayed Surgical
Complication in a Patient Operated on a Giant
Neuroma of the Vagus Nerve: Case Report and
Management Considerations
Pseudoaneurisma gigante como complicação cirúrgica
em paciente operado com neuroma gigante do nervo
vago: relato de caso e considerações
Demian Manzano-Lopez1 Pablo Rubino2
Gerardo Conesa Bertran1
Pablo Mendivil Teran1
1 Neurosurgery Department, Hospital del Mar, Parc de Salut Mar,
Barcelona, Spain
2 Neurosurgery Department, Hospital El Cruce, Dr. Néstor Kirchner,
Buenos Aires, Argentina
Jesús Lafuente Baraza1
Address for correspondence Demian Manzano Lopez Gonzalez, MD,
Neurosurgery Department, Hospital del Mar, Parc de Salut Mar,
Passeig Maritim 23-25, Barcelona, Spain Zip: 08003
(e-mail: [email protected]; [email protected]).
Abstract
Keywords
► posterior fossa
approach
► pseudoaneurysm
► vertebral artery
► endovascular
treatement
Resumo
Palavras-chave
► acesso à fossa
posterior
► pseudoaneurisma
► artéria vertebral
► tratamento
endovascular
received
January 20, 2014
accepted
August 7, 2015
published online
October 28, 2015
The vertebral artery has four segments. The horizontal portion of the V3 segment is the
most exposed portion of the vertebral artery to potential iatrogenic injuries during
surgical approaches to the posterior fossa. We present an unusual case of a patient who
was operated on a giant neuroma of the left vagus nerve, with incidental vertebral
artery iatrogenic injury, the development of a delayed giant pseudoaneurysm, and the
treatment for this complication. We conclude that endovascular treatment may be a
good option for the management of this serious surgical complication.
A artéria vertebral tem quarto segmentos. A porção horizontal do segmento V3 é a
mais exposta a potenciais lesões iatrogênicas durante procedimento cirúrgico de
acesso à fossa posterior. Apresentamos caso incomum de paciente submetido à
cirurgia para neuroma gigante no nervo vago esquerdo, com acidental lesão da artéria
vertebral iatrogênica, desenvolvimento de posterior pseudoaneurisma gigante e
tratamento para esta complicação. Concluímos que o tratamento endovascular
pode ser uma boa opção para o cuidado desta grave complicação cirúrgica.
10.1055/s-0035-1564580.
ISSN 0103-5355.
321
322
Pseudoaneurysm as Delayed Complication in Vagus Nerve Neuroma Surgery
Introduction
Manzano-Lopez et al.
delayed giant pseudoaneurysm, and the treatment for this
complication.
The vertebral artery (VA) has four segments. Segment V1
runs from the vertebral artery origin to the C-6 transverse
process. Segment V2 is the portion of the artery that courses
through the C-6 to the C-2 transverse processes. Segment V3
runs from the C-2 transverse process to the entry in the dura
mater. The segment V4, which is the intradural portion of the
artery, ends in the confluence with the basilar artery.1–8
The V3 segment, or suboccipital segment, is in turn
divided into three parts. First, the vertical part runs between
the C-1 and C-2 transverse processes and contains the
proximal loop. The second is the horizontal part, formed
by the segment of the artery that courses in the groove of the
posterior arch of the atlas, and that contains the distal loop.
Third, there is the oblique part, which projects superomedially from C-1 and enters the dura mater.1–3,7
The horizontal part of the V3 segment is the most exposed
portion of the vertebral artery to potential iatrogenic injuries
during surgical approaches to the posterior fossa.3,7
We present an unusual case of a patient who was operated
on a giant neuroma of the left vagus nerve, with incidental
vertebral artery iatrogenic injury, the development of a
Case Report
A 34-year-old man with history of neurofibromatosis extending throughout the central and peripheral nervous
system had been operated on multiple spinal dorsal schwannomas that caused cord compression. He presented with
worsening of gait disturbance in a myelopathy context due to
his neurological history. Upon physical examination, the
stability of his myelopathy was verified and, instead, we
found an affectation of the 7th, 8th, 9th and 10th left cranial
nerves, together with a worsening of the previous gait
disturbance.
Upon cranial magnetic resonance (MR), two tumors were
found. Both were located bilaterally in the cerebellomedullary cisterns. The right tumor was small and of insignificant
size. The left tumor was very voluminous, with significant
brain stem compression, and with important extracranial
extension through the jugular foramen. We suspected the
tumors were lower cranial nerves neuromas, most probably
from the vagus nerve on the left side (►Fig. 1).
Fig. 1 Preoperative cranial MR. (A) Coronal view showing bilateral lower cranial nerves neuromas located at both cerebellomedullary cisterns.
The right one is very small and insignificant in size. On the other hand, the left tumor shows significant size and compression of the brain stem. (B)
Coronal view showing compression and distortion of the brain stem by the left vagus nerve neuroma. No hydrocephalus is apparent. (C) Coronal
view showing important extracranial extension of the left tumor through the jugular foramen. (D) Axial view showing the left tumor at the
cerebellomedullary cistern. The tumor is multilobulated and shows significant brain stem compression.
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Fig. 2 Postoperative studies. (A) Immediate postoperative Angio-CT scanner performed to rule out any complication on the vertebral artery
injured during surgery. No thrombosis, dissection, pseudoaneurysm, or any other complication develop in the immediate postoperative period.
Red arrow showing indemnity of the left vertebral artery at V3 portion. (B) Postoperative MR showing gross subtotal removal of the intracranial
portion of the left tumor. A very small portion of the tumor had to be left because of its adherences to the facial nerve and brain stem, when the
intraoperative neurophysiological potentials were affected. The procedure achieved satisfactory brain stem decompression and restoration of
normal anatomy. Histopathological findings confirm schwannoma. (C) Compact cellular pattern in Antoni A fiber areas (hematoxylin-eosin stain).
(D) Negativity for neurofilaments. (E) Positivity for S100 protein.
No new spinal tumors were found upon the spinal MR.
The patient underwent surgery to achieve brain stem
decompression.
We performed a lateral suboccipital retrosigmoid approach. Patient positioning was “park bench,” and intraoperative neurophysiological monitoring was set up.
During muscular dissection, the left vertebral artery was
accidentally injured in its third portion. The hemorrhage
was controlled with tamponade and hemostatic agents,
and the rest of the surgery was performed without incidents. We achieved a gross subtotal removal of the
intracranial tumor extension, obtaining satisfactory brain
stem decompression. A very little portion of the tumor
was left because of its adherences to the facial nerve and
the brain stem, when intraoperative neurophysiological
potentials were affected (left 7th cranial nerve and right
upper limb) (►Fig. 2B).
We employed an Angio-CT scanner in the immediate postoperatory period to rule out any complication of the injured
vertebral artery. We found no thrombosis, dissection, pseudoaneurysm, or any other complication. The CT-angiography
showed indemnity of both vertebral arteries (►Fig. 2A).
The postoperative course was favorable and the patient
recovered from the 7th and 8th cranial nerve affectation and
his gait disturbance diminished. On the other hand, the 9th
and 10th cranial nerves remained affected, and the patient
was sent to rehabilitation therapy.
The pathologist reported schwannoma, confirming the
presumptive diagnosis (►Figs. 2C, 2D, 2E).
Four weeks later, the patient developed a sudden painful
lump with important tension on the left retroauricular
region. A CT scanner showed a soft tissue hematoma
Fig. 3 A CT scanner four weeks after surgery showing a soft tissue
hematoma on the left retroauricular region as the patient develops a
sudden painful lump with important tension.
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324
Fig. 4 An angiogram demonstrates a giant pseudoaneurysm originating from the horizontal portion of the V3 segment of the left vertebral
artery. The pseudoaneurysm is 25 40 mm in size, and has a proximal and a distal lobule.
(►Fig. 3). An angiogram was made and it demonstrated a
giant pseudoaneurysm of the V3 portion of the left vertebral
artery (►Fig. 4). The pseudoaneurysm was treated by coil
embolization in the same act. The postembolization angiogram showed exclusion of the pseudoaneurysm and permeability of the vertebral artery (►Fig. 5).
The postoperative course was favorable and the lump
diminished in size and tension, no longer inflicting pain on
the patient.
Three months later, the patient no longer had the lump.
Two years later, the postoperative studies, MR-angiography, and Angiogram, still showed exclusion of the pseudoaneurysm and permeability of the vertebral artery (►Fig. 6).
Discussion
Although surgical injuries on the vertebral artery (SIVA) are
rare, they can lead to various different clinical outcomes. If
the initial hemorrhage is controlled well, the patient may
remain asymptomatic (especially if the injured vertebral
artery is not dominant or the patient has good intracranial
and
extracranial collateral circulation).9 On the other
hand, surgical injuries on the vertebral artery may also lead
to catastrophic consequences when they are associated with
serious complications, such as arteriovenous fistula, lateonset hemorrhage, pseudoaneurysm, thrombosis, embolism,
cerebral ischemia, and death.8,10–15
Once the injury occurs, the intraoperative treatment options
are: hemostatic tamponade/compression, microvascular repair
of the injured artery, and ligation of the vertebral artery.
