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抗精神病药物所致迟发性运动障碍的治疗。

Treatment of neurolept-induced tardive dyskinesia.

作者信息

Jankelowitz Stacey K

机构信息

Central Clinical School, University of Sydney, Sydney, NSW, Australia.

出版信息

Neuropsychiatr Dis Treat. 2013;9:1371-80. doi: 10.2147/NDT.S30767. Epub 2013 Sep 16.

Abstract

Tardive dyskinesia (TDK) includes orobuccolingual movements and "piano-playing" movements of the limbs. It is a movement disorder of delayed onset that can occur in the setting of neuroleptic treatment as well as in other diseases and following treatment with other drugs. The specific pathophysiology resulting in TDK is still not completely understood but possible mechanisms include postsynaptic dopamine receptor hypersensitivity, abnormalities of striatal gamma-aminobutyric acid (GABA) neurons, and degeneration of striatal cholinergic interneurons. More recently, the theory of synaptic plasticity has been proposed. Considering these proposed mechanisms of disease, therapeutic interventions have attempted to manipulate dopamine, GABA, acetylcholine, norepinephrine and serotonin pathways and receptors. The data for the effectiveness of each class of drugs and the side effects were considered in turn.

摘要

迟发性运动障碍(TDK)包括口颊舌运动和肢体的“弹钢琴”样运动。它是一种起病延迟的运动障碍,可发生于抗精神病药物治疗过程中,也可发生于其他疾病及使用其他药物治疗之后。导致TDK的具体病理生理学机制仍未完全明确,但可能的机制包括突触后多巴胺受体超敏、纹状体γ-氨基丁酸(GABA)神经元异常以及纹状体胆碱能中间神经元变性。最近,有人提出了突触可塑性理论。考虑到这些提出的疾病机制,治疗干预措施试图调节多巴胺、GABA、乙酰胆碱、去甲肾上腺素和5-羟色胺途径及受体。依次考虑了各类药物有效性的数据及副作用。

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