Early-onset Post-stroke Depression Research Articles

Lesion location and serum levels of homocysteine are associated with early-onset post-stroke depression in acute ischemic stroke.

It is well known that post-stroke depression (PSD) is a psychiatric complication after stroke which leads to worse functional outcome and poorer quality of life. Some risk factors including gender, stroke severity, lesion location, homocysteine (HCY), and so on are associated with PSD. This study aims to further explore the possible relationship between serum levels of HCY and early-onset PSD and the predictive value of HCY combined with stroke characteristics for early-onset PSD. Two hundred forty-five patients with acute ischemic stroke who met the criteria were included in this study from March 2015 to March 2017. PSD was diagnosed at 2weeks after stroke. The severity of depressive symptoms was evaluated with the Hamilton depression scale 17 items (HAMD-17), and patients with HAMD scores ≥7 were included in the PSD group. The demographic data, clinical characteristics, serum levels of HCY, and detailed radiological variables (e.g., lesion location and quantity of the brain infarct) were also examined. In total, 97 (39.6%) patients of the 245 patients were diagnosed with depression. The univariate analyses suggested that patients in PSD group had a higher NIHSS score, modified Rankin Scale score, and HCY levels than patients in non-PSD group (p < .001). The patients with PSD had higher proportion of multiple-site acute infarcts and frontal lobe lesion (p < .05). In multivariate logistic regression analysis, NIHSS score at admission, serum levels of HCY, and multiple-site lesions were independently related to early-onset PSD. Based on receiver operating characteristic curves analysis, the combination of HCY, NIHSS scores, multiple-site lesions, and lesion location revealed a highest area under the curve of 0.807 (95% confidence interval [CI]: 0.748-0.865, p < .001). Furthermore, there was a significantly increased risk of early-onset PSD associated with serum levels of HCY ≥16.98μmol/L (odds ratio [OR]=10.976, 95% CI: 5.585-21.573, p < .001). Our study indicated that higher NIHSS score, elevated serum levels of HCY, and multiple-site lesions may be independent risk factors of early-onset PSD. The combination of HCY, NIHSS scores, multiple-site lesions, and lesion location may provide greater predictive value than HCY alone for early-onset PSD. Early intervention for elevated serum levels of HCY may be a potential target for the intervention and prevention of PSD.

The role of indoleamine 2,3-dioxygenase 1 in early-onset post-stroke depression.

The immune-inflammatory response has been widely considered to be involved in the pathogenesis of post-stroke depression (PSD), but there is ambiguity about the mechanism underlying such association. According to Diagnostic and Statistical Manual of Mental Disorders (5th edition), depressive symptoms were assessed at 2 weeks after stroke onset. 15 single nucleotide polymorphisms (SNPs) in genes of indoleamine 2,3-dioxygenase (IDO, including IDO1 and IDO2) and its inducers (including pro-inflammatory cytokines interferon [IFN]-γ, tumor necrosis factor [TNF]-α, interleukin [IL]-1β, IL-2 and IL-6) were genotyped using SNPscan™ technology, and serum IDO1 levels were detected by double-antibody sandwich enzyme-linked immune-sorbent assay. Fifty-nine patients (31.72%) were diagnosed with depression at 2 weeks after stroke onset (early-onset PSD). The IDO1 rs9657182 T/T genotype was independently associated with early-onset PSD (adjusted odds ratio [OR] = 3.008, 95% confidence interval [CI] 1.157-7.822, p = 0.024) and the frequency of rs9657182 T allele was significantly higher in patients with PSD than that in patients with non-PSD (χ2 = 4.355, p = 0.037), but these results did not reach the Bonferroni significance threshold (p > 0.003). Serum IDO1 levels were also independently linked to early-onset PSD (adjusted OR = 1.071, 95% CI 1.002-1.145, p = 0.044) and patients with PSD had higher serum IDO1 levels than patients with non-PSD in the presence of the rs9657182 T allele but not homozygous C allele (t = -2.046, p = 0.043). Stroke patients with the TNF-α rs361525 G/G genotype had higher serum IDO1 levels compared to those with the G/A genotype (Z = -2.451, p = 0.014). Our findings provided evidence that IDO1 gene polymorphisms and protein levels were involved in the development of early-onset PSD and TNF-α polymorphism was associated with IDO1 levels, supporting that IDO1 which underlie strongly regulation by cytokines may be a specific pathway for the involvement of immune-inflammatory mechanism in the pathophysiology of PSD.

