Xiao W, Xie Y
Institute of Basic Medical Sciences, Beijing.
Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 1990 Apr;12(2):110-4.
Peripheral nerve injury by chronic compression caused a decrease in conductive velocity or a delay in the transmission of the action potential, later blocking it completely following demyelination of the damaged nerve region. Abnormal firing activities were recorded from the injured peripheral nerve fibers after the 6-7th postoperative day. There were different patterns of abnormal firing from fibers. Regular tonic ectopic firings with high frequency were always recorded from A beta fibers. A delta/C fibers, however, had burst or irregular spikes. A single antidromic shock to the damaged region sometimes induced ectopic spikes following the expected one. The demyelinated region of the damaged nerve was very sensitive to both tetraethylammonium, a K+ channel blocker, and noradrenaline. The authors suggest that new ion channels or receptors, absent in normal, form in the damaged region.
慢性压迫导致的周围神经损伤会使传导速度降低或动作电位传导延迟,随后在受损神经区域脱髓鞘后完全阻断传导。术后第6 - 7天,在受损的周围神经纤维上记录到异常放电活动。不同纤维有不同的异常放电模式。Aβ纤维总是记录到高频规则的紧张性异位放电。然而,Aδ/C纤维有爆发性或不规则的尖峰。对受损区域进行单次逆向冲击有时会在预期的尖峰之后诱发异位尖峰。受损神经的脱髓鞘区域对钾通道阻滞剂四乙铵和去甲肾上腺素都非常敏感。作者认为,正常情况下不存在的新离子通道或受体在受损区域形成。