Authors: Jie-Min Li, Su-Sheng Long, Teng-Xiang Lu, Yi-Chun Jiang, Xiao-Wei Zhang, You-Quan Ren
Categories: Observational Study, Stroke, Depression, Anxiety, Mental health, Functional outcomes, Observational study, Psychiatric symptoms, Rehabilitation
Source: World Journal of Psychiatry
Authors: Jie-Min Li, Su-Sheng Long, Teng-Xiang Lu, Yi-Chun Jiang, Xiao-Wei Zhang, You-Quan Ren
Post-stroke psychiatric complications, particularly depression and anxiety, significantly impact rehabilitation outcomes and quality of life. Despite their prevalence and clinical significance, these conditions often remain underrecognized in routine stroke care. Understanding their clinical features and temporal patterns is crucial for improving patient outcomes.
To investigate the prevalence, temporal evolution, and clinical correlates of depression and anxiety post-stroke and their impact on functional recovery.
In this prospective observational study, 127 patients first-ever ischemic stroke were enrolled between June 2022 and June 2024. Depression and anxiety were assessed using the Hamilton Depression Rating Scale and Hamilton Anxiety Rating Scale at baseline and follow-up intervals (2 weeks, 1 month, 3 months, and 6 months). Stroke severity was evaluated using the National Institutes of Health Stroke Scale, and functional outcomes were measured using the modified Rankin Scale.
Among 120 patients who completed follow-up (94.5% completion rate), 37.5% had depression (mild: 18.3%, 12.5%, 6.7%) and 41.7% had anxiety at baseline. Depression prevalence showed a biphasic pattern, peaking at 2 weeks (37.5%), declining at 3 months (28.3%), and slightly increasing at 6 months (30.8%). Stroke severity significantly correlated with both depression (odds ratio = 1.18, 95%CI: 1.06-1.31, P = 0.003) and anxiety (odds ratio = 1.15, 95%CI: 1.04-1.27, P = 0.008). Left hemisphere lesions had a stronger association with psychiatric symptoms than right hemisphere lesions (P = 0.035). Patients with psychiatric complications demonstrated poorer functional outcomes at 6 months (median modified Rankin Scale 3 vs 2, P = 0.015) and longer hospital stays (mean 3.2 days, P = 0.002).
Identifying the clinical and neuroanatomical correlates of depression and anxiety will enable effective risk stratification and patient management. Integrating routine psychiatric screening and early intervention is essential in stroke care.
Core Tip: Depression and anxiety are prevalent post-stroke psychiatric complications that significantly affect functional recovery and rehabilitation outcomes. This observational study highlights a biphasic pattern in the prevalence of depression, with the highest incidence at 2 weeks post-stroke. Stroke severity and left hemisphere lesions are closely associated with these psychiatric symptoms. Patients with depression and anxiety showed poorer functional outcomes and longer hospital stays. These findings emphasize the need for early psychiatric screening and intervention in stroke care to improve patient outcomes.
Stroke is a leading cause of disability and mortality worldwide and represents a significant global health challenge. Recent epidemiological data indicate that approximately 12.2 million new stroke cases occur annually, with ischemic stroke accounting for approximately 80% of all cases[1]. Beyond immediate physical consequences, a stroke can cause significant psychological effects such as mood disorders and anxiety symptoms during the post-stroke period[2].
Post-stroke psychiatric complications have garnered increasing attention in recent years, as they can significantly influence rehabilitation outcomes and overall quality of life. In particular, depression and anxiety have been recognized as prevalent psychological sequelae of stroke. Recent meta-analyses have shown that an estimated 33% of stroke survivors experience depression and 25%-30% develop anxiety disorders within the first year post-stroke[3]. These psychological complications often manifest alongside physical disabilities, creating a complex condition that requires comprehensive management approaches[4].