Psychopathological network for early-onset post-stroke depression symptoms

BackgroundPost-stroke depression (PSD) can be conceptualized as a complex network where PSD symptoms (PSDS) interact with each other. The neural mechanism of PSD and interactions among PSDS remain to be elucidated. This study aimed to investigate the neuroanatomical substrates of, as well as the interactions between, individual PSDS to better understand the pathogenesis of early-onset PSD.MethodsA total of 861 first-ever stroke patients admitted within 7 days poststroke were consecutively recruited from three independent hospitals in China. Sociodemographic, clinical and neuroimaging data werecollected upon admission. PSDS assessment with Hamilton Depression Rating Scale was performed at 2 weeks after stroke. Thirteen PSDS were included to develop a psychopathological network in which central symptoms (i.e. symptoms most strongly correlated with other PSDS) were identified. Voxel-based lesion-symptom mapping (VLSM) was performed to uncover the lesion locations associated with overall PSDS severity and severities of individual PSDS, in order to test the hypothesis that strategic lesion locations for central symptoms could significantly contribute to higher overall PSDS severity.ResultsDepressed mood, Psychiatric anxiety and Loss of interest in work and activities were identified as central PSDS at the early stage of stroke in our relatively stable PSDS network. Lesions in bilateral (especially the right) basal ganglia and capsular regions were found significantly associated with higher overall PSDS severity. Most of the above regions were also correlated with higher severities of 3 central PSDS. The other 10 PSDS could not be mapped to any certain brain region.ConclusionsThere are stable interactions among early-onset PSDS with Depressed mood, Psychiatric anxiety and Loss of interest as central symptoms. The strategic lesion locations for central symptoms may indirectly induce other PSDS via the symptom network, resulting in higher overall PSDSseverity.Trial registrationURL: http://www.chictr.org.cn/enIndex.aspx; Unique identifier: ChiCTR-ROC-17013993.

Association of homocysteine and polymorphism of methylenetetrahydrofolate reductase with early-onset post stroke depression.

Homocysteine (Hcy) has been indicated to be involved in pathophysiology of post stroke depression (PSD). There is a lack of research to study the relationship between Hcy metabolism genes and PSD. Our study aims to investigate the relationship among Hcy metabolism genes, Hcy, and early-onset PSD. We recruited 212 patients with stroke and collected their peripheral blood sample, clinical data, and laboratory test on admission. 12 single nucleotide polymorphisms (SNPs) in methylenetetrahydrofolate reductase (MTHFR), methionine synthase reductase (MTRR), and methionine synthase (MTR) genes were genotyped by high-resolution melt analysis. PSD was diagnosed by DSM-V at 2 weeks after stroke. Binary logistic regression and haplotype analysis were used to examine the association between Hcy metabolism genes and PSD. Mediation analysis was performed to clarify whether the SNPs exerted their effect on PSD by affecting the Hcy level. 81 patients were diagnosed with PSD, and the incidence rate was 38.2%. Hcy level in PSD group was significantly higher than it in non-PSD group (p = 0.019). MTHFR rs1801133 AA genotype an A allele were associated with an elevated risk of PSD after adjustment for some confounding factors (OR = 4.021, 95% CI: 1.459∼11.080, p = 0.007 for AA genotype; OR = 1.808, 95% CI: 1.172∼2.788, p = 0.007 for A allele). Furthermore, the effect of MTHFR rs1801133 AA genotype on PSD was mediated by Hcy (OR = 1.569, 95% CI: 0.013∼3.350, p < 0.05). MTHFR rs1801133 and Hcy were associated with PSD, and MTHFR rs1801133 may exert an effect on PSD via mediating Hcy level. This offers a new perspective for treating PSD and understanding the mechanism of PSD.

