Brain Advance Access originally published online on January 16, 2009
Brain 2009 132(3):749-755; doi:10.1093/brain/awn348
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Disordered plasticity in the primary somatosensory cortex in focal hand dystonia
1 Human Motor Control Section, Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA 2 Department of Neurology, Jikei University School of Medicine, Tokyo 3 Human Brain Research Center, Kyoto University Graduate School of Medicine, Kyoto 4 Department of Integrative Physiology, National Institute of Physiological Sciences, Okazaki, Japan
Correspondence to: Dr. Mark Hallett, MD, Human Motor Control Section, Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Building 10, Room 7D37, 10 Center Drive, MSC 1428, Bethesda, MD 20892-1428, USA E-mail: hallettm{at}ninds.nih.gov
Interventional paired associative stimulation (PAS) can induce plasticity in the cortex, and this plasticity was previously shown to be disordered in the primary motor cortex in focal hand dystonia (FHD). This study aimed to test whether associative plasticity is abnormal in the primary somatosensory cortex (S1) in FHD and whether PAS modulates excitatory or inhibitory interneurons within the cortex. Ten FHD patients and 10 healthy volunteers were studied. We investigated the changes in single- and double-pulse somatosensory-evoked potentials before and after PAS, which consisted of peripheral electrical nerve stimulation and subsequent transcranial magnetic stimulation over S1. Four sessions of somatosensory-evoked potentials recordings were performed: before PAS, and immediately, 15 and 30 min after PAS. We compared the time course of the somatosensory-evoked potentials between the FHD and healthy groups. In the single-pulse condition, the P27 amplitudes were significantly higher in FHD immediately after PAS than before PAS, while no changes were observed in healthy subjects. In the double-pulse condition, significant differences in the suppression ratio of P27 were found immediately after and 15 min after PAS, while there were no significant differences in healthy subjects. The P27 suppression tended to normalize toward the level of the healthy volunteer group. In FHD, PAS transiently induced an abnormal increase in excitability in S1. In addition, intracortical inhibition in S1 was found to increase as well. This abnormal plasticity of the intracortical neurons in S1 may contribute to the pathophysiology of dystonia.
Key Words: associative plasticity; paired associative stimulation; focal hand dystonia; somatosensory-evoked potential
Abbreviations: APB, abductor pollicis brevis; BA, Brodmann area; EEG, electroencephalogram; FHD, focal hand dystonia; ISI, interstimulus-interval; LTD, long-term depression; LTP, long-term potentiation; M1, primary motor cotex; MD, musician's dystonia; PAS, paired associative stimulation; S1, primary somatosensory cotex; SICI, short-latency intracortical inhibition; TMS, transcranial magnetic stimulation; WC, writer's cramp
Received August 5, 2008. Revised November 22, 2008. Accepted November 24, 2008.
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