ObjectiveLittle is known about the relevance of lesion in neural circuits reported to be associated with major depressive disorder. We investigated the association between lesion stroke size in the limbic-cortical-striatal-pallidal-thalamic (LCSPT) circuit and incidence of major depressive episode (MDE).MethodsWe enrolled 68 patients with first-ever ischemic stroke and no history of major depressive disorder. Neurological and psychiatric examinations were performed at three time-points. We diagnosed major depressive episode, following DSM-IV criteria. Lesion location and volume were determined with magnetic resonance imaging, using a semi-automated method based on the Brodmann Cytoarchitectonic Atlas.ResultsTwenty-one patients (31%) experienced major depressive episode. Larger lesions in the left cortical regions of the LCSPT circuit (3,760 vs. 660 mm3; P = 0.004) were associated with higher incidence of MDE. Secondary analyses revealed that major depressive episode was associated with larger lesions in areas of the medial prefrontal cortex including the ventral (BA24) and dorsal anterior cingulate cortex (BA32) and subgenual cortex (BA25); and also the subiculum (BA28/36) and amygdala (BA34).ConclusionsOur findings indicate that depression due to stroke is aetiologically related to the disruption of the left LCSPT circuit and support the relevance of the medial prefrontal cortex dysfunction in the pafhophysiology of depression.

INTRODUÇÃOO acidente vascular cerebral (AVC) pode limitar de modo significativo o desempenho funcional, com conseqüências negativas nas relações pessoais, familiares, sociais e sobretudo na qualidade de vida. Essa limitação, entretanto, nem sempre se deve ao déficit neurológico em si. Complicações psiquiátricas têm sido indicadas como fatores determinantes da incapacitação do paciente após o AVC. Dentre as complicações psiquiátricas, a depressão é a mais prevalente e a que mais tem sido associada a um pior prognóstico.Conhecer a natureza desta depressão e seus fatores de risco torna-se essencial para aprimorar seu diagnóstico e tratamento.A participação de fatores psicológicos é difícil de ser questionada. Somente o impacto RESUMO -A depressão é a complicação psiquiátrica mais freqüen-te nos pacientes com acidente vascular cerebral (AVC). Vários aspectos têm sido detectados como fatores de risco para a sua ocorrência. Neste artigo faz-se uma revisão dos fatores envolvidos na depressão pós-AVC e o estado atual de seu tratamento, a fim de estimular sua detecção e adequado tratamento pelo médico não-psiquiatra.A prevalência da depressão maior pós-AVC é de 10% a 34%, variando conforme as diferenças dos métodos de pesquisa. O período do pós-AVC, o tipo de população avaliada e o tratamento recebido pelos pacientes, assim como o critério utilizado para o diagnóstico da depressão, podem influir a sua prevalência.Fatores de risco associados à ocorrência da depressão pós-AVC têm sido detectados, tais como: prejuízo funcional, prejuízo cognitivo, história de depressão no passado, idade, sexo, AVC prévio, hipercortisolemia, precária rede de suporte social e características neuroanatômicas do AVC. Estes têm fornecido suporte para formulação de um mecanismo fisiopatológico da depressão pós-AVC, relacionado às vias prefrontosubcortical e à neurotransmissão das aminas biogênicas.As repercussões da depressão são significativas, incorrendo em um maior grau de prejuízo funcional, retardo do processo de reabilitação, complicações na evolução e maior risco de mortalidade. A isto se soma o seu subdiagnóstico e subtratamento.Com o advento da ressonância magnética, pesquisadores devem investigar a associação de regiões cerebrais específicas com a manifestação depressiva e resposta terapêutica. Aspectos metodológicos devem ser levados em consideração para uma análise mais confiável.

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The relationship between depression and cognitive impairment, frequent after stroke, is complex and has not been sufficiently elucidated.ObjectiveTo review the relationship between post-stroke depression and cognitive impairment.MethodsWe performed a PubMed database search spanning the last ten years, using the terms post-stroke depression, cognitive dysfunction, cognitive impairment and neuropsychological tests. Our target studies were original quantitative studies that investigated the relationship between post-stroke depression (PSD) and cognitive impairment in stroke patients. Articles published in English, Spanish, Italian and Portuguese were considered. Selection criteria were the use of neuropsychological tests to assess cognitive function, and of either instruments to diagnose major depression, or scales to assess depressive symptoms, within the first three months after stroke.ResultsSix original quantitative studies fulfilled the criteria. The prevalence of PSD within the first three months after stroke ranged from 22% to 31%. Incidence ranged from 25% to 27% and was evaluated in only two studies. PSD was associated with increased cognitive impairment. Cognitive impairment was reported in 35.2% to 87% of the patients. Post-stroke cognitive deficits were reported mostly in executive function, memory, language, and speed of processing.ConclusionExecutive dysfunction and depression occur in stroke survivors, are frequently coexistent, and also associated with worse stroke prognosis. Healthcare professionals need to address and provide adequate treatment for depression and executive dysfunctions in stroke patients early in the first three months after stroke. Future studies should evaluate the efficacy of programs evaluating the early detection and treatment of PSD and executive dysfunction in stroke survivors.

