神经传导速度对糖尿病周围神经病的诊断价值

目的 :探讨神经传导速度 (NCV)对糖尿病周围神经病 (DPN)的诊断价值。方法 :对 5 0例糖尿病患者分为有症状组和无症状组 ,进行周围神经NCV的测定 ,与健康人对照 ,同时行相关因素分析。结果 :糖尿病患者运动神经传导速度 (MCV)、感觉神经传导速度 (SCV)与健康人比较存在明显差异 ,且有症状组更显著 (P <0 0 5 ) ;患者的NCV与空腹血糖无明显相关 ,而与病程长短呈正相关。结论 :周围神经NCV的检测有助于DPN的早期诊断     

神经电生理检查在糖尿病前期周围神经病变的应用进展

糖尿病前期周围神经病的早期诊断重点依赖于对小纤维的评价.传统的神经传导检测只能反映大的有髓纤维的功能,而对于与痛觉及自主神经病变有关的小纤维病变缺乏敏感性.近年来随着神经电生理诊断技术的发展,糖尿病前期周围神经病的早期诊断不断提高.临床中常用小纤维病变的检测方法主要包括皮肤交感反应、定量感觉检查、接触性热痛诱发电位及定量催汗轴突反射等.就糖尿病前期周围神经病的发病机制、神经功能的病理学改变及神经电生理技术在糖尿病前期周围神经病变的应用进展加以综述,旨在为糖尿病前期周围神经病变的早期诊断提供客观依据.     

红花注射液治疗糖尿病周围神经病变临床观察

目的观察红花注射液治疗糖尿病周围神经病（DPND）的疗效。方法将52例DPND患者随机分成2组,对照组采用DPND的常规治疗方法,治疗组在对照组用药基础上加用红花注射液,每日静滴20 ml治疗2周,并在治疗12周后观察患者症状和体征、血糖情况。结果治疗12周后,红花注射液治疗组对改善DPND患者的肢体疼痛、麻木、发凉、感觉异常和/或减退等临床症状的总有效率为73.03%,较对照组50.0%,有显著性差异（P〈0.01）。结论红花注射液对改善DPND患者的临床症状有明显疗效,是治疗DPND的有效方法之一。     

感觉电流阈值在糖尿病周围神经病变诊断中的临床应用

目的:探讨感觉电流阈值(CPT)在糖尿病周围神经病变(DPN)诊断中的价值.方法:选取符合入选条件的52例2型糖尿病( T2DM)患者和50例健康人的感觉电流阈值.以神经传导速度检查( NCV)为诊断糖尿病周围神经病变的“金标准”,使用X 2检验评价电流感觉阈值的灵敏度、特异度、阳性预测值、阴性预测值及Kappa值.结果:以NCV为标准,电流感觉阈值的灵敏度61.1％,特异度62.5％,阳性预测值78.6％,阴性预测值41.7％,Kappa值0.207.结论:电流感觉阈值能评估个体感觉通路功能,有助于筛查DPN患者.     

神经传导速度对Ⅱ型糖尿病周围神经病的早期诊断价值

目的:探讨神经传导速度(NCV)对Ⅱ型糖尿病性周围神经病(DPN)的早期诊断价值。方法:对80例Ⅱ型糖尿病患者行周围神经NCV的测定,以本室正常值为标准进行判定,同时行相关因素分析。结果:Ⅱ型糖尿病患者神经传导速度与正常值比较存在明显差异(p(0.01)。本组NCV异常63例,占78.8%,且以感觉神经传导速度(SCV)改变最明显。在所检神经中,下肢腓肠神经的异常率最高,为57例,占90.5%。患者NCV异常与有无临床症状及病程长短呈正相关。结论:周围神经NCV的检测有助于DPN的早期诊断。     

