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.     

William Feinberg lecture 2002: emotions,mood, and behavior after stroke

While emotional outcome is a critical factor influencing early evolution and late prognosis after stroke, few relevant studies have been performed on this subject. However, mood changes, modified judgment, and emotional reactions may also dramatically alter recruitment into clinical trials; for instance, up to one third of patients with acute stroke may have altered time perception, inappropriate self-evaluation of their condition, and attentional or memory dysfunction, with a subsequent increase in referral-to-hospital delays. In addition, the value of the "informed" consenting process may be questionable in the setting of urgent randomization into an acute stroke clinical trial. Data from ongoing studies suggest that behavior and emotional reactions in acute stroke patients may be classified into a few broad categories, with considerable overlap. Correlations between mood changes and the type, location, and severity of stroke may provide useful information for improving patient management, including the prediction of functional evolution and late prognosis. While depressive reactions have been widely studied in the recovery-rehabilitation phase after stroke, significant depression is uncommon shortly after stroke. On the other hand, related, though different, emotional behavioral changes may be more frequent; these have often been confused with depression and include catastrophic reaction, emotionalism, and athymhormia. Late depression is the most common mood alteration during the first year after stroke and has specific characteristics that differentiate it from classic endogenous and reactive depression, thus emphasizing the critical role of brain damage in the pathogenesis of poststroke depression. Early recognition and management of mood disorders after stroke are critical for the functional improvement of individual patients. However, little is known about specific indications for different antidepressant drugs in poststroke depression and related disorders. Ongoing research has identified a "new" emotional-behavioral disorder, poststroke fatigue, which is clearly distinct from depression in most instances. It is especially disabling and frustrating in that it typically involves patients with total or near-total neurological recovery, who should have been able to go back to their previous activities but who become severely disabled because of early and persisting exhaustion. Preliminary neuropsychological and MR and PET imaging studies suggest that disruption of subtle mechanisms underlying attention, in the absence of significant cognitive and mood alterations, may be responsible. Research projects are now being launched to better delineate poststroke fatigue and its management.     

Treatment of cognitive impairment after poststroke depression : a double-blind treatment trial

BACKGROUND AND PURPOSE: Patients with poststroke major depression have a greater severity of cognitive impairment than nondepressed patients even when matched for size and location of stroke lesion. Prior treatment studies have consistently failed to show an improvement in cognitive function even when poststroke mood disorders responded to antidepressant therapy. We examined the response of cognitive function to treatment with nortriptyline or placebo in a double-blind trial. METHODS: Patients with major (n=33) or minor (n=14) depression participated in a double-blind treatment study with nortriptyline or placebo. They were examined for change in depressive mood, measured by the Hamilton Rating Scale for Depression (HAM-D), and change in cognitive impairment, assessed by the Mini-Mental State Examination (MMSE), after treatment with nortriptyline or placebo. Cognitive treatment response, as measured by the MMSE, was compared between patients whose depression did and did not respond to treatment. RESULTS: Patients whose poststroke depression remitted (predominantly associated with nortriptyline treatment) had significantly greater recovery in cognitive function over the course of the treatment study than patients whose mood disorder did not remit (predominantly associated with placebo treatment). CONCLUSIONS: Our findings support the contention that poststroke major depression leads to a "dementia of depression." Prior studies failed to show an effect of treatment because the effect size was too small. Successful treatment of depression may constitute one of the major methods of promoting cognitive recovery in victims of stroke.     

Little evidence for different phenomenology in poststroke depression

Cumming TB, Churilov L, Skoog I, Blomstrand C, Linden T. Little evidence for different phenomenology in poststroke depression. Objective: It remains unclear whether mood depressive disorders after stroke have a distinct phenomenology. We evaluated the symptom profile of poststroke depression (PSD) and assessed whether somatic symptoms were reported disproportionately by stroke patients. Method: The sample was 149 stroke patients at 18 months poststroke and 745 age‐ and sex‐matched general population controls. A comprehensive psychiatric interview was undertaken and depression was diagnosed according to DSM‐III‐R criteria. Results: Depressed controls reported more ‘inability to feel’ (P = 0.002) and ‘disturbed sleep’ (P = 0.008) than depressed stroke patients. Factor analysis of the 10 depressive symptoms identified two main factors, which appeared to represent somatic and psychological symptoms. There was no difference in scores on these two factors between stroke patients and controls. Conclusion: Phenomenology of depression at 18 months poststroke is broadly similar but not the same as that described by controls. Somatic symptoms of depression were not over‐reported by stroke patients.     