Direct hemostatic tamponade/compression may be an
effective, quick, and easy measure. However, several cases
of delayed hemorrhage and arteriovenous fistula formation
have been reported.16,17 Microvascular primary repair restores normal blood flow and minimizes the risk of immediate or delayed ischemic complications.16,17 However, it is
technically demanding. Ligation of the vertebral artery is
associated with significant morbidity and mortality, such as
Fig. 5 Endovascular coil embolization of the pseudoaneurysm is performed. Only the proximal lobule of the pseudoaneurysm is treated. A
complete exclusion of the pseudoaneurysm is achieved and vertebral artery permeability is maintained. Immediately after the procedure the
patient is relieved from pain. Three months after the endovascular procedure, the patient no longer has the lump.
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surgery.20 In this situation, patients can be followed up with
MR-angiography or CT-angiography to evaluate the vessel
situation and exclude the possibility of a growing pseudoaneurysm formation.
Progressively, there has been greater introduction of
endovascular management, such as coil embolization,
stent-assist coil embolization, and the use of stent grafts or
covered stents.11,13,15,18 An ideal situation would be to be
able to rely on an intraoperative angiogram and an endovascular team for the immediate evaluation and treatment of
the SIVA. However, this is not the usually standard situation.
On a separate issue, considering that the horizontal
portion of the V3 segment of the vertebral artery is the
most exposed to potential injuries during surgical approaches to the posterior fossa, it is important to briefly
comment on patient positioning during the surgery to help
avoid this serious complication. Perhaps Neurosurgery is the
surgical specialty in which patient position is one of the most
critical aspects of the surgical act itself. The case we present
is a good example of this. Patient positioning can minimize
the risk of surgical injury to the horizontal portion of the V3
segment of the VA. It is important to open up the interval
between the artery and the occipital bone with adequate
neck flexion, head rotation, and dropping the vertex of the
head toward the floor. These maneuvers displace the superior surface of the horizontal portion of the V3 segment away
from the lower occiput, minimizing the risk of arterial
injury.3,6,21,22
Conclusion
Fig. 6 MR-Angiography two years after the embolization still shows
exclusion of the pseudoaneurysm and permeability of both vertebral
arteries. Arrows show the horizontal portion of the V3 segment of the
left vertebral artery where the pseudoaneurysm developed.
The horizontal portion of the V3 segment of the vertebral
artery is the most exposed to accidental surgical injuries
during surgical approaches to the posterior fossa.
Patient positioning is a matter of utmost importance in
preventing potentially fatal complications during this type of
surgery.
If intraoperative vertebral artery injury occurs, initial
control of bleeding may be obtained with hemostatic tamponade. However, there is a risk of developing a growing
pseudoaneurysm leading to possibly fatal bleeding. An angiogram or CT-angiography should be performed in such
cases, although if normal, these cannot rule out delayed
formation of pseudoaneurysm.
The endovascular treatment is a good option in the
management of this serious surgical complication.
References
Wallenberg’s syndrome, cerebellar infarction, cranial nerve
paresis, quadriparesis, and hemiplegia.12,18,19
Immediate angiogram is recommended after surgical
vertebral artery injury to detect vascular complications
and confirm adequate collateral circulation to the brain.
However, a normal angiogram after SIVA does not rule out
the subsequent formation of a pseudoaneurysm, and there
have been reports of rebleeding days and even years after
1 Aota Y, Honda A, Uesugi M, et al. Vertebral artery injury in C-1
lateral mass screw fixation. Case illustration. J Neurosurg Spine
2006;5(6):554
2 George B, Cornelius J. Vertebral artery: surgical anatomy. In:
Spetzler RF (ed): Operative Techniques in Neurosurgery. Philadelphia: WB Saunders; 2001:168–181
3 Ulm AJ, Quiroga M, Russo A, et al. Normal anatomical variations of
the V3 segment of the vertebral artery: surgical implications.
J Neurosurg Spine 2010;13(4):451–460
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4 Argenson C, Francke JP, Sylla S, Dintimille H, Papasian S, di Marino
14 Gluf WM, Schmidt MH, Apfelbaum RI. Atlantoaxial transarticular
V. The vertebral arteries (segments V1 and V2). Anat Clin 1980;
2:29–41
Francke JP, Dimarino V, Pannier M, Argenson C, Libersa C. The
vertebral arteries (arteria vertebralis): the V3 atlanto-axoidal
and V4 intracranial segments-collaterals. Anat Clin 1981;
2:229–242
George B. Exposure of the upper cervical vertebral artery. In:
Dickman CA, Spetzler RF, Sontag VKH (eds): Surgery of the
Craniovertebral Junction. New York: Thieme; 1998:545–567
Tubbs RS, Shah NA, Sullivan BP, Marchase ND, Cohen-Gadol AA.
Surgical anatomy and quantitation of the branches of the V2 and
V3 segments of the vertebral artery. Laboratory investigation.
J Neurosurg Spine 2009;11(1):84–87
Peng CW, Chou BT, Bendo JA, Spivak JM. Vertebral artery injury in
cervical spine surgery: anatomical considerations, management,
and preventive measures. Spine J 2009;9(1):70–76
Inamasu J, Guiot BH. Iatrogenic vertebral artery injury. Acta
Neurol Scand 2005;112(6):349–357
Prabhu VC, France JC, Voelker JL, Zoarski GH. Vertebral artery
pseudoaneurysm complicating posterior C1-2 transarticular
screw fixation: case report. Surg Neurol 2001;55(1):29–33, discussion 33–34
Cosgrove GR, Théron J. Vertebral arteriovenous fistula following
anterior cervical spine surgery. Report of two cases. J Neurosurg
1987;66(2):297–299
Shintani A, Zervas NT. Consequence of ligation of the vertebral
artery. J Neurosurg 1972;36(4):447–450
Daentzer D, Deinsberger W, Böker DK. Vertebral artery complications in anterior approaches to the cervical spine: report of two
cases and review of literature. Surg Neurol 2003;59(4):300–309,
discussion 309
screw fixation: a review of surgical indications, fusion rate,
complications, and lessons learned in 191 adult patients. J Neurosurg Spine 2005;2(2):155–163
Méndez JC, González-Llanos F. Endovascular treatment of a vertebral
artery pseudoaneurysm following posterior C1-C2 transarticular
screw fixation. Cardiovasc Intervent Radiol 2005;28(1):107–109
de los Reyes RA, Moser FG, Sachs DP, Boehm FH. Direct repair of an
extracranial vertebral artery pseudoaneurysm: case report and
review of the literature. Neurosurgery 1990;26(3):528–533
Neo M, Fujibayashi S, Miyata M, Takemoto M, Nakamura T.
Vertebral artery injury during cervical spine surgery: a survey
of more than 5600 operations. Spine 2008;33(7):779–785
Choi JW, Lee JK, Moon KS, et al. Endovascular embolization of
iatrogenic vertebral artery injury during anterior cervical spine
surgery: report of two cases and review of the literature. Spine
2006;31(23):E891–E894
Golueke P, Sclafani S, Phillips T, Goldstein A, Scalea T, Duncan A.
Vertebral artery injury—diagnosis and management. J Trauma
1987;27(8):856–865
Diaz-Daza O, Arraiza FJ, Barkley JM, Whigham CJ. Endovascular
therapy of traumatic vascular lesions of the head and neck.
Cardiovasc Intervent Radiol 2003;26(3):213–221
Bruneau M, George B. Foramen magnum meningiomas: detailed
surgical approaches and technical aspects at Lariboisière Hospital
and review of the literature. Neurosurg Rev 2008;31(1):19–32,
discussion 32–33
Kawashima M, Tanriover N, Rhoton AL Jr, Ulm AJ, Matsushima T.
Comparison of the far lateral and extreme lateral variants of the
atlanto-occipital transarticular approach to anterior extradural
lesions of the craniovertebral junction. Neurosurgery 2003;53(3):
662–674, discussion 674–675
5
6
7
8
9
10
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12
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THIEME
Síndrome do trefinado: relato de caso
Syndrome of Trephined: A Case Report
Augusto Santos1 Diego Oliveira da Mata2
Thiago Oliveira Lemos de Lima4
Rayane Toledo Simas2
1 Neurocirurgião do Hospital João XXIII, Belo Horizonte, MG, Brasil
2 Acadêmicos de Medicina da Faculdade Ciências Médicas de Minas
Gerais (CMMG), Belo Horizonte, MG, Brasil
Rodrigo Moreira Faleiro3
Address for correspondence Rayane Toledo Simas, MS 4y, Rua
Paineiras 1117, Eldorado, Contagem, MG, Brasil CEP: 32310-400
3 Chefe do Serviço de Neurocirurgia e Neurologia do Hospital João
XXIII e neurocirurgião do Hospital Felício Rocho, Belo Horizonte, MG,
Brasil
4 Médico Residente da Fundação Hospitalar do Estado de Minas Gerais
(FHEMIG), Belo Horizonte, MG, Brasil
Resumo
Palavras-Chave
► craniectomia
descompressiva
► traumatismos
encefálicos
► síndrome
Abstract
Keywords
► descompressive
craniectomy
► brain injuries
► syndrome
Síndrome do trefinado é atualmente uma complicação comum na neurotraumatologia,
sendo descrita como uma síndrome na qual ocorre deterioração neurológica acompanhada de sinais e sintomas após a remoção de uma parte considerável de osso do
crânio, assim como ocorre na hemicraniectomia. Neste artigo, juntamente com a
revisão de literatura, será relatado o caso de um paciente adulto, vítima de acidente
automobilístico, com história de traumatismo cranioencefálico (TCE) grave que foi
submetido à craniectomia terapêutica, cursando com a síndrome do trefinado.
