Poststroke depression: prevalence, diagnosis, treatment, and disease progression.

In recent years, poststroke depression has attracted worldwide interest. This review focuses on the major research themes that have emerged. Pooled data from studies conducted throughout the world have found prevalence rates for major depression of 19.3% among hospitalized patients and 23.3% among outpatient samples. The diagnosis of poststroke depression is most appropriately based on a structured mental state exam and DSM-IV criteria for depression due to stroke with major depressive-like episode or depressive features. Rarely, poststroke patients may also develop bipolar mood disorder. The treatment of poststroke depression has been examined in several placebo-controlled randomized clinical trials with both nortriptyline and citalopram showing efficacy. The progression of recovery following stroke can be altered by treating depression, which has been shown to improve recovery in activities of daily living and cognitive impairment and to decrease mortality. In addition, two studies have demonstrated that poststroke depression can be prevented using antidepressant medication, which also decreases the frequency of associated physical illness. Furthermore, two studies have shown that premorbid depression can significantly increase the risk of stroke over the subsequent 10-15 years. The mechanisms underlying the association of cerebrovascular diseases and mood disorder are important areas for future investigation.     

Pathological correlates of poststroke depression in elderly patients.

OBJECTIVE: The authors examined the relationship between poststroke depression and location of stroke. METHODS: They performed a clinicopathological analysis of 95 consecutively autopsied elderly initial-stroke survivors. RESULTS: The severity of brain vessel arteriosclerosis and frequency of brain vascular lesions were not significantly different between 21 cases with poststroke depression and 74 cases without. Earlier death was the only variable significantly associated with poststroke depression. No lesion pattern characterized the depression group. CONCLUSIONS: Neuropathological data confirm that depression is associated with worse prognosis in elderly stroke patients and lend support to the hypothesis that psychological rather than neurological factors are the main determinants of poststroke depression.     

The Effect of Poststroke Depression on Recovery from Stroke

Background : Stroke is a major health problem and poststroke depression is known to be one of the frequent and severe psychiatric complications following stroke.
Methods : Based on the results of structured psychiatric mental state exams and DSM diagnostic criteria, the prevalence of poststroke depression has been examined in numerous study populations throughout the world. Longitudinal examinations have documented the effect of poststroke depression on recovery from stroke.
Results : The mean prevalence of poststroke major depression was 21.1 % and minor depression was 17.1% among hospitalized or outpatient samples. Community samples showed a slightly lower rate of 14.1% and 9.1%, respectively. Furthermore, the existence of poststroke depression leads to poorer physical recovery, greater cognitive impairment, and worse recovery in activities of daily living compared with non-depressed patients. Several studies have also found that poststroke depression is associated with increased mortality compared with non-depressed patients who had comparable strokes and similar premorbid risk factors. Finally, several studies have found that successful treatment of poststroke depression improves both cognitive and physical recovery and decreases mortality.
Conclusion : The current review documents the beneficial effect of identifying and treating poststroke depression on both recovery and survival following stroke.     

Impact of medical comorbid disease on antidepressant treatment of major depressive disorder

A major factor in evaluating and treating depression is the presence of comorbid medical problems. In this paper, the authors will first evaluate studies showing that medical illness is a risk factor for depression. The authors will review a series of randomized, controlled studies of antidepressant treatment in subjects with major depressive disorder (MDD) and comorbid medical illnesses (myocardial infarction, stroke, diabetes, cancer, and rheumatoid arthritis). Most of these studies report an advantage for an active antidepressant over placebo in improvement of depressive symptoms. The authors also will review a series of studies in which the outcome of antidepressant treatment is compared between subjects with MDD with and without comorbid medical illness. In these studies, subjects with medical illness tend to have lower improvement of depressive symptoms and higher rates of depressive relapse with antidepressant treatment compared with MDD subjects with no medical comorbidity. In addition, the authors will review hypotheses on the mechanism of the interaction between medical illness and clinical response in MDD. The paper will conclude that medical comorbidity is a predictor of treatment resistance in MDD.     

