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Vitamin E treatment of tardive dyskinesia
Adler LA; Peselow E; Rotrosen J; Duncan E; Lee M; Rosenthal M; Angrist B
OBJECTIVE: The authors studied the effects of vitamin E treatment of tardive dyskinesia; earlier studies have produced contradictory results. METHOD: Twenty-eight patients with tardive dyskinesia were treated in a double-blind, parallel-group comparison study of 8-12 weeks of treatment with vitamin E (1600 IU/day) or matching placebo capsules. RESULTS: The Abnormal Involuntary Movement Scale scores of the patients treated with vitamin E improved significantly compared to the scores of the patients given placebo. CONCLUSIONS: These results support earlier findings of the efficacy of vitamin E in treating tardive dyskinesia
PMID: 8102511
ISSN: 0002-953x
CID: 8277
ELEVATED PLA-2 ACTIVITY IN SCHIZOPHRENICS AND PSYCHIATRIC CONTROLS [Meeting Abstract]
NOPONEN, M; SANFILIPO, M; SAMANICH, K; FUKUI, T; RYER, H; KO, G; ROTROSEN, J
ISI:A1993LA41700221
ISSN: 0006-3223
CID: 54175
Negative symptoms and hypofrontality in chronic schizophrenia
Wolkin A; Sanfilipo M; Wolf AP; Angrist B; Brodie JD; Rotrosen J
Frontal lobe dysfunction is widely suspected to underlie negative symptoms of schizophrenia. This hypothesis is based largely on long-standing observations of the similarities between the effects of frontal lobe lesions and negative symptoms. However, there is little direct evidence specifically for such an association in schizophrenic patients. We measured the relationship between decreased relative prefrontal cortex glucose metabolism (hypofrontality) using positron emission tomography and evaluated the severity of negative symptoms in 20 chronic schizophrenics who underwent scanning while not receiving neuroleptic drugs. We found a close relationship between negative symptoms and prefrontal hypometabolism, particularly in the right dorsolateral convexity. This association was regionally specific. Furthermore, there was no evidence that this relationship was an artifact of age, cerebral atrophy, or severity of positive symptoms
PMID: 1360200
ISSN: 0003-990x
CID: 57503
Acute neuroleptic-induced akathisia
Chapter by: Adler, Lenard A; Angrist, Burt; Rotrosen, John
in: Drug-induced movement disorders by Lang AE; Weiner WJ [Eds]
Mt. Kisco NY : Futura, 1992
pp. ?-?
ISBN: 0879935251
CID: 5274
SERUM IRON AND AKATHESIA - REPLY [Letter]
NEMES, Z; ROTROSEN, J; WHITE, T; ANGRIST, B; PESELOW, E; SHOENTAG, R; BROWN, KW
ISI:A1991GQ04800013
ISSN: 0006-3223
CID: 51532
Efficacy of betaxolol in neuroleptic-induced akathisia
Adler LA; Angrist B; Rotrosen J
Betaxolol, a beta 1-selective antagonist, produced marked improvement in eight patients with neuroleptic-induced akathisia. No further improvement was seen with subsequent propranolol treatment. These findings, along with the results of prior studies of betaxolol and metoprolol, suggest that blockade of central beta 1-receptors may be sufficient for efficacy in akathisia
PMID: 1686812
ISSN: 0165-1781
CID: 23586
Stability of resting deoxyglucose metabolic values in PET studies of schizophrenia
Bartlett EJ; Barouche F; Brodie JD; Wolkin A; Angrist B; Rotrosen J; Wolf AP
Positron emission tomography (PET) and the deoxyglucose method were used to determine the test-retest stability of regional cerebral glucose metabolism in 8 male schizophrenic patients and 11 normal control subjects, scanned twice under baseline (resting) conditions. Normal and schizophrenic subjects showed comparable stability of regional metabolism. When the regional values were scaled to compensate for the effects of changes in whole brain metabolism, the resulting mean regional changes were reduced to about 1-2% in both groups. This study demonstrates that the baseline resting state is an appropriate reference state for schizophrenic subjects in deoxyglucose PET experiments
PMID: 1946838
ISSN: 0165-1781
CID: 14038
Disappearance of memory deficits in outpatient depressives responding to imipramine
Peselow ED; Corwin J; Fieve RR; Rotrosen J; Cooper TB
We evaluated learning and memory in 50 depressed patients prior to and following 4 week treatment with imipramine compared to 21 normal controls tested at corresponding times. At baseline, the depressives did worse than normals on most memory tasks with the difficult memory tasks, regardless of store, modality or type of task best distinguishing between depressive and normal memory. Following imipramine treatment, responders performed better than nonresponders on the difficult memory tasks, and not significantly differently from controls on most tasks. This, as well as the fact that the responders improved to a greater degree than controls on most measures (in a few cases the difference was statistically significant) and the fact that at 4 weeks complete responders to imipramine did significantly better than partial responders to imipramine, indicates that relief from depression is highly related to improved memory functioning. The finding that complete responders to imipramine were not significantly worse than normal controls suggests that imipramine did not have significant adverse effects on memory
PMID: 1829740
ISSN: 0165-0327
CID: 14124
Serum iron levels and akathisia [see comments] [Comment]
Nemes ZC; Rotrosen J; Angrist B; Peselow E; Schoentag R
PMID: 1674665
ISSN: 0006-3223
CID: 14130
Lack of efficacy of d-propranolol in neuroleptic-induced akathisia
Adler LA; Angrist B; Fritz P; Rotrosen J; Mallya G; Lipinski JF Jr
d-Propranolol lacks clinically significant beta-adrenergic receptor blocking properties, but has the same membrane stabilizing effects as racemic (d,l) propranolol. To assess the role of beta-blockade versus membrane stabilization or other shared nonspecific effects in the therapeutic action of propranolol in neuroleptic-induced akathisia (NIA) we treated 11 patients with NIA in a crossover, double-blind study of d-propranolol versus placebo. Akathisia scores were unchanged after both d-propranolol and placebo. Eight patients were subsequently treated in a nonblind manner with racemic propranolol, with a significant reduction in akathisia scores. These findings suggest that beta-blockade, not membrane stabilization or other shared nonspecific effects, contributes to the efficacy of propranolol in NIA
PMID: 1673844
ISSN: 0893-133x
CID: 23587