Luisa de Marillac Niro Terroni

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

Abstract 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.

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 ressonance, 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.

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.

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.

Depressão pós-AVC: aspectos psicológicos, neuropsicológicos, eixo HHA, correlato neuroanatômico e tratamento

CONTEXTO: A depressao pos-AVC (DPAVC) possui uma prevalencia elevada. Apesar disso, ela e pouco detectada e tratada. Muitos fatores de risco e repercussoes negativas na recuperacao dos pacientes estao associados a DPAVC. OBJETIVO: Revisar alguns aspectos da DPAVC como: qualidade de vida, prejuizos cognitivos, eixo HHA, localizacao do AVC e tratamento. METODOS: Pesquisa dos ultimos 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 prevalencia de DPAVC e de 23% a 60%. Ha poucos estudos sobre a incidencia de DPAVC. A DPAVC esta associada a pior prognostico e evolucao, agravo das disfuncoes cognitivas e reducao da qualidade de vida. O hipercortisolismo esta associado a DPAVC que ocorre tardiamente ao AVC. AVC em gânglios da base, regiao frontal esquerda e estruturas do circuito prefrontosubcortical esta relacionado a frequencia e a gravidade da DPAVC. CONCLUSOES: E necessario melhoria na metodologia dos estudos para maior esclarecimento sobre a fisiopatologia da incidencia da DPAVC. Programas objetivando o aumento das taxas de deteccao dos pacientes deprimidos se fazem necessarios inclusive para a reducao dos impactos negativos na recuperacao desses pacientes.

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.

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.

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.

Depression affecting moral judgment

Depressive mood can be involved in the moral judgments made by people with depression. Here, we focus on the negative judgments depressed patients have of themselves and the world. Possibly, the alterations in moral judgment in subjects with depression can be understood by taking into account the neural basis of depression.

Associação entre o episódio depressivo maior após acidente vascular cerebral isquêmico e comprometimento de circuitos neuronais pela lesão: um estudo prospectivo de 4 meses

INTRODUCAO: Alteracoes em circuito neural tem sido associadas com o transtorno depressivo maior. Entretanto, ate o momento nao se tem estudos investigando a associacao entre a lesao do acidente vascular cerebral neste circuito e a incidencia do episodio depressivo maior apos o acidente vascular cerebral. Este estudo teve como objetivo principal investigar de modo prospectivo a associacao entre o volume da lesao no circuito neural limbico-cortico-estriado-palido-talâmico no hemisferio esquerdo e a incidencia de episodio depressivo maior nos primeiros quatro meses posteriores ao acidente vascular cerebral isquemico. Como objetivo secundario, visou investigar a associacao entre o volume da lesao em regioes especificas do circuito e a incidencia do episodio depressivo maior apos o acidente vascular cerebral isquemico. METODOS: Neste estudo foram triados de modo consecutivo 326 pacientes admitidos na enfermaria de neurologia do Hospital das Clinicas de Sao Paulo. Destes, foram elegiveis 68 pacientes e foram acompanhados prospectivamente. A avaliacao psiquiatrica consistiu na aplicacao da entrevista clinica estruturada para diagnostico pelo DSM-IV e no manual estruturado para entrevista da Escala de Hamilton para Depressao; o grau de comprometimento nas atividades de vida diaria foi medido pelo Indice 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 avaliacoes ocorreram em 3 momentos sendo a primeira em media 12,4 dias (+ 4,5) apos o acidente vascular cerebral, a segunda em media 37 dias (+ 6) e, a terceira em media e 91,6 dias (+ 5,4) apos o acidente vascular cerebral. As imagens por ressonância magnetica foram realizadas dentro dos 15 dias posteriores ao acidente vascular cerebral em um aparelho de 1.5 Tesla (GE-Horizon LX) com protocolo especifico. A localizacao 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, Sao 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...