Bloem B R, Beckley D J, van Dijk J G, Zwinderman A H, Remler M P, Roos R A
Department of Neurology, Leiden University Hospital, The Netherlands.
Mov Disord. 1996 Sep;11(5):509-21. doi: 10.1002/mds.870110506.
It is still unclear why balance impairment in Parkinson's disease (PD) often responds insufficiently to dopaminergic medication. We have studied this issue in 23 patients with idiopathic PD and 24 healthy controls. Our specific purposes were (a) to investigate the contribution of abnormal automatic postural responses to balance impairment in PD and (b) to assess the influence of dopaminergic medication on abnormal automatic postural responses and balance impairment. Standing subjects received 4 degrees "toe-up" rotational perturbations of a supporting forceplate. We bilaterally recorded posturally destabilizing medium latency (ML) responses from the stretched gastrocnemius muscles and functionally corrective long latency (LL) responses from the shortened tibialis anterior (TA) muscles. We also assessed changes in the center of foot pressure (CFP) and the center of gravity (COG). All patients were tested in the "off" and "on" phases. All controls were tested and retested after 1 h. During the off phase, we found enlarged ML amplitudes and diminished LL amplitudes in patients, together with a markedly increased posterior displacement of the COG. The abnormal ML and LL responses were partially responsible for the increased body sway in patients because the initial forward (destabilizing) displacement of the CFP was increased, while the subsequent backward displacement of the CFP (a measure of the corrective braking action of LL responses) was delayed. Abnormal late automatic or possibly more voluntary postural corrections also contributed substantially to the increased body sway. During the on phase, ML amplitudes were reduced in patients but remained increased compared with controls. LL amplitudes no longer differed between both groups due to a modest, possibly dopamine-related increase in patients and a simultaneous decrease in controls. The abnormal CFP displacement was only partially improved by dopaminergic medication. The later postural corrections were not improved at all. Consequently, the increased posterior COG displacement was not ameliorated during the on phase. We conclude that (a) a combination of abnormal automatic and perhaps more voluntary postural corrections contributes to increased body sway in PD and (b) dopaminergic medication fails to improve balance impairment in PD because early automatic postural responses are only partially corrected, while later occurring postural corrections are not improved at all. These electrophysiological results support clinical observations and suggest that nondopaminergic lesions play a significant role in the pathophysiology of postural abnormalities in PD.
帕金森病（PD）患者的平衡障碍为何常常对多巴胺能药物反应不足，目前仍不清楚。我们对23例特发性PD患者和24名健康对照者进行了研究。我们的具体目的是：（a）研究异常自动姿势反应对PD患者平衡障碍的影响；（b）评估多巴胺能药物对异常自动姿势反应和平衡障碍的影响。站立的受试者接受支撑测力平台4度的“足尖上抬”旋转扰动。我们双侧记录了被拉伸的腓肠肌产生的姿势失稳中潜伏期（ML）反应，以及缩短的胫骨前肌（TA）产生的功能性矫正长潜伏期（LL）反应。我们还评估了足压力中心（CFP）和重心（COG）的变化。所有患者均在“关”期和“开”期接受测试。所有对照者在1小时后进行测试和重新测试。在“关”期，我们发现患者的ML波幅增大、LL波幅减小，同时COG的向后位移明显增加。异常的ML和LL反应部分导致了患者身体摆动增加，因为CFP最初向前（失稳）的位移增加，而随后CFP向后的位移（一种衡量LL反应矫正制动作用的指标）延迟。异常的晚期自动或可能更多的自主姿势矫正也在很大程度上导致了身体摆动增加。在“开”期，患者的ML波幅降低，但与对照者相比仍升高。两组之间的LL波幅不再有差异，因为患者有适度的、可能与多巴胺相关的增加，而对照者同时出现降低。多巴胺能药物仅部分改善了CFP的异常位移。后期的姿势矫正根本没有改善。因此，在“开”期，COG增加的向后位移并未得到改善。我们得出结论：（a）异常自动和可能更多的自主姿势矫正共同导致了PD患者身体摆动增加；（b）多巴胺能药物未能改善PD患者的平衡障碍，因为早期自动姿势反应仅得到部分矫正，而后期出现的姿势矫正根本没有改善。这些电生理结果支持了临床观察，并表明非多巴胺能损伤在PD姿势异常的病理生理学中起重要作用。
