Reciprocal inhibition and corticospinal transmission in the arm and leg in patients with autosomal dominant pure spastic paraparesis (ADPSP)
Reciprocal inhibition and corticospinal transmission in the arm and leg in patients with autosomal dominant pure spastic paraparesis (ADPSP)
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DOI：
10.1093/brain/awh319
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发表时间：
2004-12-01
期刊：
影响因子：
14.5
通讯作者：
Nielsen, JB
中科院分区：
文献类型：
--
作者：
Crone, C;Petersen, NT;Nielsen, JB
痉挛发生的病理生理机制尚不清楚，但许多不同来源的痉挛患者的突触相互作用抑制通路的兴奋性受到影响。患有遗传性常染色体显性遗传性纯痉挛性截瘫 (ADPSP) 的患者会出现腿部痉挛和轻瘫，但手臂通常没有症状。因此，比较这些患者的腿部和手臂的脊柱和脊柱上控制可能提供有关痉挛病理生理学的有价值的信息。在本研究中，我们测试了以下假设：这些患者痉挛的病理生理机制之一是皮质脊髓传递异常，这可能导致相互抑制减少。对 10 名患者和 15 名健康年龄匹配的对照对象进行了调查。患者均出现腿部痉挛（腱反射亢进、肌张力增高和巴宾斯基征），但手臂无神经症状（除一名患者外）。测量桡侧腕屈肌 (FCR) 和比目鱼肌 (SOL) 运动神经元的突触相互 Ia 抑制（作为背景 FCR 和 SOL EMG 活动的抑制，以及由桡神经和腓神经刺激引起的 FCR 和 SOL H 反射的短潜伏期抑制）。此外，还测量了 FCR 肌肉和胫骨前肌 (TA) 的运动诱发电位 (MEP) 潜伏期。在患者中，手臂的平均相互抑制是正常的，而腿部的平均相互抑制与健康受试者相比显着下降。在患者中，FCR 肌肉中 MEP 的平均潜伏期正常，而 TA 肌肉中 MEP 的潜伏期明显长于健康受试者。然而，四名患者与其他患者的不同之处在于腿部有显着的相互抑制，并且 TA MEP 的潜伏期比其他患者明显短。相反，与健康受试者和四名保留相互抑制的患者相比，腿部没有相互抑制的六名患者具有显着的短潜伏期促进 SOL H 反射和更长的 TA MEP 潜伏期。这些发现支持这样的假设，即突触相互抑制和短潜伏期促进与痉挛的发展有关，此外，它们表明皮质脊髓传递受损与相互抑制/相互促进出现的减少之间存在正相关。
The pathophysiological mechanisms underlying the development of spasticity are not clear, but the excitability of the disynaptic reciprocal inhibitory pathway is affected in many patients with spasticity of different origin. Patients with genetically identified autosomal dominant pure spastic paraparesis (ADPSP) develop spasticity and paresis in the legs, but usually have no symptoms in the arms. Comparison of the spinal and supraspinal control of the legs and arms in these patients may therefore provide valuable information about the pathophysiology of spasticity. In the present study, we tested the hypothesis that one of the pathophysiological mechanisms of spasticity in these patients is abnormal corticospinal transmission and that this may lead to decreased reciprocal inhibition. Ten patients and 15 healthy age-matched control subjects were investigated. The patients were all spastic in the legs (with hyperactive tendon reflexes, increased muscle tone and Babinski sign), but had no neurological symptoms in the arms (except for one patient). Disynaptic reciprocal Ia inhibition of flexor carpi radialis (FCR) and soleus (SOL) motoneurons was measured (as the depression of the background FCR and SOL EMG activity and as the short latency inhibition of the FCR and SOL H-reflex evoked by radial and peroneal nerve stimulation). In addition, the latency of motor evoked potentials (MEPs) in the FCR muscle and the tibialis anterior (TA) muscle was measured. In the patients, the mean reciprocal inhibition was normal in the arms, while it was significantly decreased in the leg compared with the healthy subjects. In the patients, the average latency of MEPs in the FCR muscle was normal, while the latency to the MEP in TA muscle was significantly longer than that found in healthy subjects. Four patients, however, differed from the other patients by having significant reciprocal inhibition in the leg and a significantly shorter latency of TA MEPs than found in the other patients. The six patients without reciprocal inhibition in the leg instead had significant short latency facilitation of the SOL H-reflex and a longer TA MEP latency than seen in the healthy subjects and in the four patients with retained reciprocal inhibition. These findings support the hypothesis that disynaptic reciprocal inhibition and short latency facilitation are involved in the development of spasticity and, furthermore, they suggest a positive correlation between impairment of corticospinal transmission and decrease of reciprocal inhibition/appearance of reciprocal facilitation.