Occurrence Of Post-stroke Depression Research Articles

Diffusion Tensor Tractography Characteristics of White Matter Tracts are Associated with Post-Stroke Depression.

PurposeTo analyze the changes in white matter tracts in patients with post-stroke depression (PSD), and the correlation between these changes and the depressive state.Patients and MethodsThe numbers of white matter tracts and corresponding fractional anisotropy (FA) in the acute phase (the onset time <72 hours) were examined in each subject by diffusion tensor tractography (DTT). Diffusion tensor imaging (DTT), a new development of diffusion tensor imaging (DTI), enables visualization of white matter fiber tracts, which are thought to be closely related to the occurrence of PSD, According to the scores of Hamilton Depression Scale (HAMD) recorded at the 2nd week, 1st month, 3rd month, 6th month, and 12th month, forty patients were randomly selected and were classified into PSD group (n=20), non-depression post-stroke group (N-PSD, n=20), and control normal group (NORM, n=20), respectively. Correlations between the number of bundles (lines) in the white matter tract and corresponding FA, and HAMD score were finally assessed.Results1) FAs of the ipsilesional crossed corticocerebellar tract, the corticospinal tract, and the anterior thalamic radiation in PSD group were significantly lower than those in N-PSD and NORM groups (P<0.01); 2) Lines in the three areas in the PSD group were significantly lower than those in the N-PSD and NORM groups (P<0.01); and 3) FA and lines in the three areas of PSD patients were negatively correlated to HAMD scores (correlation coefficient=−0.586, −0.793, −0.626, −0.533, −0.642, and −0.524, respectively, all P<0.05).ConclusionFA and lines of the ipsilesional crossed corticocerebellar tract, the corticospinal tract, and the anterior thalamic radiation in PSD patients are significantly correlated to the depressive state. The crossed corticocerebellar tract, the corticospinal tract and the anterior thalamic radiation are involved in the development of PSD.

Differential Association of Serum BDNF With Poststroke Depression and Poststroke Anxiety

ObjectivesTo investigate the correlation between brain-derived neurotrophic factor (BDNF) and risk factors, as well as functional outcome in poststroke depression (PSD) or poststroke anxiety (PSA). DesignCohort study. SettingStroke patients admitted to an urban rehabilitation hospital. ParticipantsStroke patients (N=162) without any previous history of depression and anxiety. InterventionsNot applicable. Main Outcome MeasuresSociodemographic information and comorbidities were recorded during hospital admission. Functional outcomes were assessed using FIM scores at time of admission and discharge. The influence of various factors such as BDNF and patient characteristics on functional outcome was investigated. Single-factor effect was examined using simple logistic regression, as was multi-factor effect using multiple logistic regression. The goodness-of-fit of those regression models was evaluated by the integrated area under ROC curve. ResultsPSD was diagnosed in 61 (37.7%) patients, and PSA was diagnosed in 40 (24.7%). Multiple logistic analysis showed that BDNF, divorce or separation, and history of smoking were significantly associated with the occurrence of PSD but not with the occurrence of PSA. The model combining low BDNF level and divorce or separation improved the prediction for PSD. Among the variables analyzed for prediction of functional outcome, serum BDNF had a minimum correlation with motor FIM scores in PSD but no significant correlation with motor FIM scores in PSA. ConclusionsBDNF is a valuable prediction for the occurrence of PSD but not for PSA. More strikingly, ischemic stroke patients who are divorced or separated with low serum BDNF have a much higher risk for PSD. BDNF has a minimum correlation with motor function outcome in PSD but no significant correlation with motor outcome in PSA.

Predictive value of inflammatory indicators for post-stroke depression in patients with ischemic stroke

