Topka H, Konczak J, Schneider K, Boose A, Dichgans J
Department of Neurology, University of Tübingen, Germany.
Exp Brain Res. 1998 Apr;119(4):493-503. doi: 10.1007/s002210050365.
In cerebellar ataxia, kinematic aberrations of multijoint movements are thought to originate from deficiencies in generating muscular torques that are adequate to control the mechanical consequences of dynamic interaction forces. At this point the exact mechanisms that lead to an abnormal control of interaction torques are not known. In principle, the generation of inadequate muscular torques may result from an impairment in generating sufficient levels of torques or from an inaccurate assessment and prediction of the mechanical consequences of movements of one limb segment on adjacent joints. We sought to differentiate the relative contribution of these two mechanisms and, therefore, analyzed intersegmental dynamics of multijoint pointing movements in healthy subjects and in patients with cerebellar degeneration. Unrestrained vertical arm movements were performed at three different target movement velocities and recorded using an optoelectronic tracking system. An inverse dynamics approach was employed to compute net joint torques, muscular torques, dynamic interaction torques and gravitational torques acting at the elbow and shoulder joint. In both groups, peak dynamic interaction forces and peak muscular forces were largest during fast movements. In contrast to normal subjects, patients produced hypermetric movements when executing fast movements. Hypermetric movements were associated with smaller peak muscular torques and smaller rates of torque change at elbow and shoulder joints. The patients' deficit in generating appropriate levels of muscular force were prominent during two different phases of the pointing movement. Peak muscular forces at the elbow were reduced during the initial phase of the movement when simultaneous shoulder joint flexion generated an extensor influence upon the elbow joint. When attempting to terminate the movement, gravitational and dynamic interaction forces caused overshooting extension at the elbow joint. In normal subjects, muscular torque patterns at shoulder and elbow joint were synchronized in that peak flexor and extensor muscular torques occurred simultaneously at both joints. This temporal pattern of muscular torque generation at shoulder and elbow joint was preserved in patients. Our data suggest that an impairment in generating sufficient levels of phasic muscular torques significantly contributes to the patients' difficulties in controlling the mechanical consequences of dynamic interaction forces during multijoint movements.
在小脑共济失调中,多关节运动的运动学异常被认为源于产生肌肉扭矩的不足,而这种不足无法充分控制动态相互作用力的机械效应。目前,导致相互作用扭矩异常控制的确切机制尚不清楚。原则上,肌肉扭矩不足可能是由于产生足够扭矩水平的能力受损,或者是由于对一个肢体节段运动对相邻关节的机械效应评估和预测不准确所致。我们试图区分这两种机制的相对贡献,因此分析了健康受试者和小脑变性患者多关节指向运动的节段间动力学。在三种不同的目标运动速度下进行无约束的垂直手臂运动,并使用光电跟踪系统进行记录。采用逆动力学方法计算作用于肘关节和肩关节的净关节扭矩、肌肉扭矩、动态相互作用力扭矩和重力扭矩。在两组中,快速运动时的峰值动态相互作用力和峰值肌肉力最大。与正常受试者相比,患者在执行快速运动时会产生动作过度的运动。动作过度的运动与肘关节和肩关节处较小的峰值肌肉扭矩以及较小的扭矩变化率相关。患者在产生适当水平肌肉力方面的缺陷在指向运动的两个不同阶段较为突出。在运动的初始阶段,当肩关节同时屈曲对肘关节产生伸展影响时,肘关节处的峰值肌肉力会降低。当试图终止运动时,重力和动态相互作用力会导致肘关节过度伸展。在正常受试者中,肩关节和肘关节处的肌肉扭矩模式是同步的,即两个关节处的峰值屈肌和伸肌肌肉扭矩同时出现。患者在肩关节和肘关节处产生肌肉扭矩的这种时间模式得以保留。我们的数据表明,产生足够水平的相位性肌肉扭矩的能力受损,显著导致了患者在多关节运动中控制动态相互作用力的机械效应时遇到困难。