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- W1966195483 abstract "It has been 50 years since the first patients with tardive dyskinesia (TD) were described, but the pathophysiology is only partially understood and effective treatments have remained elusive. Newer atypical antipsychotics with less nonspecific activity at dopamine receptors have not heralded the end of tardive dyskinesia and merely highlight the incomplete understanding of the disorder. We present an overview of the existing pathophysiology of the disorder and incorporate recent developments in genetics and the study of human synaptic plasticity in other hyperkinetic movement disorders. We propose a hypothesis that dopamine-receptor sensitization and altered function of the N-methyl-D-aspartate receptor produces maladaptive synaptic plasticity, which allows the encoding of abnormal motor programs, and propose studies that would falsify or support this hypothesis. In conclusion, a maladaptive synaptic plasticity hypothesis goes some way toward filling in the gaps of existing theories of TD with the pathophysiology of other hyperkinetic movement disorders. © 2012 Movement Disorder Society." @default.
- W1966195483 created "2016-06-24" @default.
- W1966195483 creator A5019155615 @default.
- W1966195483 creator A5029342491 @default.
- W1966195483 creator A5078261834 @default.
- W1966195483 date "2012-08-01" @default.
- W1966195483 modified "2023-10-18" @default.
- W1966195483 title "Tardive dyskinesia is caused by maladaptive synaptic plasticity: A hypothesis" @default.
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