Antidepressants in bipolar disorder: the case for caution

The 2002 American Psychiatric Association (APA) guidelines for the treatment of bipolar disorder recommended more conservative use of antidepressants. This change in comparison with previous APA guidelines has been criticized, especially from some groups in Europe. The Munich group in particular has published a critique of assumptions underlying the conservative recommendations of the recent APA treatment guidelines. In this paper, we re-examine the argument put forward by the Munich group, and we demonstrate that indeed, conceptually and empirically, there is a strong rationale for a cautious approach to antidepressant use in bipolar disorder, consistent with, and perhaps even more strongly than, the APA guidelines. This rationale is based on support for the following four propositions: (i) The risk of antidepressant induced mood-cycling is high, (ii) Antidepressants have not been shown to definitively prevent completed suicides and reduce mortality, whereas lithium has, (iii) Antidepressants have not been shown to be more effective than mood stabilizers in acute bipolar depression and have been shown to be less effective than mood stabilizers in preventing depressive relapse in bipolar disorder and (iv) Mood stabilizers, especially lithium and lamotrigine, have been shown to be effective in acute and prophylactic treatment of bipolar depressive episodes. We therefore draw three conclusions from this interpretation of the evidence: (i) There are significant risks of mania and long-term worsening of bipolar illness with antidepressants, (ii) Antidepressants should generally be reserved for severe cases of acute bipolar depression and not routinely used in mild to moderate cases and (iii) Antidepressants should be discontinued after recovery from the depressive episode, and maintained only in those who repeatedly relapse after antidepressant discontinuation (a minority we judge to represent only about 15–20% of bipolar depressed patients).     

Do Stroke Patients have an Increased Risk of Developing Suicidal Ideation or Dying by Suicide? An Overview of the Current Literature

Stroke is a leading cause of death that affects 15 million people worldwide each year. Increasing evidence suggests that stroke confers substantial risk for suicide and following a stroke, patients frequently develop poststroke depression, which is a well‐established risk factor for suicide. In this overview of the current literature, we examined the association between suffering a stroke and subsequent risk for suicide and suicidal ideation. We performed a careful MedLine, Excerpta Medica, PsycLit, PsycInfo, and Index Medicus search to identify all articles and book chapters in English. We initially selected 31 articles published between 1990 and 2011; however, only 16 studies were included in this review. All articles identified stroke as a significant risk factor for suicide, especially among depressed patients, providing further support for poststroke depression and suicidality. The results also indicated that there were differences between patients who developed acute‐onset suicidal plans and those who reported delayed‐onset plans, which occurred more frequently. Many of the stroke patients who died by suicide suffered from depression prior to their death, suggesting that being diagnosed with a mood disorder contributes to an increased risk of suicide in this population. Suffering from a stroke increases the risk of dying by suicide and developing suicidal ideation, particularly in young adults and women. The factors found to confer the most risk for suicidality were depression, previous mood disorder, prior history of stroke, and cognitive impairment.     

The prospective impact of sleep duration on depression and mania

OBJECTIVE: Many patients report sleeping less than 6 h per night during episodes of depression and mania. This type of sleep deficit may also be a risk factor for subsequent mood episodes; however, the long-term impact of sleep deficit remains unclear. The current study is among few longitudinal studies to assess the prospective effect of sleep deficit on depression and mania. METHODS: A subsample of 54 individuals from a longitudinal study of bipolar I disorder was selected. Participants entered the study during a mood episode. Baseline symptom data were collected at month 4 to allow for recovery from the initial episode, sleep was assessed at month 6, and follow-up symptom data were obtained during months 7-12. RESULTS: Sleep deficit predicted depressive symptoms across the 6-month follow-up but not mania. CONCLUSIONS: It is likely that the impact of sleep deficit on mania was probably missed because assessments covered a full month. Monitoring sleep duration may help predict depression in bipolar disorder and provide an opportunity for targeting intervention.     