To investigate the association of venous blood neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) and levels of interleukin-17 (IL-17) and IL-6 at 2 weeks after admission with the occurrence of post-stroke depression (PSD) in patients with first-ever acute ischemic stroke. The hospitalized patients with first-ever acute ischemic stroke were recruited consecutively from the Department of Neurology of Yijishan Hospital from March, 2015 to September, 2017. The demographic and baseline clinical data on admission and the imaging data were collected. The diagnosis of PSD was established in line with DSM-IV (SCID-I-R) at 3 months during the follow-up. The severity of PSD was assessed using the Hamilton Depression Scale (HAMD-17). Multivariate logistic regression analysis was used to investigate the correlation of NLR, PLR, IL-17, and IL-6 with PSD in these patients. A total of 376 patients with acute ischemic stroke were enrolled, including 224 male patients (59.57%) and 152 female patients (40.43%), whose mean age was 61.37±10.34 years. Of these patients 104 (27.66%) were found to have PSD. Univariate analysis showed that gender, years of education, BMI, widowhood, NIHSS score, MMSE score, mRS score, and laboratory indexes (NLR, PLR, IL-17, and IL-6) were all significantly correlated with PSD (all P &lt; 0.05). Multivariate logistic regression analysis showed that, after adjusting for the compounding factors, the third quartile of NLR (P &lt; 0.001), the third quartile of PLR (P=0.002), IL-17 (P=0.025) and IL-6 (P=0.016) were independent factors that predicted the occurrence of PSD. Elevated NLR and PLR at admission and levels of IL-17 and IL-6 at 2 weeks after admission are all independent predictors of the occurrence of PSD at 3 months after stroke.

A Middle Cerebral Artery Occlusion Technique for Inducing Post-stroke Depression in Rats.

Post-stroke depression (PSD) is the most recurrent of all psychiatric complications resulting from an ischemic stroke. A greater majority (about 60%) of all ischemic stroke patients suffer from PSD, a disorder considered to be an ischemic stroke-related precursor for increased death and degradation in health. The pathophysiology of PSD is still obscure. To study the mechanism of development and occurrence of PSD further, and to find out a therapy, we attempted to develop a new protocol that requires occluding the middle cerebral artery (MCA) via the internal carotid artery (ICA) in rats. This protocol describes a model of PSD induced in rats through the middle cerebral artery occlusion (MCAO). Also used in the experiment are the Porsolt forced swim test and the sucrose preference test to confirm and evaluate the depressive mood of the rats under investigation. Rather than inserting the catheter through the external carotid artery (ECA), as stipulated for the original procedure, this MCAO technique has the monofilament passing directly through the ICA. This MCAO technique was developed a few years ago and leads to a reduction in mortality and variability. It is generally accepted that the criteria used are preferred in the selection of biological models. The data obtained with this protocol show that this model of MCAO could be a way of inducing PSD in rats and could potentially lead to the understanding of the pathophysiology and the future development of new drugs and other neuroprotective agents.

Chronic Unexpected Mild Stress Destroys Synaptic Plasticity of Neurons through a Glutamate Transporter, GLT-1, of Astrocytes in the Ischemic Stroke Rat.

Background and Objective Chronic unexpected mild stress (CUMS) destroys synaptic plasticity of hippocampal regenerated neurons that may be involved in the occurrence of poststroke depression. Astrocytes uptake glutamate at the synapse and provide metabolic support for neighboring neurons. Currently, we aim to investigate whether CUMS inhibits synaptic formation of regenerated neurons through a glutamate transporter, GLT-1, of astrocytes in the ischemic stroke rats. Method We exposed the ischemic stroke rats to ceftriaxone, during the CUMS intervention period to determine the effects of GLT-1 on glutamate circulation by immunofluorescence and mass spectrometry and its influences to synaptic plasticity by western blot and transmission electron microscopy. Result CUMS evidently reduced the level of astroglial GLT-1 in the hippocampus of the ischemic rats (p < 0.05), resulting in smaller amount of glutamate being transported into astrocytes surrounding synapses (p < 0.05), and then expression of synaptophysin was suppressed (p < 0.05) in hippocampal dentate gyrus. The ultrastructures of synapses in dentate gyrus were adversely influenced including decreased proportion of smile synapses, shortened thickness of postsynaptic density, reduced number of vesicles, and widened average distance of the synaptic cleft (all p < 0.05). Moreover, ceftriaxone can promote glutamate circulation and synaptic plasticity (all p < 0.05) by raising astroglial GLT-1 (p < 0.05) and then improve depressive behaviors of the CUMS-induced model rats (p < 0.05). Conclusion Our study shows that CUMS destroys synaptic plasticity of regenerated neurons in the hippocampus through a glutamate transporter, GLT-1, of astrocytes in the ischemic stroke rats. This may indicate one potential pathogenesis of poststroke depression.

