Cheron G, Piette T, Thiriaux A, Jacquy J, Godaux E
Department of Neurophysiology, University of Mons, Faculty of Medicine, Belgium.
Electroencephalogr Clin Neurophysiol. 1994 Nov;92(6):491-501. doi: 10.1016/0168-5597(94)90133-3.
Studies attempting to relate the abnormalities of the frontal N30 components of the somatosensory evoked potentials (SEPs) to motor symptoms in Parkinson's disease (PD) have shown contradictory results. We recorded the frontal and parietal SEPs to median nerve stimulation in 2 groups 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 with a group of 10 non-parkinsonian patients. All parkinsonian and non-parkinsonian patients were studied before ("off" condition) and after a subcutaneous injection of apomorphine ("on" condition). The gating effects of a voluntary movement (clenching of the hand) on the SEPs were also studied for the wearing-off group of PD patients (in states off and on) in comparison with the healthy subjects. At rest and in the off condition the amplitude of the frontal N30 was significantly reduced in the 2 groups of PD patients. We demonstrate that the movement gating ability of the PD patient is preserved in spite of the reduced amplitude of the frontal N30. This result suggests that the specific change in the frontal N30 in PD is not the consequence of a continuous gating of the sensory inflow by a motor corollary discharge. Clinical motor improvement induced by apomorphine was associated with a significant enhancement of the frontal N30 wave. In contrast, the subcortical P14 and N18 waves and the cortical N20, P22, P27 and N45 were not statistically modified by the drug. Apomorphine infusion did not change the absolute reduced voltage of the N30 reached during the movement gating. While the frontal N30 component of the non-parkinsonian patients was significantly lower in comparison to healthy subjects, this wave did not change after the apomorphine administration. In the wearing-off PD patient group the frontal N30 increment was positively correlated with the number of off hours per day. This specific apomorphine sensitivity of the frontal N30 was interpreted as a physiological index of the dopaminergic modulatory control exerted on the neuronal structures implicated in the generation of the frontal N30.
试图将帕金森病（PD）体感诱发电位（SEP）的额叶N30成分异常与运动症状联系起来的研究结果相互矛盾。我们记录了两组PD患者正中神经刺激后的额叶和顶叶SEP：一组17例出现剂末现象的患者，以及一组10例未经治疗的PD患者。将结果与一组13名年龄相仿的健康志愿者以及一组10名非帕金森病患者进行比较。所有帕金森病患者和非帕金森病患者均在皮下注射阿扑吗啡之前（“关”状态）和之后（“开”状态）进行研究。还研究了PD患者剂末组（关和开状态）与健康受试者相比，自主运动（握拳）对SEP的门控效应。在静息和关状态下，两组PD患者额叶N30的波幅均显著降低。我们证明，尽管额叶N30波幅降低，但PD患者的运动门控能力仍得以保留。这一结果表明，PD患者额叶N30的特异性变化并非运动伴随放电对感觉传入持续门控的结果。阿扑吗啡诱导的临床运动改善与额叶N30波的显著增强相关。相比之下，皮层下P14和N18波以及皮层N20、P22、P27和N45波在用药后无统计学改变。阿扑吗啡输注并未改变运动门控期间N30达到的绝对降低电压。虽然非帕金森病患者的额叶N30成分与健康受试者相比显著降低，但用药后该波并未改变。在剂末PD患者组中，额叶N30的增量与每天的关期小时数呈正相关。额叶N30对阿扑吗啡的这种特异性敏感性被解释为多巴胺能对参与额叶N30产生的神经元结构进行调节控制的生理指标。
