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
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.