“Syndrome of the Trephined” or “Sinking Skin Flap Syndrome” is an usual syndrome in
which neurological deterioration occurs following removal of a large skull bone flap (for
example, in descompressive craniectomy). In this article, we will report the case of a
24 years old male, victim of an automobile accident with severe traumatic brain injury
(TBI), which developed the Syndrome of the Trephined.
Introdução
Relato de Caso
Síndrome do trefinado (ST) é uma síndrome em que ocorre
deterioração neurológica após a remoção de uma parte
considerável do crânio.1,2 A ST é frequentemente não diagnosticada, e seus sintomas são melhorados após a cranioplastia. Conceitualmente, essa síndrome pode ser definida
como a conversão de uma caixa fechada (closed box) para
uma caixa aberta (open box).2
Assim, reportaremos o caso de um adulto jovem, vítima de
trauma automobilístico, submetido à craniectomia, seguido
de complicações da ST.
Paciente homem de 24 anos de idade, vítima de acidente
automobilístico em novembro de 2013, com história de
craniectomia bifrontotemporal devido a TCE grave. Evoluiu
bem, apresentando-se apenas confuso na alta hospitalar,
sendo programada cranioplastia eletiva posterior. Dois meses depois cursou com rebaixamento do sensório e abaulamento da área de craniectomia. Foi internado, e a tomografia
de crânio evidenciou hidrocefalia tetraventricular com transudação ependimária importante (►Fig. 1). Após exame de
líquor sem evidências de infecção, foi realizado implante de
received
November 10, 2013
accepted
August 7, 2015
published online
October 7, 2015
10.1055/s-0035-1564822.
ISSN 0103-5355.
327
328
Síndrome do trefinado
Santos et al.
Fig. 2 Pós-operatório de DVP.
paciente foi submetido à cranioplastia heteróloga bifrontal
com metilmetacrilato, em ato sem intercorrências, com
melhora do quadro.
Após 10 dias, o paciente evoluiu com rebaixamento de
sensório e formação de coleção sob a pele, levantando-se a
hipótese de disfunção de válvula. A tomografia de crânio
mostrou higroma subdural à direita e coleção hemorrágica à
esquerda, e optou-se por tratamento conservador. (►Fig. 4).
Poucos dias depois, o paciente apresentou drenagem de
secreção purulenta pela ferida operatória.
No exame físico, o paciente mostrava-se sonolento, despertando a estímulo doloroso e localizando a dor bilateralmente, com pupilas 3 þ /3 þ . Houve ainda deiscência da
ferida operatória com secreção purulenta de odor fétido,
Fig. 1 Hidrocefalia tetraventricular com transudação ependimária
importante.
derivação ventriculoperitoneal (DVP) (►Fig. 2). No pós-operatório, o paciente apresentava boa evolução, com escala de
coma de Glasgow (ECG) igual a 11. Porém, uma semana após
a DVP, ele cursou com piora neurológica importante, com
rebaixamento do sensório, ECG igual a 3, e depressão da
craniolacuna.
No entanto, apresentava razoável padrão respiratório em
ar ambiente, sugerindo-se a hipótese de síndrome do trefinado (►Fig. 3).
Dessa maneira, realizou-se cranioplastia externa (com
capacete de gesso), melhorando o quadro neurológico no
dia seguinte. Subsequentemente, o paciente foi submetido à
ligadura da DVP, com proposta de reabertura após cranioplastia, realizando-se apenas observação do quadro. Assim, o
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No. 4/2015
Fig. 3 Depressão de craniectomia bilateral.
Fig. 4 Higroma subdural à direita e coleção hemorrágica à esquerda.
sendo sugerida infecção em sítio de cranioplastia. A conduta
foi a retirada da cranioplastia, desbridamento do sítio da
cranioplastia, acompanhada de tratamento com antibiótico
(vancomicina e amicacina) e drenagem do empiema extradural. Além disso, houve a retirada da DVP e colocação de
derivação ventricular externa (DVE), a qual foi monitorada no
pós-operatório, necessitando de abertura constante durante
a evolução.
Após controle da infecção, o paciente foi submetido à DVP
de alta pressão à direita, com posterior retirada da DVE
parietal esquerda.
A evolução neurológica do paciente foi estável, com janela
da craniectomia abaulada, mas deprimível ou não tensa.
Referente ao quadro neurológico, o paciente apresentavase alerta, localizava dor e emitia sons incompreensíveis.
Atualmente, convive com quadro sequelar funcional
moderado.
Santos et al.
Além disso, desidratação prolongada e posição ortostática
podem precipitar esse fenômeno.7
A fisiopatologia alterada encontrada em um crânio convertido a partir de uma “caixa fechada” para uma “caixa
aberta” traz benefícios e riscos, como no caso relatado. Em
alguns pacientes que realizaram craniectomia, as forças da
pressão atmosférica e da gravidade sobrecarregam a pressão
intracraniana, consequentemente o cérebro parece afundado. Isto pode levar à hérnia de paradoxal e à síndrome
do trefinado, que é uma emergência neurológica.2,7–9
A craniectomia descompressiva é frequentemente realizada em caráter de urgência no cenário de pressões intracranianas incontroláveis a partir de uma variedade de causas.
Os relatos iniciais focam seu benefício na definição das
massas ou edema cerebral localizado. No entanto, as indicações estão se expandindo e agora incluem: lesão cerebral
traumática com pressões refratárias intracranianas, hematomas subdurais, inchaço cerebral por vasoespasmo após
hemorragia subaracnóidea, encefalite, sangramentos ou hematomas hipertensos intracerebrais, trombose venosa cerebral e acidentes vasculares encefálicos.2 No entanto, este
procedimento pode levar à síndrome do trefinado que deve
ser suspeita quando houver deterioração neurológica após
craniectomia, especialmente quando a pele do sítio de
craniectomia é afundada.10
De acordo com Shirley et al,11 outras complicações são:
!Complicações perioperatórias
• Expansão hemorrágica de contusões é inerente ao processo de lesão e tem sido demonstrada em tomografias
computadorizadas em pacientes com TCE.
• Craniectomia descompressiva para TCE pode levar a uma
nova lesão em massa, contralateral ou remota, para o
hemisfério descomprimido.
• Expansão do cérebro com hérnia cerebral externa através
do defeito da craniectomia é frequentemente observada
no início do período após a descompressão (►Fig. 5).
Discussão
Yamaura e Makina3 definiram a síndrome do trefinado como
alterações neurológicas que poderiam ser explicadas unicamente devido à concavidade do retalho de pele e à pressão da
atmosfera sobre o tecido cerebral subjacente.
Outros investigadores têm procurado explicar a fisiopatologia desse fenômeno. Uma teoria seria de que a pressão
atmosférica a ser transmitida diretamente para a cavidade
intracraniana deslocaria o couro cabeludo ao longo do sítio
de craniectomia para o interior.4
Recentemente, vários autores5,6 propuseram que um
gradiente negativo entre a pressão atmosférica e intracraniana, que é agravada por alterações no compartimento do
líquido cefalorraquidiano (LCR), seria o mecanismo de deterioração neurológica após craniectomia.
A drenagem do LCR em um paciente que sofre de hidrocefalia e meningite exacerba este efeito por meio da criação
de um gradiente de pressão através do sítio de craniectomia.
Fig. 5 Higroma subdural associado à herniação cerebral externa.
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Santos et al.
!Complicações pós-operatórias (dentro de 30 dias)
• Higromas subdurais: craniectomia altera a dinâmica da
circulação do LCR (►Fig. 5).
• Hérnia paradoxal, com compressão do tronco cerebral e
deterioração neurológica, pode apresentar-se de forma
atrasada após uma punção lombar em pacientes com a
craniectomia descompressiva.
efeito imediato ajuda na diminuição dos efeitos pressóricos
externos e na programação da cranioplastia definitiva.
Portanto, a cranioplastia deve ser realizada o mais precocemente possível, diminuindo as chances de complicações da
craniectomia descompressiva, tal como a síndrome do trefinado, melhorando a sobrevida do paciente e auxiliando na
recuperação dos danos neurológicos.
Conflitos de Interesse
Os autores declaram não haver conflitos de interesse.
!Complicações tardias, após 1 mês
• Hidrocefalia e síndrome do trefinado são as complicações
mais frequentes da craniectomia descompressiva após 1
mês. Além disso, foi identificada como fator de risco para
alterações no LCR e desenvolvimento de hidrocefalia póstraumática.
• Infecções.
• Na craniectomia descompressiva, a reabsorção de retalhos
ósseos livres é comum e pode aproximar-se de uma
incidência tão alta quanto 50% no acompanhamento a
longo prazo.
• Estado vegetativo persistente.
