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Brain Advance Access originally published online on August 18, 2006
Brain 2006 129(10):2709-2721; doi:10.1093/brain/awl221
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© The Author (2006). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

The two sides of associative plasticity in writer's cramp

David Weise1, Axel Schramm1, Katja Stefan1,3, Alexander Wolters2, Karlheinz Reiners1, Markus Naumann1,4 and Joseph Classen1

1 Human Cortical Physiology and Motor Control Laboratory, Department of Neurology, University of Wuerzburg Wuerzburg, Germany 2 Department of Neurology, University of Rostock Rostock, Germany 3 Present addresses: Department of Neurology, University of Rostock Rostock, Germany 4 Present addresses: Neurologische Klinik und klinische Neurophysiologie Augsburg, Germany

Correspondence to: Prof. Dr. Joseph Classen, Human Cortical Physiology and Motor Control Laboratory, Department of Neurology, University of Wuerzburg, Josef-Schneider Strauss 11, 97080 Wuerzburg, Germany E-mail: classen_j{at}klinik.uni-wuerzburg.de

Neuronal plasticity is to be kept within operational limits to serve its purpose as a safe memory system that shapes and focuses sensory and motor representations. Temporal and spatial properties of motor cortical plasticity were assessed in patients with writer's cramp using a model of long-term potentiation (LTP) and long-term depression (LTD) of synaptic efficacy. Paired associative stimulation (PAS) combined repetitive electric stimulation of the median or ulnar nerve (MN or UN) with subsequent transcranial magnetic stimulation of the contralateral dominant motor cortex at 21.5 ms (MN-PAS21.5; UN-PAS21.5) or 10 ms (MN-PAS10). Motor-evoked potentials were recorded from abductor pollicis brevis (APB) muscle and abductor digiti minimi (ADM) muscles in 10 patients with writer's cramp and 10 matched healthy control subjects. Following MN-PAS21.5 or UN-PAS21.5 in non-dystonic subjects, motor responses increased if the afferent PAS-component came from a homologous peripheral region and remained stable with a non-homologous input. In contrast, following either MN-PAS21.5 or UN-PAS21.5, both APB- and ADM-amplitudes increased in patients. Compared with controls, this increase started earlier, its magnitude was larger and its duration longer. Following MN-PAS10 in controls, APB-amplitudes decreased, while ADM-amplitudes increased. In writer's cramp, the decrease of APB-amplitudes started earlier and lasted longer. Of note, ADM-amplitudes were decreased, too. LTP-like as well as LTD-like plasticity is abnormal with respect to both gain and spatial organization. These findings may help to develop a pathophysiological model explaining core features of focal dystonia.

Key Words: dystonia; long-term depression; long-term potentiation; paired associative stimulation; plasticity; transcranial magnetic stimulation

Abbreviations: ADM, abductor digiti minimi; ANOVARM, repeated measures analyses of variance; APB, abductor pollicis brevis; LTD, long-term depression; LTP, long-term potentiation; MEPs, motor-evoked potentials; PAS, paired associative stimulation; TMS, transcranial magnetic stimulation

Received March 8, 2006. Revised July 11, 2006. Accepted July 12, 2006.


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