皮神经感觉传导速度和波幅检测对糖尿病周围神经病的诊断作用

目的：探讨皮神经感觉传导速度（SCV）,波幅（Amp)检测对糖尿病患者周围神经远端受损的早期诊断价值。方法：受试者为糖悄病患者组和正常对照组各25例,对前臂外侧皮神经和腓肠神经共100条,就其感觉传导速度（SVC）及其诱发的波幅（Amp)进行分析,并与胫神经,正中神经进行比较,结果：混合神经的异常率明显低于皮神经,尤以无周围神经症状的糖尿病者更加明显（P＜0．01）,结论：皮神经的SCV,Amp检测,对糖尿病周围神经远端受损的早期诊断可靠,灵敏度高。     

糖尿病性周围神经病患者的运动神经传导阻滞现象

目的：观察糖尿病性周围神经病（DPN）患者运动神经传导阻滞（CB）的发生率及其与其它神经电生理参数的关系。方法：对346例糖尿病患者的神经电生理检测数据，包括运动神经传导速度（MCV）、F反应、感觉神经传导速度（SCV）等作回顾性分析。并对MCV测定时近、远端刺激引出的复合肌肉动作电位（CMAP）波幅和波面积进行比较，判断是否存在CB。结果：①在346例糖尿病患者中，有CB的病例为57例占16.5％，受检的1345条神经中，有62条神经异常，占4.6％，胫神经异常率最高（13.6％）。②出现CB的患者受检的225条神经中，SCV、F反应、MCV的异常率依次为52.9％、47.4％和45.1％。③出现CB的神经有67.9％伴有F波潜伏期延长和/或F波传导速度减慢，32.1％出现F波时间离散度增加。结论：部分糖尿病患者存在运动神经传导阻滞现象（CB）、胫神经CB出现率最高；运动神经CB多伴有MCV其它参数异常。     

银杏达莫注射液治疗糖尿病周围神经病变临床观察

目的观察银杏达莫注射液治疗糖尿病周围神经病的疗效。方法将57例周围神经病变患者随机分成2组,对照组采用周围神经病变的常规治疗方法,治疗组在对照组用药基础上加用银杏达莫注射液,每日静滴20ml治疗3周,并在治疗12周后观察患者症状和体征、血糖情况。结果治疗12周后,银杏达莫注射液治疗组对改善周围神经病变患者的肢体疼痛、麻木、发凉、感觉异常和/或减退等临床症状的总有效率为78.57%,较对照组51.72%,有显著性差异(P<0.01)。结论银杏达莫注射液对改善周围神经病变患者的临床症状有明显疗效,是治疗周围神经病变的有效方法之一。     

糖尿病神经病变与微循环的关系

为研究糖尿病神经病变与微循环的关系，对１１７例非胰岛素依赖型糖尿病（ＮＩＤＤＭ）并发糖尿病周围神经病变（ＤＰＮ）患者甲襞微循环进行了观察，并与无ＤＰＮ组（３６例）进行比较。结果显示，ＤＰＮ患者有明显的微循环障碍，ＤＰＮ组微血管形态、流态和袢周状态均有显著异常。与无ＤＰＮ组比较，ＤＰＮ患者血液流速明显减慢（Ｐ＜０．０５），并有明显的血细胞聚集（Ｐ＜０．０５）、袢周渗出（Ｐ＜０．０１）与出血（Ｐ＜０．０５）。Ｌｏｇｉｓｔｉｃ逐步回归分析显示，微循环障碍是糖尿病神经病变发病的独立危险因素（ＯＲ：１．５７；９５％ＣＩ：１．１８２．０９）。     

神经传导速度早期诊断糖尿病性周围神经病

本文对58例糖尿病人进行了神经传导速度(NCV)测定,其中有周围神经损害的症状和体征,临床诊断为糖尿病并发周围神经病者32例,临床无周围神经损害的糖尿病者26例。其结果表明,NCV测定为判断周围神经损害的一种客观指标,且感觉神经测定比运动神经敏感,下肢胫神经测定比上肢敏感,也可提示亚临床期的周围神经病变,有助于糖尿病性周围神经病的早期诊断。     

