Impaired modulation of quadriceps tendon jerk reflex during spastic gait: differences between spinal and cerebral lesions
Impaired modulation of quadriceps tendon jerk reflex during spastic gait: differences between spinal and cerebral lesions
复制标题
DOI：
10.1093/brain/122.3.567
复制
发表时间：
1999-03-01
期刊：
影响因子：
14.5
通讯作者：
Dietz, V
中科院分区：
文献类型：
--
作者：
Faist, M;Ertel, M;Dietz, V
在健康受试者中，短潜伏期腿部肌肉反射的功能适当调节发生在步态过程中。这种调节在一定程度上归因于Ia传入神经突触前抑制的变化。我们将健康受试者与半麻痹性或旁麻痹性痉挛患者步态时股四头肌肌腱抽搐反射调节的变化进行了比较。痉挛分别由单侧脑梗死和外伤性脊髓损伤引起。本文研究了股四头肌肌腱抽搐反射在步进循环的16个阶段的调节。在跑步机上行走时获得的反射反应与模仿步态的站立姿势获得的控制值进行比较，这些姿势具有相应的随意肌收缩水平和膝关节角度。在健康受试者中，反射的大小被深刻调节，并且在整个阶跃循环中普遍被抑制。在脊柱病变患者中，步态中的反射抑制几乎被消除，并且与步进周期中的弱调节或无调节有关；在大脑病变患者中，与健康受试者相比，反射大小的抑制较少，与受影响侧反射调节减少有关。在“未受影响”的一侧，这些患者的反射调节与健康受试者相似，但步态时的反射大小与站立控制值没有显著差异。这些观察结果表明，导致健康人正常步态中反射大小下降和调节的机制在脊髓或脑源性痉挛中不同程度地受损，可能是由于偏瘫患者单侧纤维束的保留。
In healthy subjects, functionally appropriate modulation of short latency leg muscle reflexes occurs during gait. This modulation has been ascribed, in part, to changes in presynaptic inhibition of Ia afferents, The changes in modulation of quadriceps tendon jerk reflexes during gait of healthy subjects were compared with those of hemi- or paraparetic spastic patients. The spasticity was due to unilateral cerebral infarction or traumatic spinal cord injury, respectively. The modulation of the quadriceps femoris tendon jerk reflex at 16 phases of the step cycle was studied. The reflex responses obtained during treadmill walking were compared with control values obtained during gait-mimicking standing postures with corresponding levels of voluntary muscle contraction and knee angles. In healthy subjects the size of the reflexes was profoundly modulated and was generally depressed throughout the step cycle. In patients with spinal lesion the reflex depression during gait was almost removed and was associated with weak or no modulation during the step cycle, In patients with cerebral lesion there was less depression of the reflex size associated with a reduced reflex modulation on the affected side compared with healthy subjects. On the 'unaffected' side of these patients reflex modulation was similar to that of healthy subjects, but the reflex size during gait was not significantly different from standing control values. These observations suggest that the mechanisms responsible for the depression of reflex size and the modulation normally seen during gait in healthy subjects are impaired to different extents in spasticity of spinal or cerebral origin, possibly due to the unilateral preservation of fibre tracts in hemiparesis.