Simon S R, Deutsch S D, Nuzzo R M, Mansour M J, Jackson J L, Koskinen M, Rosenthal R K
J Bone Joint Surg Am. 1978 Oct;60(7):882-94.
Using high-speed motion pictures, electromyography, a dynamic piezoelectric force plate, and computer analysis of the data, the gait patterns of fifteen children, four to sixteen years old, with spastic cerebral palsy and genu recurvatum were analyzed to determine the mechanisms producing genu recurvatum and the effect of fixed-ankle below-the-knee orthoses. In all children the recurvatum during stance phase began when the tibia stopped moving forward and disappeared when tibial movement resumed. In six patients (Group I), excessive activity of the calf muscles in response to the increasing dorsiflexion moment about the ankle produced by the foot-floor reaction force arrested the forward motion of the tibia. In six others (Group II), the contraction of the calf muscles was not sufficiently strong to resist the dorsiflexion moment and the tibia moved forward until maximum dorsiflexion had occurred and then stopped. In both instances recurvatum was produced when the femur continued to move forward over the stationary tibia and an extension moment was produced at the knee. In no patient did activity of the knee flexors prevent recurvatum, which was eliminated only by resumption of forward movement of the tibia. This movement of the tibia was produced either by heel-off (Group I) or by sudden unweighting of the limb due to opposite heel-strike (Group II). In Group I, when tibial motion stopped in the first half of stance phase the position of the hip rapidly changed from flexion to extension and there was forward leaning of the trunk, while in Group II the change from hip flexion to extension occurred with backward leaning of the trunk. The fixed-ankle below-the-knee orthosis, by preventing excessive dorsiflexion and plantar flexion, produced more normal moments about all joints, especially the knee. In the three children (Group III) whose recurvatum was permanently corrected by the brace, no explanation for the improvement was evident in these studies.
利用高速动态影片、肌电图、动态压电测力板以及数据的计算机分析，对15名4至16岁患有痉挛性脑瘫并伴有膝反屈的儿童的步态模式进行了分析，以确定产生膝反屈的机制以及固定踝关节的膝下矫形器的作用。在所有儿童中，站立期的膝反屈始于胫骨停止向前移动时，并在胫骨恢复移动时消失。在6名患者（第一组）中，小腿肌肉因足底反作用力产生的踝关节背屈力矩增加而过度活动，从而阻止了胫骨的向前移动。在另外6名患者（第二组）中，小腿肌肉的收缩力量不足以抵抗背屈力矩，胫骨继续向前移动，直到出现最大背屈然后停止。在这两种情况下，当股骨在静止的胫骨上继续向前移动并在膝关节处产生伸展力矩时，就会出现膝反屈。在任何患者中，膝关节屈肌的活动都未能阻止膝反屈，只有胫骨恢复向前移动才能消除膝反屈。胫骨的这种移动要么是通过足跟离地（第一组），要么是由于对侧足跟触地导致肢体突然失重（第二组）产生的。在第一组中，当胫骨运动在站立期的前半段停止时，髋关节的位置迅速从屈曲变为伸展，躯干向前倾斜，而在第二组中，从髋关节屈曲到伸展的变化伴随着躯干向后倾斜。固定踝关节的膝下矫形器通过防止过度的背屈和跖屈，在所有关节尤其是膝关节处产生了更正常的力矩。在3名儿童（第三组）中，矫形器永久性地矫正了他们的膝反屈，但在这些研究中，对于这种改善的原因并不明确。