A new nomogram including total cerebral small vessel disease burden for individualized prediction of early-onset depression in patients with acute ischemic stroke.

ObjectivesThe present study was designed to evaluate the effects of total cerebral small vessel disease (CSVD) on early-onset depression after acute ischemic stroke (AIS), and to develop a new nomogram including total CSVD burden to predict early-onset post-stroke depression (PSD).MethodsWe continuously enrolled patients with AIS who were hospitalized at the First Affiliated Hospital of Soochow University between October 2017 and June 2019. All patients were assessed for depressive symptoms using the 17-item Hamilton Depression Scale (HAMD-17) at 14 ± 2 days after the onset of AIS. The diagnosis for depression was made according to the American Diagnostic and Statistical Manual of Mental Disorders Version 5 (DSM-5). The demographic and clinical data were collected including total CSVD burden. On the basis of a multivariate logistic model, the independent factors of early-onset PSD were identified and the predictive nomogram was generated. The performance of the nomogram was evaluated by Harrell's concordance index (C-index) and calibration plot.ResultsA total of 346 patients were enrolled. When contrasted to a 0 score of total CSVD burden, the score ≥2 (moderate to severe total CSVD burden) was an independent risk factor for early-onset PSD. Besides, gender, cognitive impairments, baseline Barthel Index (BI), and plasma fibrinogen were independently associated with early-onset PSD. The nomogram based on all these five independent risk factors was developed and validated with an Area Under Curve (AUC) of 0.780. In addition, the calibration plot revealed an adequate fit of the nomogram in predicting the risk of early-onset depression in patients with AIS.ConclusionsOur study found the total CSVD burden score of 2–4 points was an independent risk factor of early-onset PSD. The proposed nomogram based on total CSVD burden, gender, cognitive impairments, baseline BI, and plasma fibrinogen concentration gave rise to a more accurate and more comprehensive prediction for early-onset PSD.

The potential risk factors of early-onset post-stroke depression from immuno-inflammatory perspective.

BackgroundMounting evidence strongly uncovered that peripheral immuno-inflammatory response induced by acute stroke is associated with the appearance of post-stroke depression (PSD), but the mechanism remains unclear.Methods103 stroke patients were assessed at 2 weeks after onset using Diagnostic and Statistical Manual of Mental Disorders, 5th edition and then divided into PSD and non-PSD groups. Polymorphisms of inflammatory molecules (interleukin [IL]-1β, IL-6, IL-10, IL-18, tumor necrosis factor-α [TNF-α], interferon-γ [IFN-γ] and C-reactive protein [CRP]), complete blood count parameters, splenic attenuation (SA) and splenic volume (SV) on unenhanced chest computed tomography, demographic and other clinical characteristics were obtained. Binary logistic regression model was used to analyze the associations between inflammation-related factors and the occurrence of PSD at 2 weeks after stroke.Results49 patients were diagnosed with PSD at 2 weeks after onset (early-onset PSD). The C/T genotypes of CRP rs2794520 and rs1205 were less in PSD group than non-PSD group (both adjusted odds ratio = 3.364; 95%CI: 1.039-10.898; p = 0.043). For CRP rs3091244, the frequency of G allele was higher (80.61% vs. 13.89%) while the frequency of A allele was lower (6.12% vs. 71.30%) in PSD patients than non-PSD patients (χ2 = 104.380; p<0.001). SA of PSD patients was lower than that of non-PSD patients in the presence of CRP rs2794520 C/T genotype and rs1205 C/T genotype (both t = 2.122; p = 0.039). Peripheral monocyte count was less in PSD group than non-PSD group (adjusted odds ratio = 0.057; 95%CI: 0.005-0.686; p = 0.024).ConclusionsCRP polymorphisms, SA based on CRP genotype, and peripheral monocytes are associated with the risk of early-onset PSD, suggesting peripheral immuno-inflammatory activities elicited by stroke in its aetiology.