Post-Stroke Depression at Teaching Hospital Center of Libreville

Introduction: Post-stroke depression occurs in a context of stroke characterized by sadness, loss of interest, feelings of guilt, loss of appetite, a feeling of tiredness, and a lack of concentration. Material and Methods: We conducted a descriptive cross-sectional study from January 1, 2013 to September 30, 2016. For the diagnosis of post-stroke depression, neuropsychological tests (DSM-IV and MADRS) were used. The collection approach was a maintenance survey followed by an examination. Results: From 153 stroke patients, 48.4% (n = 74) had post-stroke depression. Depressed mood was noted in 50.3% and 43.8% had a marked decrease in interest. 67.9% of these patients had a primary level of education. Widows had 4.2 times the risk of post-stroke depression, and married and retired patients were 3 times more likely than public servants. The occurrence of post-stroke depression was significantly related to the presence of motor deficit in our patients, p < 0.0001. Conclusion: These results suggest that the risk of developing depression after stroke increases with the motor deficit. The DSM-IV and MADRS scores remain neuropsychological examinations of choice for the diagnostic approach.

Genetic variations in the p11/tPA/BDNF pathway are associated with post stroke depression

BackgroundThe effects of BDNF on post stroke depression (PSD) may be influenced by genetic variations in intracellular signal transduction pathways, such as the p11/tPA/BDNF pathway. In this study, we aimed to determine the association of polymorphisms in candidate genes of the gene transduction pathway with PSD, as well as the effects of the interactions between genes in our Chinese sample. MethodsTwo-hundred-fifty-four Chinese samples with acute ischaemic stroke included 122 PSD patients and 132 nonPSD patients. Sixty-five single nucleotide polymorphisms (SNPs) in six genes (p11, tPA, PAI-1, BDNF, TrkB and p75NTR) of the p11/tPA/BDNF pathway with minor allele frequencies > 5% were successfully genotyped from an initial series of 76 SNPs. The severity of depressive symptoms was assessed by the 17-item Hamilton Depression Rating scale score. Environmental factors were measured with the life events scale and social support rating scale for all patients. SNP and haplotype associations were analysed using gPLINK software. Gene-gene interactions were evaluated with generalized multifactor dimensionality reduction software. ResultsThe results showed that TrkB polymorphisms (rs11140793AC genotype, rs7047042CG genotype, rs1221CT genotype, rs2277193TC genotype and rs2277192AG genotype) were significantly associated with PSD. Three haplotypes (AT, GG, and AAT) of TrkB were significantly associated with PSD. Seven haplotypes (GC, AG, ACG, CGC, GCT, ACGC and ACAT) of BDNF were significantly correlated with PSD. We identified significant gene-gene interactions between the p11 (rs11204922 SNP), tPA (rs8178895, rs2020918 SNPs) and BDNF (rs6265, rs2049046, rs16917271, rs727155 SNPs) genes in the PSD group. We also identified significant gene-gene interactions between the BDNF (rs2049046, rs7931247 SNPs) and TrkB (rs7816 SNP) genes with increased occurrence of PSD and sig gene-gene interactions between the BDNF gene (rs6265, rs56164415, rs2049046, rs4923468, rs2883187, rs16917271, rs1491850, rs727155, rs2049048 SNPs) and p75NTR gene (rs2072446, rs11466155) in the PSD group. ConclusionThese findings provides evidence that the TrkB gene, BDNF and TrkB haplotypes, and gene-gene interactions between p11, tPA and BDNF are all associated with PSD, which suggests that genetic variations in the p11/tPA/BDNF pathway may play a central role in regulating the underlying mechanism of PSD.

Risk Factors for Post-stroke Depression: A Meta-analysis.

Background: Stroke not only impacts patients physically but also economically. Post-stroke depression (PSD), as a common complication of stroke, always obstructs the process of stroke rehabilitation. Accordingly, defining the risk factors associated with PSD has extraordinary importance. Although there have been many studies investigating the risk factors for PSD, the results are inconsistent.Objectives: The objectives of this study were to identify the risk factors for PSD by evidence-based medicine.Data sources: A systematic and comprehensive database search was performed of PubMed, Medline, CENTRAL, EMBASE.com, the Cochrane library and Web of Science for Literature, covering publications from January 1, 1998 to November 19, 2016.Study Selection: Studies on risk factors for PSD were identified, according to inclusion and exclusion criteria. The risk of bias tool, described in the Cochrane Handbook version 5.1.0, was used to assess the quality of each study. Meta-analysis was performed using RevMan 5.3 software.Results: Thirty-six studies were included for review. A history of mental illness was the highest ranking modifiable risk factor; other risk factors for PSD were female gender, age (<70 years), neuroticism, family history, severity of stroke, and level of handicap. Social support was a protective factor for PSD.Conclusion: There are many factors that have effects on PSD. The severity of stroke is an important factor in the occurrence of PSD. Mental history is a possible predictor of PSD. Prevention of PSD requires social and family participation.