Neurobiological and psychosocial factors both influence the association between stroke and subsequent psychiatric symptoms. Research has demonstrated that the location and extent of cerebral infarction can directly impact mood regulation, with lesions in specific brain regions, particularly the left frontal lobe and basal ganglia, showing stronger associations with post-stroke depression[5]. In addition, the sudden onset of physical disability, cognitive impairment, and changes in social roles can contribute to the development of anxiety and depressive symptoms[6].
Post-stroke psychiatric symptoms affect mental health outcomes and can significantly impair rehabilitation engagement, increase healthcare burden, and negatively affect functional recovery[7]. Moreover, they are associated with higher mortality rates and increased risk of recurrent stroke events[8]. The economic burden of post-stroke care is substantially higher in patients who develop psychiatric complications, highlighting the importance of early identification and intervention[9].
However, current clinical practices often emphasize physical rehabilitation while potentially overlooking the psychological aspects of recovery. The heterogeneous presentation of post-stroke depression and anxiety combined with communication difficulties in some patients can make accurate diagnosis challenging[10]. Furthermore, the temporal relationship between stroke onset and the development of psychiatric symptoms varies considerably among patients, necessitating continuous monitoring throughout the recovery period[11].
Recent advances in neuroimaging and psychiatric assessment tools have enhanced our understanding of the biological basis of post-stroke psychiatric symptoms. Specific neural network disruptions are associated with post-stroke mood disorders, suggesting potential therapeutic targets[12]. Additionally, the development of validated screening tools has improved the ability to identify at-risk patients, though the optimal timing and frequency of psychological assessment remain uncertain[13].
The interaction between traditional stroke risk factors and psychiatric symptoms adds another layer of complexity to patient care. Vascular risk factors, such as hypertension and diabetes, are associated with both stroke occurrence and increased susceptibility to mood disorders, suggesting shared pathophysiological mechanisms[14]. Understanding these interactions is crucial for developing integrated treatment approaches that address both physical and mental health aspects of stroke recovery[15].
Given the substantial impact of psychiatric complications on stroke outcomes and the current gaps in clinical practice, research examining the clinical characteristics of depression and anxiety in stroke patients is imperative. In this observational study, we aimed to investigate the prevalence, clinical features, and correlates of depression and anxiety among patients with ischemic stroke, focusing on identifying patterns that could inform more targeted therapeutic interventions and improve patient care strategies.
This prospective observational study was conducted at the Department of Neurology of Linquan County People’s Hospital between June 2022 and June 2024. The study protocol was approved by the institutional ethics committee, and written informed consent was obtained from all participants or their legal guardians. The study was conducted in accordance with the Declaration of Helsinki and followed the Strengthening the Reporting of Observational Studies in Epidemiology guidelines for observational studies.
The study enrolled patients diagnosed with ischemic stroke who were admitted to the Department of Neurology or attended outpatient follow-up clinics. Ischemic stroke was diagnosed based on clinical presentation and confirmed through neuroimaging (computed tomography or magnetic resonance imaging) by experienced neurologists based on the World Health Organization criteria.
**Inclusion criteria ** (1) Age ≥ 18 years; (2) First-ever ischemic stroke confirmed with computed tomography or magnetic resonance imaging within the last 14 days; (3) Clinical stability allowing psychiatric evaluation; (4) Adequate cognitive function to complete psychological assessments (Mini-Mental State Examination score ≥ 24); and (5) Ability to provide informed consent.
**Exclusion criteria ** (1) History of major psychiatric disorders prior to stroke; (2) Severe aphasia or cognitive impairment preventing reliable assessment; (3) Other neurological conditions that could affect mental status; (4) Severe systemic diseases with life expectancy < 6 months; and (5) Participation in other clinical trials.
All participants underwent comprehensive clinical evaluations within 48 hours of admission or during their scheduled outpatient visits. Demographic data, medical history, and stroke-related information were collected through standardized case report forms. Stroke severity was assessed by certified neurologists using the National Institutes of Health Stroke Scale (NIHSS). Functional status was evaluated using the modified Rankin Scale (mRS). Neuroimaging data were analyzed by two independent neuroradiologists blinded to the patients' clinical status. Stroke location was classified according to vascular territory, and lesion volume was calculated using standardized methods. Any discrepancies in interpreting the images were resolved through discussion until a consensus was reached.
