The Impact of Post-Stroke Depressive Symptoms on Cognitive Performance in Women and in Men: A 4 Month Prospective Study.

Background: Depressive symptoms have been associated with cognitive impairment after stroke, and women may be specifically affected. Objective: The aim of this study was to investigate gender-specific characteristics in the relationship between changes in depression severity and changes in cognitive performance after stroke. Methods: We prospectively evaluated 73 patients without a previous history of depression in the first and fourth months after a first ischemic stroke. The severity of depressive symptoms was assessed using the 31-item version of the Hamilton Rating Scale for Depression, and executive function, attention, working memory, and verbal fluency were assessed using a neuropsychological battery. Results: We included 46 (63.0%) men and 27 (36.9%) women, with mean ages of 55.2 (SD ± 15.1) and 46.8 (SD ± 14.7) years, respectively. We found significant improvement in the digit span forward and Stroop dots from month 1 to month 4 post stroke for both men and women. Women, but not men, presented a correlation between changes in phonemic verbal fluency and changes in the 31-item version of the Hamilton Rating Scale for Depression scores. Improvement in depression was correlated with improvement in verbal fluency, and worsening in depression was correlated with worsening in verbal fluency. Conclusions: Our results suggest that women might be more vulnerable to the relationship between depressive symptoms and cognitive performance, and improvement of depression may be necessary for women's improvement in phonemic verbal fluency from the first to the fourth month after a stroke. We did not adjust the results for multiple comparisons. Thus, our findings might be considered preliminary, and confirmatory studies, also focusing on specific characteristics of women that could explain these differences, are warranted.

Primary angiitis of the central nervous system as a mimic of multiple sclerosis: A case report.

BACKGROUND: Primary angiitis of the central nervous system is a rare inflammatory vasculopathy and it is a difficult diagnosis to make because of its kaleidoscopic presentation and its multiple mimics, including multiple sclerosis. CASE PRESENTATION: A 21-year-old men presented a four-year history of progressive gait deterioration. Magnetic resonance imaging of the brain and spine showed hyperintense round-shaped lesions on T2 images, many with contrast enhancement, in supra/infratentorial and spinal segments. He received treatment for multiple sclerosis but presented clinical worsening, and follow-up neuroimaging showed persistent contrast enhancement lesions and a cerebellar hematoma. Brain biopsy was performed and demonstrated inflammatory infiltrations in blood vessels. The patient received 6 monthly schedules of 5 g methylprednisolone and 1 g cyclophosphamide with clinical stabilization. DISCUSSION: Our patient presented a primary angiitis central nervous system according to the Birnbaum and Hellmann proposed criteria. This case reinforces the importance of advancing the differential diagnosis of patients that present red flags in brain neuroimaging. CONCLUSION: The presence of the micro/macrobleeds and persistent contrast enhancing lesions should raise the suspicion of vasculitis in the differential diagnosis of multiple sclerosis.

Anticoagulation and Stroke.

In 2019, the American Heart Association did not recommend the emergent use of anticoagulation to prevent recurrence or progression of acute ischemic stroke. However, its indication in patients with extracranial artery intraluminal thrombus with artery-to-artery cerebral embolization must be analyzed. In this article, we will also discuss other indications of anticoagulation. This treatment could be indicated in patients with ischemic stroke caused by embolization from cervical artery dissection, catastrophic antiphospholipid antibodies syndrome (APS) and some cases of Covid 19. For secondary prevention, anticoagulation is recommended for Cardioembolic stroke such as nonvalvular atrial fibrillation and other cardiopathies, some patients with cervical artery dissection, stroke associated with cancer, and thrombophilia such as APS. The timing to restart anticoagulation after a large ischemic stroke or after a cerebral hemorrhagic transformation always represent a challenge. Even in patients with high risk of thromboembolism it should be delayed at least two weeks, ideal after four weeks.

Anticoagulation and Stroke / Anticoagulação e AVC

Abstract In 2019, the American Heart Association did not recommend the emergent use of anticoagulation to prevent recurrence or progression of acute ischemic stroke. However, its indication in patients with extracranial artery intraluminal thrombus with artery-to-artery cerebral embolization must be analyzed. In this article, we will also discuss other indications of anticoagulation. This treatment could be indicated in patients with ischemic stroke caused by embolization from cervical artery dissection, catastrophic antiphospholipid antibodies syndrome (APS) and some cases of Covid 19. For secondary prevention, anticoagulation is recommended for Cardioembolic stroke such as nonvalvular atrial fibrillation and other cardiopathies, some patients with cervical artery dissection, stroke associated with cancer, and thrombophilia such as APS. The timing to restart anticoagulation after a large ischemic stroke or after a cerebral hemorrhagic transformation always represent a challenge. Even in patients with high risk of thromboembolism it should be delayed at least two weeks, ideal after four weeks.