The related factors of post-stroke depression and nursing intervention in patients with motor aphasia

Objective To explore the related factors and nursing interventional methods of depression in patients with motor aphasia after stroke. Methods The Stroke Aphasic Depression Questionnaire-Hospital version (SADQ-H) was used to diagnose depression of 271 patients with motor aphasia after stroke. The association of post-stroke depression with social factors, vascular risk factors and stroke features were analyzed. The relationship between depression severity and aphasia severity were analyzed. A total of 166 patients with depression were divided into the control group and the observation group to carry out different nursing interventional methods. Results The incidence of post-stroke depression in patients with motor aphasia was 61.3% (166/271). The occurrence of post-stroke depression was correlated with female (χ2=5.580, P=0.02) , age less than 60 years old (χ2=4.390, P=0.04) , living alone (χ2=5.400, P=0.02) , recent negative events (χ2=4.420, P=0.04). The multi-factor Logistic regression analysis showed that the occurrence of post-stroke depression was independently associated with female (OR= 2.58, 95%CI 2.12-3.86, P < 0.01), age less than 60 years old (OR= 2.62, 95%CI 2.16-3.94, P < 0.01), living alone (OR= 2.59, 95%CI 2.13-3.92, P < 0.01). After 4 weeks of nursing intervention, there were significant differences in SADQ-H scores (t=2.94, P = 0.002) and distribution of Boston Diagnostic Aphasia Examination (BDAE) (χ2= 14.045, P=0.000) between the control group and the observation group. Conclusions Female, ages less than 60 years old, living alone are independent risk factors of post-stroke depression in motor aphasia patients. The degree of depression is associated with aphasia severity. The early nursing intervention can improve the depression status and promote recovery of the language function of patients with motor aphasia after stroke. Key words: Aphasia, broca; Stroke; Risk factors; Nursing care; Post-stroke depression

Estrogen therapy increases BDNF expression and improves post-stroke depression in ovariectomy-treated rats.

The present study investigated the effect of exogenous estrogen on post-stroke depression. Rats were exposed to chronic mild stress following middle cerebral artery occlusion. The occurrence of post-stroke depression was evaluated according to the changes in preference for sucrose and performance in a forced swimming test. Estrogen therapy significantly improved these neurological symptoms, indicating that estrogen is effective in treating post-stroke depression. Increased brain-derived neurotrophic factor (BDNF) expression was reported in the hippocampus of rats that had been treated with estrogen for two weeks, suggesting that BDNF expression may be an important contributor to the improvement of post-stroke depression that is observed following estrogen therapy.

Association of post stroke depression with social factors, insomnia, and neurological status in Chinese elderly population.

The purpose of this study was to investigate the association of post stroke depression (PSD) with social factors, insomnia, and neurological status among elderly Chinese patients with ischemic stroke. Six hundred and eight patients over 60years of age, who had suffered from a first episode of ischemic stroke within 7days, were enrolled into the study. They were divided into PSD and non-PSD groups according to the Self-rating Depression Scale (SDS) scores. The association of PSD with social factors, insomnia, and neurological status was analyzed using multivariable logistic regression analysis. Compared with the patients who did not develop PSD, those with PSD reported adverse life events more frequently, and more subjects with PSD lived alone, had left carotid artery infarction and cortical infarction (P<0.05), history of insomnia, and high National Institute of Health Stroke Scale (NIHSS) scores and low Barthel Index (BI) scores (P<0.01). The multivariable logistic regression analysis showed that the occurrence of PSD was associated with a history of insomnia (HR=1.59, 95% CI 1.12-2.36, P<0.01), NIHSS scores (HR=2.45, 95% CI 1.42-3.91, P<0.01) and BI scores (HR=2.56, 95% CI 1.39-4.25, P<0.01). Insomnia and the degree of neurological deficit were associated with PSD in an elderly population of Chinese people.