Symptomatic plaque enhancement is associated with early-onset post-stroke depression

BackgroundThe association between imaging features closely associated with symptomatic intracranial atherosclerotic plaques and early-onset post-stroke depression (PSD) is currently unclear. Materials and methods76 ischemic stroke patients who underwent high-resolution vessel wall magnetic resonance imaging (HR-VWI) were divided into PSD and non-PSD groups according to their DSM-V diagnoses and HAMD-17 scores at 14 days after onset. Clinical data and the imaging features associated with symptomatic plaques (including the enhancement index (EI), remodeling index, and plaque surface irregularity) were compared between groups. Multifactorial logistic regression analysis was used to find independent predictors of early-onset PSD. Spearman rank correlation analysis explores the association between clinical data, symptomatic plaque imaging features, and HAMD-17 in patients. ResultsThe sample comprised 36 patients with early-onset PSD. The symptomatic plaque EI and infarct volume were significantly higher in depressed patients than in patients without depression (P < 0.05). Multivariate logistic regression showed that symptomatic plaque EI could be used as an independent predictor of early-onset PSD after correcting for the confounding factor of infarct volume (OR = 1.034, 95% CI:1.014–1.055, P = 0.001). In the total sample, symptomatic plaque EI, infarct volume, and HAMD-17 had a significant positive correlation with each other (P < 0.05). LimitationsThis study focused only on the patients' symptomatic plaques and did not monitor patients' systemic inflammation levels at the time of HR-VWI. ConclusionsThe degree of symptomatic plaque enhancement is an independent predictive imaging marker of early-onset PSD and can be used the early diagnosis of early-onset PSD.

Early-Onset Depression in Stroke Patients: Effects on Unfavorable Outcome 5 Years Post-stroke.

Background: Post-stroke depression (PSD) constitutes an essential complication of stroke and is associated with high-risk unfavorable outcome after stroke. The main objective of this prospective study was to determine the relationship between early-onset PSD (1 month after stroke) and functional outcomes 5 years after baseline enrollment.Methods: Four hundred thirty-six patients who met the criteria were included in this study from October 2013 to February 2015. The follow-up time for each patient was ~5 years, with follow-up every 3 months. Patients received questionnaires including the 17-item Hamilton Depression Scale (HAMD), the Mini-Mental State Examination (MMSE), the National Institutes of Health Stroke Scale (NIHSS), the modified Rankin Scale (mRS), and the Barthel Index (BI).Results: Of the 436 patients, 154 (35.3%) patients with the prevalence of PSD status at baseline, 26 (7.2%) patients with the prevalence of PSD status, and 73 (20.1%) had an unfavorable outcome 5 years after stroke. The odds ratio (OR) for unfavorable outcome at 5 years in the PSD group was ~2.2 relative to the non-PSD group after adjusting for potential risk factors [OR = 2.217, 95% confidence interval (CI) = 1.179–4.421, P = 0.015]. In the early-onset PSD group, HAMD scores were independently associated with 5-year unfavorable outcome rates (OR = 1.168, 95% CI = 1.015–1.345, P = 0.031).Conclusions: Our findings indicate that early-onset PSD status in Chinese patients is an independent risk factor for unfavorable outcome 5 years after stroke, and that the severity of PSD is also related to unfavorable outcome.

Admission Heart Rate Variability Is Associated With Poststroke Depression in Patients With Acute Mild-Moderate Ischemic Stroke.

