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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous investigations by our group and others have demonstrated that poststroke depressions are not fully explained by the severity of associated impairment. We have consistently found, however, a strong association between development of major depression and left anterior brain injury. Recent studies have demonstrated that either left anterior cortical or subcortical lesions may lead to the development of major depression and that preexisting subcortical atrophy may play an important permissive role in the development of major depression. Patients with a mild degree of ventricular enlargement perhaps related to perinatal damage may be more likely to develop poststroke major depression following a lesion of the left frontal cortex or left basal ganglia than a patient without preexisting atrophy. Poststroke mania, on the other hand, is strongly associated with right hemisphere lesions as well as a preexisting subcortical atrophy and sometimes a family history of affective disorder. Thus, mania following brain injury may require the convergence of two factors: a right hemisphere brain injury and either a preexisting subcortical atrophy or a genetic vulnerability. PET scan findings have suggested that the biochemical response of the two hemispheres to stroke may be different. Right hemisphere stroke produces an increase in serotonin receptor binding, which is not found following comparable left hemisphere strokes. Within the left hemisphere, the lower the serotonin binding, the more severe the depression. This suggests that the right but not the left hemisphere may have an ability to increase serotonin binding in noninjured regions, producing a biochemical "compensation" for damage. This differential biochemical response to injury between the right and left hemisphere may partially explain why left hemisphere injury leads to depression and right hemisphere injury (in special circumstances) lead to mania. There remain, however, numerous unanswered questions and many important areas for future research. Although this area of neuropsychiatry is just beginning to develop, it is hoped that insights gained from studying mood disorders in brain-injured patients may also help to illuminate mechanisms involved in affective disorder in patients without brain injury.
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PMID:Mood disorders following stroke: new findings and future directions. 260 85

Depression is a serious complication of stroke. Although tricyclic antidepressants have well-established efficacy in the treatment of functional depression, they are not often used to treat depression following stroke. Studies have identified two types of depression in patients following stroke: major depression and minor depression. Longitudinal studies indicate that untreated major depression may last about 1 year, whereas untreated minor depression may last more than 2 years. Patients with depression who are not treated with antidepressant medication have been found to do more poorly on several measures of physical and cognitive rehabilitation than depressed patients who are treated. Two double-blind drug treatment studies of depression following stroke have been done. Although adverse side effects were reported in both studies, serious side effects were no more common in the active drug group than in the placebo group. Both studies, however, reported significantly better outcome, measured by depression scores or activities of daily living, in patients treated with nortriptyline or trazodone than in placebo-treated controls. Thus, although the use of antidepressant medication requires caution, the recognition and treatment of depression in patients who have had a stroke may result in a significant enhancement of both physical and cognitive recovery as well as emotional state.
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PMID:Tricyclic antidepressants in the treatment of poststroke depression. 266 48

Historical approaches of psychotherapy for depression are contrasted with current psychotherapeutic strategies. Now more strategies are focused, structured, time-limited, observable, testable, researchable and data based. The following depressive syndromes are reviewed in terms of the literature that demonstrates the effectiveness of psychotherapy: major depressive disorder, bipolar depressive disorder, depression associated with medical illness such as cancer, myocardial infarction and stroke, resistant depression post-traumatic stress disorder, grief reactions and depression during adolescence, mid-life and the geriatric period of the life cycle. A conceptual model favoring tripartite focus of intervention is recommended. Psychodynamic psychotherapy for depression must consider intrapsychic, interpersonal and family dynamics as well as social supports. A model for each population needs to be studied and developed further. Recommendations for current research are suggested. In the individual modification of psychotherapeutic approaches we must consider the varying maturity of ego defenses and the ego strength of the individual patient. Forty well-designed studies that demonstrate the effectiveness of psychotherapy in the depressive syndromes are quoted in this paper.
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PMID:Psychodynamic psychotherapy for the depressive syndrome. 266 95

Empirical studies have recently demonstrated that major and minor depressive disorders occur in 30-50% of stroke patients, and last more than one year without treatment, although they do respond to tricyclic antidepressants. These mood disorders are not strongly associated with severity of impairment, demographic characteristics, social supports or prior personal history, but major depression is often strongly associated with left frontal or left basal ganglia lesions and pre-existing subcortical atrophy. While the aetiology of these mood disorders remains unknown, serotonergic or noradrenergic dysfunction may play a role. Mania is a rare complication of stroke: the clinical presentation and response to treatment are usually the same as mania without brain injury. Post-stroke mania is strongly associated with both a right hemisphere lesion in a limbic-connected area and a second predisposing factor, such as genetic loading for affective disorder, pre-existing subcortical atrophy or seizure disorder. This disorder may be mediated through frontal lobe dysfunction. The lesion method represents a potentially fruitful technique for investigating the mechanisms of affective disorder.
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PMID:Affective disorders and cerebral vascular disease. 267 74

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.
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PMID:Lateralization of dementia of depression in stroke patients. 271 68

