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.

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.

Association among depression, cognitive impairment and executive dysfunction after stroke / Associação entre depressão, comprometimento cognitivo e disfunção executiva após acidente vascular cerebral

The relationship between depression and cognitive impairment, frequent after stroke, is complex and has not been sufficiently elucidated. Objective: To review the relationship between post-stroke depression and cognitive impairment. Methods: We 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. Results: Six 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. Conclusion: Executive dysfunction and depression occur in stroke survivors, are frequently coexistent, and also associated with worse stroke prognosis. Healthcare professionals need to address andprovide adequate treatment for depression and executive dysfunctions in stroke patients early in the first three monthsafter stroke. Future studies should evaluate the efficacy of programs evaluating the early detection and treatment of PSD and executive dysfunction in stroke survivors.

A depressão e o déficit cognitivo são frequentes após o acidente vascular cerebral. A relação entre as duas condições é complexa e não tem sido suficientemente elucidada. Objetivo: Fazer uma revisão da relação entre a depressão pós-AVC e prejuízo cognitivo. Métodos: Foi realizada uma pesquisa no banco de dados PubMed nos últimos dez anos. Nosso foco foi estudos quantitativos originais que investigaram a relação entre depressão e comprometimento cognitivoem pacientes com AVC. Os termos depressão, disfunção cognitiva, comprometimento cognitivo e testes neuropsicológicos foram usados para pesquisa. Foram considerados artigos publicados em Inglês, Espanhol, Italiano e Português. Os critérios de seleção foram o uso de testes neuropsicológicos para avaliar a função cognitiva com também o uso de instrumentos para diagnosticar a depressão maior ou escalas para avaliar sintomas depressivos nos primeiros três meses após o AVC. Resultados: Seis estudos quantitativos originais preencheram os critérios de seleção. A prevalência de depressão pós-AVC nos primeiros três meses após o AVC variou de 22% a 31%. A incidência de depressão pós-AVC variou de 25% a27% e foi avaliada apenas em dois estudos. A depressão pós-AVC esteve associada com comprometimento cognitivo maisacentuado. Disfunção cognitiva pós-AVC foi relatada em 35,2% a 87% dos pacientes. Déficits cognitivos pós-AVC foramencontrados principalmente em função executiva, memória, linguagem e velocidade de processamento. Conclusão: Adisfunção executiva e a depressão ocorrem em pacientes de AVC, sendo frequentemente concomitantes e associadas a um pior prognóstico. Os profissionais de saúde devem diagnosticar e fornecer um tratamento adequado para a depressão e disfunção executiva nos primeiros três meses após o AVC. Mais estudos devem avaliar a efetividade de programas de detecção precoce e tratamento da depressão e disfunção executiva pós-AVC.

Association among depression, cognitive impairment and executive dysfunction after stroke.

The relationship between depression and cognitive impairment, frequent after stroke, is complex and has not been sufficiently elucidated. OBJECTIVE: To review the relationship between post-stroke depression and cognitive impairment. METHODS: We 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. RESULTS: Six 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. CONCLUSION: Executive 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.

A depressão e o déficit cognitivo são frequentes após o acidente vascular cerebral. A relação entre as duas condições é complexa e não tem sido suficientemente elucidada. OBJETIVO: Fazer uma revisão da relação entre a depressão pós-AVC e prejuízo cognitivo. MÉTODOS: Foi realizada uma pesquisa no banco de dados PubMed nos últimos dez anos. Nosso foco foi estudos quantitativos originais que investigaram a relação entre depressão e comprometimento cognitivo em pacientes com AVC. Os termos depressão, disfunção cognitiva, comprometimento cognitivo e testes neuropsicológicos foram usados para pesquisa. Foram considerados artigos publicados em Inglês, Espanhol, Italiano e Português. Os critérios de seleção foram o uso de testes neuropsicológicos para avaliar a função cognitiva com também o uso de instrumentos para diagnosticar a depressão maior ou escalas para avaliar sintomas depressivos nos primeiros três meses após o AVC. RESULTADOS: Seis estudos quantitativos originais preencheram os critérios de seleção. A prevalência de depressão pós-AVC nos primeiros três meses após o AVC variou de 22% a 31%. A incidência de depressão pós-AVC variou de 25% a 27% e foi avaliada apenas em dois estudos. A depressão pós-AVC esteve associada com comprometimento cognitivo mais acentuado. Disfunção cognitiva pós-AVC foi relatada em 35,2% a 87% dos pacientes. Déficits cognitivos pós-AVC foram encontrados principalmente em função executiva, memória, linguagem e velocidade de processamento. CONCLUSÃO: A disfunção executiva e a depressão ocorrem em pacientes de AVC, sendo frequentemente concomitantes e associadas a um pior prognóstico. Os profissionais de saúde devem diagnosticar e fornecer um tratamento adequado para a depressão e disfunção executiva nos primeiros três meses após o AVC. Mais estudos devem avaliar a efetividade de programas de detecção precoce e tratamento da depressão e disfunção executiva pós-AVC.

