Biomedical subjects
Publications and source records attributed to B Angrist.
Six hospitalized patients with neuroleptic-induced akathisia were treated with clonidine under single-blind conditions. Akathisia and anxiety at maximum clonidine dose were significantly lower than at baseline, although it was difficult to differentiate specific therapeutic effects from sedation.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Positron emission tomography (PET) with 11C-2-deoxyglucose (11DG) was used to compare regional brain metabolism in four patients with chronic schizophrenia who had no history of psychotropic medication and in 12 normal controls. Patients had a second PET scan after an injection of thiothixene to evaluate the effects of acute neuroleptics on glucose metabolism. The patients showed higher glucose metabolic values than the normals and did not show the metabolic hypofrontality reported in chronic medicated patients with schizophrenia. Administration of the neuroleptic did not have a significant effect in the metabolic pattern of the patients. These results give support to the hypothesis that prolonged medication may contribute to the metabolic hypofrontal pattern seen in patients with schizophrenia.
Twelve patients with neuroleptic-induced akathisia were treated in a randomised, double-blind, cross-over design with propranolol and matching placebo. Propranolol caused significant decrements in both subjective and objective ratings of akathisia, but not in anxiety scores. This confirms prior findings of the efficacy of propranolol in akathisia induced by neuroleptic treatment.
Twenty-five schizophrenic outpatient subjects in a depot neuroleptic discontinuation study received an amphetamine challenge approximately 6 weeks after their last dose. Only five of these showed greater than three-point increases in positive symptoms on the BPRS, and all five relapsed within 30 days of the challenge. The 20 with less than three-point increases in positive symptoms showed extremely variable stability, relapsing from 20- greater than 600 days after the challenge. Thus, increase in positive symptoms after amphetamine may identify a group at risk for rapid relapse after neuroleptic discontinuation, but lack of such a response gives little prognostic information.
Six normal adults were administered an oral dose of 0.25 mg/kg of dextroamphetamine, and their learning performance on a paired-associate task and drug blood level were measured at hourly intervals for 5 hours postdrug intake. Dextroamphetamine plasma concentration peaked at 2 to 3 hours following the oral dose, and learning errors were lowest during the same period. A self-report measure of mood also yielded findings consistent with peak plasma concentration. Similar findings obtained with hyperactive children treated with methylphenidate (Ritalin) lead the authors to conclude that the paired-associate learning task may be useful as an indicator of psychostimulant plasma levels, as a predictor of clinical response after an acute dose, and as a highly controlled task for studying psychostimulant drug effects on learning.
The effects of propranolol, 20 to 30 mg/day, on neuroleptic-induced akathesia were compared with those of lorazepam, 2 mg/day, and periods of no treatment. Raters were blind to treatment condition. As reported in prior open studies, propranolol was found to be dramatically effective in reducing akathesia induced by neuroleptic treatment.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In stable schizophrenic outpatients with predominantly "defect state" symptomatology amphetamine caused a reduction in negative symptoms that was statistically significant but not complete (i.e. these symptoms remained clinically discernible). The possibility that dopaminergic hypofunction contributes some elements to the schizophrenic defect state is presented, along with some limited data compatible with this concept. These findings are compared to prior studies in recently hospitalized schizophrenic subjects, and discussed with respect to recent theoretical concepts regarding the role of dopamine in schizophrenic psychopathology.
Explore the source record for details and available documents.
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.
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.
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.
Explore the source record for details and available documents.