Diversiform Etiologies for Post-stroke Depression.
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ABSTRACT:
SUBMITTER: Wang Z
PROVIDER: S-EPMC6351464 | biostudies-literature | 2018
REPOSITORIES: biostudies-literature
Publications
Diversiform Etiologies for Post-stroke Depression.
Wang Zan Z Shi Yanmin Y Liu Fangfang F Jia Nan N Gao Junya J Pang Xiaomin X Deng Fang F
Frontiers in psychiatry 20190123
After the onset of stroke, many patients suffer from emotional behavior changes. Approximately, one-third of stroke survivors are affected by post-stroke depression (PSD), making it a serious social and public health problem. Post-stroke depression (PSD) has an important impact on the course, recovery, and prognosis of stroke. The pathogenesis of PSD is very complex, involving many factors such as biological mechanism and social psychological mechanisms. This article provides a brief review of t ...[more]
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Project description:ObjectiveSleep disturbance and depression are common in stroke patients, however, little is known about the role of sleep in post-stroke depression. This study examined the association between pre-stroke sleep duration and depression at 90 days post-stroke in a population-based bi-ethnic sample.MethodsThe study included 1369 stroke patients from the Brain Attack Surveillance in Corpus Christi project who survived 90 days post-stroke. Depression at 90 days post-stroke was assessed by the 8-item Patient Health Questionnaire, and pre-stroke sleep duration was self-reported shortly after stroke in reference to the pre-stroke state. Multiple imputation and inverse probability weighting were used to deal with missing data and attrition. Weighted logistic regression models were fit to examine the association between pre-stroke sleep duration and post-stroke depression.ResultsThe mean age was 68.2 years, and 63.6% were Mexican American. The prevalence of post-stroke depression was highest among participants reporting less than 6 hours of sleep before stroke (52.4%, 95% confidence interval = 45.7%-59.0%). Compared with participants reporting 7-8 hours of sleep before stroke, those with short sleep duration had significantly increased odds for post-stroke depression (odds ratio = 1.96; 95% confidence interval = 1.38-2.79), after adjustment for sociodemographic, stroke and pre-stroke characteristics including pre-stroke depression.ConclusionsPre-stroke short sleep duration may be an independent risk factor for post-stroke depression.
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Project description:BackgroundLittle is known about ethnic differences in poststroke depression (PSD) in the United States. This study aims to estimate the prevalence of PSD at 90 days after first-ever stroke and to examine ethnic differences in the prevalence between Mexican Americans (MAs) and non-Hispanic whites (NHWs).Methods and resultsStroke cases from 2011 to 2015 were identified from the BASIC project (Brain Attack Surveillance in Corpus Christi)-a population-based stroke surveillance study in south Texas. Participants were interviewed at the onset of stroke (baseline interview) and ≈90 days post-stroke (outcome interview). PSD was assessed by the Patient Health Questionnaire-8. Inverse probability weights were generated to account for differential attrition, and weighted logistic regression was used to investigate the association between ethnicity and PSD. The study sample consisted of 586 first-ever stroke patients who completed nonproxy baseline and outcome interviews and had depression assessment. Approximately, 60% of them were MAs, and 40% were NHWs. After accounting for attrition, the prevalence of depression at 90 days post-stroke was 30.4% for MAs (95% confidence interval, 25.0%-35.9%) and 20.7% for NHWs (95% confidence interval, 15.7%-25.7%). The crude odds of PSD in MAs was 1.69 times greater than that in NHWs (95% confidence interval, 1.13-2.51). The odds ratio decreased by 23.6% after adjustment for education (odds ratio, 1.29; 95% confidence interval, 0.82-2.02) and was further attenuated with additional adjustment for other covariates.ConclusionsMAs had a higher prevalence of PSD at 90 days than NHWs. The ethnic difference was explained by sociodemographic and health factors, especially low educational attainment.
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Project description:Ischemic Stroke precedes depression. Post-stroke depression (PSD) is a major driver for poor recovery, negative quality of life, poor rehabilitation outcomes and poor functional ability. In this systematic review, we analysed the inflammatory basis of post-stroke depression, which involves bioenergetic failure, deranged iron homeostasis (calcium influx, Na influx, potassium efflux etc), excitotoxicity, acidotoxicity, disruption of the blood brain barrier, cytokine-mediated cytotoxicity, reactive oxygen mediated toxicity, activation of cyclooxygenase pathway and generation of toxic products. This process subsequently results in cell death, maladapted, persistent neuro-inflammation and deranged neuronal networks in mood-related brain regions. Furthermore, an in-depth review likewise reveals that anatomic structures related to post-stroke depression may be localized to complex circuitries involving the cortical and subcortical regions.
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Project description: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 were collected 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 PSDS severity.Trial registrationURL: http://www.chictr.org.cn/enIndex.aspx ; Unique identifier: ChiCTR-ROC-17013993.
| S-EPMC9945689 | biostudies-literature
Project description:Stroke is one of the most common cerebrovascular diseases, which is the cause of long-term mental illness and physical disability, Post-stroke depression (PSD) is the most common neuropsychiatric complication after stroke, and its mechanisms are characterized by complexity, plurality, and diversity, which seriously affects the quality of survival and prognosis of patients. Studies have focused on and recognized neurotransmitter-based mechanisms and selective serotonin-reuptake inhibitors (SSRIs) can be used to treat PSD. Neuroinflammation, neuroendocrinology, neurotrophic factors, and the site of the stroke lesion may affect neurotransmitters. Thus the mechanisms of PSD have been increasingly studied. Pharmacological treatment mainly includes SSRIs, noradrenergic and specific serotonergic antidepressant (NaSSA), anti-inflammatory drugs, vitamin D, ect, which have been confirmed to have better efficacy by clinical studies. Currently, there is an increasing number of studies related to the mechanisms of PSD. However, the mechanisms and pharmacologic treatment of PSD is still unclear. In the future, in-depth research on the mechanisms and treatment of PSD is needed to provide a reference for the prevention and treatment of clinical PSD.