Referências
1 Joseph V, Reilly P. Syndrome of the trephined. J Neurosurg 2009;
111(4):650–652
2 Akins PT, Guppy KH. Sinking skin flaps, paradoxical herniation,
3
4
5
O objetivo do tratamento do paciente com a síndrome do
trefinado é a restauração da pressão exercida pela depressão
do sítio de craniectomia.7
Segal et al12 sugeriram que a cranioplastia melhora os
déficits neurológicos por uma diminuição da pressão intracraniana local e correção da dinâmica anormal do LCR. No
entanto, a cranioplastia para grave defeito no crânio pode
resultar em disfunção do cérebro subjacente, risco de formação de coleção líquida e de formação de hematoma no espaço
subdural, devido ao grande espaço morto.7 Os métodos
cirúrgicos seguros e eficazes para expandir a depressão no
couro e para eliminar o espaço morto no contexto do shunt
ventrículo-ponte são: oclusão temporária ou remoção do
dispositivo de derivação antes da cranioplastia.13
Fodstad et al14 propuseram que apenas sintomas aliviados
por cranioplastia devem ser incluídos na definição de síndrome do trefinado. Outros sintomas associados a esta
síndrome são: queixas subjetivas, hemiparesia, defeitos no
sensório, disfasia, convulsões, síndrome do mesencéfalo,
disfunção mesodiencefálica e mutismo acinético.
Conclusão
7
8
9
10
11
12
13
A compreensão aprofundada da síndrome do trefinado se
constitui relevante, uma vez que é uma das temíveis complicações da craniectomia descompressiva.
O tratamento da ST com a cranioplastia temporária (calota
de gesso externa) tem mostrado grandes resultados, e seu
6
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14
and external brain tamponade: a review of decompressive craniectomy management. Neurocrit Care 2008;9(2):269–276
Yamaura A, Makino H. Neurological deficits in the presence of the
sinking skin flap following decompressive craniectomy. Neurol
Med Chir (Tokyo) 1977;17(1 Pt 1):43–53
Langfitt TW. Increased intracranial pressure. Clin Neurosurg
1969;16:436–471
Oyelese AA, Steinberg GK, Huhn SL, Wijman CA. Paradoxical
cerebral herniation secondary to lumbar puncture after decompressive craniectomy for a large space-occupying hemispheric
stroke: case report. Neurosurgery 2005;57(3):E594, discussion
E594
Schwab S, Erbguth F, Aschoff A, Orberk E, Spranger M, Hacke W.
[“Paradoxical” herniation after decompressive trephining]. Nervenarzt 1998;69(10):896–900
Han PY, Kim JH, Kang HI, Kim JS. “Syndrome of the sinking skinflap” secondary to the ventriculoperitoneal shunt after craniectomy. J Korean Neurosurg Soc 2008;43(1):51–53
Romero FR, Zanini MA, Ducati LG, Gabarra RC. Sinking skin
flap syndrome with delayed dysautonomic syndrome-An
atypical presentation. Int J Surg Case Rep 2013;4(11):
1007–1009
Gadde J, Dross P, Spina M. Syndrome of the trephined (sinking skin
flap syndrome) with and without paradoxical herniation: a series
of case reports and review. Del Med J 2012;84(7):213–218
Chalouhi N, Teufack S, Fernando Gonzalez L, Rosenwasser RH,
Jabbour PM. An extreme case of the syndrome of the trephined
requiring the use of a novel titanium plate. Neurologist 2012;
18(6):423–425
Stiver SI. Complications of decompressive craniectomy for traumatic brain injury. Neurosurg Focus 2009;26(6):E7
Segal DH, Oppenheim JS, Murovic JA. Neurological recovery
after cranioplasty. Neurosurgery 1994;34(4):729–731, discussion 731
Liao CC, Kao MC. Cranioplasty for patients with severe depressed
skull bone defect after cerebrospinal fluid shunting. J Clin Neurosci 2002;9(5):553–555
Fodstad H, Love JA, Ekstedt J, Fridén H, Liliequist B. Effect of
cranioplasty on cerebrospinal fluid hydrodynamics in patients
with the syndrome of the trephined. Acta Neurochir (Wien) 1984;
70(1–2):21–30
THIEME
Traumatic Cervical Artery Dissection and
Ischemic Stroke: Anticoagulation or Antiplatelet
Therapy? The Controversies Remain
Dissecção traumática da artéria cervical e AVC
isquêmico: anticoagulação ou terapia antiplaquetária?
A polêmica continua
Leonardo Christiaan Welling1 Camila Mariana Fukuda2 Edek Francisco de Mattos da Luz2
Mariana Schumacher Welling2 Eberval Gadelha Figueiredo3
1 Neurosurgeon; Professor at Universidade Estadual de Ponta Grossa,
Ponta Grossa, PR, Brazil
2 Medical School Students at Universidade Estadual de Ponta Grossa,
Ponta Grossa, PR, Brazil
3 Neurosurgeon; Professor at Universidade de São Paulo, São Paulo,
SP, Brazil
Address for correspondence Leonardo Christiaan Welling, MD, Rua
Tiradentes, 976, Centro, Ponta Grossa, PR, Brazil CEP: 84010-190
Abstract
Keywords
► ischemia
► carotid artery
► dissection
Resumo
Palavras-chave
► isquemia
► carótida interna
► dissecação
received
November 10, 2013
accepted
August 7, 2015
published online
October 13, 2015
Arterial dissection of the wall of the carotid artery is a recognized and significant cause
of stroke. We described a 22-year-old man presented to the emergency department
after a motorcycle accident. He had a right acetabular fracture and had not complained
of other symptoms. A few minutes after being admitted, the patient developed left side
hemiparesis. Emergency brain magnetic resonance imaging (MRI) revealed an acute
ischemia in the left basal ganglia. Conventional angiography confirmed almost
complete occlusion of carotid artery lumen. We treated the patient with antiplatelet
therapy and he is currently followed at the outpatient clinic with good recovery of
motor symptoms. Early identification and management of cervical artery dissection is
important, as it is one of the major causes of ischemic stroke in young adults. Despite
previous published articles, the best treatment of carotid artery dissection, especially
after trauma, remains controversial.
Dissecação da parede da artéria carótida interna é uma causa reconhecida de acidente
vascular cerebral. Descrevemos um jovem de 22 anos admitido na emergência após
acidente motociclístico. Inicialmente foi diagnosticado somente fratura acetabular,
sem nenhuma outra queixa pelo paciente. Poucos minutos após admissão, o paciente
evoluiu com hemiparesia esquerda. Encaminhado a ressonância magnética do encéfalo
em caráter de urgência, identificou-se isquemia aguda nos gânglios da base à esquerda.
Angiografia convencional demonstrou oclusão quase completa da artéria carótida
interna. O caso foi tratado com terapia antiagregante plaquetária e atualmente o
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Traumatic Cervical Artery Dissection
Welling et al.
paciente está em acompanhamento ambulatorial com boa recuperação dos sintomas
motores. Como uma das maiores causas de acidente vascular cerebral isquêmico em
jovens, a identificação precoce e manejo da dissecação cervical é importante. A depeito
dos trabalhos previamente publicados, o melhor tratamento para a dissecação
carótidea, especialmente após trauma, permanece controversa.
Introduction
Case Report
Arterial dissection of the wall of the carotid artery causing
narrowing or occlusion of the arterial lumen or acting as a
source of emboli is a recognized and significant cause of
cerebral ischemia and stroke.1 Dissections may be precipitated
by neck or head movement and neck manipulation, including
bouts of violent coughing, sneezing, or sudden deceleration.2
Alternatively, they may result from significant trauma, including non-penetrating injury to the head and neck as well as
direct arterial injury.2 Although the clinical presentation of
traumatic cervical artery dissection (TCAD) can sometimes
appear benign in cases of isolated pain or Horner’s syndrome,
dissections are a major cause of ischemic stroke in young and
middle-aged adults. Therefore, early recognition and appropriate management of this disorder are of great importance.3
A 22-year-old man presented to the emergency department after a motorcycle accident. The patient had a right
acetabular fracture and no complaints of any other symptoms. A few minutes after being admitted, he developed
left side hemiparesis. Emergency magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) of
neck and brain revealed an acute ischemia in the left basal
ganglia (►Fig. 1). The wall hematoma resulted in almost
complete occlusion of the arterial lumen, as observed in
conventional angiography (►Fig. 2). He received treatment
with antiplatelet therapy and is currently undergoing
follow-up in the outpatient clinic with good recovery of
motor symptoms.
Fig. 1 Brain Magnetic resonance imaging (MRI) revealed an acute ischemia in left basal ganglia.
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Welling et al.
Fig. 2 Conventional angiography shows complete occlusion of the arterial lumen.
Discussion
The clinical presentation of cerebral ischemia caused by
TCAD does not differ from that of cerebral ischemia attributable to other factors. Nonetheless, the pathophysiology of
cervical artery dissection (CAD) remains poorly understood.
Some researchers have postulated that patients with CAD
could have a constitutional, at least in part, genetically
determined weakness of the vessel wall and that environmental factors, such as acute infection or minor trauma, act
as triggers.4
Traumas are important predisposing factors for CAD.
