Activity-dependent hyperpolarization and impulse conduction in motor axons in patients with carpal tunnel syndrome
Activity-dependent hyperpolarization and impulse conduction in motor axons in patients with carpal tunnel syndrome
复制标题
DOI：
10.1093/brain/awg087
复制
发表时间：
2003-04-01
期刊：
影响因子：
14.5
通讯作者：
Burke, D
中科院分区：
文献类型：
--
作者：
Cappelen-Smith, C;Lin, CSY;Burke, D
轴突衰减、缺血、脱髓鞘和髓鞘再生对腕管综合征病理生理的不同作用仍未得到解决。以往的研究表明，自发性收缩引起的运动轴突超极化可能导致慢性获得性脱髓鞘性多发性神经病的传导阻滞。本研究调查了这种轴突超极化是否可以产生或加重腕管综合征的传导阻滞，从而暗示脱髓鞘是其发病机制中的一个重要因素。研究在12名轻度至中度腕管综合征患者中进行，并与12名健康对照组进行比较。采用阈值追踪技术，记录拇短展肌（APB）的复合肌肉动作电位（CMAP）对腕部正中神经的超大刺激的反应，交替测量轴突兴奋性。主动收缩APB 60 s后，患者超极化阈值增加（18%）较对照组（37%）少。强度持续时间常数和超常度的变化在患者中适当较小。最大CMAP的幅度和面积在两组中均无显著改变。活动依赖性传导阻滞并没有沉淀在腕管综合征患者，即使这种程度的轴突超极化足以产生传导阻滞慢性炎症性脱髓鞘性多发性神经病。这些研究支持了这样的观点：脱髓鞘可能不是轻度至中度腕管综合症冲动传导减慢的关键因素。
The differing contributions of axonal attenuation, ischaemia, demyelination and remyelination to the pathophysiology of carpal tunnel syndrome remain unresolved. Previous studies indicate that the hyperpolarization of motor axons produced by voluntary contractions may precipitate conduction block in chronic acquired demyelinating polyneuropathies. The present study investigated whether this axonal hyperpolarization can produce or accentuate conduction block in carpal tunnel syndrome, thereby implicating demyelination as a significant factor in its pathogenesis. Studies were performed in 12 patients with mild to moderate carpal tunnel syndrome and compared with 12 healthy control subjects. Using the technique of threshold tracking, the compound muscle action potential (CMAP) of abductor pollicis brevis (APB) was recorded in response to supramaximal stimuli to the median nerve at the wrist, alternating with measurements of axonal excitability. After a voluntary contraction of APB for 60 s, there was a lesser hyperpolarizing threshold increase in the patients (similar to18%), than in controls (similar to37%). The changes in strength-duration time constant and supernormality were appropriately smaller in the patients. The amplitude and area of the maximal CMAP was not significantly altered in either group. Activity-dependent conduction block was not precipitated in the carpal tunnel syndrome patients even though this degree of axonal hyperpolarization was sufficient to produce conduction block in chronic inflammatory demyelinating polyneuropathy. These studies support the view that demyelination may not be a critical factor in the slowing of impulse conduction in mild to moderate carpal tunnel syndrome.