Inflammation and the Silent Sequelae of Stroke

Depression and fatigue are common after stroke and negatively impact the quality of life of stroke survivors. The biological bases of these symptoms are unknown, but an abundance of data point to a role for inflammation. This review highlights evidence supporting the contribution of inflammation to poststroke depression and poststroke fatigue. Potential treatments for poststroke depression and poststroke fatigue are explored, with a special emphasis on those that modulate the immune response.     

Risk factors for and correlates of poststroke depression following discontinuation of antidepressants

The authors randomly assigned nondepressed patients at least 3 months poststroke to receive nortriptyline, fluoxetine, or placebo for 3 months using double-blind methodology. Patients were followed at 3, 6, 9, and 21 months for new onset of depression. In patients treated with antidepressants, lesion volume and degree of social impairment were associated with subsequent late-onset of poststroke depression at 6 and 9 months. In the placebo group, severity of impairment in activities of daily living, at 3 and 9 months, was associated with late onset poststroke depression. Differences in the clinical/pathological correlates may reflect subtle differences in the pathophysiology of poststroke depression following prophylactic antidepressants.     

Depression and other mental health diagnoses increase mortality risk after ischemic stroke

OBJECTIVE: Poststroke depression has been linked to higher mortality after stroke. However, the effect of other mental health conditions on poststroke mortality has not been examined. The objective of this study was to evaluate the effect of poststroke depression and other mental health diagnoses on mortality after ischemic stroke. METHOD: The authors examined a national cohort of veterans hospitalized after an ischemic stroke at any U.S. Department of Veterans Affairs (VA) medical center from 1990 to 1998. Demographic, admission, and all-cause mortality data were abstracted from VA administrative databases. Chronic conditions present at discharge and new poststroke depression and other mental health diagnoses within 3 years after the stroke were identified with ICD-9 codes. Mortality hazard ratios were modeled by using Cox regression models. RESULTS: A total of 51,119 patients hospitalized after an ischemic stroke who survived beyond 30 days afterward were identified; 2,405 (5%) received a diagnosis of depression, and 2,257 (4%) received another mental health diagnosis within 3 years of their stroke. Patients with poststroke depression were younger, more often white, and less likely to be alive at the end of the 3-year follow-up period. Both poststroke depression (hazard ratio=1.13, 95% CI=1.06-1.21) and other mental health diagnoses (hazard ratio=1.13, 95% CI=1.07-1.22) independently increased the hazard for death even after other chronic conditions were controlled. CONCLUSIONS: Despite being younger and having fewer chronic conditions, a higher 3-year mortality risk was seen in patients with poststroke depression and other mental health diagnoses after hospitalization for an ischemic stroke. The biological and psychosocial mechanisms driving this greater risk should be further explored, and the effect of depression treatment on mortality after stroke should be tested.     

The dexamethasone suppression test and mood following stroke

Dexamethasone suppression tests (DSTs) were given to 65 acute and chronic stroke patients. For patients who had had a stroke less than 1 year earlier, nonsuppression on the DST was significantly associated with the presence of poststroke depression. The authors, who used the DSM-III symptom criteria for major depression, found that DST sensitivity was 67% but specificity was only 70%. False positive tests in the stroke patients seemed related to large lesion volume. The DST, although of limited clinical utility in this population because of false positive tests, may help define more homogeneous subtypes of poststroke depression for research.     

Methylphenidate in treating poststroke depression

The authors retrospectively studied the charts of 25 patients with poststroke depression who were treated with methylphenidate. The 13 patients (52%) who recovered completely from their depression did not differ significantly from the 12 nonresponders on demographic characteristics, location of cerebrovascular accident, and other variables. Mood usually improved within 48 hours; only 3 (12%) patients had side effects. Rapid response to treatment and lack of significant side effects indicate that methylphenidate may be a valuable treatment for poststroke depression.     

Phenomenological comparison of poststroke depression and functional depression

The authors used structured clinical interviews to compare depressive symptoms in 43 patients with poststroke major depression and 43 patients with major depression without a known medical cause. The depressive syndrome profiles in the two patient groups were highly similar.