Traumatic cervical artery dissection can occur as a result
of major penetrating or non-penetrating traumas.5 In published works, CAD has been shown to occur in 1–2% of
patients who have had blunt trauma, and the risk is also
increased with trauma-associated injuries such as severe
facial fractures and skull-base fractures.1–5
Medical treatment and prevention strategies currently
rely solely on empirical data. Patients with cervical artery
dissection should be treated with antiplatelets or anticoagulants to prevent future cerebrovascular ischemic events.
The risk of early recurrence of stroke has led many clinicians
to advocate the use of anticoagulation from presentation
until 3 or 6 months after dissection. However, others believe
that antiplatelet drugs might be sufficient.6 Anticoagulants
might prevent embolism from a fresh thrombus; however,
they are also more hazardous than antiplatelet drugs and
may result in extension of the intramural hemorrhage, which
occurs in a third of patients, according to MRI.7
A Cochrane review found no completed randomized
trials comparing antiplatelet agents to anticoagulants. In
Fig. 3 Proposed diagnostic algorithm in trauma patients.
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Welling et al.
the 36 observational studies reviewed, there were no
differences in the odds of death or recurrence of ischemic
stroke, although there was a non-significant trend in favor
of anticoagulants for the death or disability outcome
(odds ratio, 1.77; 95% confidence interval, 0.98–3.22).
There was a 0.8% risk of symptomatic intracranial hemorrhage and 1.6% risk of major extracranial hemorrhage only
in the anticoagulant group. 8 In an effort to solve this
question, the Cervical Artery Dissection In Stroke Study
(CADISS) was established to compare the effectiveness of
antiplatelet drugs with anticoagulant drugs for the prevention of recurrent stroke in patients with carotid and
vertebral dissection. The results of this study shows that a
recurrent stroke at 3 months is rare, with no significant
difference between the two treatments. Although more
strokes occurred in the antiplatelet group than in the
anticoagulant group, this difference was counterbalanced
by one major subarachnoid hemorrhage in the anticoagulant group.9 It is important to emphasize that the risk of
recurrent events in this trial was lower than that reported
in some observational studies.9,10
All the previous studies include spontaneous and traumatic causes of carotid dissections. Schneidereit et al.
proposed a diagnostic algorithm and a choice of antithrombotic therapy that can be useful in trauma patients 11
(►Fig. 3).
best treatment of carotid artery dissection, especially after
trauma, remains controversial.
References
1 Rubinstein SM, Peerdeman SM, van Tulder MW, Riphagen I,
2
3
4
5
6
7
8
9
Conclusion
Early identification and management of cervical artery dissection is important, as it is one of the major causes of
ischemic stroke in young adults. Aside from trauma, several
environmental and genetic risk factors have been suggested
to underlie TCADs, but current evidence is limited to small
series. Despite the recently published trial, the CADISS, the
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10
11
Haldeman S. A systematic review of the risk factors for cervical
artery dissection. Stroke 2005;36(7):1575–1580
Redekop GJ. Extracranial carotid and vertebral artery dissection: a
review. Can J Neurol Sci 2008;35(2):146–152
Dziewas R, Konrad C, Dräger B, et al. Cervical artery dissection—
clinical features, risk factors, therapy and outcome in 126 patients. J Neurol 2003;250(10):1179–1184
Lee VH, Brown RD Jr, Mandrekar JN, Mokri B. Incidence and
outcome of cervical artery dissection: a population-based study.
Neurology 2006;67(10):1809–1812
Kim YK, Schulman S. Cervical artery dissection: pathology,
epidemiology and management. Thromb Res 2009;123(6):
810–821
Arauz A, Hoyos L, Espinoza C, Cantú C, Barinagarrementeria F,
Román G. Dissection of cervical arteries: Long-term follow-up
study of 130 consecutive cases. Cerebrovasc Dis 2006;22(2-3):
150–154
Beletsky V, Nadareishvili Z, Lynch J, Shuaib A, Woolfenden A,
Norris JW; Canadian Stroke Consortium. Cervical arterial dissection: time for a therapeutic trial? Stroke 2003;34(12):
2856–2860
Lyrer P, Engelter S. Antithrombotic drugs for carotid artery
dissection. Cochrane Database Syst Rev 2003;(3):CD000255
Markus HS, Hayter E, Levi C, Feldman A, Venables G, Norris J;
CADISS trial investigators. Antiplatelet treatment compared with
anticoagulation treatment for cervical artery dissection (CADISS):
a randomised trial. Lancet Neurol 2015;14(4):361–367
Georgiadis D, Arnold M, von Buedingen HC, et al. Aspirin vs
anticoagulation in carotid artery dissection: a study of 298
patients. Neurology 2009;72(21):1810–1815
Schneidereit NP, Simons R, Nicolaou S, et al. Utility of screening for
blunt vascular neck injuries with computed tomographic angiography. J Trauma 2006;60:209–215, discussion 215–216
THIEME
Criptococoma cerebral e pulmonar em paciente
imunocompetente: relato de caso
Cerebral and Pulmonary Cryptococcoma in an
Immunocompetent Pacient: Case Report
Caio Sander Andrade Portella Júnior1 Marcelle Rehem Machado2 Lucas Chaves Lelis2
Jefferson Fonseca Dias2 Luiz Eduardo Ribeiro Wanderley Filho3 Carlos Antonio Guimarães Bastos4
1 Neurocirurgião do Hospital Luis Eduardo Magalhães, Porto Seguro, BA, Brasil
2 Médico Residente em Neurocirurgia do Hospital São Rafael,
Salvador, BA, Brasil
3 Neurocirurgião do Hospital Regional de Irecê, Irecê, BA, Brasil
4 Neurocirurgião do Hospital Universitário Prof. Edgard Santos,
Address for correspondence Caio Sander Andrade Portella Junior, MR,
Departamento de Neurocirurgia, Hospital São Rafael, Av. São Rafael,
2152–São Marcos, Salvador, Bahia, Brasil CEP: 41253-190
Salvador, BA, Brasil
Resumo
Palavras-Chave
►
►
►
►
cérebro
infecção
criptococose
neurocirurgia
Abstract
Keywords
►
►
►
►
brain
infection
cryptococcosis
neurosurgery
received
July 18, 2014
accepted
August 7, 2015
published online
October 2, 2015
Neurocriptococose é uma infecção fúngica do sistema nervoso central e sua principal
apresentação clínica é a meningoencefalite. Lesões sólidas com aspecto tumoral,
denominadas criptococoma, podem manifestar-se principalmente em imunodeprimidos. É relatado caso de paciente jovem, imunocompetente, com lesão tumoral frontal
direita com grande efeito de massa e lesão menor em lobo occipital esquerdo, assim
como lesão tumoral em pulmão direito. A paciente e seus cuidadores concordaram e
autorizaram a publicação do caso. Foi feita revisão da literatura quanto à epidemiologia, tratamento e prognóstico. A paciente foi tratada com anfotericina B lipossomal e
submetida à ressecção cirúrgica das lesões cerebrais e pulmonar, em tempos distintos,
com bom desfecho clínico. A criptococose é infecção comum que pode acometer
indivíduos tanto imunocomprometidos quanto imunocompetentes. Embora a meningoencefalite seja a forma mais comum de acometimento do SNC, existem outras
formas mais raras como criptococoma cerebral. Há evidência de que a abordagem
cirúrgica das lesões expansivas é benéfica e recomendada.
Neurocryptococcosis is a fungal infection of the central nervous system and its major
clinical manifestation is meningoencephalitis. Solid tumor-like lesions, referred as
cryptococcoma, usually occurs in immunocompromised patients. This paper reports a
young immunocompetent female with a tumor-like lesion on the right frontal region
and another one on the left occipital lobe, as well as a tumor lesion on her right lung.
The patient and her caregivers have agreed and authorized the publishing of the case.
Literature review was made regarding the epidemiology, treatment and prognosis. The
patient was treated with anfotericine B and underwent surgical resection of the brain
and lung lesions, at different times, with good clinical outcome. C. neoformans is a
common fungal infection that can affect both immunocompetent and
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Portella Júnior et al.
immunocompromised individuals. Although meningoencephalitis is the most common
presentation of CNS involvement, there are other rarer forms such as cerebral
cryptococcoma. There is evidence that the surgical treatment of mass lesions is
beneficial and recommended.
Introdução
Criptococose é infecção sistêmica causada pelo fungo leveduriforme encapsulado Cryptococcus neoformans, que ocorre por
contato com solo contaminado com dejeções de aves. É a
infecção fúngica mais comum do sistema nervoso central
(SNC) e indivíduos imunocomprometidos são vulneráveis à
manifestação disseminada da doença.1 A apresentação clínica
mais comum da criptococose é a meningoencefalite, e granulomas do SNC são raros. Além disso, o indivíduo imunocompetente com meningite criptocócica pode não apresentar
sintomas clássicos como cefaleia e irritação meníngea.2 Neste
artigo, descrevemos o caso de uma paciente com criptococose
do SNC apresentando-se como lesão tumoral cerebral e
pulmonar.