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.

Associação entre o episódio depressivo maior após acidente vascular cerebral isquêmico e comprometimento de circuitos neuronais pela lesão: um estudo prospectivo de 4 meses / Association between post-stroke major depressive episode and neural circuits affected by lesion: a four-month prospective study

INTRODUÇÃO: Alterações em circuito neural têm sido associadas com o transtorno depressivo maior. Entretanto, até o momento não se tem estudos investigando a associação entre a lesão do acidente vascular cerebral neste circuito e a incidência do episódio depressivo maior após o acidente vascular cerebral. Este estudo teve como objetivo principal investigar de modo prospectivo a associação entre o volume da lesão no circuito neural límbico-córtico-estriado-pálido-talâmico no hemisfério esquerdo e a incidência de episódio depressivo maior nos primeiros quatro meses posteriores ao acidente vascular cerebral isquêmico. Como objetivo secundário, visou investigar a associação entre o volume da lesão em regiões específicas do circuito e a incidência do episódio depressivo maior após o acidente vascular cerebral isquêmico. MÉTODOS: Neste estudo foram triados de modo consecutivo 326 pacientes admitidos na enfermaria de neurologia do Hospital das Clinicas de São Paulo. Destes, foram elegíveis 68 pacientes e foram acompanhados prospectivamente. A avaliação psiquiátrica consistiu na aplicação da entrevista clinica estruturada para diagnóstico pelo DSM-IV e no manual estruturado para entrevista da Escala de Hamilton para Depressão; o grau de comprometimento nas atividades de vida diária foi medido pelo Índice de Barthel; o grau de gravidade do acidente vascular cerebral foi mensurado pela escala para acidente vascular cerebral do National Institutes of Health e, a capacidade cognitiva foi avaliada pelo Miniexame do estado mental. As avaliações ocorreram em 3 momentos sendo a primeira em média 12,4 dias (+ 4,5) após o acidente vascular cerebral, a segunda em média 37 dias (+ 6) e, a terceira em média e 91,6 dias (+ 5,4) após o acidente vascular cerebral. As imagens por ressonância magnética foram realizadas dentro dos 15 dias posteriores ao acidente vascular cerebral em um aparelho de 1.5 Tesla (GE-Horizon LX) com protocolo específico. A localização do acidente...

BACKGROUND: Dysfunction in the neural circuit has been etiologically related to major depressive disorder. However no study has investigated the role of lesion in these circuits and post-stroke major depression. The objective of this study was to prospectively investigate the association between stroke volume in left limbiccortical- striatal-pallidal-thalamic neural circuit and incidence of major depressive episode after stroke, and secondary to investigate the association between stroke volume in specific areas of the neural circuit and the incidence of major depressive episode after stroke. METHODS: From 326 consecutively screened patients admitted in the neuroclinical unit of Clinics Hospital, São Paulo, 68 were eligible and followed. The Structured Clinical Interview for DSM-IV and Hamilton Depression Scale were applied in the psychiatry evaluations. The stroke severity was evaluated using the National Institutes of Health Stroke Scale and the activities of daily living limitations were measured using Barthel Index. Cognitive capacity was measured using Mini Mental State Examination. The evaluations were done in three timepoints the first in mean of 12.4 (+ 4.5) days after stroke, the second in 37 (+ 6) days and, the third, 91.6 (+ 5.4) days after stroke. Magnetic resonance scans were performed within 2 weeks after stroke in a 1.5 Tesla (GE-Horizon LX) scanner. Stroke localization and volume quantification were performed using a semi-automated method based on the Brodmann Cytoarchitectonic Atlas. The depressed and non depressed patients were compared. RESULTS: Twenty-one patients (31%) experienced a new onset of major depressive episode within a four-month period after stroke. No differences were found between depressed and non depressed patients regarding age, gender distribution, marital status, employment status, ischemic lesion hemispheric lateralization, stroke severity, level of limitations in activities of daily living and cognitive...

Depressão pós-AVC: aspectos psicológicos, neuropsicológicos, eixo HHA, correlato neuroanatômico e tratamento: [revisão] / Post-stroke depression: psychological, neuropsychological, HHA axis, localization of stroke aspects and treatment: [review]

CONTEXTO: 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 palavras-chave post-stroke depression, stroke, quality of life, hypercortisolism, cogntitive dysfunction e treatment. RESULTADOS: A prevalência de DPAVC é de 23 por cento a 60 por cento. 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.

BACKGROUND: 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 percent to 60 percent. 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 frequency and severity of PSD. DISCUSSION: Some programs can be used to assist the medical care researcher with these patients in diagnosis and treatment of PSD. The research needs to be continued with clear methodological protocols in order to understand the physiopathology related to the incident PSD.

[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