SOMATOSENSORY-EVOKED POTENTIALS AT REST AND DURING MOVEMENT IN PARKINSONS-DISEASE - EVIDENCE FOR A SPECIFIC APOMORPHINE EFFECT ON THE FRONTAL N30 WAVE

Citation
G. Cheron et al., SOMATOSENSORY-EVOKED POTENTIALS AT REST AND DURING MOVEMENT IN PARKINSONS-DISEASE - EVIDENCE FOR A SPECIFIC APOMORPHINE EFFECT ON THE FRONTAL N30 WAVE, Electroencephalography and clinical neurophysiology, 92(6), 1994, pp. 491-501
Citations number
39
Categorie Soggetti
Neurosciences
ISSN journal
00134694
Volume
92
Issue
6
Year of publication
1994
Pages
491 - 501
Database
ISI
SICI code
0013-4694(1994)92:6<491:SPARAD>2.0.ZU;2-H
Abstract
Studies attempting to relate the abnormalities of the frontal N30 comp onents of the somatosensory evoked potentials (SEPs) to motor symptoms in Parkinson's disease (PD) have shown contradictory results. We reco rded-the frontal and parietal SEPs to median nerve stimulation in 2 gr oups of PD patients: a group of 17 patients presenting the wearing-off phenomenon, and a group of 10 untreated PD patients. The results were compared with a group of 13 healthy volunteers of the same age and wi th a group of 10 non-parkinsonian patients. All parkinsonian and non-p arkinsonian patients were studied before (''on'' condition) and after a subcutaneous injection of apomorphine (''on'' condition). The gating effects of a voluntary movement (clenching of the hand) on the SEPs w ere also studied for the wearing-off group of PD patients (in states o ff and on) in comparison with the healthy subjects. At rest and in the off condition the amplitude of the frontal N30 was significantly redu ced in the 2 groups of PD patients. We demonstrate that the movement g ating ability of the PD patient is preserved in spite of the reduced a mplitude of the frontal N30. This result suggests that the specific ch ange in the frontal N30 in PD is not the consequence of a continuous g ating of the sensory inflow by a motor corollary discharge. Clinical m otor improvement induced by apomorphine was associated with a signific ant enhancement of the frontal N30 wave. In contrast, the subcortical P14 and N18 waves and the cortical N20, P22, P27 and N45 were not stat istically modified by the drug. Apomorphine infusion did not change th e absolute reduced voltage of the N30 reached during the movement gati ng. While the frontal N30 component of the non-parkinsonian patients w as significantly lower in comparison to healthy subjects, this wave di d not change after the apomorphine administration. In the wearing-off PD patient group the frontal N30 increment was positively correlated w ith the number of off hours per day. This specific apomorphine sensiti vity of the frontal N30 was interpreted as a physiological index of th e dopaminergic modulatory control exerted on the neuronal structures i mplicated in the generation of the frontal N30.