Relato de Caso
Paciente do sexo feminino, procedente do interior da Bahia,
com relato de cefaleia em região frontal bilateral com predomínio do lado direito, pulsátil, de forte intensidade, persistente, associada a astenia, adinamia, perda de peso,
náuseas e vômitos, iniciada há cerca de 3 meses. Os sintomas
evoluíram com piora da frequência e intensidade. A paciente
apresentou paralisia do nervo craniano VI à esquerda, o que
motivou a realização de tomografia computadorizada do
crânio que mostrou lesão expansiva em região frontal direita
e occipital esquerda exercendo efeito de massa (►Fig. 1).
Admitida no serviço de neurocirurgia bastante emagrecida,
mantendo o quadro clínico e papiledema bilateral. Submetida à ressecção microcirúrgica para exérese da lesão frontal
direita em caráter de urgência. O exame anatomopatológico
evidenciou Cryptococcus neoformans (►Fig. 2). Foram reali-
zadas pesquisas para HIV e outras imunodeficiências, com
resultado negativo. A radiografia do tórax mostrou lesão
pulmonar à direita, sendo introduzida anfotericina B lipossomal por 3 meses. A paciente evoluiu sem apresentar
resposta clínica ou radiológica. Optou-se, então, por realizar
a exérese da lesão pulmonar e cerebral remanescentes. Após
os procedimentos cirúrgicos, em tempos distintos, a paciente
apresentou melhora clínica e resolução dos sinais e sintomas.
Discussão
Cryptococcus neoformans é organismo encapsulado de distribuição mundial encontrado nas fezes de aves e mamíferos.2 É um fungo oportunista que acomete o sistema nervoso
central principalmente em indivíduos com HIV ou outras
imunodeficiências.2 Os principais locais de infecção são
pulmões, SNC e doença disseminada.3 Caracteriza-se esta
última como a presença de C. neoformans no sangue, em
fluidos estéreis e tecidos outros que não o pulmonar.3 É a
infecção micótica mais comum do SNC, sendo a meningoencefalite sua principal forma de acometimento.4 Outra manifestação mais raramente encontrada é o criptococoma – um
pseudocisto encapsulado formado de substância gelatinosa,
que pode acometer o cérebro e espaço subaracnoideo.4,5
Acredita-se que tal acometimento se deva à disseminação
hematogênica pelo pulmão.4 Cefaleia é o sintoma mais
comum, mas pode apresentar também sinais meníngeos,
confusão mental, convulsão, alterações visuais e mais raramente déficits focais.2 Indivíduos imunocompetentes podem
não apresentar os sintomas clássicos de cefaleia e sinais
meníngeos, e ter achados mais incomuns.2 A pressão liquórica encontra-se frequentemente aumentada, e o líquor pode
Fig. 1 Tomografia computadorizada do crânio sem contraste evidenciando lesões hipodensas frontal à direita e occipital à esquerda.
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Criptococose cerebral e pulmonar
Portella Júnior et al.
Fig. 2 Lâmina de microscopia demonstrando presença de Cryptococcus neoformans. Aumento de 75X, coloração em hematoxilina eosina.
apresentar leucocitose leve a moderada com diminuição dos
níveis de glicose e elevação na proteinorraquia.4 Pacientes
infectados podem ainda ter testes antigênicos positivos no
sangue ou líquor.1,4 Este teste tem sensibilidade de 97% e
especificidade de 93-100% quando se trata de paciente com
criptococose disseminada, mas pode ser falso negativo no
criptococoma ou indivíduos imunocompetentes.6 A cultura
do líquor no meio ágar dextrose Sabouraud pode evidenciar o
crescimento de C. neoformans.3 A ressecção da lesão seguida
de anfotericina B lipossomal intravenosa por longa duração é
recomendada como tratamento do criptococoma do SNC.3
No caso relatado, a paciente recebeu o diagnóstico logo após
a ressecção cirúrgica pelo exame anatomopatológico, não
sendo necessária a realização de exames sorológicos.
Conclusão
Criptococoma é uma apresentação incomum da criptococose
cerebral, podendo acometer tanto imunodeficientes como
imunocompetentes e o tratamento clínico com antifúngicos
associado à ressecção cirúrgica é preconizado.
Referências
1 Patro SN, Kesavadas C, Thomas B, Kapilamoorthy TR, Gupta
2
3
4
5
6
AK. Uncommon presentation of intracranial cryptococcal
infection
mimicking
tuberculous
infection
in
two
immunocompetent patients. Singapore Med J 2009;50(4):
e133–e137
Saigal G, Post MJD, Lolayekar S, Murtaza A. Unusual presentation of central nervous system cryptococcal infection in an
immunocompetent patient. AJNR Am J Neuroradiol 2005;26(10):2522–2526
Taneja J, Bhargava A, Loomba P, Dogra V, Thakur A, Mishra B.
Cryptococcal granulomas in an immunocompromised HIVnegative patient. Indian J Pathol Microbiol 2008;51(4):
553–555
Caldemeyer KS, Mathews VP, Edwards-Brown MK, Smith RR.
Central nervous system cryptococcosis: parenchymal calcification and large gelatinous pseudocysts. AJNR Am J Neuroradiol
1997;18(1):107–109
Lizarazo-Nino J. Criptococosis del sistema nervioso central
en pacientes inmunocompetentes. Rev Neurol 2008;47(6):
335
Eric Searls D, Sico JJ, Bulent Omay S, Bannykh S, Kuohung V,
Baehring J. Unusual presentations of nervous system infection by
Cryptococcus neoformans. Clin Neurol Neurosurg 2009;111(7):
638–642
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THIEME
338
Technical Note | Nota Técnica
Cranioplastia externa para a síndrome do
trefinado – nota técnica
External Cranioplasty for the Syndrome of Trephined –
Technical Note
Rodrigo Moreira Faleiro1
Luiz Alberto Otoni Garcia2
1 Chefe do Serviço de Neurocirurgia e Neurologia do Hospital João
XXIII; Neurocirurgião do Hospital Felício Rocho, Belo Horizonte, MG,
Brasil
2 Residente em Neurocirurgia da Fundação Hospitalar do Estado de
Minas Gerais, Belo Horizonte, MG, Brasil
3 Acadêmica de Medicina da Universidade Federal de Minas Gerais,
Belo Horizonte, MG, Brasil
Luanna Rocha Vieira Martins3
Address for correspondence Rodrigo Moreira Faleiro, MD, Rua
Caraça, 518, apto 201, Serra, Belo Horizonte, MG, Brasil CEP: 30220260 (e-mail: [email protected]).
Resumo
Palavras-Chave
► craniectomia
descompressiva
► síndrome do
trefinado
► cranioplastia externa
Abstract
Keywords
► decompressive
craniectomy
► syndrome of
trephined
► external cranioplasty
received
November 10, 2013
accepted
August 7, 2015
published online
October 2, 2015
A craniectomia descompressiva (CD) é método cirúrgico amplamente utilizado para
tratar a hipertensão intracraniana. Entre as complicações decorrentes da CD, a
hidrocefalia é uma das mais frequentes, ocorrendo em até 30% dos casos. A
implantação de derivação liquórica, necessária em alguns casos de hidrocefalia, resulta
em agravamento da depressão do couro cabeludo, que ocorre após CD – síndrome do
trefinado (ST). A realização de cranioplastia convencional é inviável em algumas
situações, como ST com derivação liquórica, que não melhora após ligadura ou
aumento de pressão do sistema, ou ST com depressão acentuada do couro cabeludo.
Nestes casos, propomos uma nova técnica que foi aplicada em quatro casos e que
consiste na confecção de uma prótese temporária com material gessado ou polimetilmetacrilato para se eliminar o efeito da pressão atmosférica. Em todos os casos,
houve melhora da ST.
The decompressive craniectomy (DC) is a surgical method widely used to treat
intracranial hypertension. Among the complications of CD, hydrocephalus is one of
the most frequently occurring in up to 30% of cases. The implantation of CSF shunt,
required in some cases of hydrocephalus results in worsening of the scalp depression,
which occurs after CD – syndrome of trephined (ST). The performance of conventional
cranioplasty is impossible in some situations, such as ST with CSF shunt that does not
improve after ligation or increment of system pressure or ST with severe depression of
the scalp. In these cases, we propose a new technique that has been applied in four
cases and consists in molding a temporary prosthesis with cast material or polymethylmetacrilate to eliminate the effect of atmospheric pressure. In all cases, there was
improvement in ST.
10.1055/s-0035-1564823.
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Cranioplastia externa para a síndrome do trefinado
Introdução
A craniectomia descompressiva (CD) é método cirúrgico
amplamente utilizado para tratar a hipertensão intracraniana (HIC) após trauma cranioencefálico (TCE) ou doença
cerebrovascular. Consiste em craniectomia e ampliação da
dura-máter para se acomodar o cérebro tumefeito.
Faleiro et al.
A CD pode gerar complicações em aproximadamente 50%
dos casos. As complicações mais frequentes são expansão do
hematoma ou da contusão (6-58%); aparecimento de um novo
hematoma contralateral ao defeito ósseo (6-28%); epilepsia
(3-22%); herniação de tecido cerebral através do defeito ósseo
(15-51%); fístula liquórica (2-4%); infecção (4-16%); efusão
subdural (11-62%); reabsorção óssea (17%); hidrocefalia
Tabela 1 Variação da síndrome do trefinado
Paciente
Sexo
Idade
Etiologia
Hidrocefalia
DVP
Síndrome do trefinado – tempo
de surgimento
1. NLLF
Masculino
27
TCE
Sim
Sim
1 mês
2. CNL
Masculino
33
TCE
Sim
Sim
4,5 meses
3. PHRA
Masculino
18
TCE
Sim
Sim
3 meses
4. RMSN
Feminino
40
HSAE
Sim
Sim
1 mês
Fig. 1 Prótese externa temporária com material gessado ou com PMMA (40 gramas) utilizada para eliminar efeito da pressão atmosférica.