BackgroundStroke has been shown to cause cardiac autonomic dysfunction. Depression is common complication after acute ischemic stroke (AIS). The purpose of this study was to investigate whether decreased heart rate variability (HRV) was related to poststroke depression (PSD) in patients with mild-moderate AIS.MethodsIn this study, we assessed autonomic function of ischemic stroke patients within 72 h from symptom onset by fractal dimension (FD). 503 patients (mean age 65.93 ± 10.19) with mild-moderate AIS underwent FD test after admission. Depressive symptoms were assessed using 17-item Hamilton Depression Rating Scale (HDRS) at baseline (within 7 days) and 3 months. Depression were defined if HDRS >6 points. According to the data of FD, we investigated association with early-onset PSD status and 3-month PSD.Results59.24% (293/503) of patients had early-onset PSD status at baseline, and 38.66% (184/476) of patients had PSD at 3 months. ROC curve analysis shown that the optimal cut point of FD for early-onset PSD status and 3-month PSD were FD ≤ 1.27 and FD ≤ 1.19, respectively. In fully adjusted models, higher NIHSS [adjusted odd ratios (OR), 1.15; 95% confidence interval (CI), 1.05–1.27; P=0.005], younger age (adjusted OR, 1.18; 95% CI, 1.01–1.13; P=0.046), and FD ≤ 1.27 (adjusted OR, 3.31; 95% CI, 2.23–4.92; P<0.001) were associated with increased risk of early-onset PSD status. Higher NIHSS (adjusted OR, 1.21; 95% CI, 1.09–1.43; P<0.001) and FD ≤ 1.19 (adjusted OR, 2.68; 95% CI, 1.79–4.03; P=0.000) were associated with increased risk of 3-month PSD.ConclusionsPSD is common after mild-moderate AIS and is highly correlated with decreased HRV, FD could serve as an objective tool to help in prediction of PSD.

Severe Periodontitis Is Associated with Early-Onset Poststroke Depression Status

BackgroundPoststroke depression (PSD) is one of the most common complications after ischemic stroke, and periodontitis is associated with depression. However, whether severe periodontitis is associated with early-onset PSD status remains unknown. In this study, we aimed to investigate whether there is an association between severe periodontitis and PSD status in acute ischemic stroke patients. Material and MethodsWe recruited 202 acute ischemic stroke patients within 7 days after stroke onset. Pocket depth and clinical attachment loss were assessed by oral examination to define the severe periodontitis. On the basis of diagnosis of PSD status according to DSM-5 criteria and a 24-item Hamilton Depression Rating Scale score greater than or equal to 8 within 2 weeks after stroke onset, we stratified patients into PSD status or non-PSD status groups and identified the independent predictors for the development of PSD status in multivariate logistic analysis. Results77 (38.1%) patients were diagnosed as early-onset PSD status. PSD status group showed more severe periodontitis, lower income, lower Barthel Index (BI) score and Montreal Cognitive Assessment score, higher National Institutes of Health Stroke Scale score and modified Rankin scale (mRS) score compared with non-PSD status group. Multivariate logistic regression showed that severe periodontitis (odds ratio 2.401) and NIHSS score (>4, odds ratio 2.130) were independent predictors for early-onset PSD status. ConclusionsSevere periodontitis is found to be an important independent predictor of early-onset PSD status in patients with acute ischemic stroke, in addition to the well-known prognostic factors such as nonminor stroke assessed by NIHSS greater than 4.

MicroRNA-140-5p: A novel circulating biomarker for early warning of late-onset post-stroke depression

We aimed to explore the circulating microRNAs biomarkers in the acute stage following cerebral ischemia to earlier warn late-onset post-stroke depression (PSD). A total of 251 consecutive patients with acute ischemic stroke were recruited. They were divided into three groups depending on whether PSD had occurred at 2 weeks or 3 months since stroke: early-onset PSD, late-onset PSD, and non-depressed group. Microarray assay was conducted to identify the different expression profiles of plasma miRNAs. Comprehensive bioinformatics analysis for their integrating putative target genes was performed. The key miRNA was validated in a larger cohort and its function was further studied in ischemic mice brain. We screened three differentially expressed miRNAs in the late-onset PSD individuals, miR-140-5p and miR-221-3p were significantly upregulated while miR-1246 was downregulated. The bioinformatics analysis demonstrated that their predicted target genes were mainly enriched in axon development and Ras signaling pathway. Logistic regression analysis revealed that miR-140-5p was an independent risk factor for late-onset PSD (P = 0.017, OR = 2.313, 95%CI 1.158 to 4.617). The miR-140-5p expression on admission was significantly positively correlated with HDRS scores assessed at 3 months after stroke (P = 0.0007). The predictive value of miR-140-5p for late-onset PSD is 83.3% sensitivity and 72.6% specificity (AUC = 0.8127, P < 0.0001). AAV-mediated overexpression of miR-140-5p decreased the protein level of IL1rap, IL1rapl1, VEGF, and MEGF10 in the ischemic mouse hippocampus and inhibited neurogenesis and capillary density. MiR-140-5p might be involved in the pathogenesis of late-onset PSD and used as a novel early warning biomarker.

