Di Fabio R P, Graf B, Badke M B, Breunig A, Jensen K
Department of Otolaryngology, University of Minnesota, Minneapolis 55455.
Exp Brain Res. 1992;90(1):189-200. doi: 10.1007/BF00229271.
The onset latency and discharge amplitude of preprogrammed postural responses were evaluated in order to determine if the structure of synergistic activation could be altered by ligamentous laxity at the knee joint. Twelve subjects with unilateral and one subject with bilateral anterior cruciate ligament (ACL) insufficiency were tested while standing on a moveable platform. External balance perturbations (6 cm anterior or posterior horizontal displacements of the platform) were presented at velocities ranging from 15 to 35 cm/s. Perturbations were presented under the following experimental conditions: unilateral and bilateral stance, knees fully straight or flexed, and with ankle motion restricted or free. These stance, knee position, and ankle motion conditions were introduced to alter the stress transmitted to the knee joint during movement of the support surface. The automatic postural response was recorded from the tibialis anterior (T), quadriceps (Q), and medial hamstrings muscles (H) bilaterally. The normal response to an externally induced backward sway involved the automatic activation of T and Q at latencies of 80 ms and 90 ms respectively. Activation of the hamstrings in the non-injured extremity was not coupled with the postural response. Hamstrings are not typically involved in the correction posterior sway because H activation would tend to pull the center of mass further backwards. However, when the response in the ACL-deficient extremity was compared to the non-injured limb: (1) the automatic postural response in the ACL-deficient extremity was restructured to include hamstrings activation (100 ms latency), (2) H activation time was faster and less variable in the ACL-deficient limb, and (3) the ratio of H/Q discharge amplitude integrated over 100 ms and 200 ms from the onset of EMG activation showed a dominance of hamstring activity during unilateral stance on the lax limb. In addition, H/Q ratios integrated over 200 ms showed dominant hamstring activity in the ACL-deficient limb during bilateral stance. (4) Cross-limb comparisons showed greater normalized IEMG amplitudes for T, H, and Q during unilateral stance on the lax limb. These results suggest that a capsular-hamstring reflex is integrated into the existing structure of a preprogrammed postural synergy in order to compensate for ligamentous laxity. Furthermore, the generalized increase of response gain observed during perturbations of unilateral stance on the lax limb indicates that joint afference can modulate central programming to control localized joint hypermobility. A concept of postural control is discussed with respect to the capsular reflex, joint loading and displacement of the center of gravity.
为了确定膝关节韧带松弛是否会改变协同激活的结构,对预编程姿势反应的起始潜伏期和放电幅度进行了评估。12名单侧和1名双侧前交叉韧带(ACL)功能不全的受试者在可移动平台上站立时接受测试。在15至35厘米/秒的速度范围内施加外部平衡扰动(平台向前或向后水平位移6厘米)。在以下实验条件下施加扰动:单侧和双侧站立、膝关节完全伸直或屈曲,以及踝关节运动受限或自由。引入这些站立、膝关节位置和踝关节运动条件是为了改变支撑面运动期间传递到膝关节的应力。双侧记录胫骨前肌(T)、股四头肌(Q)和内侧腘绳肌(H)的自动姿势反应。对外部诱发的向后摆动的正常反应分别涉及T和Q在80毫秒和90毫秒潜伏期的自动激活。未受伤肢体的腘绳肌激活与姿势反应没有关联。腘绳肌通常不参与纠正向后摆动,因为H的激活会倾向于将重心进一步向后拉。然而,当将ACL缺陷肢体的反应与未受伤肢体进行比较时:(1)ACL缺陷肢体的自动姿势反应被重新构建,包括腘绳肌激活(潜伏期100毫秒),(2)ACL缺陷肢体中H的激活时间更快且变异性更小,(3)从肌电图激活开始在100毫秒和200毫秒内积分的H/Q放电幅度比显示,在松弛肢体上单侧站立期间腘绳肌活动占主导。此外,在双侧站立期间,ACL缺陷肢体中200毫秒内积分的H/Q比值显示腘绳肌活动占主导。(4)跨肢体比较显示,在松弛肢体上单侧站立期间,T、H和Q的归一化肌电积分幅度更大。这些结果表明,为了补偿韧带松弛,囊 - 腘绳肌反射被整合到预编程姿势协同作用的现有结构中。此外,在松弛肢体上单侧站立扰动期间观察到的反应增益普遍增加表明,关节传入信号可以调节中枢编程以控制局部关节活动过度。关于囊反射、关节负荷和重心位移,讨论了姿势控制的概念。