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Tardive dyskinesia is caused by maladaptive synaptic plasticity: A hypothesis
Author(s) -
Teo James T.,
Edwards Mark J.,
Bhatia Kailash
Publication year - 2012
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.25107
Subject(s) - tardive dyskinesia , neuroscience , psychology , dyskinesia , synaptic plasticity , plasticity , neuroplasticity , neurological disorder , medicine , psychiatry , central nervous system disease , schizophrenia (object oriented programming) , parkinson's disease , disease , physics , receptor , thermodynamics
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