Predictors of Remission of Early-Onset Poststroke Depression and the Interaction Between Depression and Cognition During Follow-Up.

Objectives: This study aimed to examine the rate of remission in individuals experiencing early-onset poststroke depression (PSD) in China and to identify predictors of remission during a 3-month follow-up. This study also explored the interaction between cognitive impairment and depression.Methods: A total of 820 patients with PSD from a massive multicenter prospective cohort project in China (PRIOD) were included in the present study. Depressive symptoms were measured with the Hamilton Depression Rating Scale (17 Items, HDRS-17) at 2 weeks and the endpoint of the 3-month follow-up. The cut-off score of HDRS-17 (< 8) was used to define remission of depression at the endpoint. The Mini-Mental State Exam (MMSE) was used to evaluate the cognitive impairment of the patients (at the 2-week follow-up and 3-month endpoint). The National Institutes of Health Stroke Scale (NIHSS) was used to measure the severity of stroke.Results: (1) Six hundred and forty-two patients completed the 3-month follow-up, and 332 (51.7%) patients remitted by the end of the study. Univariate analyses indicated that there was a higher proportion of patients who had hypertension, frontal lobe lesion, basal ganglia lesion, poor outcome at 2 weeks, high scores on the NIHSS at 2 weeks, major life events within 3 months, and major medical diseases within 3 months in the nonremission group. In stepwise multiple logistic regression analyses, remission was significantly predicted by lower NIHSS scores at 2 weeks (p = 0.001, OR = 1.086, 95% CI 1.035–1.139), fewer major life events (p = 0.036, OR = 5.195, 95% CI 1.111–27.283), fewer major medical comorbidities (p = 0.015, OR = 2.434, 95% CI 1.190–4.979), and fewer frontal lobe lesions (p = 0.042, OR = 1.717, 95% CI 1.019–2.891). (2) After controlling for confounding variables, repeated measures analysis of variance revealed a significant interaction between time (2 weeks vs. 3 months) and group (remitters vs. nonremitters) on MMSE scores [F(1, 532) = 20.2, p < 0.001].Conclusions: Early-onset PSD patients with milder neurological impairment, fewer major life events, fewer major medical comorbidities and no frontal lobe lesion at baseline were more likely to achieve remission 3 months after stroke. Only remitters of PSD improved significantly in cognitive impairment after stroke.The PRIOD trial is registered at http://www.isrctn.com/, number ISRCTN62169508.

Age-Related Frontal Periventricular White Matter Hyperintensities and miR-92a-3p Are Associated with Early-Onset Post-Stroke Depression.

Objective: To explore the correlationship among white matter hyperintensities (WMHs), miR-92a-3p and early-onset post-stroke depression (PSD).Methods: We recruited consecutively 238 patients with acute cerebral infarction and MRI examination in the Department of neurology, Ruijin hospital, Shanghai Jiaotong University School of Medicine. The diagnosis of early-onset PSD was made in accordance with DSM-IV criteria for depression in 2 weeks after stroke. Clinical information and assessments of stroke severity were recorded on admission. The analysis of plasma miR-92a-3p was performed using quantitative PCR at the same time. WMHs were evaluated by the Fazekas and Scheltens visual rating scales. The relationship among WMHs, miR-92a-3p and PSD were analyzed by SPSS 22.0 software.Results: Logistic regression demonstrated that periventricular WMHs (PVWMHs) in frontal caps was an independent risk factor with early-onset PSD (OR = 1.579, 95% CI: 1.040–2.397, p = 0.032). The age and numbers of lacunes were related to frontal PVWMHs. Plasma miR-92a-3p in the PSD group was higher compared with the non-depressed group. Receiver operating curve analysis revealed that miR-92a-3p could predict early-onset PSD with 90% sensitivity and 90% specificity. The higher miR-92a-3p trended toward association with greater frontal PVWMHs.Conclusion: Acute ischemic stroke patients with frontal PVWMHs or a high plasma miR-92a-3p at baseline were more likely to develop early-onset PSD. MiR-92a-3p might be involved in the white matter impairment and post-stroke depression.

