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Biomedical subjects

J Rotrosen

Publications and source records attributed to J Rotrosen.

At least 55 records · Page 3Linked to original sources
PubMed1989

Neuroleptic-induced akathisia: a review.

Neuroleptic-induced akathisia (NIA) is a relatively common side effect of neuroleptics, in which patients complain of a subjective sense of restlessness usually referable to the legs and have characteristic motor movements. This paper will review: 1) history of spontaneously occurring syndromes of pathologic restlessness and NIA, 2) the clinical significance of NIA, 3) issues concerning the diagnosis and quantification of NIA, 4) treatments of NIA and 5) possible future directions for research in this area. Special attention will be paid to newer treatments for this syndrome, specifically beta-blockers.

Akathisia, Drug-Induced↗
PubMed1989

Effects of a specific beta 2-receptor blocker in neuroleptic-induced akathisia.

To assess the role of blockade of beta-receptor subpopulations in the treatment of neuroleptic-induced akathisia (NIA), the specific beta 2-antagonist ICI 118,551 was compared to placebo in a double-blind study. After a baseline evaluation on placebo, patients were treated with ICI 118,551 or placebo. Five of six patients treated with ICI 118,551 showed improvements in NIA, while only one of four patients improved on placebo. Patients were then treated openly with propranolol, a mixed beta 1, beta 2-antagonist. Compared to ICI 118,551, no further improvement on objective measures of akathisia was seen on propranolol. Mean subjective assessments of NIA declined on propranolol, but changes were variable and not statistically significant.

Adrenergic beta-Antagonists↗
PubMed1989

ECT and Parkinson's disease revisited: a "naturalistic" study.

In an open study, seven patients with Parkinson's disease received ECT for major depression. Both the motor dysfunction and the mood impairment of these patients improved following an average of seven ECT sessions. Significant improvement in motor function occurred after only two treatments. All aspects of Parkinson's disease improved significantly after ECT. Older patients showed greater improvement in motor function. The authors conclude that the therapeutic utility of ECT in depressed and nondepressed patients with Parkinson's disease should be further evaluated.

Aged↗
PubMed1989

Neuroleptic augmentation with alprazolam: clinical effects and pharmacokinetic correlates.

Alprazolam added to stable doses of neuroleptics in nine schizophrenic patients was associated with a 20%-30% mean reduction in positive and negative symptoms, although clinical response was variable and in some patients particularly brisk. The authors examined the possibilities of a pharmacokinetic effect of alprazolam on neuroleptic plasma levels and of a clinical effect of alprazolam. The modest increase in mean neuroleptic plasma levels did not correlate with clinical change, but those patients with the highest alprazolam plasma levels tended to show more robust clinical responses.

Adult↗
PubMed1989

Dopamine blockade and clinical response: evidence for two biological subgroups of schizophrenia.

Because CNS neuroleptic concentration cannot be directly measured in patients, the relation between clinical response and extent of dopamine receptor blockade is unknown. This relationship is critical in ascertaining whether nonresponse to neuroleptics is the result merely of inadequate CNS drug levels or of more basic biological differences in pathophysiology. Using [18F]N-methylspiroperidol and positron emission tomography, the authors assessed dopamine receptor occupancy in 10 schizophrenic patients before and after treatment with haloperidol. Responders and nonresponders had virtually identical indices of [18F]N-methylspiroperidol uptake after treatment, indicating that failure to respond clinically was not a function of neuroleptic uptake or binding in the CNS.

Adolescent↗
PubMed1989

Efficacy of low-dose metoprolol in neuroleptic-induced akathisia.

Recent studies have shown that the beta-blockers can be effective treatments for neuroleptic-induced akathisia. However, the relative contributions of beta-1 versus beta-2 blockade to the therapeutic effect of beta-blockers remains unclear. We treated nine patients who had neuroleptic-induced akathisia with low doses (25-100 mg/day) of the beta-blocker metoprolol. At these doses metoprolol causes selective blockade of beta-1 receptors. Seven patients improved after metoprolol; no further substantial changes were seen after subsequent treatment with propranolol. This finding suggests that neuroleptic-induced akathisia can be improved by selective beta-1 blockade.