The domains of retardation and interest/fatigue are the most relevant for the diagnosis of major depressive episode after stroke.

ResumoContexto: A depressão pós-AVC (DPAVC) possui uma prevalência elevada. Apesar disso, ela é pouco detectada e tratada. Muitos fatores de risco e repercussões negativas na recuperação dos pacientes estão associados à DPAVC. Objetivo: Revisar alguns aspectos da DPAVC como: qualidade de vida, prejuízos cognitivos, eixo HHA, localização do AVC e tratamento. Métodos: Pesquisa dos últimos 10 anos da base de dados MedLine/PubMed usando as palavraschave post-stroke depression, stroke, quality of life, hypercortisolism, cogntitive dysfunction e treatment. Resultados: A prevalência de DPAVC é de 23% a 60%. Há poucos estudos sobre a incidência de DPAVC. A DPAVC está associada a pior prognóstico e evolução, agravo das disfunções cognitivas e redução da qualidade de vida. O hipercortisolismo está associado à DPAVC que ocorre tardiamente ao AVC. AVC em gânglios da base, região frontal esquerda e estruturas do circuito prefrontosubcortical está relacionado à frequência e à gravidade da DPAVC. Conclusões: É necessário melhoria na metodologia dos estudos para maior esclarecimento sobre a fisiopatologia da incidência da DPAVC. Programas objetivando o aumento das taxas de detecção dos pacientes deprimidos se fazem necessários inclusive para a redução dos impactos negativos na recuperação desses pacientes.Terroni LMN, et al. / Rev Psiq Clín. 2009;36(3):100-8 Palavras-chave: depressão pós-AVC, acidente vascular cerebral, qualidade de vida, disfunção cognitiva, hipercortisolismo, tratamento. AbstractBackground: The prevalence of post-stroke depression (PSD) is elevated. Some risk factors and poor outcome have been associated with PSD. The treatment of PSD reduced the negative impact in patients recovery. Appart from these data the PSD has been under diagnosed and under treated. Objective: Review some aspects such as quality of life, cognitive dysfunction, hypercortisolism, stroke localization and treatment of PSD. Methods: MedLine/PubMed database search using the terms post-stroke depression, stroke, quality of life, hypercortisolism, cognitive dysfunction and treatment, published in MedLine in the last 10 years. Results: PSD has a high rate of prevalence, from 23% to 60%. Few incidence rates are investigated. PSD is associated with poor outcome, increase of cognitive dysfunction and reduced quality of life. The hypercortisolism seems to be associated with PSD in the latter period of stroke. Stroke in the left frontal region, basal ganglia and some structures of prefrontosubcortical circuits have been related with

The depression-executive dysfunction syndrome, a late-onset depression of vascular origin with executive dysfunction and psychomotor retardation, has also been described after stroke. We verified whether this syndrome also occurs in nonelderly stroke patients by investigating the association between domains of depressive symptoms with executive functions in 87 first-ever ischemic stroke patients. The retardation domain of the 31-item Hamilton Rating Scale for Depression was associated with decreased performance on verbal fluency (assessed with FAS). The association was maintained for younger patients (aged <60 years) after adjusting for confounders. This result supports the clinical presentation of depression-executive dysfunction syndrome in younger stroke patients. Confirmation of this finding, its neural correlates, and clinical implication deserve further investigation.

BackgroundAnhedonia constitutes a coherent construct, with neural correlates and negative clinical impact, independent of depression. However, little is known about the neural correlates of anhedonia in stroke patients. In this study, we investigated the association of post-stroke anhedonia with salivary cortisol levels and stroke location and volume.Patients and methodsA psychiatrist administered the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition to identify anhedonia in 36 inpatients, without previous depression, consecutively admitted in a neurology clinic in the first month after a first-ever ischemic stroke. Salivary cortisol levels were assessed in the morning, evening, and after a dexamethasone suppression test. We used magnetic resonance imaging and a semi-automated brain morphometry method to assess stroke location, and the MRIcro program according to the Brodmann Map to calculate the lesion volume.ResultsPatients with anhedonia had significantly larger diurnal variation (P-value =0.017) and higher morning levels of salivary cortisol (1,671.9±604.0 ng/dL versus 1,103.9±821.9 ng/dL; P-value =0.022), and greater stroke lesions in the parahippocampal gyrus (Brodmann area 36) compared to those without anhedonia (10.14 voxels; standard deviation ±17.72 versus 0.86 voxels; standard deviation ±4.64; P-value =0.027). The volume of lesion in the parahippocampal gyrus (Brodmann area 36) was associated with diurnal variation of salivary cortisol levels (rho=0.845; P-value =0.034) only in anhedonic patients.ConclusionOur findings suggest that anhedonia in stroke patients is associated with the volume of stroke lesion in the parahippocampal gyrus and with dysfunction of the hypothalamic–pituitary–adrenal axis.