The combination of plasma glutamate and physical impairment after acute stroke as a potential indicator for the early-onset post-stroke depression

ObjectsThe present study aimed to investigate the relationship of plasma glutamate levels with the early-onset of post-stroke depression (PSD) and to further explore the prognostic value of plasma glutamate combined with clinical characteristics for the early-onset PSD in the acute ischemic stroke patients. MethodsSeventy-four patients who admitted to the hospital within 24h of acute ischemic stroke were consecutively recruited and followed up for 2weeks. The Beck Depression Inventory (BDI) and 17-item Hamilton Depression Rating Scale (HAMD-17) were used to screen for depressive symptoms 14days after stroke. Diagnoses of depression were made in accordance with DSM-IV. Plasma glutamate levels were determined by High Performance Liquid Chromatography (HPLC) on days 1 and 14 after stroke for all patients. ResultsPlasma glutamate levels were significantly lower in PSD patients than those of non-PSD patients on day 1 after stroke. ROC curve analyses revealed an AUC (area under the ROC curve) of 0.724 (95% CI: 0.584–0.863, p=0.004) and of 0.669 (95% CI: 0.523–0.814, p=0.030) for National Institute of Health Stroke Scale (NIHSS) scores and plasma glutamate levels on day 1 respectively. Combined ROC analyses using the two factors revealed the highest AUC of 0.804 (95% CI: 0.685–0.922, P<0.0001). ConclusionsThese results indicated an association between the early-onset PSD and a low plasma glutamate level following acute ischemic stroke. The combination of reduced plasma glutamate levels and physical impairment (determined by NIHSS) 1day after acute ischemic stroke was a potential diagnostic indicator for early-onset PSD.

Clinical predictor and circulating microRNA profile expression in patients with early onset post-stroke depression

ObjectiveWe aim to explore the clinical factors and blood biomarker for predicting the early-onset post-stroke depression (PSD). Methods251 acute ischemic stroke patients were divided into PSD group and non-PSD group by Hamilton depression scale in 2 weeks after stroke. The clinical data, the severity, etiology and location of stroke were recorded. The analysis of inflammatory mediator, glycose and lipid metabolism was performed on the day of admission. The association between clinical factors and early onset PSD was studied by logistic regression analysis. In addition, the differentially expressed miRNAs in plasma between the two groups were screened by gene chip and the bio-information was further investigated by GO and KEEG analysis. ResultsAmong 251 patients, 45 (17.93%) were diagnosed as early onset PSD. NIHSS score (>3) and carotid stenosis were independent relative factors with early-onset PSD (OR 3.479 and 2.617, p=0.000 and 0.009, respectively). Moreover, lower LDL trended toward association with early onset PSD in minor stroke subgroup (p=0.084). MiRNA profile demonstrated 25 differential expressed circulating miRNAs with FC≥2 and P≤0.05 between the two groups. The target genes of these miRNAs were enriched in pathways of cancer and MAPK signaling. LimitationsThe sample of the study was small. The results should be further confirmed in large cohort patients. ConclusionsEarly onset PSD was more likely in patients with severe neurological deficits and carotid artery stenosis, also note the possible association between lower LDL and depression in minor stroke. Blood miRNAs may be served as a potential biomarker for PSD diagnosis.

Depression after minor stroke: the association with disability and quality of life--a 1-year follow-up study.