基于一维卷积神经网络的糖尿病周围神经病变预测模型研究

为了实现对糖尿病周围神经病变(DPN)的早期预防,辅助医生进行早期诊断与决策,提出了一种基于一维卷积神经网络的DPN预测模型,对原始数据进行了一系列的预处理工作以提高数据的质量,此外数据集的特征维度较高,为了进一步提高预测模型的准确性,进行了主成分分析(PCA)降维处理,通过自主学习数据的特征信息,从中挖掘其有价值的医学信息与规律,来实现DPN的预测。通过支持向量机、BP神经网络和一维卷积神经网络分别建立了DPN预测模型。实验结果表明,一维卷积神经网络模型预测效果优于其他两个模型,其准确率、召回率、F1值、AUC值分别达到了0.983、0.916、0.923、0.98。     

Morphology of diabetic neuropathy

The morphological findings in peripheral nerves in diabetic subjects are reviewed. Diabetes is probably the most frequent cause of neuropathy. However it does not constitute a single nosological entity but is comprised of a variety of clinical and morphological changes. These are considered to be the consequences of metabolic derangements resulting from chronic hyperglycemia. Distal symmetrical neuropathies, which are most common, are characterized by axonal degeneration and segmental demyelination with loss of nerve fibres and fibrosis. Remyelination and axonal sprouting occur. Microvascular changes consist of thickening and hyalinization of the walls of the vessels. On electron microscopy these vessels appear thickened and show reduplication of the basal lamina that surrounds the endothelial cells and pericytes. The morphological bases of proximal symmetrical motor neuropathy, as well as of focal and multifocal neuropathies are briefly described. The synopsis of current knowledge can be helpful in diagnosis and differential diagnosis of disorders of the peripheral nervous system.     

改良的下肢SLSEP检测方法对糖尿病近端神经病的诊断意义

目的：探讨改良的短潜伏期体感诱发电位（SLSEP）（改变记录点）的检测方法对糖尿病性近端神经病的诊断意义。方法：排除脑卒中、腰颈椎病及其它疾病引起的神经肌肉疾病,肌电图检查排除有神经病变体征同时常规神经传导检测异常的糖尿病（DM）患者,将符合标准的61例2型DM患者分为3组：有神经病体征而常规神经传导检测正常（Ⅰ组）20例,无神经病体征且常规神经传导检测正常（Ⅱ组）21例和无神经病体征而常规神经传导检测异常（Ⅲ组）20例,与30例正常人均行改良的SLSEP测定。结果：改良的胫神经SLSEP反映下肢感觉神经近端功能的参数总异常率以DM有神经病变症状肢体亚组（Ⅰ组）（n=27）所占的比例最高（85％,23／27）,SLSEP反映神经近端功能的N13、N24峰的感觉神经传导速度（SCV）和N13N24、N9-N24峰间SCV,与对照组比较差异均有显著意义（P〈0．01）;DMⅡ组虽然无神经病变体征并且神经传导测定无异常,但与对照组比较,N13-N24峰间SCV异常肢体率却有显著差异（P〈0．01）。DMⅢ组SLSEP各参数异常率普遍较高（20％～72．5％）,但以反映神经远端功能的N9峰SCV异常率最高。结论：改良的SLSEP检测是对常规SCV检测的一种补充,可以提供感觉纤维近端信息,对有周围神经损害症状而常规SCV测定正常的DM患者其诊断意义尤为显著。SLSEP还有利于发现DM患者亚临床症状。     

Auditory neuropathy in streptozotocin-induced diabetic mouse

An investigation of the mechanism of damage to the peripheral nervous system and central nervous system in diabetes mellitus (DM) is highly important in current neurological research. Auditory neuropathy is a hearing disorder in which the auditory brainstem evoked potential is absent or severely abnormal. This study investigated auditory neuropathy caused by streptozotocin in mouse model. In order to assess diabetic auditory neuropathy, we evaluated auditory brainstem response (ABR) for the evaluation of sensorineural function in peripheral auditory nerve. Auditory middle latency response (AMLR) was employed to assess the middle response in the midbrain. STZ groups significantly increased the absolute latencies IV and the interpeak latencies I-III and I-IV of ABR compared with STZ 0 group. Pa latency of AMLR also significantly increased in proportion to STZ dosage. Taken together, our results demonstrate that STZ-induced DM may impair the auditory pathway from peripheral auditory nerve to midbrain in the mouse model. We suggest that the STZ-induced diabetic mouse model may be useful for the evaluation of auditory pathway impairment by using ABR and AMLR tests.     