The number (Bmax) and affinity (Kd) of platelet-tritiated imipramine binding sites was determined in young and middle-aged controls 50 years of age and younger (n = 25), elderly normal controls over 60 years of age (n = 18), patients who fulfilled DSM-III criteria for major depression who were under 50 years of age (n = 29), patients who fulfilled DSM-III criteria for major depression who were 60 years of age and older (n = 19), and patients who fulfilled both DSM-III criteria for primary degenerative dementia and National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorders Association criteria for probable Alzheimer's disease (n = 13). Both groups of depressed patients (under 50 and over 60 years of age) exhibited significant reductions (decreases 42%) in the number of platelet-tritiated imipramine binding sites with no change in affinity, when compared with their age-matched controls. There was little overlap in Bmax values between the elderly depressed patients and their controls. The patients with probable Alzheimer's disease showed no alteration in platelet-tritiated imipramine binding. There was no statistically significant relationship between postdexamethasone plasma cortisol concentrations and tritiated imipramine binding. These results indicate that platelet-tritiated imipramine binding may have potential utility as a diagnostic adjunct in geriatric depression, and moreover that the reduction in the number of platelet-tritiated imipramine binding sites is not due to hypercortisolemia.
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PMID:Marked reduction in the number of platelet-tritiated imipramine binding sites in geriatric depression. 284 32

Patients who developed major depression within two years following stroke (n = 13) were compared with patients who did not become depressed in the same period (n = 13) but who did have a similar size and location of lesion as in the depressed group. Although the depressed patients were not significantly different from the nondepressed patients in background characteristics, history of depressive disorder, neurological impairment, or social functioning, the depressed group had greater cognitive impairment as measured by Mini-Mental State score. In addition, the depressed group had significantly larger lateral and third ventricular to brain ratios than nondepressed patients on computed tomographic scan analysis. The results suggest that poststroke depression itself may produce an intellectual impairment; subcortical atrophy, which likely preceded the stroke lesion, may produce a vulnerability for depression following stroke.
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PMID:Comparison of patients with and without poststroke major depression matched for size and location of lesion. 334 79

In a prospective study of mood disorders in 103 stroke patients, we examined the predictive value of affective, cognitive, social and neurologic variables obtained in-hospital and at six months poststroke in terms of outcome as determined by the same measures at one and two years follow-up. The following factors were found to have prognostic significance: 1) Lesion Location: proximity of the lesion on CT scan to the frontal pole in patients with left anterior infarcts showed a strong positive relationship with severity of depression at one year but not at two years poststroke. 2) Affective Status: depression (in-hospital and at 6 months) strongly predicted depression at one year but not at two years poststroke. Additionally, in-hospital depression significantly correlated with physical impairment at two years, while depression at six months bore a moderate relationship to physical impairment at one year. 3) Physical Impairment: impairment in activities of daily living in-hospital bore a modest relationship to depression at one year while such impairment at six months correlated strongly with depression at both one and two years. These findings may reflect the natural course of major depression which remits between one and two years poststroke. Although stroke lesion location is the strongest predictor of subsequent depression, there appears to be a reciprocal relationship between physical impairment and depression (i.e., depression predicts impairment and impairment predicts depression). Since poststroke depressions are amenable to therapeutic intervention, these prognostic factors may have implications for the treatment and rehabilitation of stroke patients.
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PMID:A two year longitudinal study of poststroke mood disorders: prognostic factors related to one and two year outcome. 339 25

As part of a prospective study of 103 stroke patients, we have analyzed the relation between depression and associated variables at 3 months, 6 months, 1 year, and 2 years after stroke. At all intervals up to and including 1 year poststroke, patients with left hemisphere strokes showed a strong relation between severity of depression and distance of the lesion on computed tomography scan from the frontal pole. At 2 years poststroke, this relation was no longer significant. The correlation between depression and impairment in activities of daily living peaked at 6 months and thereafter fell but remained significant at 1 and 2 years poststroke. The correlation between depression and cognitive impairment and between depression and social functioning fluctuated--with most correlations at 1 and 2 years follow-up nonsignificant. Although the conclusions that can be drawn from this study are limited by the fact that less than half of the original patients were followed up at each time, these declining correlations between depression and associated variables at 1 and 2 years follow-up may reflect the natural course of major depression which spontaneously remits between 1 and 2 years after stroke. The persisting significant association of impairment in activities of daily living with depression may reflect the effect of severe depression in sustaining and possibly retarding recovery from physical impairment.
Stroke
PMID:Two-year longitudinal study of post-stroke mood disorders: dynamic changes in correlates of depression at one and two years. 359 Feb 49

As part of a prospective study of mood disorders in stroke patients, interviews were obtained from 37 patients at 1 year and 48 patients at 2 years follow-up. In-hospital evaluations for these 65 follow-up patients found that 9 patients (14%) had symptom clusters of major depression, 12 patients (18%) had symptom clusters of dysthymic or minor depression, and 44 patients (68%) did not meet the DSM III diagnostic criteria for depression. Although overall prevalence of depression did not change significantly over time, the prognosis for individual patients, depending on diagnostic group, was different. All of the follow-up patients with major depression in-hospital were improved by 2 years, with a significant reduction in their mean depression scores and improvement in their activities of daily living, whereas only 30% of follow-up patients with dysthymic depression improved by this time. There was no significant improvement in their mean depression scores or mean activities of daily living score. Of the patients followed up who were not depressed in-hospital, 34% had developed major or minor depression by 2 years, and their mean depression scores were significantly increased. These data suggest that the prevalence of depression among the follow-up patients remains high (between 30 and 40%) for the first 2 years after stroke, but that untreated poststroke major depression has a natural course of about 1-2 years, with associated improvement in activity of daily living scores, whereas the prognosis for poststroke dysthymic depression is frequently unfavorable and often persists for greater than 2 years.
Stroke
PMID:Two-year longitudinal study of poststroke mood disorders: diagnosis and outcome at one and two years. 362 40


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