Resumo Anticoagulação na fase aguda do acidente vascular isquêmico (AVCI) ainda é um tema bastante controverso. Em 2019, a American Heart Association (AHA) não recomendou o uso precoce da anticoagulação para evitar a progressão ou recorrência de AVCIs de grandes artérias. Mas sugere que a anticoagulação em pacientes com AVCI por embolização a partir de trombos intraluminais aderidos a parede de vasos extracranianos fosse analisada. Tanto a antiagregação como anticoagulação são opções terapêuticas nos casos de AVCI por dissecção arterial cervical. Mas em pacientes com AVCI por mecanismo de embolização, a anticoagulação poderia ser indicada. Pacientes com AVCI e sindrome catastrófica por anticorpos antifosfolípides devem ser anticoagulados além de receber tratamento específico. Outra indicação seriam casos de trombofilia como Covid 19. Nesse artigo de revisão será discutida a prevenção secundária de AVCI em situações específicas (AVCI cardioembólico em pacientes com fibrilação atrial não valvular ou outras cardiopatias, AVCI em casos oncológicos, além de outras trombofilias), além do período ideal para se introduzir ou reiniciar a anticoagulação após transformação hemorrágica.

The association of post-stroke anhedonia with salivary cortisol levels and stroke lesion in hippocampal/parahippocampal region.

BACKGROUND: Anhedonia 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 METHODS: A 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. RESULTS: Patients 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. CONCLUSION: Our 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.

The influence of depressive symptoms on quality of life after stroke: a prospective study.

BACKGROUND: Poststroke depressive symptoms have prospectively predicted impairment of health-related quality of life (HRQOL). However, it is not known whether such predictive effect is independent of HRQOL at 1 month after stroke. This study aimed to investigate the impact of depressive symptoms at 1 and 3 months after stroke on the 3-month poststroke HRQOL and to investigate the influence of the HRQOL measured at 1 month after stroke on these relationships. METHODS: We prospectively evaluated 67 patients at 1 and 3 months after a first-ever ischemic stroke from 106 eligible patients who have been consecutively admitted to the neurology ward of a teaching hospital. A psychiatrist assessed the presence of depressive symptoms using the 31-item version of the Hamilton Rating Scale for Depression and the HRQOL was assessed with the 36-item Short-Form Health Survey from the Medical Outcomes Study. We used linear regression to measure the impact of depressive symptoms, HRQOL at 1 month, and potential confounders on HRQOL at 3 months. RESULTS: We found an association between depressive symptoms at 1 month and HRQOL at 3 months after the stroke; however, this association was not significant when adjusting for the 1 month poststroke HRQOL. Depressive symptoms at 3 months were associated with HRQOL at 3 months after stroke, independently of the poststroke HRQOL at 1 month and potential confounders. CONCLUSIONS: Current depressive symptoms at 3 months are important for HRQOL at 3 months after stroke; however, regarding the prospective prediction, HRQOL at 1 month is the most relevant factor.

Executive function and depressive symptoms of retardation in nonelderly stroke patients.

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.

Stroke lesion in cortical neural circuits and post-stroke incidence of major depressive episode: a 4-month prospective study.

OBJECTIVE: Little 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). METHODS: We 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. RESULTS: Twenty-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). CONCLUSIONS: Our 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 pathophysiology of depression.

Importance of retardation and fatigue/interest domains for the diagnosis of major depressive episode after stroke: a four months prospective study.

OBJECTIVE: Post-stroke major depressive episode is very frequent, but underdiagnosed. Researchers have investigated major depressive episode symptomatology, which may increase its detection. This study was developed to identify the depressive symptoms that better differentiate post-stroke patients with major depressive episode from those without major depressive episode. METHOD: We screened 260 consecutive ischemic stroke patients admitted to the neurology clinic of a university hospital. Seventy-three patients were eligible and prospectively evaluated. We assessed the diagnosis of major depressive episode using the Structured Clinical Interview for DSM-IV and the profile of depressive symptoms using the 31-item version of the Hamilton Depression Rating Scale. For data analysis we used cluster analyses and logistic regression equations. RESULTS: Twenty-one (28.8%) patients had a major depressive episode. The odds ratio of being diagnosed with major depressive episode was 3.86; (95% CI, 1.23-12.04) for an increase of one unit in the cluster composed by the domains of fatigue/interest and retardation, and 2.39 (95% CI, 1.21-4.71) for an increase of one unit in the cluster composed by the domains of cognitive, accessory and anxiety symptoms. The domains of eating/weight and insomnia did not contribute for the major depressive episode diagnosis. CONCLUSION: The domains of retardation and interest/fatigue are the most relevant for the diagnosis of major depressive episode after stroke.