Serotonin system and post-stroke depression

Objective To investigate the effect of the 5-hydroxytryptamine (5-HT) on the occurrence, development of post-stroke depression (PSD). Methods The literatures on the relationship between 5-HT and PSD were selected from databases such as Wanfang Data , CNKI and PubMed before in 2010-2014. According to absorption and exclusion criteria of the literature, collect literatures, and summary, induce and analyze on them. Results Search 258 literatures and accept 44 literatures accorded with the criteria, including the relationship between 5-HT and PSD, the relationship between 5-hydroxytryptamine receptor (5-HTR) gene polymorphism and PSD, the relationship between 5-hydroxytryptamine transporter linked promoter region(5-HTTLPR) and PSD, and the treatment of selective serotonin reuptake inhibitors (SSRIs) in PSD. Conclusion Reduced levels of 5-HT lead to the occurrence of PSD, and they had a negative correlation; 5-HTR1A, 5-HTR2A are related genes of PSD; S allele and S/S genotype is susceptible factors of PSD, while the L allele is the protective factors of PSD; SSRIs can increase the level of 5-HT in the synaptic gap so as to improve the depressive symptoms of PSD. In the future, it is necessary to increase the sample size to confirm the relationship between 5-HT and PSD, and combine with other factors to explore the relationship between them. Key words: Serotonin; Post stroke depression; Gene polymorphism

Serotonin Transporter Gene 5-HTTLPR Polymorphism as a Protective Factor Against the Progression of Post-Stroke Depression.

Polymorphisms in the 5-HTT and BDNF genes are shown to affect their function at the molecular and serum level. Prior work has tried to correlate the polymorphisms with post-stroke depression (PSD), the results nevertheless remain indefinitive. A plausible reason accounting for the uncertainty relates to the small sample of each published trial. In this study, we have performed a comprehensive meta-analysis in order to evaluate the effects of 5-HTT and BDNF polymorphisms (5-HTTLPR, STin2 VNTR, 5-HTR2a 102 T/C, Val66Met) on genetic risk of PSD. Human case-control trials were identified by computer-assisted and manual searches. The article search was performed until October 2014. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using the fixed effects meta-analysis to measure the effects 5-HTT and BDNF polymorphisms exerted on PSD. We also performed test of heterogeneity, test of publication bias, and sensitivity analysis to examine the reliability and stability of combined effects. 5-HTTLPR was clearly associated with genetic risk of PSD. The association seemed to be more pronounced in the homozygous model (OR = 0.34, 95% CI = 0.23-0.51, P(Q-test) = 0.63). Both the heterozygous model and the recessive model showed 50% decreased risk of PSD (OR = 0.50, 95% CI = 0.37-0.67, P(Q-test) = 0.91; OR = 0.50, 95% CI = 0.36-0.70, P(Q-test) = 0.43, respectively). Such significant association was also detected for Caucasian and Asian. These results were reliable and stable based on related analyses. Taken together, 5-HTTLPR polymorphism of the 5-HTT gene seems to protect against the occurrence of PSD. Small sample size for the polymorphisms within 5-HTT and BDNF genes may have caused underestimated associations, and a larger study is required to further assess the relations.

Abstract W P132: Poststroke Depression After Intracerebral Hemorrhage At Young Age

Background and Purpose: Poststroke depression (PSD) is an important complication of stroke. We studied long-term PSD after intracerebral hemorrhage (ICH) at young age, as well as the quality of life of the survivors. Methods: We gathered clinical and imaging data on young ICH patients between age 16 and 49 treated in the Helsinki University Central Hospital between January 2000 and March 2010. The survivors were interviewed with structural questionnaires including Beck Depression Inventory II (BDI-II), Hospital Anxiety and Depression Scale (HADS), EuroQol (EQ-5D), Pain Anxiety Symptoms Scale (PASS-20), Brief Pain Inventory (BPI), and Montreal Congnitive Assessment (MOCA). Univariate analysis was performed to identify baseline factors associated with PSD (BDI-II score &gt; 13). Correlation between degree of disability measured by modified Rankin Scale score and PSD was analyzed. Results: Median follow-up time was 9.7 [7.0-12.0] years. PSD was present among 30 (23.1%) out of 130 patients included. Mild or moderate emotional distress was present in 47 (36.2%) patients (HADS score &gt; 7). Discomfort or pain was reported by 55 (42.3%) patients (measured by EQ-5D). Higher degree of disability was associated with symptoms of depression (higher BDI-II scores, p=0.001), and emotional distress (higher HADS scores, p=0.004). The only baseline factor identified to associate with PSD was hydrocephalus (p=0.014). Median PASS-20 score was 9 (IQR 0-25), median BPI score was 5 (0-23), and median MOCA score was 26 (22-28). Conclusions: One out of four survivors of ICH at young age suffers long-term PSD. Higher degree of disability predicted occurrence of PSD.