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Faleiro et al.
(8-29%) e síndrome do trefinado (1-13%). As duas últimas
ocorrem geralmente após um mês do procedimento.1–6
A hidrocefalia é uma complicação relativamente comum
após a realização de CD. Sua incidência difere de acordo com
o estudo analisado. Quando ocorre, pode ser necessária a
inserção de uma derivação liquórica, o que agrava a depressão do couro cabeludo que geralmente ocorre após a CD –
síndrome do trefinado (ST). Nestes casos, realiza-se cranioplastia no local da falha óssea com o propósito de eliminar o
efeito da pressão atmosférica e melhorar o estado neurológico do paciente.4
Em nosso serviço, percebeu-se que, em alguns casos, a
realização da cranioplastia convencional é inviável em
decorrência da presença de ST com derivação liquórica,
que não melhora após ligadura ou aumento da pressão do
sistema (no caso de válvula regulável), e ST sem derivação
liquórica e com depressão profunda do couro cabeludo.
Nestes casos, propomos uma nova técnica que consiste na
confecção de uma prótese externa com material gessado ou
com polimetilmetacrilato (PMMA) para se eliminar o efeito
da pressão atmosférica. A seguir, é relatada a série de casos
que envolvem as situações descritas, em que optamos pela
realização desta técnica, a que denominamos cranioplastia
externa.
Relato de Casos
Trata-se de descrição da técnica (cranioplastia externa) que
foi aplicada em quatro casos.
Fig. 2 Tomografia computadorizada realizada em até 72 horas.
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Quanto ao perfil epidemiológico dos pacientes analisados,
três eram do sexo masculino, e a faixa etária variava de 18 a
40 anos. Três pacientes eram vítimas de TCE e um possuía
hemorragia subaracnóidea decorrente de aneurisma cerebral. Na evolução do quadro, todos os pacientes foram
submetidos à CD, cursando com hidrocefalia. Em todos os
pacientes foi necessária a implantação de derivação liquórica
– derivação ventriculoperitoneal (DVP). A ST foi observada
em todos os casos, sendo que seu tempo de aparecimento
variou de um a quatro meses e meio. (►Tabela 1).
Em todos os pacientes, foi confeccionada uma prótese
externa temporária com material gessado ou com PMMA (40
gramas), que foi utilizada com o objetivo de eliminar o efeito
da pressão atmosférica. Na confecção da prótese, são utilizadas duas compressas para preencher a depressão da pele,
facilitando, assim, o molde de gesso ou PMMA. Tomografia
computadorizada realizada em até 72 horas evidenciou
melhora da ST (►Figs. 1 e 2). Esta prótese foi mantida até a
realização da cranioplastia convencional, com troca diária de
curativo. Não houve complicações diretamente relacionadas
à técnica ou ao material utilizado.
Discussão
A CD é uma técnica cirúrgica amplamente utilizada para o
tratamento da HIC secundária ao TCE ou a doenças cerebrovasculares. A CD pode resultar em inúmeras complicações,
sendo a hidrocefalia uma das mais frequentes, ocorrendo em
até 30% dos casos.
O líquor é um fluido aquoso e incolor que ocupa o espaço
subaracnóideo e as cavidades ventriculares e tem como
principal função a proteção mecânica do sistema nervoso
central. É formado nos plexos corioides e pelo epêndima das
paredes ventriculares. O volume total de líquor é de 100 a 150
cm3, renovando-se completamente a cada 8 horas. É absorvido nas granulações aracnóideas que se projetam no interior
dos seios da dura-máter, sendo predominante no seio sagital
superior. Para que esta absorção ocorra, deve haver uma
diferença pressórica entre o espaço subaracnóideo e os seios
da dura-máter. A pressão do líquor no espaço subaracnóideo
é em torno de 0-10mmHg no adulto, e a pressão dos seios
durais é negativa, refletindo a pressão da cavidade
torácica.6,7
Segundo Bateman et al, estados de hiperemia encefálica
cursam com aumento da pressão venosa, ou seja, da pressão
nos seios da dura-máter.8 Como a CD é realizada em casos de
brain swelling, ou seja, hiperemia encefálica, e sabidamente
causa uma queda abrupta da pressão subaracnóidea, temos a
possível explicação da formação da hidrocefalia após realização de CD.
Para tratar a hidrocefalia, deve ser implantada uma
derivação liquórica, que pode ser interna ou externa.
Este procedimento causa um aumento da depressão no
local da craniectomia como resultado do gradiente de
pressão atmosférica – ST. Dessa forma, deve-se tentar
aliviar o efeito da pressão atmosférica no local da craniectomia, o que pode ser feito com cranioplastia. Contudo, em
alguns casos, como já relatado, a realização da cranioplastia convencional é inviável em decorrência da presença de
ST com derivação liquórica, que não melhora após ligadura
do sistema ou aumento de pressão (no caso de válvula
Faleiro et al.
regulável), e ST sem derivação liquórica e com depressão
profunda do couro cabeludo. Outra situação seria a presença de ST com extensa necrose de pele. Para diminuir o
grau de depressão, optou-se, em nosso serviço, pela realização de cranioplastia externa com material gessado ou
polimetilmetacrilato, com bons resultados.
Referências
1 Yang XF, Wen L, Shen F, et al. Surgical complications secondary to
2
3
4
5
6
7
8
decompressive craniectomy in patients with a head injury: a
series of 108 consecutive cases. Acta Neurochir (Wien) 2008;
150(12):1241–1247, discussion 1248
Flint AC, Manley GT, Gean AD, Hemphill JC III, Rosenthal
G. Post-operative expansion of hemorrhagic contusions
after
unilateral
decompressive
hemicraniectomy
in
severe traumatic brain injury. J Neurotrauma 2008;25(5):
503–512
Ban SP, Son YJ, Yang HJ, Chung YS, Lee SH, Han DH. Analysis of
complications following decompressive craniectomy for
traumatic brain injury. J Korean Neurosurg Soc 2010;48(3):
244–250
Faleiro RM, Faleiro LC, Caetano E, et al. Decompressive craniotomy: prognostic factors and complications in 89 patients. Arq
Neuropsiquiatr 2008;66(2B):369–373
Honeybul S, Ho KM. Long-term complications of decompressive
craniectomy for head injury. J Neurotrauma 2011;28(6):
929–935
Honeybul S. Complications of decompressive craniectomy for
head injury. J Clin Neurosci 2010;17(4):430–435
Machado A, Haertel LM. Neuroanatomia funcional. 3. Ed. São
Paulo: Atheneu; 2006
Bateman G. Hyperemic hydrocephalus: a new form of childhood
hydrocephalus analogous to hyperemic intracranial hypertension
in adults. J Neurosurg Pediatr 2010;5(1):20–26
Vol. 34
No. 4/2015
341
THIEME
342
Letter to the Editor | Carta ao Editor
Hospital do Câncer de Barretos
Carlos Afonso Clara, MD, PhD1
1 Departamento de Neurocirurgia, Hospital de Câncer de Barretos,
Barretos, SP, Brasil
Arq Bras Neurocir 2015;34:342.
Prezado Editor-Chefe Dr. Eberval Gadelha Figueiredo,
Referente ao artigo publicado na revista Brazilian Neurosurgery (volume 34, número 2, 2015): Remote Cerebellar
Hemorrhage after Surgery for Spinal Column Tumor: An Unusual Cause of Impaired Consciousness.
Como é de seu conhecimento através do contato que
fizemos com a Sociedade Brasileira de Neurocirurgia
(SBN), o autor publicou um caso tratado no Hospital de
Câncer de Barretos (HCB) sem o conhecimento e autorização
da Instituição e do Departamento de Neurocirurgia. O projeto não foi avaliado ou aprovado pelo Comitê de Ética do
HCB. Não foi obtido termo de consentimento do paciente. O
received
July 24, 2015
accepted
August 18, 2015
published online
October 28, 2015
10.1055/s-0035-1564420.
ISSN 0103-5355.
Address for correspondence Carlos Afonso Clara, MD, PhD,
Departamento de Neurocirurgia, Hospital de Câncer de Barretos,
Avenida 27, n° 956, Barretos, SP, Brasil CEP: 14784-400
autor não é médico do HCB, foi estagiário como médico
observador por 90 dias em 2014. Os coautores também
não são médicos do HCB e consta que desconheciam o envio
da publicação. Acreditamos que houve um problema de
ordem ética. Já sabemos das providências que estão sendo
tomadas pela SBN e pela revista para solucionar esse caso.
Gratos pela atenção.
