Funding agencies: This study was supported by the Guarantors of Brain Clinical Fellowship Scheme (A.S.) and the Japan Society for the Promotion of Science Postdoctoral Fellowships for Research Abroad (M.H.).
A reflection on plasticity research in writing dystonia
Article first published online: 13 MAY 2014
© 2014 International Parkinson and Movement Disorder Society
Volume 29, Issue 8, pages 980–987, July 2014
How to Cite
Sadnicka, A., Hamada, M., Bhatia, K. P., Rothwell, J. C. and Edwards, M. J. (2014), A reflection on plasticity research in writing dystonia. Mov. Disord., 29: 980–987. doi: 10.1002/mds.25908
Relevant conflicts of interest/financial disclosures: Nothing to report.
Full financial disclosures and author roles may be found in the online version of this article.
- Issue published online: 17 JUL 2014
- Article first published online: 13 MAY 2014
- Manuscript Accepted: 11 APR 2014
- Manuscript Revised: 21 MAR 2014
- Manuscript Received: 2 OCT 2013
- writing dystonia;
- writers' cramp;
- paired associative stimulation;
Much attention has focused on the hypothesis that there is enhanced plasticity of sensorimotor circuits in patients with dystonia. A common experimental method to assess plasticity in dystonia research is paired associative stimulation (PAS). Excessive, nonfocal effects of PAS were observed in early studies of dystonia; however, these large effects have not been uniformly replicated. In this viewpoint, data from 15 patients with writing dystonia are presented. We suggest that, as in healthy individuals, the effects of PAS are highly variable. A review of previous studies examining PAS in writing dystonia highlights the range of results that have been observed. We conclude that current experimental evidence cannot be fully explained by the notion that PAS responses in writing dystonia are consistently excessive or nonspecific. The variability of PAS responses is such that enhanced plasticity should not be considered a dystonic fingerprint, because the direction of response can vary, and there is overlap between patient and healthy data. We also discuss evidence questioning the assumption that PAS responses are a clear correlate to levels of synaptic plasticity; we need to define more specifically what PAS responses signify in the dystonic brain. Our conclusions are limited to PAS in writing dystonia; however, much variation exists with other plasticity protocols. Large multicenter studies of both focal and generalized forms of dystonia, probing variability of individual neurophysiological profiles, are encouraged. This will reveal the true role of plasticity in the pathophysiology of dystonia and may expose subject-specific therapeutic interventions that are currently concealed. © 2014 International Parkinson and Movement Disorder Society