Abnormalities of somatosensory evoked potentials in spasmodic torticollis
Identifieur interne : 002B80 ( Istex/Curation ); précédent : 002B79; suivant : 002B81Abnormalities of somatosensory evoked potentials in spasmodic torticollis
Auteurs : Mazzini [Italie] ; M. Zaccala [Italie] ; C. Balzarini [Italie]Source :
- Movement Disorders [ 0885-3185 ] ; 1994.
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Abstract
This study examined the N20 and N30 waves of somatosensory evoked potentials (SEPs) from median nerve stimulation at three different stimulation rates (1, 3, and 6 Hz) in patients with idiopathic spasmodic torticollis (ST). The data were compared with those collected from a group of patients affected by Parkinson's disease (PD) and normal age‐matched subjects. N30 amplitude was significantly decreased in both groups of patients with respect to the controls. The decrease was larger in patients with ST. The N20 wave remained stable. The latencies of both waves were unchanged. When the stimulus rate was increased, the N30 amplitude decreased significantly, with a similar trend observed in both patients and controls. The isolated abnormalities of the N30 wave in both ST and PD support the hypothesis of a common physiopathogenetic mechanism that involves the basal ganglia or their connections with the supplementary motor area.
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DOI: 10.1002/mds.870090408
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<front><div type="abstract" xml:lang="en">This study examined the N20 and N30 waves of somatosensory evoked potentials (SEPs) from median nerve stimulation at three different stimulation rates (1, 3, and 6 Hz) in patients with idiopathic spasmodic torticollis (ST). The data were compared with those collected from a group of patients affected by Parkinson's disease (PD) and normal age‐matched subjects. N30 amplitude was significantly decreased in both groups of patients with respect to the controls. The decrease was larger in patients with ST. The N20 wave remained stable. The latencies of both waves were unchanged. When the stimulus rate was increased, the N30 amplitude decreased significantly, with a similar trend observed in both patients and controls. The isolated abnormalities of the N30 wave in both ST and PD support the hypothesis of a common physiopathogenetic mechanism that involves the basal ganglia or their connections with the supplementary motor area.</div>
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