Carlos Afonso Clara, MD, PhD
Departamento de Neurocirurgia,
Hospital de Câncer de Barretos,
Barretos, SP, Brasil
THIEME
Retraction Notice | Retratação
Remote Cerebellar Hemorrhage after Surgery
for Spinal Column Tumor: An Unusual Cause of
Impaired Consciousness
Hemorragia cerebelar remota após cirurgia para tumor
da coluna vertebral: causa não habitual de
rebaixamento de consciência
Juliano Nery Navarro1
Telmo Augusto Barba Belsuzarri1
1 Department of Neurosurgery, Hospital Celso Pierro/PUC-Campinas,
Campinas, São Paulo, Brazil
João Flávio Mattos Araujo1
Address for correspondence Juliano Nery Navarro, MD, Rua Morgado
de Mateus, n° 314, Apartamento 31, São Paulo, SP, Brazil CEP: 04015-050
Arq Bras Neurocir 2015;34:343.
Retraction Notice
As author to the article Remote Cerebellar Hemorrhage after
surgery for spinal column tumor: an unusual cause of impaired
consciousness, published on Brazilian Neurosurgery, Volume
34, Number 2, hereby request its retraction for the mistakes on
editing authors list, as well as for other mistakes on its
translation, for the lack of informed consent from the patient,
for the lack of approval by the Ethics Committee of the Hospital
de Câncer de Barretos (HCB), and for not having the approval
from the neurosurgery department from HCB.
I would like to express my sincere apologies to Dr. Carlos A.
Clara and his entire Neurosurgery staff at Hospital de Câncer
de Barretos, to which I have admiration, respect and gratitude.
For these reasons, I humbly request the Editor of this
journal to retract/suspend the publication of this article.
Juliano Nery Navarro
Retratação
cause of impaired consciousness, publicado na revista
Arquivos Brasileiros de Neurocirurgia, volume 34, número
2, venho por meio deste documento me retratar em
relação aos erros por mim cometidos na edição dos autores
deste artigo e outros erros que ocorreram na tradução do
mesmo, pela falta do consentimento informado pelo paciente em relação à publicação do caso, pela falta da
aprovação do Comitê de Ética do Hospital de Câncer de
Barretos (HCB), bem como pela ausência de autorização da
publicação deste pelo departamento de neurocirurgia do
HCB.
Peço minhas sinceras desculpas pelo ocorrido ao Dr.
Carlos A. Clara e a toda equipe de Neurocirurgia do Hospital
de Câncer de Barretos, aos quais tenho muita admiração,
respeito e agradecimento.
Diante do exposto, solicito aos editores da revista o
imediato cancelamento/suspensão da publicação deste artigo.
Na qualidade de autor do artigo Remote Cerebellar Hemorrhage after surgery for spinal column tumor: an unusual
received
October 2, 2015
accepted
October 6, 2015
published online
October 28, 2015
10.1055/s-0035-1554900.
ISSN 0103-5355.
Juliano Nery Navarro
Copyright © 2015 by Thieme Medical
Publishers, 333 Seventh Avenue, New
York, NY 10001, USA.
343
ISSN 0103-5355
Instructions to Authors
Brazilian Neurosurgery (Arquivos Brasileiros
de Neurocirurgia), an official journal of the
Brazilian Society of Neurosurgery (Sociedade
Brasileira de Neurocirurgia) and Portuguese
Language Neurosurgery Society (Sociedades
de Neurocirurgia de Língua Portuguesa),
aims to publish scientific works in Neurosurgery and related fields, unpublished and exclusive. The journal publishes papers written in
Portuguese with abstracts in English or written
in English with Portuguese abstracts.
Submitted articles shall be placed as one of
the following categories:
• Original: result of clinical, epidemiological or
experimental research. Abstracts of theses
and dissertations.
• Review: review and update synthesis of specific themes, with critical analysis and conclusions. Databases and the period range
must be specified.
• Case Report: presentation, analysis and discussion of cases that present relevant interest.
• Technical Note: note on surgery techniques
and/or surgical instruments.
• Miscellaneous: neurosurgery history, professional practice, medical ethics and other
pertinent matters to the journal purpose.
• Letter to the Editor: critics and comments presented in a brief ethical and instructive manner about published content in this journal.
The copyright is safe to authors of the aimed
subject. Letters, when accepted, will be published with authors reply.
General standards for publishing
• Article files for publishing must be submitted to the Editor, via http://www.editorialmanager.com/bns/.
• All articles will be submitted to a double
blinded peer-review process.
• Only new unpublished manuscripts will be
acceptable. Submitted articles to Brazilian
Neurosurgery must not be fully or partially
submitted to any other journal.
• The editorial board may reject or suggest
changes in order to improve the clarity and
structure of the text and maintain uniformity with the journal policy.
• Copyrights of articles published in the
journal will belong exclusively to the
Brazilian Neurosurgery and Thieme
Publicações Ltda. The reproduction of
articles or illustrations without prior
consent is prohibited.
Standards for submission
Authors must send the following files:
1. Pub Letter (Word – Microsoft Office) stating the article has not yet been published
partially or fully or submitted concomitantly
to other journal.
2. Manuscript (Word – Microsoft Office).
Theses and dissertations
3. Figures (Tiff, Jpeg, Pdf, Indd) sent in separate
files with minimum resolution of 300 dpi.
Pimenta CAM. Aspectos culturais, afetivos e
terapêuticos relacionados à dor no câncer.
[thesis]. São Paulo: Escola de Enfermagem da
Universidade de São Paulo; 1995.
4. Tables, charts and graphics (Word – Microsoft Office) sent separately.
Standards for articles structure
Articles must be structured with all the following items and paginated accordingly:
1. Title page: article title both in Portuguese
and English; full name of all authors; academic or
professional degree of each author (maximum
of two degrees per author); institutions names
where the study took place; running title; corresponding author name, degree, full address,
e-mail and phone number.
2. Abstract: original articles need structured
abstract with 250 words at the most: objective, methods, results and conclusions; review
articles, case reports, technical notes and
miscellaneous need no structured abstract.
Following the abstract comes keywords (six at
the most), based on MeSH (Medical Subject
Headings), published in Medline and available
at: www.ncbi.nlm.nih.gov/mesh/.
3. Portuguese abstract: Portuguese version
of title, abstract and keywords based on DeCS
(Descritores em Ciências da Saúde, http://
decs.bvs.br).
4. Main text: introduction; casuistry or material and methods; results; discussion; conclusion; acknowledgments.
5. References: number references as they are
first cited in the text with Arabic numerals.
Use Vancouver style; list all authors until the
sixth, using et al. after the third when more
than six; when reference authors are cited in
the text cite the first and et al. for references
with more that two authors; unpublished data
or personal communication must be cited as
such between parentheses and cannot be listed as reference; use journal abbreviation from
Index Medicus; use the following examples:
Journal Article
Agner C, Misra M, Dujovny M, Kherli P, Alp
MS, Ausman JI. Experiência clínica com oximetria cerebral transcraniana. Arq Bras Neurocir
1997;16(1):77–85
Book Chapter
Peerless SJ, Hernesniemi JA, Drake CG. Surgical
management of terminal basilar and posterior
cerebral artery aneurysms. In: Schmideck HH,
Sweet WH, editors. Operative neurosurgical
techniques. 3rd ed. Philadelphia: WB Saunders;
1995:1071–86.
Book
Melzack R. The puzzle of pain. New York: Basic
Books Inc Publishers; 1973.
Annals and other congresso publications
Corrêa CF. Tratamento da dor oncológica. In:
Corrêa CF, Pimenta CAM, Shibata MK, editores.
Arquivos do 7º Congresso Brasileiro e Encontro
Internacional sobre Dor; 2005 outubro 19–22;
São Paulo, Brasil. São Paulo: Segmento Farma.
pp. 110–20.
Available Article in ahead of print
International Committee of Medial Journal
Editors. Uniform requirements for manuscripts
submitted to biomedical journals. Writing and
editing for biomedical publication. Updated
October 2007. Available at: http://www.icmje.
org. Access in: June 12, 2008.
6. Tables and charts: numbered by Arabic
numerals according to its citation in the text;
edited in double space, using separate sheets
per table/chart; title right above; note, abbreviations, legends must follow right under; introduce only essential tables and charts; files
must come separately.
8. Figures: digital formats (Tiff, Jpeg, Pdf,
Indd) with minimum resolution of 300 dpi
(trim 7.5 or 15 cm).
9. Legends and captions: numbered by Arabic numerals according to its citation in the
text; edited in double space, using separate files;
identify eventual labels present in the figure
(arrows, characters, lines etc.); image previously published must have publisher authorization and credits.
10. Other information: PDF proof will be
sent to corresponding authors for eventual
queries reply and/or approval limited by
72 hours due date; except measure units,
acronyms must be spelled out the first time
mentioned; commercial marks should be
avoided; no data or image that can identify
a patient can be used; studies using human
beings must follow ethical standards with
formal consent and approval of an Ethics
Committee from the institution of origin;
authors are the sole responsible for opinions
and concepts in the published articles, as well
as for the reference accuracy.
Secretariat: Rua Abílio Soares, 233, cj. 143,
Paraíso. 04005-001, São Paulo, SP, Brazil.
Phone: (+55 11) 3051-6075. Home page:
www.sbn.com.br. e-mail: arquivosbrasileiros@
sbn.com.br

Volume 34 - Número 4 - Sociedade Brasileira de Neurocirurgia

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