Biomedical subjects
Publications and source records attributed to E Peselow.
A new self-rating scale, the General Behavior Inventory (GBI), was lower in eight controls and 61 patients in remission than in 32 depressed patients. Scores of depressed patients decreased over treatment time. GBI score correlated significantly with the past occurrence of manic plus depressive symptoms per visit and past mean mood shift per visit.
Platelet [3H]imipramine binding (Bmax) was determined in 67 patients with major affective illness (33 euthymic bipolar, 34 depressed unipolar) and 58 normal control subjects. Bipolar patients had significantly lower Bmax values than did control subjects. The mean Bmax in the unipolar patients was lower than in the control subjects, but the difference was not statistically significant. Dissociation constant (Kd) values did not distinguish patients in either category from control subjects. The significantly lower Bmax in euthymic bipolar patients and the apparent state independence of Bmax in some but not all unipolar patients suggest that platelet imipramine binding may be a trait marker in a subset of affective disorders.
Preclinical and clinical observations suggest that enhancement of prostaglandin activity inhibits catecholamine release and may have antidyskinetic effects. A double-blind therapeutic trial with prostaglandin precursor essential fatty acids was conducted in 16 patients with tardive dyskinesia. No beneficial effects were seen.
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.
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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.
A theoretical argument proposes that thresholds for visual perception of movement should be abnormally high in schizophrenia. This may reflect a central vestibular dysfunction, consisting of abnormally high levels of extraneous noise within the neural activity of the central vestibulo-cerebellar complex. Two experiments are reported with results that support the hypothesis. To some extent, the disorder may explain the smooth pursuit eye movement dysfunction in schizophrenia. Relations to the dopamine hypothesis in schizophrenia are discussed.
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.
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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.
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Components of emotional processing were examined in psychiatric and neurological populations: communication channel (face/voice), processing mode (expression/perception), and emotional valence (positive/negative). These were assessed with an experimental affect battery which was administered to schizophrenic, unipolar depressive, right-brain-damaged, Parkinson's disease, and normal control right-handed adults. For expression, subjects were taped while producing facial and vocal emotional expressions. Judges rated the expressions for accuracy and intensity. For perception, subjects were asked to identify and discriminate facial and vocal emotions. Using correlational techniques, relationships between facial and vocal channels and between expressive and perceptual modes were explored. The test battery has good psychometric properties and discriminates among diagnostic groups.
Neuropsychological research in major depression has generally been limited to the realm of cognition. This study focuses instead on the neuropsychology of affect. Emotional facial expression was examined in light of its presumed right cerebral hemisphere mediation and evidence for right hemisphere disorganization in major depression. Posed facial emotional expressions of four emotions were elicited and dynamically photographed in 30 unipolar depressives and 30 normal controls. Accuracy and emotional intensity of the expressions were rated by blind raters. Depressed patients were significantly impaired in the production of emotional facial expressions, particularly for positive ones. Several alternative explanations for the findings are discussed and further studies recommended.