Effects of dopamine on postural control in Parkinsonian subjects: Scaling, set, and tone
Effects of dopamine on postural control in Parkinsonian subjects: Scaling, set, and tone
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DOI：
10.1152/jn.1996.75.6.2380
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发表时间：
1996-06-01
影响因子：
2.5
通讯作者：
Nutt, J
中科院分区：
文献类型：
--
作者：
Horak, FB;Frank, J;Nutt, J
1.本研究探讨帕金森综合征和多巴胺替代疗法（左旋多巴）的影响缩放的幅度自动姿势反应的基础上感觉反馈和预测的中央集。在帕金森综合征患者和老年对照组中，比较了左旋多巴治疗前后的表面反应性扭矩和肌电图（EMG）活动对向后表面平移的反应。最早的姿势反应之间的相关性[扭矩和综合肌电图（IEMG）的初始变化率]和平移速度提供了一个措施的姿势幅度缩放使用体感反馈。反应与预期平移幅度的相关性提供了依赖于预测中心集的缩放度量，因为反应先于幅度完成。6条腿和躯干肌肉的帕金森氏肌电图反应不晚于老年对照组。事实上，股四头肌拮抗剂laerobic早于正常，导致在膝关节的共激活不存在于对照受试者。EMG激活是分段的，具有短爆发持续时间和高强直水平，通常在多次爆发后恢复到基线。此外，帕金森反应表现出比正常小的激动性伸肌爆发和比正常大的胫骨肌和股直肌拮抗性屈肌激活。虽然帕金森病患者的位移速度和振幅缩放姿势反应，他们的扭矩反应小于老年对照组，特别是在响应位移振幅。帕金森病患者和对照受试者的姿势反应幅度缩放位移速度的增益（斜率）相似。尽管帕金森患者的扭矩较小。帕金森病患者也能够使用预测来缩放对小的预期位移幅度的响应，但是许多患者在较大的位移幅度下没有产生所需的较大的跖屈扭矩。大幅度扭矩降低与腓肠肌IEMG激动剂减少、胫骨肌拮抗剂爆发反应增加和胫骨肌紧张性背景活动增加相关。左旋多巴进一步降低了帕金森病患者已经很低的初始扭矩和IEMG对位移速度和振幅的反应。对速度反馈的姿势反应的能力不受左旋多巴的影响。但是左旋多巴使基于中心集对大位移幅度的响应进行缩放的能力变差。左旋多巴还显著降低了肌电图的紧张性背景水平，特别是远端腓肠肌和胫骨肌的活动。高基线肌张力在帕金森病患者中是明显的，因为他们在安静站立时的高背景EMG活动，特别是在胫骨肌和四头肌，以及响应位移的质心下降的缓慢初始速度。通过降低音调，左旋多巴降低了对扰动的被动刚度，而不增加EMG爆发幅度，导致对外部位移的阻力较小，因此身体质量中心（COM）位移更快。帕金森病患者最大的姿势缺陷不是反应潜伏期、模式或反应幅度的反应性或预测性缩放，而是快速产生足够水平的姿势力。多巴胺改善了紧张性背景姿势音，但进一步削弱了对外部位移的自动姿势反应。因此，基底神经节可以通过调节适当水平的背景姿势张力和通过使足够的力产生抵抗外部位移来参与姿势控制。
1. This study investigates the effects of parkinsonism and of dopamine replacement therapy (levodopa) on scaling the magnitude of automatic postural responses based on sensory feedback and on predictive central set. Surface reactive torques and electromyographic (EMG) activity in response to backward surface translations were compared in patients with parkinsonism ON and OFF levodopa and in elderly control subjects. Correlations between the earliest postural responses [initial rate of change of torque and integrated EMG (IEMG)] and translation velocity provided a measure of postural magnitude scaling using somatosensory feedback. Correlations of responses with expected translation amplitude provided a measure of scaling dependent on predictive central set because the responses preceded amplitude completion.2. Parkinsonian EMG responses in six leg and trunk muscles were not later than in elderly control subjects. In fact, quadriceps antagonist latencies were earlier than normal, resulting in coactivation at the knee not present in control subjects. EMG activation was fragmented, with short burst durations and high tonic levels that often returned to baseline with multiple bursts. In addition, parkinsonian responses showed smaller-than-normal agonist extensor bursts and larger-than-normal activation in tibialis and rectus femorus antagonist flexors.3. Although parkinsonian subjects scaled postural responses to both displacement velocities and amplitudes, their torque response were smaller than those of elderly controls, especially in response displacement amplitudes. The gain (slope) of postural response magnitude scaling to displacement velocity was similar for parkinsonian and control subjects. although parkinsonian subjects had smaller torques. Parkinsonian subjects were also able to use prediction to scale responses to small expected displacement amplitudes, but many patients did not generate the larger plantar-flexion torques required at larger displacement amplitudes. Reduced torque at large amplitudes was associated with less agonist gastrocnemius IEMG; increased tibialis antagonist burst responses, and increased tibialis tonic background activity.4. Levodopa further reduced the already low magnitude of initial torque and IEMG responses to displacement velocities and amplitudes in parkinsonian patients. The ability to scale postural responses to velocity feedback was not affected by levodopa. but the ability to scale responses to large displacement amplitudes based on central set was worsened by levodopa. Levodopa also significantly reduced the tonic, background levels of EMG, particularly the distal gastrocnemius and tibialis activity.5. High baseline muscle tone was apparent in parkinsonian subjects from their high background EMG activity in quiet stance, especially in tibialis and quadriceps, and the slow initial velocity of center of mass falling in response to displacements. By reducing a tone, levodopa reduced passive stiffness to perturbations without increasing EMG burst magnitudes, resulting in less resistance to external displacements and thus faster center of body mass (COM) displacements.6. The biggest postural deficit in parkinsonian subjects was not in response latency, pattern, or reactive or predictive scaling of response magnitude, but in quickly generating an adequate level of postural force. Dopamine improved tonic background postural tone but further weakened automatic postural responses to external displacements. Thus the basal ganglia may participate in postural control by regulating appropriate levels of background postural tone and by enabling adequate force generation for resisting external displacements.