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Phenytoin potentiation of neuroleptic‐induced dyskinesias
Author(s) -
Sethi K. D.,
Hitri Ana,
Diamond Bruce I.
Publication year - 1990
Publication title -
movement disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.352
H-Index - 198
eISSN - 1531-8257
pISSN - 0885-3185
DOI - 10.1002/mds.870050413
Subject(s) - tardive dyskinesia , phenytoin , dopamine , dopamine receptor , dyskinesia , chlorpromazine , pharmacology , dopaminergic , dopamine receptor d2 , long term potentiation , medicine , receptor , epilepsy , psychology , neuroscience , schizophrenia (object oriented programming) , psychiatry , parkinson's disease , disease
Clinically phenytoin‐induced movement disorders may resemble neuroleptic‐induced tardive dyskinesia (TD). Neuroleptic‐induced TD is thought to be related to an increase in the number and affinity of dopamine D 2 receptors. We investigated the interaction of phenytoin with dopaminergic systems by measuring dopamine behavior and receptor changes in animals treated with phenytoin alone or in combination with chlorpromazine. Phenytoin alone or in combination produced significant behavioral supersensitivity without alteration of dopamine D2 receptor density or affinity. This animal study suggests that phenytoin may aggravate neuroleptic‐induced tardive dyskinesia through mechanisms other than the dopamine D 2 receptors.