Sethi K D, Hitri A, Diamond B I
Department of Neurology, Medical College of Georgia, Augusta.
Mov Disord. 1990;5(4):325-7. doi: 10.1002/mds.870050413.
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 D2 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 D2 receptors.
临床上,苯妥英钠所致运动障碍可能类似于抗精神病药物所致迟发性运动障碍(TD)。抗精神病药物所致TD被认为与多巴胺D2受体数量及亲和力增加有关。我们通过测量单独使用苯妥英钠或与氯丙嗪联合使用的动物的多巴胺行为及受体变化,研究了苯妥英钠与多巴胺能系统的相互作用。单独使用苯妥英钠或联合使用时均产生了显著的行为超敏反应,而多巴胺D2受体密度或亲和力未发生改变。这项动物研究表明,苯妥英钠可能通过多巴胺D2受体以外的机制加重抗精神病药物所致迟发性运动障碍。