Search

Patients with ischaemic lesions of the left cerebral hemisphere were examined for depression and intellectual impairment: in non-depressed patients, the severity of impairment was related to both lesion volume and location, as assessed by CT scan analysis. Cognitive impairment in patients with major depression was greater than predicted by lesion volume alone, and when patients were matched for severity of impairment, depressed patients had smaller lesion volumes than the non-depressed. After six months, non-depressed patients had significantly less cognitive impairment than depressed patients who showed no improvement. Both depression and lesion volume were significantly and independently related to cognitive impairment. These findings suggest that post-stroke depression can produce a true dementia in its own right, and that treatment of post-stroke depression might benefit cognitive function. [ABSTRACT FROM AUTHOR]

Fifteen patients with bilateral hemisphere brain injury secondary to thromboembolic stroke or trauma were evaluated for depression, cognitive impairment, and functional physical impairment. Analysis of CT scans and standardized mood scales revealed that patients with left anterior brain injury were significantly more depressed than patients without such injury. Depression severity was directly and significantly correlated with left lesion proximity to the frontal pole. Left lesion age, lesion temporal sequence, right lesion location, cognitive impairment, and functional physical impairment did not significantly correlate with depression. Depressive symptomatology previously shown to be associated with single left frontal lobe lesions appeared to dominate post-brain injury psychopathology regardless of location or temporal sequence of other brain lesions. [ABSTRACT FROM AUTHOR]

Sertraline, a selective serotonin reuptake inhibitor, was used to treat two consecutive cases of genetically confirmed Huntington's disease in which severe irritability and aggressiveness required inpatient admission. The complete cessation of aggressive behavior in both cases has been maintained on follow-up. This report adds to the literature implicating serotonergic mechanisms in irritability and aggressiveness in both neuropsychiatric and idiopathic psychiatric disorders.

Objective: This study was undertaken to test the reliability and validity of the Pathological Laughter and Crying Scale and the effectiveness of nortriptyline treatment for patients with emotional lability following stroke., Method: Eighty-two patients with ischemic brain injury-54 who had been hospitalized with acute stroke and 28 others who requested treatment for pathological laughing and crying--were given standardized psychiatric and neurological assessments and then administered the Pathological Laughter and Crying Scale. The 54 acute stroke patients were used to evaluate the Pathological Laughter and Crying Scale, and the 28 patients with pathological emotional display were randomly assigned to nortriptyline treatment or placebo in a 6-week double-blind trial to assess the efficacy of a tricyclic antidepressant in treatment of this disorder., Results: The interrater reliability on the Pathological Laughter and Crying Scale for a subgroup of 15 patients was 0.93, and the test-retest reliability of the scale was excellent. After 4 and 6 weeks of treatment, scores on the Pathological Laughter and Crying Scale showed significantly greater improvement in the 14 patients given nortriptyline than in the 14 given placebo. Although almost one-half of these patients also had major depression, the improvement in emotional lability was independent of depression status. In addition, response to treatment was not significantly affected by lesion location or time since stroke., Conclusions: The severity of symptoms in pathological emotional display can be reliably quantified with the Pathological Laughter and Crying Scale, and treatment with nortriptyline can effectively ameliorate this emotional disorder.

A 69-year-old male with severe coronary artery disease, ankylosing spondylitis, and severe major depression was scheduled for electroconvulsive therapy (ECT). The patient had previously failed or proved intolerant of antidepressant drug therapy. The nature and severity of the patient's diseases and complexity of potential interactions with ECT and anesthesia required sequential assessment of hemodynamic and airway tolerances with successive treatments. Despite substantial risks for particular patients, ECT may provide the only treatment option for life-threatening psychiatric illness and warrants innovative approaches to anesthetic management.

Objective: Although many investigators have studied mood disorders following myocardial infarction, the prevalence, severity, and persistence of depression have been disputed, and standard rating scales and criteria for depressive disorders have infrequently been utilized. The authors' goal was to determine how frequently depressive disorders occur after myocardial infarction, and to investigate predisposing factors for such disorders., Method: Structured clinical interviews were administered to 129 inpatients within ten days of myocardial infarction. Patients were also evaluated using standardized rating scales for depression, social function, cognition, and physical impairment. DSM-III diagnoses were derived from the structured interview., Results: Major depressive syndromes were present in 19 percent (n = 25) of the patients and were associated with prior history of mood disorder, female sex, large infarcts, and functional physical impairment., Conclusion: Major depression is common in the acute post-myocardial infarction period. Such disorders confer significant psychiatric morbidity and, if sustained, require psychiatric intervention.

Patients with major depression admitted to hospital with acute stroke (n = 44), acute myocardial infarction (n = 25), or acute spinal cord injury (n = 12) were examined for differences in their phenomenological presentation of major depression. Depressed stroke patients were found to have significantly higher scores on the syndrome clusters for generalized anxiety and ideas of reference than depressed cardiac or spinal cord injury patients. In addition, significantly more stroke patients met diagnostic criteria for generalized anxiety disorder compared with the other two groups. Although spinal cord injury patients were younger, more likely to be treated with benzodiazepines, and less likely to be treated with beta-blockers, none of these factors distinguished stroke patients with anxious depression from stroke patients with depression only. These findings are consistent with the hypothesis that the etiology of depression following stroke may be different from that associated with myocardial infarction or spinal cord injury.

