No abstract

Cognitive function, once improved after remission of poststroke depression, is likely to remain stable over the next 2 years in the absence of subsequent reinjury to the central nervous system. Cognitive impairment due to poststroke depression is reversible and can be quantified separately from cognitive impairment on the basis of the location and extent of ischemic brain damage.

This study examined the effect of antidepressants in preventing depression after stroke. Nondepressed poststroke patients (N = 48) were randomly assigned to receive nortriptyline, fluoxetine, or placebo for 3 months by using double-blind methodology and were followed-up for 21 months by using a naturalistic design. During the treatment period, one minor depression developed in the nortriptyline group (n = 13 at 3 months), one minor depression developed in the fluoxetine group (n = 13), and five minor depressions developed in the placebo group (n = 15; p <.05). When treatment was discontinued, nortriptyline-treated patients were more likely to develop depression and had significantly more severe depressive symptoms during the next 6 months compared with patients in the other two groups. Both nortriptyline and fluoxetine appeared to be efficacious in preventing depression after stroke. However, nortriptyline produced an increased vulnerability to depression for more than 6 months after it was discontinued. This finding suggests the need to extend prophylactic treatment and monitor patients carefully after the discontinuation of nortriptyline.

A recent publication based on a meta-analysis concluded that there was no association between poststroke depression (PSD) and lesion location. This study, therefore, was undertaken to reappraise the hypothesis using meta-analysis of the correlation between severity of depression following stroke and proximity of the lesion to the frontal pole, an issue that was not examined in the prior meta-analysis. Results showed there was a significant inverse correlation between severity of depression and distance of the lesion from the frontal pole among 163 patients with left hemisphere stroke but not among 106 patients with right hemisphere stroke. This study supports the hypothesis that risk of poststroke depression is related to the location of brain injury.

Antidepressant treatment fosters long-term improvement of executive function following stroke. This phenomenon is consistent with a reorganisation of neuronal networks associated with prefrontal functions based on modulation of monoaminergic neurotransmission and the activity of neurotrophins.

Impairments in activities of daily living (ADL) are common after stroke and may be related to poststroke depression. We have demonstrated that remission of poststroke major depression was associated with improvement in ADL. The administration of antidepressants within the first 3 months after stroke has been shown to prevent poststroke depression, early administration might also improve recovery of ADL among patients with stroke. This study examines the effect of early versus late treatment with antidepressants on recovery in ADL. Among 62 patients after stroke, the therapeutic effect of a 3-month course of antidepressants begun during the first month after stroke was compared with the effect of treatment begun after 1 month. The severity of impairment was measured using the Functional Independence Measure (FIM) and post-treatment outcome was assessed over the following 21 months. Although both the early and late treatment groups showed improvements in FIM scores during the 3 months of treatment, the early treatment group improved significantly more than the late treatment group. After the treatment, the early treatment group maintained this improvement over 2 years while the late treatment group deteriorated over time. There were no significant differences in the 2 groups that would explain the findings. Recovery in ADL impairment after stroke appeared to be enhanced by the use of antidepressant medication if treatment was started within the first month after stroke. These findings are consistent with the hypothesis that there may be a time-related therapeutic window in the treatment of physical impairment associated with poststroke depression.

Repetitive transcranial magnetic stimulation (rTMS) is an effective treatment for depression. Increased metabolism in the anterior cingulate cortex (ACC) is a known predictor for antidepressant response. The authors assessed whether increased theta power within the ACC predicts rTMS response in participants with vascular depression. Sixty-five participants were randomized to active or sham rTMS. Outcome was assessed using the Hamilton Depression Rating Scale. Electroencephalography was obtained, and comparisons were made among each group with a normative database using low-resolution electromagnetic tomography. Results suggest that vascular depression participants respond well to rTMS and that increased low-theta power in the subgenual ACC predicts response to rTMS.A modern apparatus of repetitive transcranial magnetic stimulation (rTMS) was developed in Great Britain in 1985. 1 Since then, rTMS has been utilized to provide noninvasive brain stimulation for research and treatment purposes. The most frequent application of rTMS in psychiatry has been as a treatment for major depression, and the first controlled treatment study was published in 1996. 2 Although a large number of studies have suggested that rTMS is efficacious against depression, a recent review found that the efficacy can be quite variable. 3 This may be due to the fact that the etiological factors underlying major depression are heterogeneous, causing some forms of depression to respond better to rTMS than others. Repetitive transcranial magnetic stimulation has already been approved as a standard treatment procedure for depression in some countries such as Canada and Israel; however, it has only recently been approved by the Food and Drug Administration in the United States.The term "vascular depression" has been used to describe depression in elderly patients with cerebrovascular disease. A causal relationship between cerebrovascular disease and late-life depression is supported by evidence such as coexistence of depression with hypertension, coronary artery disease, and multiple hyperintensities on brain imaging. 4 Patients with latelife depression often have a chronic, treatment resistant course and frequently meet criteria for vascular depression. 5 Predictors of response to different antidepressant treatment modalities are a growing area of clinical research interest. Higher than normal activity in the rostral anterior cingulate cortex (ACC) has been shown to predict response to antidepressant medication in patients with major depression. 6-9 High theta power in the rostral ACC has also been found to predict response in a similar population. 10 This same group found that metabolism and theta activity are linked in this region. 11 However, functional abnormalities in this region do not change in response to antidepressant treatment. Treatment response to antidepressants has been correlated to change in the subgenual region of the ACC. 12 It is unclear whether this is a normalization of high metabolism or a resetting to a new lower l...

Repetitive transcranial magnetic stimulation (rTMS) is an effective treatment for depression. Increased metabolism in the anterior cingulate cortex (ACC) is a known predictor for antidepressant response. The authors assessed whether increased theta power within the ACC predicts rTMS response in participants with vascular depression. Sixty-five participants were randomized to active or sham rTMS. Outcome was assessed using the Hamilton Depression Rating Scale. Electroencephalography was obtained, and comparisons were made among each group with a normative database using low-resolution electromagnetic tomography. Results suggest that vascular depression participants respond well to rTMS and that increased low-theta power in the subgenual ACC predicts response to rTMS.