Importance of retardation and fatigue/interest domains for the diagnosis of major depressive episode after stroke: a four months prospective study / Lentificação e fadiga/interesse no diagnóstico do episódio depressivo maior após o acidente vascular cerebral: um estudo prospectivo de quatro meses

OBJECTIVE: Post-stroke major depressive episode is very frequent, but underdiagnosed. Researchers have investigated major depressive episode symptomatology, which may increase its detection. This study was developed to identify the depressive symptoms that better differentiate post-stroke patients with major depressive episode from those without major depressive episode. METHOD: We screened 260 consecutive ischemic stroke patients admitted to the neurology clinic of a university hospital. Seventy-three patients were eligible and prospectively evaluated. We assessed the diagnosis of major depressive episode using the Structured Clinical Interview for DSM-IV and the profile of depressive symptoms using the 31-item version of the Hamilton Depression Rating Scale. For data analysis we used cluster analyses and logistic regression equations. RESULTS: Twenty-one (28.8 percent) patients had a major depressive episode. The odds ratio of being diagnosed with major depressive episode was 3.86; (95 percent CI, 1.23-12.04) for an increase of one unit in the cluster composed by the domains of fatigue/interest and retardation, and 2.39 (95 percent CI, 1.21-4.71) for an increase of one unit in the cluster composed by the domains of cognitive, accessory and anxiety symptoms. The domains of eating/weight and insomnia did not contribute for the major depressive episode diagnosis. CONCLUSION: The domains of retardation and interest/fatigue are the most relevant for the diagnosis of major depressive episode after stroke.

OBJETIVO: O episódio depressivo maior após acidente vascular cerebral é muito frequente, mas é subdiagnosticado. Pesquisas têm investigado a sintomatologia do episódio depressivo maior pós-acidente vascular cerebral, o que pode facilitar sua identificação. Este estudo foi desenvolvido para identificar os sintomas depressivos que melhor diferenciam pacientes com episódio depressivo maior daqueles sem episódio depressivo maior após o acidente vascular cerebral. MÉTODO: Foram triados consecutivamente 260 pacientes com acidente vascular cerebral admitidos à enfermaria de neurologia de um hospital universitário, dos quais 73 pacientes foram acompanhados. Para investigar o diagnóstico de episódio depressivo maior foi utilizada a Entrevista Clinica Estruturada para DSM-IV e para a sintomatologia depressiva a Escala de Avaliação para Depressão de Hamilton, versão 31 itens. Para a análise dos dados foi utilizada a análise de clusters e regressão logística. RESULTADOS: Vinte e um (28,8 por cento) pacientes tiveram episódio depressivo maior. O odds ratio para o diagnóstico de episódio depressivo maior foi 3,86; (95 por cento IC, 1,23-12,04) para um aumento de uma unidade no cluster dos domínios interesse/fadiga e lentificação, e 2,39 (95 por cento IC, 1,21-4,71) para um aumento de uma unidade no cluster de domínios de sintomas cognitivos, acessórios e ansiedade. Os domínios apetite/peso e insônia não contribuíram para o diagnóstico de episódio depressivo maior. CONCLUSÃO: Os domínios de lentificação e interesse/fadiga são os mais relevantes para o diagnóstico do episódio depressivo maior após acidente vascular cerebral.

[Poststroke depression: risk factors and antidepressant treatment]. / Depressão pós-AVC: fatores de risco e terapêutica antidepressiva.

Depression is the most frequent psychiatric complication among stroke survivors. Several aspects have been indicated as risk factors for its occurrence. This review investigates the risk factors and the state of the art of the treatment for poststroke depression, in order to stimulate its detection and adequate treatment by the physician. The point prevalence of Major Depression after stroke varies from 10% to 34%, varying according to differences among the research methods. The length of poststroke period, characteristics of the sample, type of treatment received by patients and diagnostic criteria used can influence the reported prevalence of poststroke depression. The risk factors that have been associated with the occurrence of poststroke depression, are: functional and cognitive impairment, previous history of depression and stroke, sex, age, hypercortisolism, poor social support and stroke neuroanatomic correlates. This one has supported the formulation of a pathophysiological mechanism for poststroke depression related with prefrontosubcortical circuits and neurotransmission of biogenic amines. The depression has a harmful impact on stroke prognosis. It can cause a more severe functional impairment, retardation of the rehabilitation process, outcome complications, and a higher mortality risk. In addition, poststroke depression has not been accurately diagnosed and treated. With the advantage of the magnetic resonance, researchers should focus investigations on the association of specific cerebral regions with the depressive manifestation and treatment response. Methodological issues such as previous history of depression and the type of the depressive manifestation should be considered for analysis.

Depressão pós-AVC: fatores de risco e terapêutica antidepressiva / Poststroke depression: risk factors and antidepressant treatment

A depressão é a complicação psiquiátrica mais freqüente 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 por cento a 34 por cento, 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