We followed 16 patients who developed depression immediately after a stroke for 6 months. By that time, six patients showed no depression (recovered group), while 10 patients were still depressed (nonrecovered group). There were no significant differences in demographic variables and social functioning between the groups, but the nonrecovered group showed less improvement in cognitive function and more physical impairments. Patients in the nonrecovered group had mainly cortical lesions, while

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... ose in the recovered group had mainly subcortical and posterior circulation strokes. A ffective disturbance has been recognized for L \ many years to be a common sequela of J. \ . cerebral infarction. 1 Recent empirical studies have demonstrated that the frequency of depression is approximately 50% among hospitalized poststroke populations 2 -5 and approximately 30% among outpatient stroke populations. 6 We 7 -9 have consistently found a strong relation between lesion location and poststroke major depression. Major depression is significantly more frequent among patients with left anterior lesions than among patients with lesions in any other location. 7 In a recent study, we 89 found that patients with single lesions restricted to the left frontal cortex (without involvement of deep gray nuclei) had the same high frequency of depression as patients with strokes restricted to the left basal ganglia regions. Moreover, we 89 found that patients with left frontal cortical or basal ganglia lesions (mainly on the head of the caudate) had a significantly higher frequency of major depression than patients with right cortical, right basal ganglia, or left or right thalamic stroke lesions. From the