Adult↗
PubMed1989

Akathisia: selective beta-blockers and rating instruments.

beta-Blockers, particularly propranolol, have been shown to be an effective treatment for neuroleptic-induced akathisia (NIA). To examine the relative contribution of beta-1 and beta-2 receptor blockade to the therapeutic effect of propranolol, we studied a beta-1 selective agent (low dose metoprolol) and a beta-2 specific blocker (ICI 118,551). Both agents ameliorated NIA. To further evaluate instruments for quantifying NIA we compared (a) two sets of clinical ratings during the metoprolol study and (b) clinical and electromechanical ratings of NIA during the ICI 118,551 study. The changes in clinical ratings of NIA after metoprolol were similar for most patients; however, the changes in electromechanical and clinical ratings after ICI 118,551 were similar in less than half of the patients studied.

Adrenergic beta-Antagonists↗
PubMed1988

Preliminary studies of clonidine in psychotic patients.

Twelve psychotic patients received a mean dose of 3.3 mg/day of clonidine. In four clonidine was the only treatment and in the remaining eight clonidine was superadded to a neuroleptic regimen after symptomatology was stable. Clonidine caused reduction of scores for both productive psychotic symptoms and anxiety. Negative symptoms were unaffected. These findings are discussed with respect to the small magnitude of the effects, questions as to specificity of the effects and methodologic limitations of this pilot study.

Adult↗
PubMed1988

Clinical stages of dementia and the dexamethasone suppression test.

1. This study was undertaken to evaluate the relationship between clinical aspects of primary degenerative dementia and suppression or non-suppression in the dexamethasone suppression test. 2. We studied 34 male patients with primary degenerative dementia (as diagnosed by DSM-III criteria). Dexamethasone 1 mg p.o. was administered at 11:00 PM and blood was drawn for cortisol determination at 4:00 PM the next day. 3. CLINICAL FACTORS INCLUDED: age, age at onset, duration of dementia, history of psychiatric illness, severity as measured by Global Deterioration Scale (GDS) score, and "malignancy" of dementia (rated by years of onset to institutionalization and as a ratio of Global Deterioration Scale to duration of primary degenerative dementia). 4. RESULTS: 56% of primary degenerative dementia patients failed to suppress. The highest degree of non-suppression was seen in Global Deterioration Scale 5 and 6 subjects (Table). 5. An unexpected finding was that a large number of Global Deterioration Scale 7 patients demonstrated normal post-dexamethasone suppression of the hypothalamic-pituitary-adrenal axis. 6. Some contradictions in previously reported studies may be explained by this pattern.

Aged↗
PubMed1988

Low frontal glucose utilization in chronic schizophrenia: a replication study.

Frontal/posterior ratios of cerebral glucose metabolism as determined by positron emission tomography were significantly lower in 13 chronic schizophrenic patients than in eight normal control subjects, as were absolute metabolic rates in both the frontal and posterior regions. The differences were not accounted for by cerebral atrophy.

Adult↗
PubMed1987

Effects of amphetamine on local cerebral metabolism in normal and schizophrenic subjects as determined by positron emission tomography.

The effects of d-amphetamine (0.5 mg/kg PO) on regional cerebral glucose utilization were measured with Positron Emission Tomography (PET). Subjects included ten chronic schizophrenics and six controls who received amphetamine, and six chronic schizophrenics and nine controls who received placebo or no treatment. Amphetamine decreased glucose metabolism in all regions studied (frontal, temporal, and striatal) in normal and schizophrenic subjects. The metabolic effects of amphetamine were correlated with plasma level of the drug. Cortical atrophy was associated with a blunted metabolic response.

Adult↗
PubMed1987

Double blind controlled trials of cholecystokinin octapeptide in neuroleptic-refractory schizophrenia.

A group of 14 schizophrenics who remained symptomatic after neuroleptic treatment received either 0.02 mcg/kg CCK-8 or saline placebo intravenously. Thereafter, 13 received the alternative infusion as a crossover treatment. A second group of 16 such patients received 0.04 mcg/kg CCK-8 or saline intravenously and, thereafter, 14 of these received the alternative infusion as a crossover treatment. Psychopathology was rated prior to, 2-3 h post, and on days 3, 5 and 7 after each infusion. Ratings consisted of the BPRS, the Abrams and Taylor Scale for Emotional Blunting, the Hamilton Anxiety Scale and a Schneiderian "Positive" symptom scale abstracted from the President State Examination. Parallel groups and cross over design analyses failed to show efficacy for CCK-8.

Antipsychotic Agents↗