Depression and anxiety symptoms were evaluated using standardized psychiatric assessment tools. The Hamilton Depression Rating Scale was used to assess depressive symptoms, with scores ≥ 7 indicating mild depression, ≥ 17 indicating moderate depression, and ≥ 24 indicating severe depression. Anxiety symptoms were assessed using the Hamilton Anxiety Rating Scale, with scores ≥ 7 indicating mild anxiety, ≥ 14 indicating moderate anxiety, and ≥ 21 indicating severe anxiety. All psychiatric assessments were conducted by trained psychiatrists or clinical psychologists who underwent standardized training before the study commenced. Inter-rater reliability was established through pilot assessments (Cohen’s kappa > 0.85). Assessments were performed in a quiet private setting, providing adequate time for patient comfort and accurate evaluation.
Patients were followed up at predetermined intervals (2 weeks, 1 month, 3 months, and 6 months post-stroke) to monitor the progression of psychiatric symptoms. During each follow-up visit, both psychiatric scales were readministered, and any changes in medical condition or treatment were documented. Additional clinical events, including stroke recurrence, hospital readmissions, or development of new medical conditions, were recorded.
Data were collected using electronic case report forms with built-in logic checks to ensure data quality. All assessments were performed according to standardized operating procedures, and regular monitoring visits were conducted to verify data accuracy and completeness. A dedicated research coordinator oversaw data collection and maintained regular communication with study personnel to promptly address any issues.
The sample size was calculated based on post-stroke depression prevalence identified by previous studies, assuming a 30% prevalence rate with a 5% margin of error and 95%CI; a minimum of 120 participants was determined as the sample size. Accounting for potential dropouts (15%), we aimed to recruit 138 patients.
Statistical analyses were performed using SPSS version 26.0 (IBM Corp., Armonk, NY, United States). Continuous variables are expressed as mean ± SD or medians with interquartile ranges, depending on data distribution. Categorical variables are presented as frequencies and percentages. The Kolmogorov-Smirnov test was used to assess normality of continuous variables.
The associations between psychiatric symptoms and clinical variables were analyzed using appropriate statistical tests. For continuous variables, Student’s t-test or Mann-Whitney U test was applied based on data distribution. χ^2^ or Fisher’s exact test was employed for categorical variables. Multivariate logistic regression analysis was performed to identify independent predictors of depression and anxiety, adjusting for potential confounding factors. Temporal changes in psychiatric symptoms were analyzed using repeated measures analysis of variance or Friedman’s test, as appropriate. Missing data were handled using multiple imputation techniques when the missing rate was < 20%. Statistical significance was set at P < 0.05, and all tests were two-tailed.
A total of 156 patients with ischemic stroke were screened for eligibility between June 2022 and June 2024. After applying inclusion and exclusion criteria, 127 patients were enrolled in the study, of whom 120 (94.5%) completed all follow-up assessments. The mean age of the study population was 65.7 ± 11.3 years, and 68 patients (56.7%) were male. The median NIHSS score at admission was 6 (interquartile 3-9), indicating predominantly mild to moderate stroke severity. Baseline demographic and clinical characteristics of the study population are presented in Table 1.
The overall prevalence of depression (Hamilton Depression Rating Scale score ≥ 7) at baseline assessment was 37.5% (45/120); 22 patients (18.3%) had mild depression, 15 (12.5%) had moderate depression, and 8 (6.7%) had severe depression. Anxiety symptoms (Hamilton Anxiety Rating Scale score ≥ 7) were present in 41.7% (50/120) of patients. The distribution patterns are shown in Table 2.
