Sertraline in the treatment of severe aggressiveness in Huntington's disease.

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.

Pathological laughing and crying following stroke: validation of a measurement scale and a double-blind treatment study.

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.

Management for electroconvulsive therapy of a patient with inoperable coronary artery disease and ankylosing spondylitis.

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.

Depression following myocardial infarction.

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.

Phenomenological comparisons of major depression following stroke, myocardial infarction or spinal cord lesions.

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 and indifference in patients on fluvoxamine and fluoxetine.

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.

The impact of poststroke depression on recovery in activities of daily living over a 2-year follow-up.

The impact of clinically diagnosed depression on recovery in activities of daily living over a 2-year follow-up was examined in a prospective study of 63 stroke patients. Although impairment in activities of daily living, neurologic diagnoses and findings, lesion location and volume as measured on computed tomographic scan, demographic variables, cognitive impairment, and social functioning were comparable between depressed (n = 25) and nondepressed (n = 38) patients during their acute hospitalization, the two groups had different patterns of recovery in activities of daily living. At 2 years after suffering a stroke, patients with an in-hospital diagnosis of depression (either major or minor depression) were significantly more impaired in both physical activities and language functioning than were non-depressed patients. Among patients with major depression, this disparity in the recovery profile was present even after the depression had remitted. This study emphasizes the need for early recognition and treatment of poststroke depression.

ECT for major depression in four patients infected with human immunodeficiency virus.

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

A two year longitudinal study of poststroke mood disorders: prognostic factors related to one and two year outcome.

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.

Olfactory recognition: differential impairments in early and late Huntington's and Alzheimer's diseases.

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.

Two-year longitudinal study of post-stroke mood disorders: dynamic changes in correlates of depression at one and two years.

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.

Two-year longitudinal study of post-stroke mood disorders: comparison of acute-onset with delayed-onset depression.

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.

Lateralized response to cortical injury in the rat: interhemispheric interaction.

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.

Sex dependent behavioral response to frontal cortical suction lesions in the rat.

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.

Depression influences intellectual impairment in stroke patients.

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.

Phenomenological comparison of poststroke depression and functional depression.

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.

Mood disorders in left-handed stroke patients.

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.

A two-year longitudinal study of poststroke mood disorders. In-hospital prognostic factors associated with six-month outcome.

In a prospective study of mood disorders in stroke patients, variables obtained during the acute hospitalization were examined for their relationship to outcome at either 3- or 6-month follow-up. Distance of the lesion on computerized axial tomography scan from the frontal pole in patients with left anterior infarcts was significantly associated with severity of depression at 3 and 6 months poststroke. In addition, intellectual and functional physical impairment in-hospital were significantly correlated with severity of depression and social functioning scores at 3 and 6 months poststroke. Thus, patients who develop depression during the first 6 months poststroke may be responding to the severity of their impairment whereas the patients who develop depressions during the acute poststroke period may have a neuroanatomical and neurophysiological basis for their depression. Although other explanations might be proposed, the dynamic nature of the relationship between depression and associated variables during the first 6 months poststroke indicates that etiology of poststroke depression may be different depending upon the time of onset of the depression after brain injury.