Sympathetic skin response in diabetic neuropathy

Autonomic neuropathy is a complication of diabetes mellitus (DM) in substantial proportion of cases and may cause definite autonomic symptoms. Because conventional electrophysiological methods do not assess the autonomic nervous system, simple reproducible tests were developed. One of them is sympathetic skin response (SSR) which provides useful information about the status of sympathetic postganglionic function. The aim of this study is to perform SSR in diabetic patients to see whether this test can be used as an electrophysiological method for the diagnosis and confirmation of diabetic autonomic neuropathy. 20 diabetic patients who had electrophysiologically confirmed polyneuropathy but showed no symptoms or signs referable to autonomic system dysfunction were included. 14 (70%) patients demonstrated abnormal SSR. 2 abnormal patterns were observed. An absent response in at least one tested lower extremity (50%) and prolonged foot with normal hand latency (20%). 6 patients (30%) demonstrated no abnormalities. Foot and hand latencies in diabetics did not differ significantly from those of normal controls (p: 0.4, p: 0.1) and no correlation could be found with latencies and duration of sickness, patient's age and HbA1c values. We believe latency measurement is an objective measure of conduction in multineural pathways and can detect subclinical involvement of sympathetic nervous system in diabetics who do not manifest symptoms or signs referable to autonomic system dysfunction.     

Sympathetic skin response in diabetic neuropathy

Sympathetic function test was undertaken using the sympathetic skin response (SSR), a technique for assessment of sudomotor activity, in 67 diabetics, and the results were compared with those from 45 age-matched normal subjects. The SSR was readily elicitable in normal subjects, but absent in six patients with diabetes. In 28 patients, the SSR was preserved, but their amplitude was below the normal range. The decrease in the SSR amplitude correlated well with a fall in motor and sensory conduction velocity. The SSR magnitude correlated well to the impaired R-R interval variation during deep breathing and the heart rate increase and the blood pressure change on standing, indicating a close correlation between the disturbance of sudomotor function and that of other sympathetic and parasympathetic functions. Most of the patients with clinical evidence of dysautonomia and with insulin treatment revealed diminished or absent SSR.     

Oral zinc therapy in diabetic neuropathy

The present double blind randomized study was conducted on 50 subjects; 20 age and sex matched healthy controls (Group--I); 15 patients of diabetes mellitus with neuropathy who received placebo for 6 weeks (Group--IIA); and 15 patients of diabetes mellitus with neuropathy who were given supplemental zinc sulphate (660 mg) for 6 weeks (Group--IIB). Serum zinc level, fasting blood sugar (FBS) and post prandial blood sugar (PPBS) levels and motor nerve conduction velocity (MNCV) were estimated on day 0 and after 6 weeks in all subjects. Serum zinc levels were significantly low (p < 0.001) in group IIA and IIB as compared to healthy controls (Group--I) at baseline. After 6 weeks the change in pre and post therapy values of FBS, PPBS and MNCV (median and common peroneal nerve) were highly significant (P = < 0.001) for group IIB alone with insignificant change (P = > 0.05) in group IIA. No improvement (P = > 0.05) in autonomic dysfunction was observed in either groups. Therefore, oral zinc supplementation helps in achieving better glycemic control and improvement in severity of peripheral neuropathy as assessed by MNCV.     

The role of endoneural edema in the pathogenesis of diabetic neuropathy

Average endoneurial area was correlated with measurements of myelinated fiber density in sural nerves from diabetics and controls. Although, in general, myelinated fiber density decreased with increasing endoneurial area, this relationship was not significant for diabetic nerves. The increase in endoneurial area was attributed to expansion of the endoneurial space as a result of endoneurial edema. A possible role for such edema in the pathogenesis of diabetic neuropathy is considered.