Longitudinal assessment revealed significant changes in both depression and anxiety symptoms over the 6-month follow-up period. The prevalence of depression showed a biphasic pattern, with an initial peak at 2 weeks post-stroke (37.5%), followed by a gradual decline at 1 month (32.5%) and 3 months (28.3%), before showing a slight increase at 6 months (30.8%). These temporal changes are detailed in Table 3.
Multivariate analysis identified several independent predictors of post-stroke depression and anxiety. Stroke severity (NIHSS score) was significantly positively correlated with both depression [odds ratio (OR) = 1.18, 95% confidence interval (CI): 1.06-1.31, P = 0.003] and anxiety (OR = 1.15, 95%CI: 1.04-1.27, P = 0.008). The relationship between stroke location and psychiatric symptoms are presented in Table 4.
Analysis of functional outcomes revealed that patients with depression or anxiety showed significantly poorer functional recovery at 6 months, as measured using the mRS scores (median mRS 3 vs 2, P = 0.015). Moreover, the occurrence of psychiatric symptoms was associated with longer hospital stays (mean 3.2 days, 95%CI: 1.5-4.9, P = 0.002) and higher rates of hospital readmission within 6 months (OR = 2.34, 95%CI: 1.28-4.27, P = 0.006).
This prospective observational study provides comprehensive insights into the prevalence, temporal patterns, and clinical correlates of depression and anxiety among patients with ischemic stroke. Our findings indicate that 37.5% of patients had depression and 41.7% experienced anxiety during the initial post-stroke period, thereby revealing that psychiatric complications are common sequelae of stroke. These prevalence rates align with recent systematic reviews, which report post-stroke depression rates of 31%-39% and anxiety rates of 38%-45%[16,17].
The temporal evolution of psychiatric symptoms in our study demonstrates a complex pattern that differs from traditional understanding. The biphasic pattern of depression prevalence, with an initial peak at 2 weeks post-stroke followed by a partial resolution and a subsequent slight increase at 6 months, suggests different underlying mechanisms at different stages of recovery. This pattern may reflect the initial impact of sudden functional loss and neurobiological changes, followed by a period of adjustment, and the subsequent effect of chronic stress and adaptation challenges[18]. Similar patterns have been reported in recent longitudinal studies, though with varying time courses[19].
The association between stroke severity and psychiatric symptoms observed in our study merits particular attention. Patients with higher NIHSS scores showed significantly increased risk for both depression and anxiety, supporting the hypothesis that more severe neurological deficits cause increased psychological distress[20]. However, the relationship between stroke severity and psychiatric symptoms appears to be bidirectional, as evidenced by the poorer functional outcomes observed in patients with psychiatric complications. This finding is consistent with that of recent neuroimaging studies, suggesting that depression and anxiety may interfere with neural plasticity and rehabilitation processes[21].
The location-specific analysis of stroke lesions revealed interesting patterns, with left hemisphere infarcts showing a stronger association with both depression and anxiety compared to right hemisphere lesions. This hemispheric asymmetry in psychiatric manifestations supports emerging neurobiological models of mood regulation[22]. The higher prevalence of psychiatric symptoms in patients with anterior circulation strokes, particularly those affecting the frontal-subcortical circuits, corresponds with the current understanding of the neural substrates of emotion regulation[23]. These findings provide additional support for the “vascular depression hypothesis” and suggest potential mechanisms through which stroke may precipitate psychiatric symptoms[24].
Prolonged hospital stays and increased readmission rates among patients with psychiatric complications have significant clinical and economic implications. Recent healthcare economic analyses have shown that post-stroke psychiatric complications can increase healthcare costs by 35%-45% during the first year after stroke[25]. The association between psychiatric symptoms and poorer functional outcomes, as measured using mRS scores, underscores the importance of early recognition and appropriate intervention[26].
The demographic and clinical risk factors identified in our study provide valuable insights for clinical practice. The higher prevalence of psychiatric symptoms among patients with limited social support and lower educational levels highlights the importance of psychosocial factors in post-stroke recovery[27]. These findings necessitate the implementation of comprehensive stroke care models that incorporate psychological assessment and support into standard rehabilitation protocols[28].
