Olanzapine treatment for dopaminergic‐induced hallucinations
Identifieur interne : 004366 ( Main/Exploration ); précédent : 004365; suivant : 004367Olanzapine treatment for dopaminergic‐induced hallucinations
Auteurs : William G. Ondo [États-Unis] ; Joel K. Levy [États-Unis] ; Kevin Dat Vuong [États-Unis] ; Christine Hunter [États-Unis] ; Joseph Jankovic [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2002-09.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Aged, Agonist, Antipsychotic, Antipsychotic Agents (therapeutic use), Atypical, Benzodiazepines, Chemotherapy, Cognition, Cognition Disorders (chemically induced), Cognition Disorders (diagnosis), Dopamine Agonists (adverse effects), Dopamine Agonists (therapeutic use), Dopamine receptor, Double-Blind Method, Female, Hallucination, Hallucinations (chemically induced), Hallucinations (diagnosis), Hallucinations (drug therapy), Human, Humans, Interview, Psychological, Low dose, Male, Mood, Neuroleptic, Neuropsychological Tests, Olanzapine, Parkinson Disease (drug therapy), Parkinson disease, Parkinson's disease, Pirenzepine (analogs & derivatives), Pirenzepine (therapeutic use), Treatment, atypical antipsychotics, olanzapine, organic psychosis.
- MESH :
- chemical , adverse effects : Dopamine Agonists.
- chemical , analogs & derivatives : Pirenzepine.
- chemical , therapeutic use : Antipsychotic Agents, Dopamine Agonists, Pirenzepine.
- chemically induced : Cognition Disorders, Hallucinations.
- diagnosis : Cognition Disorders, Hallucinations.
- drug therapy : Hallucinations, Parkinson Disease.
- Aged, Benzodiazepines, Double-Blind Method, Female, Humans, Interview, Psychological, Male, Neuropsychological Tests.
Abstract
Atypical antipsychotic medications with lower affinities for D2 receptors are considered useful alternatives to treat drug‐induced hallucinations in Parkinson's disease (PD). We conducted a double‐blind, placebo‐controlled, unforced titration, parallel design study (2:1 drug to placebo randomization ratio) using olanzapine (2.5–10 mg/day to effect) in 30 PD patients with drug‐induced hallucinations. We performed an extensive battery of neuropsychological tests, the Unified Parkinson's Disease Rating Scale (UPDRS), assessments of on and off time at baseline and at 9 weeks after starting the medication. Sixteen patients on olanzapine (mean dose, 4.6 mg/night) and 11 on placebo completed the study. Compared with placebo, performance on the UPDRS item 2 (thought disorder), and a structured interview for hallucinations, both tended to improve on drug but neither reached statistical significance. A neuropsychological test battery did not show any significant differences. Total on UPDRS motor scores (P < 0.05) and timed tapping (P < 0.01) worsened while on drug compared to placebo. Bradykinesia (P < 0.01) and gait (P < 0.001) items on the UPDRS largely accounted for this deterioration. After completion of the study, 8 of 16 patients randomly assigned to drug continued olanzapine at a mean dose of 2.4 mg/day. However, at the last recorded visit only 5 of 24 (20.8%) of all patients exposed to drug (including those originally randomly assigned to placebo) remained on olanzapine. In patients with PD, low‐dose olanzapine did not significantly improve hallucinations but did worsen motor function. © 2002 Movement Disorder Society
Url:
DOI: 10.1002/mds.10217
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en">Atypical antipsychotic medications with lower affinities for D2 receptors are considered useful alternatives to treat drug‐induced hallucinations in Parkinson's disease (PD). We conducted a double‐blind, placebo‐controlled, unforced titration, parallel design study (2:1 drug to placebo randomization ratio) using olanzapine (2.5–10 mg/day to effect) in 30 PD patients with drug‐induced hallucinations. We performed an extensive battery of neuropsychological tests, the Unified Parkinson's Disease Rating Scale (UPDRS), assessments of on and off time at baseline and at 9 weeks after starting the medication. Sixteen patients on olanzapine (mean dose, 4.6 mg/night) and 11 on placebo completed the study. Compared with placebo, performance on the UPDRS item 2 (thought disorder), and a structured interview for hallucinations, both tended to improve on drug but neither reached statistical significance. A neuropsychological test battery did not show any significant differences. Total on UPDRS motor scores (P < 0.05) and timed tapping (P < 0.01) worsened while on drug compared to placebo. Bradykinesia (P < 0.01) and gait (P < 0.001) items on the UPDRS largely accounted for this deterioration. After completion of the study, 8 of 16 patients randomly assigned to drug continued olanzapine at a mean dose of 2.4 mg/day. However, at the last recorded visit only 5 of 24 (20.8%) of all patients exposed to drug (including those originally randomly assigned to placebo) remained on olanzapine. In patients with PD, low‐dose olanzapine did not significantly improve hallucinations but did worsen motor function. © 2002 Movement Disorder Society</div>
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