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Poststroke depression (PSD) has been recognized by psychiatrists for more than 100 years, but controlled systematic studies did not begin until the 1970s. Meta-analyses addressing almost all major clinical issues in the field have emerged because of the relatively small number of patients included in some stroke studies. In order to build large databases, these meta-analyses have merged patients with rigorously assessed mood disorders with major depressive features with patients scoring above arbitrary cutoff points on depression rating scales, thus missing important findings such as cognitive impairment associated with major but not minor depression. Nevertheless, PSD occurs in a significant number of patients and constitutes an important complication of stroke, leading to greater disability as well as increased mortality. The most clinically important advances, however, have been in the treatment and prevention of PSD. Recent meta-analyses of randomized controlled trials for the treatment of PSD have demonstrated the efficacy of antidepressants. Similarly, randomized controlled trials for prevention of PSD have shown that antidepressants significantly decrease the incidence of PSD compared with placebo. Early antidepressant treatment of PSD appears to enhance both physical and cognitive recovery from stroke and might increase survival up to 10 years following stroke. There has also been progress in understanding the pathophysiology of PSD. Inflammatory processes might be associated with the onset of at least some depressive symptoms. In addition, genetic and epigenetic variations, white matter disease, cerebrovascular deregulation, altered neuroplasticity, and changes in glutamate neurotransmission might be relevant etiological factors. Further elucidation of the mechanism of PSD may ultimately lead to specific targeted treatments. [ABSTRACT FROM AUTHOR]

Objective: This study examined the frequency of major and minor depression in Alzheimer's disease and determined whether these types of depression have a different functional and psychopathologi- cal impact and whether there is a change in the prevalence of major and minor de- pression throughout the stages of Alzhei- mer's disease. Method: A consecutive series of 670 pa- tients with probable Alzheimer's disease were assessed with the Structured Clinical Interview for DSM-IV; specific instruments to rate the presence and severity of depres- sion, anxiety, apathy, irritability, delusions, pathological affective crying, performance of activities of daily living, and social func- tioning; and a standardized neuropsycho- logical evaluation. Diagnoses of major and minor depression were generated from DSM-IV criteria. Results: Twenty-six percent of the pa- tients had major depression, 26% had minor depression, and 48% were not depressed. Major depression was signifi- cantly associated with sad mood in all three stages of the illness, although this as- sociation dropped significantly for minor depression in severe Alzheimer's disease. Both major and minor depression were significantly associated with more severe psychopathology, functional impairments, and social dysfunction. Depressive symp- toms that most strongly discriminated be- tween Alzheimer's disease patients with and without sad mood were guilty ide- ation, suicidal ideation, toss of energy, in- somnia, weight loss, psychomotor retarda- tion/agitation, poor concentration, and loss of interest. Conclusions: Our study demonstrates that DSM-IV criteria for major and minor depression identify clinically relevant syndromes of depression in Alzheimer's disease, mild levels of depression can pro- duce significant functional impairment, and the severity of psychopathological and neurological impairments increases with increasing severity of depression. [ABSTRACT FROM AUTHOR]

Assesses whether antidepressant treatment would reduce poststroke mortality over nine years of follow-up. Use of the Kaplan-Meier method; Efficacy of fluoxetine or nortriptyline; Effects of other factors associated with mortality; Impairment in cognitive functioning.

Objective: Cognitive impairment is common after stroke and may be caused by poststroke depression. Remission of poststroke major depression after treatment has been associated with improvement in cognitive function. The current study was designed to examine how long that cognitive improvement lasts and to compare depressed patients' cognitive status with that of nondepressed patients with comparable lesions. Method: Seventeen patients with poststroke depression and cognitive impairment who had early and sustained remission of their depression during a doubleblind treatment study were compared with 42 nondepressed stroke patients who remained nondepressed throughout the follow-up. Mood and cognitive function were followed-up over 2 years with the Hamilton Depression Rating Scale and Mini-Mental State Examination (MMSE). Results: In the patients with early and sustained remission of depression, there was rapid improvement of cognitive function, which was maintained over 2 years. Their initial MMSE score of 23.3 (SD=4.2) improved to 26.6 (SD=3.5) at 3 months and was 26.1 (SD=3.6) at 2 years. The nondepressed patients showed essentially no change in cognitive function over 2 years (initial MMSE score: mean=26.3, SD=3.1; score at 2-year follow-up: mean= 25.7, SD=4.1). Conclusions: Cognitive function, once improved after remission of poststroke depression, is likely to remain stable over the next 2 years in the absence of subsequent rein jury 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. [ABSTRACT FROM AUTHOR]

Objective: This study compared nortriptyline and fluoxetine with placebo in the treatment of depression and in recovery from physical and cognitive impairments after stroke. Method: A total of 104 patients with acute stroke enrolled between 1991 and 1997 entered a double-blind randomized study comparing nortriptyline, fluoxetine, and placebo over 12 weeks of treatment. The majority of patients were recruited from a rehabilitation hospital in Des Moines, Iowa, but other enrollment sites were also used. Both depressed and nondepressed patients were enrolled to determine whether improved recovery could be mediated by mechanisms unrelated to depression. Nortriptyline in doses of 25 mg/day gradually increased to 100 mg/day or fluoxetine in doses of 10 mg/day gradually increased to 40 mg/day or identical placebo were given over 12 weeks. Response to treatment of depression for individual patients was defined as a greater-than-50% reduction in scores on the Hamilton Rating Scale for Depression and no longer fulfilling diagnostic criteria for major or minor depression. Improved recovery for a treatment group was defined as a significantly higher mean score from baseline to end of the treatment trial, compared with patients treated with placebo, on measures of impairment in activities of daily living and levels of cognitive and social functioning. Results: Nortriptyline produced a significantly higher response rate than fluoxetine or placebo in treating poststroke depression, in improving anxiety symptoms, and in improving recovery of activities of daily living as measured by the Functional Independence Measure. There was no effect of nortriptyline or fluoxetine on recovery of cognitive or social functioning among depressed or nondepressed patients. Fluoxetine in increasing doses of 10-40 mg/day led to an average weight loss of 15. 1 pounds (8% of initial body weight) over 12 weeks of treatment that was not seen with nortriptyline or placebo. Conclusions: Given the doses of medication used in this study, nortriptyline was superior to fluoxetine in the treatment of poststroke depression. Demonstrating a benefit of antidepressant treatment in recovery from stroke may require the identification of specific subgroups of patients, alternative measurement scales, or the optimal time of treatment. [ABSTRACT FROM AUTHOR]