A Prospective Study of the Incidence and Correlated Factors of Post-Stroke Depression in China

BackgroundPost-stroke depression (PSD) is commonly observed among stroke survivors. However, statistical analysis of such data is scarce in developing countries. The purpose of this study is to examine the incidence of PSD and its relationship with stroke characteristics in China.MethodsThis was a prospective hospital-based study. Stroke patients were assessed within two weeks after acute ischemic stroke onset and then reevaluated at three months. Hamilton Depression Scale (HAMD) was used for screening depression (PSD). Subjects with HAMD score of ≥7 were further assessed with the World Health Organization Composite International Diagnostic Interview. Stroke severity was measured by the National Institutes of Health Stroke Scale (NIHSS). Stroke outcome was measured by the modified Rankin Scale (mRS).ResultsOne hundred and two stroke patients were recruited, only ninety-one patients completed del period (men = 53, 63.74%), with mean age 60.0±10.4 years (range, 34–82 years). The incidence of PSD was 27.47% two weeks after stroke. The occurrence of PSD was unrelated with age, stroke type, stroke lesion and the history of disease. In univariate analysis gender, PSD was correlated with female gender. In multivariate logistic regression analysis, poor stroke outcome (mRS≥3) (OR 12.113, CI 1.169 to 125.59, P<0.05) was the important predictors of PSD.ConclusionsThe study indicated that gender, functional dependence and stroke outcome are determinants of PSD occurrence during the first 2 weeks after stroke in China.

Analysis of ¹H-MRS in patients with depression after basal ganglia infarction

To investigate the metabolic changes on proton magnetic resonance spectroscopy (¹H-MRS) in patients with first left basal ganglia infarction and their relationship with depression. Twenty-two patients with first left basal ganglia infarction and 10 matched healthy controls were recruited in the study. Patients and controls underwent (1)H MRS scan and the spectrum of N-acetyl aspartic acid (NAA), choline (Cho) and creatinine (Cr) was recorded at the first week (D7) and 1 month after onset (M1), respectively. National Institutes of Health Stroke Scale (NIHSS), Ability of daily life (ADL), Hamilton Depression Scale (HAMD) were evaluated at D7, M1 and M6 after onset. The patients were classified into two groups: post-stroke depression (PSD) and non-post-stroke depression (NPSD) according to the result of HAMD.The differences of (1)H-MRS between these two groups were compared and their relationship with NIHSS and ADL was analyzed. Among 22 patients 10 were diagnosed as PSD and 12 were NPSD. Compared to controls, NAA/Cr was significantly lower and Cho/Cr was significantly higher (P <0.05)in left prefrontal white matter and left basal ganglia in patients with infarct. Patients with PSD showed a lower NAA/Cr and higher Cho/Cr than NPSD patients (P <0.05). At M1 after onset, NAA/Cr in the left prefrontal white matter was significantly correlated with NIHSS (r=-0.551, P =0.032), while Cho/Cr was correlated with ADL (r=0.682, P=0.005)in PSD patients. Metabolic changes shown on (1)H-MRS in patients with basal ganglia infarction may predict the occurrence of PSD.

Sociodemographic profile and social support for post-stroke depression in Kinshasa: A rehabilitation based cross-sectional study

The World Health Organization has highlighted the emergence of non-communicable chronic diseases, including stroke, in developing countries. As a cause of death, stroke ranks first in Africa. Stroke is the foremost cause of neuropsychiatric disease, including post-stroke depression (PSD) which is a very common disease. Surveys of this condition in Congolese pa tients are virtually non-existent. The objectives of this study were to assess the prevalence of PSD in Congolese patients and identify associated sociodemographic factors. Age, sex, address, province of origin, social and professional status, education, religion and consumption habits were chosen as indicators or parameters of interest to be examined in this study. The results of descriptive analyses are presented as frequencies for categorical variables and as mean ± standard deviation for quantitative variables. The association between different variables was assessed using tables of comparisons of proportions and the Chi-square test. Logistic regression was performed to predict the occurrence of PSD. There were more male than female patients. The mean age was 54.67 ± 12.51 years. Nearly 3 fourths of the patients were aged less than 65. The family was the primary source of social support. The majority was satisfied by the social support received from the family. Just over half the study patients (53.6%) had mild to severe depression as assessed by the PHQ9. Univariate analysis and logistic regression indicated a statistically significant association between low educational level and the occurrence of PSD. However, there was no relationship between age, sex or drinking habits and the onset of PSD. The majority of the subjects were satisfied by the social support from their families. Depression was common after stroke with the occurrence of 53.6%. These results highlight the need to investigate, diagnose and treat PSD, which is a risk factor for morbidity and mortality after stroke.

