Background Among asymptomatic patients with severe carotid artery stenosis but no recent stroke or transient cerebral ischaemia, either carotid artery stenting (CAS) or carotid endarterectomy (CEA) can restore patency and reduce long-term stroke risks. However, from recent national registry data, each option causes about 1% procedural risk of disabling stroke or death. Comparison of their long-term protective effects requires large-scale randomised evidence.Methods ACST-2 is an international multicentre randomised trial of CAS versus CEA among asymptomatic patients with severe stenosis thought to require intervention, interpreted with all other relevant trials. Patients were eligible if they had severe unilateral or bilateral carotid artery stenosis and both doctor and patient agreed that a carotid procedure should be undertaken, but they were substantially uncertain which one to choose. Patients were randomly allocated to CAS or CEA and followed up at 1 month and then annually, for a mean 5 years. Procedural events were those within 30 days of the intervention. Intention-to-treat analyses are provided. Analyses including procedural hazards use tabular methods. Analyses and meta-analyses of non-procedural strokes use Kaplan-Meier and log-rank methods. The trial is registered with the ISRCTN registry, ISRCTN21144362.

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

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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.