Quetiapine monotherapy for bipolar depression

Bipolar depression is more common, disabling, and difficult-to-treat than the manic and hypomanic phases that define bipolar disorder. Unlike the treatment of so-called "unipolar" depressions, antidepressants generally are not indicated as monotherapies for bipolar depressions and recent studies suggest that -even when used in combination with traditional mood stabilizers - antidepressants may have questionable value for bipolar depression. The current practice is that mood stabilizers are initiated first as monotherapies; however, the antidepressant efficacy of lithium and valproate is modest at best. Within this context the role of atypical antipsychotics is being evaluated. The combination of olanzapine and the antidepressant fluoxetine was the first treatment to receive regulatory approval in the US specifically for bipolar I depression. Quetiapine was the second medication to be approved for this indication, largely as the result of two pivotal trials known by the acronyms of BOLDER (BipOLar DEpRession) I and II. Both studies demonstrated that two doses of quetiapine (300 mg and 600 mg given once daily at bedtime) were significantly more effective than placebo, with no increased risk of patients switching into mania. Pooling the two studies, quetiapine was effective for both bipolar I and bipolar II depressions and for patients with (and without) a history of rapid cycling. The two doses were comparably effective in both studies. Although the efficacy of quetiapine monotherapy has been established, much additional research is necessary. Further studies are needed to more fully investigate dose-response relationships and comparing quetiapine monotherapy to other mood stabilizers (lithium, valproate, and lamotrigine) in bipolar depression, both singly and in combination. Head-to-head studies are needed comparing quetiapine to the olanzapine-fluoxetine combination. Longer-term studies are needed to confirm the persistence of response and to better gauge effects on metabolic profiles across months of therapy. A prospective study of patients specifically seeking treatment for rapid cycling and those with a history of treatment-emergent affective shifts also is needed. Despite the caveats, as treatment guidelines are revised to incorporate new data, the efficacy and tolerability of quetiapine monotherapy must be given serious consideration.     

Does Cognitive Impairment Cause Poststroke Depression?

Studies have demonstrated that poststroke depression is associated with cognitive impairment, but have failed to show improvement in cognitive function when mood improves. A consecutive series of patients with (n=41) or without (n=135) major depression were evaluated for cognitive functioning during acute hospitalization and either 3 or 6 months later. Patients with poststroke major depression whose mood improved at follow-up had significantly greater recovery in cognitive functioning than patients whose mood did not improve. Furthermore, patients whose cognitive functioning improved at follow-up had significantly greater improvement in mood than comparable patients whose cognitive function did not improve, suggesting that poststroke major depression leads to cognitive impairment and not vice versa. The failure of previous treatment studies to show cognitive improvement in poststroke patients with depression was probably due to the inclusion of patients with minor depression (not associated with cognitive impairment) or the failure of patients with major depression to respond to treatment.     

Electrophysiological changes in poststroke subjects with depressed mood: A quantitative EEG study

Background

We aimed to explore the electrophysiological changes in poststroke subjects with depressed mood.

Methods

Resting‐state electroencephalogram (EEG) signals of 16 electrodes in 35 poststroke depressed, 24 poststroke nondepressed, and 35 age‐matched healthy control subjects were analyzed by means of spectral power analysis, a quantitative EEG measurement of different frequency bands. The relationship among depressed mood, functional status, lesion side, and poststroke time was assessed by using variance and Spearman correlation analysis. Multiple analysis of variance was used to compare the differences among the 3 groups. Binary logistic regression analysis was used to establish a regression model to predict depressed mood in stroke subjects and to explore the association between depression and EEG band power. Receiver operating characteristic curves were used to estimate the ability of spectral power selected by binary logistic regression to indicate depressed mood in stroke subjects.

Results

We found that the hemisphere in which the lesion was located and the time since stroke onset had no effect on depressed mood. Only the patient's functional status was related to emotional symptoms. Quantitative EEG analysis revealed increased delta, theta, and beta2 power in stroke subjects with depressed mood, particularly in temporal regions. The theta and beta2 power in the right temporal area were shown to be highly sensitive to depressed mood, and these parameters showed good discriminatory ability for depressed subjects following stroke.

Conclusion

Depressed mood after stroke is associated with functional status. Quantitative EEG parameters may be a useful tool in timely screening for depressed mood after stroke.