Inshasi J S, Jose V P, van der Merwe C A, Gledhill R F
Neurosciences Department, Rashid Hospital, Dubai, United Arab Emirates.
Neuromuscul Disord. 1999 Jun;9(4):227-31. doi: 10.1016/s0960-8966(98)00129-1.
Reversible electrophysiologic abnormalities of sensory nerve function were found by chance in three patients with hypokalemic periodic paralysis, a disorder previously considered to affect the function of muscle membranes only. A formal, prospective study was therefore conducted. Serial nerve conduction studies were done in ten additional patients. Amplitude of sensory action potentials was significantly smaller during paralytic attacks, but did not differ from controls after normalization of serum potassium concentration. These apparently novel findings might be explained by previous electrodiagnostic studies either not involving the testing of sensory nerves at all, or not being repeated after recovery from an attack. Involvement of sensory nerves in hypokalemic periodic paralysis is suggested to arise through dorsal root ganglia having an incomplete blood-nerve barrier and sensory neurons being particularly vulnerable to derangements affecting nerve cell metabolism. Neuronal inexcitability is postulated to occur consequent upon possible inactivation of the sodium-potassium pump by the low concentration of extracellular potassium. In patients with acute areflexic limb weakness, the diagnosis of hypokalemic periodic paralysis should not be excluded by abnormal results of sensory nerve conduction studies.
在三名低钾性周期性麻痹患者中偶然发现了感觉神经功能的可逆性电生理异常，低钾性周期性麻痹是一种先前被认为仅影响肌膜功能的疾病。因此进行了一项正式的前瞻性研究。对另外十名患者进行了系列神经传导研究。在麻痹发作期间，感觉动作电位的幅度明显较小，但在血清钾浓度恢复正常后与对照组无差异。这些明显新颖的发现可能是由于先前的电诊断研究根本未涉及感觉神经的测试，或者在发作恢复后未重复测试。低钾性周期性麻痹中感觉神经受累被认为是由于背根神经节的血-神经屏障不完整以及感觉神经元特别容易受到影响神经细胞代谢的紊乱的影响。据推测，由于细胞外低钾浓度可能使钠钾泵失活，从而导致神经元兴奋性降低。在急性无反射性肢体无力的患者中，感觉神经传导研究结果异常不应排除低钾性周期性麻痹的诊断。