Apathy, indifference, loss of initiative, or disinhibition (without concurrent sedation or hypomania) were observed among five patients receiving the serotonin reuptake blocking antidepressants fluvoxamine or fluoxetine. These effects appeared to be dose related. They disappeared rapidly when the dose of fluvoxamine, which has a short half-life, was reduced. Fluoxetine, which has a long half-life, was more difficult to titrate. A possible relationship between mild drug-induced indifference and the therapeutic effects of serotonin reuptake blocking medication in anxiety disorders is discussed.

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.

The method of clinico-pathological correlation for drawing inferences about the localization of particular cerebral functions has a long history of use, and well established theoretical limitations. Release phenomena, loss of excitatory drive, as well as non-specific tissue responses to injury may all have a bearing on observed behavioral change. Nevertheless, the consistent observation that severity of depression in stroke patients is greater for left hemispheric strokes, and greater for left frontal versus left occipital strokes is of considerable interest. Site of lesion appears to have greater explanatory power for this emotional symptom than the obvious psychological explanations in terms of loss of self-esteem and loss of function. Depression is greater for strokes in general than would be expected for equivalent loss of motor function with orthopedic etiology. Loss of cognitive function likewise is a poorer guide to severity of depression than site of lesion. On the other hand, accuracy of lesion assessment using present static anatomical methods (CAT scan), and reliability and validity of the psychopathological examination present methodological difficulties which are discussed. As newer brain imaging techniques that are sensitive to function are developed, this line of enquiry holds considerable promise for furthering our understanding of the anatomy and physiology of emotion.

The efficacy of nortriptyline in the treatment of post-stroke depression was assessed by a double-blind study in thirty-four patients. Half of the patients had major depression. There was a significantly greater improvement in depression in patients treated with nortriptyline than in a similar group of placebo-treated patients. Depression was measured by the Hamilton depression scale, Zung depression scale, present state examination, and an overall depression scale. Successfully treated patients had serum nortriptyline levels in the therapeutic range. Post-stroke depressions are common, severe, and longstanding, and the demonstrated efficacy of nortriptyline provides an important addition to the treatments available for stroke patients.

This study was conducted to investigate the role of interhemispheric interaction in the production of spontaneous hyperactivity following right but not left frontal cortical suction lesions in the rat. Bilateral lesions, either simultaneous or left followed 1 week later by right, led to spontaneous hyperactivity and bilateral depletions of cortical norepinephrine concentrations. Rats given corpus callosum sectioning as neonates and frontal cortical suction lesions as adults developed spontaneous hyperactivity only when the right hemisphere was injured. These data suggest that lateralized spontaneous hyperactivity as elicited by small suction lesions of the right hemisphere does not depend on interhemispheric release or interaction and that at least the cortical mechanism is in the right hemisphere itself.

Patients who developed post-stroke depression 3 to 24 months after hospital discharge (N = 21) were compared with patients who developed depression during hospitalization (N = 26) and patients who never developed depression over 24 months of follow-up (N = 15). During the acute hospitalization and at follow-up, the three groups were not significantly different in their demographic characteristics, neurological impairment, intellectual impairment, or quality of social support. The acute depression group, however, showed an increased correlation between impairment and depression from hospitalization to follow-up. Findings suggest that impairment does not produce depression, but, once depression occurs, it may interact with impairment to influence post-stroke recovery.

Previous reports indicate that male rats given right (but not left) frontal cortical suction lesions develop hyperactivity accompanied by cortical norepinephrine depletions. In this study, female rats given such lesions to either hemisphere developed bilateral cortical norepinephrine depletions but no hyperactivity. Right lesion male rats developed both catecholamine depletions and hyperactivity. Thus, the lateralized hyperactivity response to these cortical lesions is sex-dependent and may involve sex differences in subcortical neural pathways.

Forty-two patients with senile dementia of the Alzheimer type (SDAT), 38 patients with Huntington's disease (HD) and matched normal controls were administered tests of olfactory, verbal, and visual recognition after being screened for normal olfactory discrimination. Early-affected Huntington's patients (EHD) with minimal chorea or cognitive deficit displayed marked deficits in olfactory recognition despite normal verbal and visual performance, even after correction for task difficulty, suggesting involvement of olfactory brain regions early in the disease process. In the early Alzheimer's group (EAD), marked deficits were seen on all recognition modalities indicating more global impairment. Both overall (early plus late) patient groups were impaired relative to controls on all recognition tasks, with the olfactory paradigm being most affected.

Thirty left-handed patients hospitalized for stroke were examined for mood disorders. Patients with left hemisphere lesions and nondominant hand impairments had significantly higher depression scores and more depressive diagnoses than patients with right hemisphere lesions and dominant hand impairments. Major depression was strongly associated with left anterior brain injury, and depression severity was significantly correlated with proximity of the lesion on CAT scan to the left frontal pole. These findings are almost identical to previously reported results from right-handed patients and suggest that cerebral lateralization of poststroke mood disorders may be independent of cerebral motor dominance and language dominance.

The authors describe four individuals infected with the human immunodeficiency virus type I (HIV) whose severe depressions were successfully treated with ECT.

The authors used structured clinical interviews to compare depressive symptoms in 43 patients with poststroke major depression and 43 patients with major depression without a known medical cause. The depressive syndrome profiles in the two patient groups were highly similar.

Dexamethasone suppression tests (DSTs) were given to 65 acute and chronic stroke patients. For patients who had had a stroke less than 1 year earlier, nonsuppression on the DST was significantly associated with the presence of poststroke depression. The authors, who used the DSM-III symptom criteria for major depression, found that DST sensitivity was 67% but specificity was only 70%. False positive tests in the stroke patients seemed related to large lesion volume. The DST, although of limited clinical utility in this population because of false positive tests, may help define more homogeneous subtypes of poststroke depression for research.