Identifies brain structures associated with emotion in normal elderly subjects. Emotional activation and increased blood flow; Brain activation as emotion-specific; Involvement of complex sensory, association and memory circuitry; Studies on identification of specific activations for emotions.

Examines patients during the first year after traumatic brain injury to determine the presence of secondary mania. Semistructured psychiatric interview; Measurement of activity impairments; Presence of temporal basal polar lesions; Severity of brain injury; Level of social functioning; Previous family or personal history of psychiatric disorder.

Tests the reliability and validity of the Pathological Laughter and Crying Scale and the effectiveness of nortriptyline treatment for patients with emotional lability following stroke, with findings confirming the reliability of the scale and the effectiveness of nortriptyline. Reliability-validity study; Treatment study.

Examines the effect of depression on mortality among a group of stroke patients followed up for 10 years. Computed tomography (CT) scans; Present State Examination; Hamilton Rating Scale for Depression; Mini-Mental State examination; Johns Hopkins Functioning Inventory; 10-item Social Ties Checklist; Social Functioning Examination; Stroke Data Bank; Method; Results; Discussion.

Objective: Some investigators have suggested that major depression might be overdiagnosed in stroke patients because of changes in appetite, sleep, or sexual interest caused by their medical illness; others have suggested that depression may be underdiagnosed in stroke patients who deny symptoms of depression because of anosognosia, neglect, or aprosody. The authors' goal was to determine how frequently depressive symptoms occur in acute stroke patients with and without depressed mood to estimate how often diagnostic errors of inclusion or exclusion may be made. Method: They examined the rate of autonomic and psychological symptoms of depression in 205 patients who were consecutively hospitalized for acute stroke. Eighty-five (41%) of these patients had depressed mood, and 120 (59%) had no mood disturbance. Forty-six (54%) of the 85 patients with depressed mood (22% of all patients) were assigned the DSM-III diagnosis of major depression. Results: The 120 patients without mood disturbance had a mean of one autonomic symptom, but the 85 patients with depressed mood had a mean of almost four. Tightening the diagnostic criteria to account for one more nonspecific autonomic symptom decreased the number of patients with major depression by only three; adding two more criteria decreased the number by only five. Thus, the rate of DSM-III major depression was 1% higher than the rate with one extra nonspecific autonomic symptom and 2% higher than the rate with two extra criteria. Conversely, loosening diagnostic criteria to account for denial of depressive illness increased the rate of major depression by only 5%. Conclusions: Both autonomic and psychological depressive symptoms are strongly associated with depressed mood in acute stroke patients. [ABSTRACT FROM AUTHOR]

In a group of stroke patients with left-hemisphere lesions, those with major depression performed significantly below nondepressed patients on four of nine cognitive domains examined with a neuropsychological test battery. Among patients with right-hemisphere stroke, those with major depression did not perform below nondepressed patients on any of the nine cognitive domains. The differential effect of depression on cognitive performance between left- and right-hemisphere lesion groups could not be accounted for by demographic variables, neurological symptoms, lesion location, or lesion size. Poststroke major depression appeared to produce a decline in cognitive performance or dementia of depression that depended on the laterality of the lesion. [ABSTRACT FROM AUTHOR]

Patients with right-hemisphere strokes (N=9) more than 1 year after injury had greater cortical binding of (3-N-[11C]methyl)spiperone than a similar group of patients with left-hemisphere strokes (N=8) or normal control subjects (N= 17). The higher S2 serotonin receptor binding occurred in uninjured regions of the right parietal and temporal cortex. The ratio of binding in the ipsilateral to contralateral cortex showed a significant negative correlation with severity of depression scores in the left temporal cortex. These findings suggest that the biochemical response of the brain may be different depending on which hemisphere is injured and that some depressions may be a consequence of the failure to upregulate serotonin receptors after stroke. [ABSTRACT FROM AUTHOR]

Patients who developed secondary mania after brain injury (N=17) had a significantly greater frequency of injury to right hemisphere areas connected with the limbic system than poststroke patients with major depression (N=31), who had injury primarily in the left frontal cortex and basal ganglia. For patients without mood disturbance after brain injury (N=28), the location of the lesion was not significant. Secondary mania patients also had a significantly greater frequency of family history of affective disorder than did the other two groups. These results suggest that an interaction between injury to certain areas of the right hemisphere and genetic factors or other neuro pathological conditions produces secondary mania. [ABSTRACT FROM AUTHOR]

The article discusses on the HIV-related secondary mania in Uganda where 141 patients were admitted to a hospital over a 6-month period with first-episode acute mania. Moreover, of the 77 patients, 55 percent were HIV positive and 61 were diagnosed for having HIV-related secondary mania because they had no personal or family history of mood disorder.

A response by Robert G. Robinson and associates to a letter to the editor about their article "Two-Year Longitudinal Study of Poststroke Mood Disorder: Comparison of Acute-Onset With Delayed-Onset Depression" in a 1986 issue of the "American Journal of Psychiatry" is presented.