Am J Psychiatry 2002 Jan;159(1):149-50
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PMID: 11772710, UI: 21633641
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J Clin Psychiatry 2001 Oct;62(10):772-5
Department of Veterans Affairs Medical Center and the University of Pennsylvania School of Medicine, Philadelphia 19104, USA.
BACKGROUND: Tardive dyskinesia (TD) remains a significant clinical problem for which there is no uniformly effective treatment. Earlier trials with acetylcholine precursors may have been disappointing because of underlying damage to striatal cholinergic neurons in patients with TD. In contrast, new cholinesterase inhibitors, developed for the treatment of dementia, may improve TD by directly increasing cholinergic synaptic transmission. METHOD: We conducted an 8-week open-label trial of donepezil in the treatment of TD. Ten patients with schizophrenia or schizoaffective disorder who received stable doses of antipsychotics and met DSM-IV criteria for TD were treated with donepezil, 5 to 10 mg/day, for 6 weeks after a 2-week baseline period. Changes in total Abnormal Involuntary Movement Scale (AIMS) scores measured every 2 weeks were assessed for significance. Patients were also assessed using the Brief Psychiatric Rating Scale, the Mini-Mental State Examination, the Barnes Akathisia Scale, and the Simpson-Angus Scale. RESULTS: Total AIMS scores decreased significantly (p = .0009), with no changes in other measures. Nine patients showed a positive response. Improvement was greatest in orofacial and upper extremity movements. No significant interactions were noted between the total AIMS scores and age (p > .29), duration of TD (p > .38), or duration of antipsychotic treatment (p > .14). CONCLUSION: Donepezil appeared to be effective in suppressing TD in this pilot study. However, placebo-controlled, double-blind studies are necessary before donepezil can be recommended as a treatment for TD.
PMID: 11816865, UI: 21591352
J Clin Psychiatry 2001 Dec;62(12):967-74
Department of Psychiatry, University of Massachusetts Medical School and Devereux Foundation, Rutland, USA. connod01@ummhc.org
BACKGROUND: Few studies have investigated the comparative risk of neuroleptic-related dyskinesias in children and adolescents receiving typical versus newer, atypical antipsychotics. This prospective study was completed to test whether clinical use of atypical antipsychotics is associated with less risk for developing neuroleptic-related dyskinesias than clinical use of typical neuroleptics in an unselected heterogeneous population of seriously emotionally disturbed youths admitted to acute residential treatment. We also tested a novel model of predictive risk for neuroleptic-related dyskinesias in children and adolescents. METHOD: 102 children and adolescents receiving typical neuroleptics, atypical antipsychotics, or the combination were studied. Youths developing neuroleptic-related dyskinesias were compared with youths free of dyskinesias over a 3-month study period on demographic, diagnostic, and treatment variables. Logistic regression was utilized to develop a novel model of predictive risk. RESULTS: Of neuroleptic-treated youths, 5.9% had probable tardive dyskinesia, a rate less than the prevalence of tardive dyskinesia in chronic neuroleptic-treated adults. Use of typical neuroleptics was significantly (p = .03) associated with dyskinesia compared with use of atypical antipsychotics. Four variables including IQ, initial Abnormal Involuntary Movement Scale score, type of antipsychotic, and cumulative number of risk factors accounted for 35.8% of the variance when predicting dyskinetic status. CONCLUSION: Use of atypical antipsychotics appears to be associated with less dyskinesia risk than typical neuroleptics in an unselected group of seriously emotionally disturbed children and adolescents. Results support a cumulative risk model of neuroleptic-related dyskinesia in youths.
PMID: 11780878, UI: 21639239
J Emerg Med 2002 Jan;22(1):67-70
Department of Emergency Medicine, St. Francis Medical Center, Pittsburgh, Pennsylvania, USA
[Medline record in process]
We present a case of a mixed ingestion of valproic acid, gabapentin, mexilitine, and ethanol with central nervous system depression that was reversed by naloxone. This report represents the fourth case demonstrating the antidotal efficacy of naloxone in reversing central nervous system depression associated with acute valproic acid overdose. Increasing clinical experience will more fully elucidate indications for, and optimal dosing of, naloxone in valproic acid toxic states.
PMID: 11809558, UI: 21668384
Lancet 2002 Jan 19;359(9302):265-7
University of North Carolina at Chapel Hill, CB 7175, 27599, Chapel Hill, NC, USA
PMID: 11812600, UI: 21671634
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