Z'Graggen W J, Lin C S Y, Howard R S, Beale R J, Bostock H
Sobell Department of Neurophysiology, Institute of Neurology, London, UK.
Brain. 2006 Sep;129(Pt 9):2461-70. doi: 10.1093/brain/awl191. Epub 2006 Aug 10.
Patients in intensive care units frequently suffer muscle weakness and atrophy due to critical illness polyneuropathy (CIP), an axonal neuropathy associated with systemic inflammatory response syndrome and multiple organ failure. CIP is a frequent and serious complication of intensive care that delays weaning from mechanical ventilation and increases mortality. The pathogenesis of CIP is not well understood and no specific therapy is available. The aim of this project was to use nerve excitability testing to investigate the changes in axonal membrane properties occurring in CIP. Ten patients (aged 37-76 years; 7 males, 3 females) were studied with electrophysiologically proven CIP. The median nerve was stimulated at the wrist and compound action potentials were recorded from abductor pollicis brevis muscle. Strength-duration time constant, threshold electrotonus, current-threshold relationship and recovery cycle (refractoriness, superexcitability and late subexcitability) were recorded using a recently described protocol. In eight patients a follow-up investigation was performed. All patients underwent clinical examination and laboratory investigations. Compared with age-matched normal controls (20 subjects; aged 38-79 years; 7 males, 13 females), CIP patients exhibited reduced superexcitability at 7 ms, from -22.3 +/- 1.6% to -7.6 +/- 3.1% (mean +/- SE, P approximately 0.0001) and increased accommodation to depolarizing (P < 0.01) and hyperpolarizing currents (P < 0.01), indicating membrane depolarization. Superexcitability was reduced both in patients with renal failure and without renal failure. In the former, superexcitability correlated with serum potassium (R = 0.88), and late subexcitability was also reduced (as also occurs owing to hyperkalaemia in patients with chronic renal failure). In patients without renal failure, late subexcitability was normal, and the signs of membrane depolarization correlated with raised serum bicarbonate and base excess, indicating compensated respiratory acidosis. It is inferred that motor axons in these CIP patients are depolarized, in part because of raised extracellular potassium, and in part because of hypoperfusion. The chronic membrane depolarization may contribute to the development of neuropathy.
重症监护病房的患者常因危重病性多发性神经病（CIP）而出现肌肉无力和萎缩，CIP是一种与全身炎症反应综合征及多器官功能衰竭相关的轴索性神经病。CIP是重症监护中常见且严重的并发症，会延迟机械通气撤机并增加死亡率。CIP的发病机制尚不清楚，且尚无特效治疗方法。本项目的目的是利用神经兴奋性测试来研究CIP中轴突膜特性的变化。对10例经电生理证实患有CIP的患者（年龄37 - 76岁；男性7例，女性3例）进行了研究。在腕部刺激正中神经，并从拇短展肌记录复合动作电位。使用最近描述的方案记录强度 - 时间常数、阈下电紧张、电流 - 阈值关系和恢复周期（不应期、超常兴奋性和后期亚兴奋性）。对其中8例患者进行了随访调查。所有患者均接受了临床检查和实验室检查。与年龄匹配的正常对照组（20名受试者；年龄38 - 79岁；男性7例，女性13例）相比，CIP患者在7毫秒时的超常兴奋性降低，从-22.3±1.6%降至-7.6±3.1%（平均值±标准误，P约为0.0001），对去极化电流（P < 0.01）和超极化电流（P < 0.01）的适应性增加，表明膜去极化。肾衰竭患者和非肾衰竭患者的超常兴奋性均降低。在前者中，超常兴奋性与血清钾相关（R = 0.88），后期亚兴奋性也降低（慢性肾衰竭患者高钾血症时也会出现这种情况）。在非肾衰竭患者中，后期亚兴奋性正常，膜去极化的体征与血清碳酸氢盐升高和碱剩余相关，表明存在代偿性呼吸性酸中毒。据推测，这些CIP患者的运动轴突发生去极化，部分原因是细胞外钾升高，部分原因是灌注不足。慢性膜去极化可能导致神经病的发展。
