糖尿病性神经病变神经兴奋性的变化  

Altered nerve excitability properties in established diabetic neuropathy

作　　者：Krishnan A.V. Kiernan M.C. 朱光明 

机构地区：[1]Prince of Wales Medical Research Institute, Barker Street, Sydney, NSW 2031, Australia,Dr.

出　　处：《世界核心医学期刊文摘（神经病学分册）》2005年第9期34-35,共2页Digest of the World Core Medical Journals:Clinical Neurology

摘　　要：The underlying cause of diabetic neuropathy remains unclear,although pathological studies have suggested an ischaemic basis related to microangiopathy, possibly mediated through effects on the energy-dependent Na+/K+pump. To investigat e the pathophysiology of diabetic neuropathy, axonal excitability techniques wer e undertaken in 20 diabetic patients with neuropathy severity graded through a c ombination of quantitative sensory testing (QST) using a vibratory stimulus, ass essment of symptom severity using the Total Neuropathy Symptom Score (T-NSS) an d measurement of glycosylated haemoglobin as a marker of disease control. To ass ess axonal excitability,compound muscle action potentials were recorded at rest from abductor pollicis brevis following stimulation of the median nerve, and sti mulus-response behaviour, threshold electrotonus,a current-threshold relationship and the recovery of excitability were recorded in each patient. All patients had established neuropathy,with abnormalities of T-NSS present in all patients and QST abnormalities present in 65%. Compared w ith controls,diabetic neuropathy patients had significant reduction in maximal C MAP amplitude (P < 0.0005), accompanied by a‘fanning in’of threshold electroto nus. In addition, the strength-duration time constant was decreased in diabetic neuropathy patients and recovery cycles were altered with reductions in refract oriness,the duration of the relative refractory period, superexcitability and su bexcitability. It is proposed that while the changes in threshold electrotonus w ith supportive findings in the currentthreshold relationship are consistent with axonal depolarization,possibly mediated by a decrease in Na +/K+pump activity , the alterations in the recovery cycle of excitability could be explained on th e basis of a smaller action potential, reflecting a limitation on the nodal driv ing current imposed by a reduction in Na+conductances.The underlying cause of diabetic neuropathy remains unclear,although pathological studies have suggested an ischaemic basis related to microangiopathy, possibly mediated through effects on the energy-dependent Na+/K+pump. To investigat e the pathophysiology of diabetic neuropathy, axonal excitability techniques wer e undertaken in 20 diabetic patients with neuropathy severity graded through a c ombination of quantitative sensory testing (QST) using a vibratory stimulus, ass essment of symptom severity using the Total Neuropathy Symptom Score (T-NSS) an d measurement of glycosylated haemoglobin as a marker of disease control. To ass ess axonal excitability,compound muscle action potentials were recorded at rest from abductor pollicis brevis following stimulation of the median nerve, and sti mulus-response behaviour, threshold electrotonus,a current-threshold relationship and the recovery of excitability were recorded in each patient. All patients had established neuropathy,with abnormalities of T-NSS present in all patients and QST abnormalities present in 65%. Compared w ith controls,diabetic neuropathy patients had significant reduction in maximal C MAP amplitude (P < 0.0005), accompanied by a‘fanning in’of threshold electroto nus. In addition, the strength-duration time constant was decreased in diabetic neuropathy patients and recovery cycles were altered with reductions in refract oriness,the duration of the relative refractory period, superexcitability and su bexcitability. It is proposed that while the changes in threshold electrotonus w ith supportive findings in the currentthreshold relationship are consistent with axonal depolarization,possibly mediated by a decrease in Na +/K+pump activity , the alterations in the recovery cycle of excitability could be explained on th e basis of a smaller action potential, reflecting a limitation on the nodal driv ing current imposed by a reduction in Na+conductances.

关 键 词：神经兴奋性 糖尿病神经病变 神经症状评分 定量感觉测试 拇短展肌 神经轴突 相对不应期 微血管病 严重度分级 电紧张 

分 类 号：R587.2[医药卫生—内分泌]