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Project description:Depression is a common outcome following stroke, associated with reduced quality of life and poorer recovery. Despite attempts to associate depression symptoms with specific lesion sites, the neural basis of post-stroke depression remains poorly understood. Resting state fMRI has provided new insights into the neural underpinnings of post-stroke depression, but has been limited to connectivity analyses exploring interregional correlations in the time-course of activity. Other aspects of resting state BOLD signal remain unexamined. Measuring the amplitude of low frequency fluctuations allows the detection of spontaneous neural activity across the whole brain. It provides complementary information about frequency-specific local neural activity. We calculated the fractional amplitude of low frequency fluctuations (fALFF) in a group of 64 participants scanned 3 months post-stroke. Twenty showed depression symptoms when assessed with the Patient Health Questionnaire (PHQ-9). We performed analyses in both the typical 0.01-0.08 Hz range, as well as separately in the slow-5 (0.01-0.027 Hz) and slow-4 (0.027-0.073 Hz) ranges. We found significantly higher fALFF in the depressed compared to non-depressed participants in the left dorsolateral prefrontal cortex (DLPFC) and the right precentral gyrus, and a significant association between higher depression scores and higher fALFF in the left insula. The group differences were detected in the slow-5 fluctuations, while the association with depression severity was observed in the slow-4 range. We conclude that post-stroke depression can be characterised by aberrant spontaneous local neural activity, which in small samples could be a more sensitive measure than lesion volume and location.
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Project description:OBJECTIVE:Depression occurs in approximately 30 percent of stroke patients, leading to increased disability, lower quality of life and increased mortality. Given new recommendations to assess depression in acute stroke patients this study evaluated rates of acute post stroke depression at a Primary Stroke Center in Doha, Qatar. METHODS:Acute stroke patients (n = 233) were given the PHQ-9 and the Mini-Cog test by stroke unit nurses within the first few days post stroke. This was part of a clinical improvement project conducted from March 2016 thru March 2017. RESULTS:Approximately 20% of acute post stroke patients (46/233) scored in the moderately depressed range on the Patient Health Questionnaire (PHQ-9 ?10 with item 1 and/or 2 endorsed). Nationality and dysarthria were significantly associated with depression. Females were twice as likely to be depressed. A significantly greater number of Middle Eastern and African patients were depressed (30.18%) than Southeast Asian and Western Pacific patients (16.76%). A PHQ-2 cut off of 2 was optimal with sensitivity of 91.3 and specificity of 71.6. CONCLUSIONS:Almost 20% of acute stroke patients were moderately depressed on the PHQ-9, with Middle Eastern/African patients almost twice as likely to be depressed. This may reflect higher baseline pre-stroke depression levels in those of Middle Eastern/African background, perhaps due to greater levels or stress or trauma exposure in these groups. Dysarthria was found to be significantly associated with depression. Initial screening with the PHQ-2 using a cut-off of 2 (versus the cut-off of 3 used in primary care settings) may be beneficial. Based on these results acute post stroke depression screening is recommended in the Middle East, coupled with culturally sensitive psychiatric care.
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Project description:Post-stroke depression (PSD) seriously affects the rehabilitation of nerve function and quality of life. However, the pathogenesis of PSD is still not clear. This study aimed to investigate the demographic, clinical, and biochemical factors in patients with PSD.Patients with an acute ischemic stroke, who met the inclusion criteria at Shanghai Tenth People's Hospital from April 2016 to September 2016, were recruited for this study. The stroke severity was assessed using the National Institutes of Health Stroke Scale (NIHSS), and the mental state was assessed using Mini-Mental State Examination (MMSE), Hamilton Depression Scale (HAMD), and Hamilton Anxiety Scale (HAMA) at 1 week of admission. The patients were divided into PSD and non-PSD groups. The demographic and clinical characteristics, as well as the biochemical factors, were compared between the two groups. A logistic regression analysis was performed to identify the risk factors for depression following stroke.A total of 83 patients with acute ischemic stroke were recruited. Of these, 36 (43.4%) developed depression. The multivariate logistic regression analysis indicated that high NIHSS [odds ratio (OR): 1.84, 95% confidence interval (CI): 1.09-3.12, P?=?0.023] and high HAMD scores (OR: 2.38, 95% CI: 1.61-3.50, P?<?0.001) were independent risk predictors for PSD and so were lower dopamine level (OR: 0.64, 95% CI: 0.45-0.91, P?=?0.014), lower 5-hydroxytryptamine level (OR: 0.99, 95% CI: 0.98-1.00, P?=?0.046), higher tumor necrosis factor-? level (OR: 1.05, 95% CI: 1.00-1.09, P?=?0.044), and lower nerve growth factor level (OR: 0.06, 95% CI: 0.01-0.67, P?=?0.022).The identification of higher NIHSS scores, higher HAMD scores, lower dopamine level, lower 5-hydroxytryptamine level, higher tumor necrosis factor-? level, and lower nerve growth factor level might be useful for clinicians in recognizing and treating depression in patients after a stroke.
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