The pattern of anxiety symptoms observed in our cohort, while closely related to depressive symptoms, showed some distinct characteristics. The slightly higher prevalence of anxiety compared to depression in the early post-stroke period suggests that anxiety may be an early indicator of psychological distress[29]. The gradual decrease in prevalence of anxiety over time, while less pronounced than the changes in depression rates, indicates different temporal dynamics for these two conditions[30].
The impact of psychiatric complications on functional recovery observed in our study has important implications for rehabilitation strategies. The significant difference in mRS scores between patients with and without psychiatric symptoms at 6 months suggests that psychological status may be a crucial determinant of rehabilitation outcomes[31]. This finding is particularly relevant given recent evidence that early psychological intervention can improve both mental health and functional outcomes post-stroke[32].
Our analysis of the relationship between stroke location and psychiatric symptoms adds to accumulating evidence regarding the neuroanatomical basis of post-stroke psychiatric complications. The higher prevalence of both depression and anxiety in patients with anterior circulation strokes, particularly those affecting the left hemisphere, provides further support for the role of specific neural circuits in mood regulation[33]. These findings may enable the development of more targeted therapeutic approaches based on stroke location and affected neural networks[34].
Although our study provides valuable insights into post-stroke psychiatric complications, it has several limitations. First, the follow-up period of 6 months is a short duration for assessing the long-term trajectory of psychiatric symptoms. Future studies should implement longer follow-up periods to better understand the chronicity of depression and anxiety and their impact on long-term recovery outcomes. Second, while we adjusted for several potential confounders, other unmeasured variables potentially influenced the results. Future research should consider additional factors, such as medication use, pre-existing subclinical psychiatric symptoms, comorbidities, and lifestyle factors that might affect both stroke outcomes and psychiatric manifestations. Third, our study focused primarily on the prevalence and correlates of psychiatric symptoms rather than on intervention strategies. Future research should explore the effectiveness of psychosocial interventions, such as cognitive-behavioral therapy and support groups, in reducing the risk of psychiatric complications and improving recovery outcomes.
The identification of a biphasic pattern in depression prevalence emphasizes the need for early and ongoing psychiatric support throughout the recovery process. Future studies should investigate the neurobiological mechanisms underlying these temporal patterns and develop targeted interventions. Additionally, the stronger association between left hemisphere lesions and psychiatric symptoms warrants further investigation into the neural pathways involved in post-stroke mood regulation. The findings of this study support the implementation of integrated care models that address both physical and psychological aspects of stroke recovery. Research on optimal approaches to include routine psychiatric screening and intervention with standard stroke care protocols could significantly impact patient outcomes and healthcare utilization. Development of prediction models incorporating the risk factors identified in this study could facilitate early identification of at-risk patients and personalized intervention strategies.
This study demonstrates that depression and anxiety are common complications following ischemic stroke, with distinct temporal patterns and significant effects on functional recovery. The identification of specific clinical and neuroanatomical correlates of post-stroke psychiatric symptoms provides valuable insights for risk stratification and patient management. The biphasic pattern observed in depression prevalence underscores the dynamic nature of psychiatric symptoms and suggests the need for early and ongoing monitoring throughout the recovery process. The strong association between psychiatric complications and poorer functional outcomes, including longer hospital stays and higher readmission rates, emphasizes the importance of integrating psychological assessment and support with standard stroke care protocols. The identification of limited social support and lower educational levels as risk factors highlights the importance of addressing psychosocial determinants of health in comprehensive stroke care. These findings support the implementation of routine screening for depression and anxiety in patients with stroke, and suggest that early identification and management of psychiatric symptoms may be crucial for optimizing recovery outcomes. The integration of psychiatric care into stroke rehabilitation represents a promising approach to improve both mental health and functional outcomes in this vulnerable patient population. Future research should further elucidate the mechanisms underlying post-stroke psychiatric symptoms and develop effective interventions to improve outcomes for stroke survivors.