Relevant conflicts of interest/financial disclosures: Nothing to report.
Article first published online: 1 AUG 2012
Copyright © 2012 Movement Disorder Society
Volume 27, Issue 10, pages 1205–1215, 1 September 2012
How to Cite
Teo, J. T., Edwards, M. J. and Bhatia, K. (2012), Tardive dyskinesia is caused by maladaptive synaptic plasticity: A hypothesis. Mov. Disord., 27: 1205–1215. doi: 10.1002/mds.25107
Full financial disclosures and author roles may be found in the online version of this article.
- Issue published online: 13 SEP 2012
- Article first published online: 1 AUG 2012
- Manuscript Accepted: 11 JUN 2012
- Manuscript Revised: 22 MAY 2012
- Manuscript Received: 10 OCT 2011
- tardive dyskinesia;
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