Neuropathological substrates and structural changes in late-life depression: the impact of vascular burden

A first episode of depression after 65 years of age has long been associated with both severe macrovascular and small microvascular pathology. Among the three more frequent forms of depression in old age, post-stroke depression has been associated with an abrupt damage of cortical circuits involved in monoamine production and mood regulation. Late-onset depression (LOD) in the absence of stroke has been related to lacunes and white matter lesions that invade both the neocortex and subcortical nuclei. Recurrent late-life depression is thought to induce neuronal loss in the hippocampal formation and white matter lesions that affect limbic pathways. Despite an impressive number of magnetic resonance imaging (MRI) studies in this field, the presence of a causal relationship between structural changes in the human brain and LOD is still controversial. The present article provides a critical overview of the contribution of neuropathology in post-stroke, late-onset, and late-life recurrent depression. Recent autopsy findings challenge the role of stroke location in the occurrence of post-stroke depression by pointing to the deleterious effect of subcortical lacunes. Despite the lines of evidences supporting the association between MRI-assessed white matter changes and mood dysregulation, lacunes, periventricular and deep white matter demyelination are all unrelated to the occurrence of LOD. In the same line, neuropathological data show that early-onset depression is not associated with an acceleration of aging-related neurodegenerative changes in the human brain. However, they also provide data in favor of the neurotoxic theory of depression by showing that neuronal loss occurs in the hippocampus of chronically depressed patients. These three paradigms are discussed in the light of the complex relationships between psychosocial determinants and biological vulnerability in affective disorders.

Serotonin Transporter Gene Polymorphism in Chinese Patients With Poststroke Depression

We sought to compare the distribution of the serotonin transporter gene SLC6A4 polymorphism between depressed and nondepressed poststroke patients. Patients with cerebral stroke admitted to hospital during a 1-year period were enrolled in a 1:1 case-control study. All cases and controls were genotyped for polymorphism of the serotonin transporter-linked promoter region and the single-nucleotide polymorphism rs25531. Among 367 patients with cerebral stroke, 57 (15.5%) were diagnosed with poststroke depression at 1 month after stroke. In the patients with poststroke depression, 7 genotypes of the serotonin transporter gene SLC6A4 were detected, and the frequency of S/S homozygotes was significantly higher (P=0.049) than that in controls. S/S homozygosity may be positively associated with the occurrence of poststroke depression in Chinese patients.

Differential Impact of Lacunes and Microvascular Lesions on Poststroke Depression

Previous studies have postulated that poststroke depression (PSD) might be related to cumulative vascular brain pathology rather than to the location and severity of a single macroinfarct. We performed a detailed analysis of all types of microvascular lesions and lacunes in 41 prospectively documented and consecutively autopsied stroke cases. Only cases with first-onset depression <2 years after stroke were considered as PSD in the present series. Diagnosis of depression was established prospectively using DSM-IV criteria for major depression. Neuropathological evaluation included bilateral semiquantitative assessment of microvascular ischemic pathology and lacunes; statistical analysis included Fisher exact test, Mann-Whitney U test, and regression models. Macroinfarct site was not related to the occurrence of PSD for any of the locations studied. Thalamic and basal ganglia lacunes occurred significantly more often in PSD cases. Higher lacune scores in basal ganglia, thalamus, and deep white matter were associated with an increased PSD risk. In contrast, microinfarct and diffuse or periventricular demyelination scores were not increased in PSD. The combined lacune score (thalamic plus basal ganglia plus deep white matter) explained 25% of the variability of PSD occurrence. The cumulative vascular burden resulting from chronic accumulation of lacunar infarcts within the thalamus, basal ganglia, and deep white matter may be more important than single infarcts in the prediction of PSD.