Minor stroke is characterized by mild neurological functional impairment and relatively good outcome. Little is known about the association between post-stroke depression (PSD) and outcomes of minor stroke. The aim of this study was to investigate the association between PSD and disability and quality of life (QoL) at 1 year after minor ischemic stroke. Patients with first-ever minor ischemic stroke (n = 747) were followed up at 14 ± 2 days, 3 months, 6 months, and 1 year after stroke. Depressive symptoms were assessed at each follow-up. Patients diagnosed with depression at 14 ± 2 days formed the early-onset PSD group; those who were diagnosed with depression at any subsequent follow-ups for the first time constituted the late-onset PSD group. The outcomes of minor stroke including disability (modified Rankin score ≥ 2) and QoL (Short Form-36 Health Survey) were assessed at the 1-year follow-up. A total of 198 (26.5%) patients were diagnosed with PSD over the 1-year follow-up; 136 and 62 patients were allocated to the early-onset PSD group and late-onset PSD group, respectively. Both early-onset and late-onset PSD were independently associated with disability and poor physical and mental health at 1 year after stroke. Recovery from depression (n = 112) within 1 year decreased the adverse impacts of PSD on functional outcome and QoL. Post-stroke depression was independently associated with disability and poor QoL at 1 year after first-ever minor ischemic stroke. Recovery from PSD decreased but did not eliminate the adverse impacts of PSD on outcomes of minor stroke.

Depression after minor stroke: Prevalence and predictors

ObjectiveSeverity of stroke and disability after stroke are major predictors of post-stroke depression (PSD). The prevalence of PSD in patients with minor stroke is expected to be low because minor stroke is characterized by mild neurological dysfunction. The aim of this study was to investigate the prevalence and predictors of PSD in patients with minor ischemic stroke. MethodsPatients with first-ever minor ischemic stroke (n=757) were followed up at 14±2days, 3months, 6months, and 1year after stroke. Depression status was assessed at each follow-up. Patients that had PSD at follow-ups were classified into two groups according to the time point of the diagnosis of PSD: patients diagnosed at 14±2days formed the early-onset PSD group, and those who were diagnosed at any subsequent follow-ups constituted the late-onset PSD group. ResultsThe 1-year prevalence of PSD in patients with minor stroke was 29.0% (95% CI, 25.2–32.8). Female gender, current smoking at stroke onset, mild global cognitive impairment at 14±2days, and stroke recurrence were independently associated with a high risk of PSD over the 1-year follow-up. Predictors of early-onset PSD included female gender, current smoking, and mild global cognitive impairment at 14±2days, while predictors of late-onset PSD were current smoking and stroke recurrence. ConclusionApproximately three in ten patients with first-ever minor ischemic stroke may develop depression during the first year after stroke. Female gender, smoking, mild global cognitive impairment, and stroke recurrence predict early-onset or late-onset PSD after minor ischemic stroke.

Long-term incidence of depression and predictors of depressive symptoms in older stroke survivors

Depression is common and an important consequence of stroke but there is limited information on the longer-term relationship between these conditions. To identify the prevalence, incidence and predictors of depression in a secondary-care-based cohort of stroke survivors aged over 75 years, from 3 months to up to 10 years post-stroke. Depression was assessed annually by three methods: major depression by DSM-IV criteria, the self-rated Geriatric Depression Scale (GDS) and the observer-rated Cornell scale. We found the highest rates, 31.7% baseline prevalence, of depressive symptoms with the GDS compared with 9.7% using the Cornell scale and 1.2% using DSM-IV criteria. Incidence rates were 36.9, 5.90 and 4.18 episodes per 100 person years respectively. Baseline GDS score was the most consistent predictor of depressive symptoms at all time points in both univariate and multivariate analyses. Other predictors included cognitive impairment, impaired activities of daily living and in the early period, vascular risk factor burden and dementia. Our results emphasise the importance of psychiatric follow-up for those with early-onset post-stroke depression and long-term monitoring of mood in people who have had a stroke and remain at high risk of depression.