Bloem B R, Beckley D J, van Dijk J G
Department of Neurology and Clinical Neurophysiology, Leiden University Medical Center, The Netherlands.
Exp Brain Res. 1999 Feb;124(4):481-8. doi: 10.1007/s002210050644.
Abnormal automatic postural responses are thought to contribute to balance impairment in Parkinson's disease. However, because postural responses are modifiable by stance, we have speculated that some postural abnormalities in patients with Parkinson's disease are secondary to their stooped stance. We have studied this assumption by assessing automatic postural responses in 30 healthy subjects who were instructed either to stand upright or to assume a typical parkinsonian posture. During both conditions, subjects received 20 serial 4 degrees 'toe-up' rotational perturbations from a supporting forceplate. We recorded short-latency (SL) and medium-latency (ML) responses from stretched gastrocnemius muscles and long-latency (LL) responses from shortened tibialis anterior muscles. We also assessed changes in the center of foot pressure (CFP) and the center of gravity (COG). The results were qualitatively compared to a previously described group of patients with Parkinson's disease who, under these circumstances, typically have large ML responses, small LL responses and insufficient voluntary postural corrections, accompanied by a slow rate of backward CFP displacement and an increased posterior COG displacement. The stooped posture resulted in unloading of medial gastrocnemius muscles and loading of tibialis anterior muscles. Onset latencies of stretch responses in gastrocnemius muscles were delayed in stooped subjects, but the onset of LL responses was markedly reduced. Amplitudes of both ML and LL responses were reduced in stooped subjects. Prestimulus COG and, to a lesser extent, CFP were shifted forwards in stooped subjects. Posterior COG displacement and the rate of backward CFP displacement were diminished in stooped subjects. Voluntary postural corrections were unchanged while standing stooped. These results indicate that some postural abnormalities of patients with Parkinson's disease (most notably the reduced LL responses) can be reproduced in healthy subjects mimicking a stooped parkinsonian posture. Other postural abnormalities (most notably the increased ML responses and insufficient voluntary responses) did not appear in stooped controls and may contribute to balance impairment in Parkinson's disease.
异常的自动姿势反应被认为是导致帕金森病平衡障碍的原因之一。然而，由于姿势反应可因站立姿势而改变，我们推测帕金森病患者的一些姿势异常是其弯腰姿势的继发结果。我们通过评估30名健康受试者的自动姿势反应来研究这一假设，这些受试者被要求要么站直，要么采取典型的帕金森病姿势。在两种情况下，受试者均从支撑测力板接受20次连续的4度“足尖向上”旋转扰动。我们记录了腓肠肌拉伸时的短潜伏期（SL）和中潜伏期（ML）反应，以及胫前肌缩短时的长潜伏期（LL）反应。我们还评估了足压力中心（CFP）和重心（COG）的变化。将结果与先前描述的一组帕金森病患者进行定性比较，在这些情况下，帕金森病患者通常具有较大的ML反应、较小的LL反应和不足的自主姿势校正，同时伴有CFP向后位移速率缓慢和COG向后位移增加。弯腰姿势导致腓肠肌内侧卸载和胫前肌加载。弯腰受试者腓肠肌拉伸反应的起始潜伏期延迟，但LL反应的起始明显减少。弯腰受试者的ML和LL反应幅度均降低。弯腰受试者刺激前的COG以及在较小程度上的CFP向前移位。弯腰受试者的COG向后位移和CFP向后位移速率减小。站立弯腰时自主姿势校正不变。这些结果表明，帕金森病患者的一些姿势异常（最明显的是LL反应降低）可以在模仿弯腰帕金森病姿势的健康受试者中重现。其他姿势异常（最明显的是ML反应增加和自主反应不足）在弯腰对照组中未出现，可能是导致帕金森病平衡障碍的原因。
