Funding agencies: Intramural National Institutes of Health.
Article first published online: 20 SEP 2011
Copyright © 2011 Movement Disorder Society
Volume 26, Issue 13, pages 2396–2403, November 2011
How to Cite
Voon, V., Brezing, C., Gallea, C. and Hallett, M. (2011), Aberrant supplementary motor complex and limbic activity during motor preparation in motor conversion disorder. Mov. Disord., 26: 2396–2403. doi: 10.1002/mds.23890
Relevant conflicts of interest/financial disclosures: Dr. Voon has not had any activities to disclose for the last 2 years. Dr. Brezing has not had any activities to disclose for the last 2 years. Dr. Gallea has not had any activities to disclose for the last 2 years. Dr. Hallett serves as Chair of the Medical Advisory Board for and receives honoraria and funding for travel from the Neurotoxin Institute. He may accrue revenue on US Patent #6,780,413 B2 (Issued: August 24, 2004): Immunotoxin (MAB-Ricin) for the treatment of focal movement disorders, and US Patent #7,407,478 (Issued: August 5, 2008): Coil for Magnetic Stimulation and methods for using the same (H-coil); in relation to the latter, he has received license fee payments from the NIH (from Brainsway) for licensing of this patent. Dr. Hallett's research at the NIH is largely supported by the NIH Intramural Program. Supplemental research funds came from the US Army via the Henry Jackson Foundation, Ariston Pharmaceutical Company via a Cooperative Research and Development Agreement (CRADA) with NIH, and the Kinetics Foundation via a Clinical Trials Agreement (CTA) with NIH. Dr. Hallett serves as Chair of the Medical Advisory Board of the Benign Essential Blepharospasm Foundation and Chair of the Medical Advisory Board of the International Essential Tremor Foundation. He serves on editorial advisory boards for Clinical Neurophysiology, Brain, Acta Neurologica Scandinavica, Journal of Clinical Neurophysiology, Italian Journal of Neurological Sciences, Medical Problems of Performing Artists, Annals of Neurology, Neurology and Clinical Neurophysiology, The Cerebellum, NeuroRx, Current Trends in Neurology, Faculty of 1000 Medicine, Brain Stimulation, Journal of Movement Disorders (Korea), and is Editor-in-Chief of World Neurology. He receives publishing royalties from Blackwell Publisher, Cambridge University Press, Springer Verlag, Taylor & Francis Group, Oxford University Press, John Wiley & Sons, Massachusetts Medical Society, Wolters Kluwer, and Elsevier. He has received honoraria for lecturing from Columbia University, the Parkinson and Aging Research Foundation, University of Maryland, University of Wisconsin, State of New York, and University of Navara.
Full financial disclosures and author roles may be found in the online version of this article.
- Issue published online: 22 NOV 2011
- Article first published online: 20 SEP 2011
- Manuscript Accepted: 3 JUL 2011
- Manuscript Revised: 20 JUN 2011
- Manuscript Received: 1 MAY 2011
- conversion disorder;
- action selection;
- motor initiation;
- supplementary motor area;
- psychogenic movement disorder
Conversion disorder (CD) is characterized by unexplained neurological symptoms presumed related to psychological issues. The main hypotheses to explain conversion paralysis, characterized by a lack of movement, include impairments in either motor intention or disruption of motor execution, and further, that hyperactive self-monitoring, limbic processing or top-down regulation from higher order frontal regions may interfere with motor execution. We have recently shown that CD with positive abnormal or excessive motor symptoms was associated with greater amygdala activity to arousing stimuli along with greater functional connectivity between the amygdala and supplementary motor area. Here we studied patients with such symptoms focusing on motor initiation. Subjects performed either an internally or externally generated 2-button action selection task in a functional MRI study. Eleven CD patients without major depression and 11 age- and gender-matched normal volunteers were assessed. During both internally and externally generated movement, conversion disorder patients relative to normal volunteers had lower left supplementary motor area (SMA) (implicated in motor initiation) and higher right amygdala, left anterior insula, and bilateral posterior cingulate activity (implicated in assigning emotional salience). These findings were confirmed in a subgroup analysis of patients with tremor symptoms. During internally versus externally generated action in CD patients, the left SMA had lower functional connectivity with bilateral dorsolateral prefrontal cortices. We propose a theory in which previously mapped conversion motor representations may in an arousing context hijack the voluntary action selection system, which is both hypoactive and functionally disconnected from prefrontal top-down regulation. © 2011 Movement Disorder Society