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Biomedical subjects

S Gershon

Publications and source records attributed to S Gershon.

At least 145 records · Page 8Linked to original sources
PubMed1980

Mental symptoms in Huntington's disease and a possible primary aminergic neuron lesion.

Monoamine oxidase activity was higher in the cerebral cortex and basal ganglia of patients dying from Huntington's disease than in controls. Enzyme kinetics and multiple substrate studies indicated that the increased activity was due to elevated concentrations of monoamine oxidase type B. Concentrations of homovanillic acid were increased in the cerebral cortex but not in the basal ganglia of brains of patients with Huntington's disease. These changes may represent a primary aminergic lesion that could underlie some of the mental symptoms of this disease.

Basal Ganglia↗
PubMed1980

Prostaglandins, platelets, and schizophrenia.

Prostaglandin (PG) E1 enhances formation of 3H-adenosine-3',5'-cyclic monophasphate (3H-cAMP) in platelets pulse-labeled with 3H-adenine. This response was assessed as an index of receptor sensitivity and of PG function. Prostagladin E1-stimulated 3H-cAMP accumulation in paltelets from schizophrenics was significantly reduced compared with control subjects. Platelet incorporation of 3H-adenine and basal 3H-cAMP accumulation. We discuss the results in terms of the possible role of PGs in the etiopathology of schizophrenia and derivative implications for treatment.

Adult↗
PubMed1980

Responses to apomorphine, amphetamine, and neuroleptics in schizophrenic subjects.

Twenty-one schizophrenic subjects, who had been neuroleptic-free, were tested for responsiveness to dopaminergic agonists: Apomorphine emesis threshold was determined and change in psychopathology after 0.5 mg/kg d-amphetamine orally was rated. The subjects' subsequent response to neuroleptic treatment were also determined. Sensitivity to apomorphine emesis was also determined in a nonschizophrenic control group. Apomorphine emesis threshold was not significantly different in the schizophrenic and control groups. Correlations were done between baseline psychopathology, apomorphine sensitivity, and changes in psychopathology after amphetamine and after neuroleptic treatment. On the Brief Psychiatric Rating Scale (BPRS), baseline psychopathology correlated with improvement after neuroleptics and, on the clinical global impressions (CGI), increase of psychopathology after amphetamine also correlated with improvement after neuroleptic treatment. An inverse correlation was found between several indices of sensitivity to amphetamine (psychopathology change) and emetic sensitivity to apomorphine. An examination of individual subjects' responses to amphetamine and, subsequently, neuroleptics, suggested that in the absence of significant clinical change after amphetamine a brisk therapeutic response to neuroleptics was rare.

Adult↗
PubMed1980

Metoclopramide: antipsychotic efficacy of a drug lacking potency in receptor models.

Metoclopramide is a substituted benzamide derivative, structurally similar to procainamide and sulpiride. In behavioral, biochemical, and neuroendocrine tests it displays classic neuroleptic dopamine (DA) antagonist properties; in contrast to other DA antagonists, it lacks potency in currently used DA receptor models. In clinical studies using low doses or dubious measures, it was considered not to be efficacious as an antipsychotic. We now find that it indeed has a clinical profile similar to known neuroleptics when used in a dose range predicted from animal models. The findings raise questions regarding the validity and universality of several predictive models, as well as hypotheses purporting to explain molecular mechanisms of action of neuroleptic agents. The drug's inactivity in receptor models suggests that an as yet unidentified DA receptor subpopulation may be important as the mediator of many DA dependent neurobiologic phenomena.

Antipsychotic Agents↗
PubMed1980

Differential effects of amphetamine and neuroleptics on negative vs. positive symptoms in schizophrenia.

Positive symptoms of schizophrenia were diminished by neuroleptics and increased by amphetamine and accounted for most of the change seen in the total Brief Psychiatric Rating Scale (BPRS). Negative symptoms in the same subjects were not affected by neuroleptics but increased after amphetamines to a degree that just attained statistical significance. This increase was due to one item (emotional withdrawal) of the negative symptom factor which responded to neuroleptics and amphetamines as did positive symptoms. These findings are discussed with respect to new ideas about the role of dopamine in schizophrenia.

Adult↗
PubMed1980

Computed tomography evaluations of brain-behavior relationships in senile dementia of the Alzheimer's type.

Neuropathological investigations have demonstrated brain-behavior relationships in senile dementia of the Alzheimer's type (SDAT), but CT studies have not produced consistent findings. We hypothesized that these discouraging results were in part due to limitations in the methods of CT scan evaluations, and to non-homogeneity of patient populations. The present study examined 43 out-patients with the presumptive diagnosis of SDAT using 37 cognitive test measures and 3 independent CT evaluation strategies. The CT methods included a new rank ordering procedure and two previously used techniques, physical measurement and 4-point rating. Highly significant (p less than or equal to 0.01) brain-behavior correlations were attained using the ranking and rating procedures for evaluation of ventricular and cortical pathology. It was found that rank ordering has high interrater reliability and is superior to the other methods for the evaluation of the ventricular system. The physical measurement of the third ventricle is the single most powerful linear correlate of cognitive impairment. Measurement of cortical sulci are of no correlational significance. Multiple regression analyses indicated that global assessments are the best cognitive predictors of both ventricular and cortical pathology. Thus the present study has demonstrated brain-behavior relationships in vivo in SDAT.

Aged↗
PubMed1980

Sodium valproate in schizophrenia: some biochemical correlates.

Sodium valproate given in doses of 750-3000 mg daily to eight schizophrenic patients produced a qualitatively similar increase in symptoms in five. CSF showed no significant change in gamma-amino-butyric acid or methoxy hydroxyphenyl glycol, but homovanillic acid increased non-significantly in five patients.

Adult↗
PubMed1980

Experimental dystonia induced by quaternary-chlorpromazine.

When quaternary-chlorpromazine (Q-CPZ) was administered intraventricularly (ICV) to rats, it induced a lateralized dystonic reaction, which progressed to head-to-tail barrel rolling. The syndrome persisted for approximately 10 minutes, was not antagonized by pretreatment with drugs used to treat extrapyramidal movement disorders, and could not be mimicked by ICV administration of dopamine antagonists. Unlike known dopamine antagonists, Q-CPZ does not alter dopamine turnover, cause prolactin release in vivo, or bind to dopamine/neuroleptic receptors in vitro. These data suggest that Q-CPZ differs substantially from CPZ in pharmacologic action, and that it elicits a behavioral syndrome of potential use for studying dystonias.

3,4-Dihydroxyphenylacetic Acid↗