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NEUROLOGY 1995;45:1671-1677
© 1995 American Academy of Neurology

Abnormal motor evoked responses to transcranial magnetic stimulation in focal dystonia

Nicolas Mavroudakis, MD, Jean Marc Caroyer, MD, Eric Brunko, PhD and Diederik Zegers de Beyl, MD, PhD

From Service de Neurologie (Drs. Mavroudakis, Caroyer, and Zegers de Beyl), Laboratoire de Neurophysiologie Clinique, Hopital Erasme, Brussels, and Laboratoire de Recherche sur le Cerveau (Dr. Brunko), Universite Libre de Bruxelles, Brussels, Belgium.
Presented in part at the 46th annual meeting of the American Academy of Neurology, Washington, DC, May 1994.
Supported by a grant from the Fondation Erasme (N. Mavroudakis).
Received August 30, 1994. Accepted in final form February 3, 1995.
Address correspondence and reprint requests to Dr. N. Mavroudakis, Service de Neurologie, Laboratoire de Neurophysiologie Clinique, Hopital Erasme, Route de Lennik, 808, Bruxelles, 1070, Belgium.

We evaluated motor responses evoked after magnetic cortical stimulation in dystonia, emphasizing the relationship between resting and facilitation state.We studied 15 normal controls (mean age, 37.9 years; range, 23 to 63) and 13 dystonic patients (mean age, 43.4 years; range, 20 to 56). Surface electrodes were placed over the right first dorsal interosseous muscle to measure motor evoked potentials and inhibitory silent periods obtained with magnetic stimulation. The amplitude ratio of motor evoked potentials measured during facilitation and at rest with low-intensity magnetic stimulation was significantly higher in dystonic patients (15.09) when compared with normal subjects (5.43; p equals 0.04). The ratio of duration of silent periods evoked with 120% motor threshold (MT) and MT plus 25% magnetic stimulus intensity was significantly higher in dystonic patients (78.4%) when compared with normal subjects (69.7%; p equals 0.04). We conclude that with low-intensity magnetic stimulation the relationship between amplitudes of motor potentials evoked at rest and during facilitation, as well as the responses of pathways that mediate silent periods, are disturbed in focal dystonia.

NEUROLOGY 1995;45: 1671-1677




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