The neural mechanisms and circuitry involved in levodopa-induced dyskinesia are unclear. Using repetitive transcranial magnetic stimulation (rTMS) over the supplementary motor area (SMA) in a group of patients with advanced Parkinson disease, the authors investigated whether modulation of SMA excitability may result in a modification of a dyskinetic state induced by continuous apomorphine infusion. rTMS at 1 Hz was observed to markedly reduce drug-induced dyskinesias, whereas 5-Hz rTMS induced a slight but not significant increase.

Koch, G., Brusa, L., Caltagirone, C., Peppe, A., Oliveri, M., Stanzione, P., et al. (2005). rTMS of supplementary motor area modulates therapy-induced dyskinesias in Parkinson disease. NEUROLOGY, 65(4), 623-625 [10.1212/01.wnl.0000172861.36430.95].

rTMS of supplementary motor area modulates therapy-induced dyskinesias in Parkinson disease

CALTAGIRONE, CARLO;STANZIONE, PAOLO;CENTONZE, DIEGO
2005-08-23

Abstract

The neural mechanisms and circuitry involved in levodopa-induced dyskinesia are unclear. Using repetitive transcranial magnetic stimulation (rTMS) over the supplementary motor area (SMA) in a group of patients with advanced Parkinson disease, the authors investigated whether modulation of SMA excitability may result in a modification of a dyskinetic state induced by continuous apomorphine infusion. rTMS at 1 Hz was observed to markedly reduce drug-induced dyskinesias, whereas 5-Hz rTMS induced a slight but not significant increase.
23-ago-2005
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore MED/26 - NEUROLOGIA
English
Con Impact Factor ISI
Dyskinesia, Drug-Induced; Treatment Outcome; Male; Middle Aged; Female; Humans; Parkinson Disease; Motor Cortex; Recovery of Function; Apomorphine; Dopamine Agonists; Neural Pathways; Aged; Transcranial Magnetic Stimulation; Dopamine
Koch, G., Brusa, L., Caltagirone, C., Peppe, A., Oliveri, M., Stanzione, P., et al. (2005). rTMS of supplementary motor area modulates therapy-induced dyskinesias in Parkinson disease. NEUROLOGY, 65(4), 623-625 [10.1212/01.wnl.0000172861.36430.95].
Koch, G; Brusa, L; Caltagirone, C; Peppe, A; Oliveri, M; Stanzione, P; Centonze, D
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/27182
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