慢性酒精中毒性周围神经病患者神经电生理变化的研究

目的 探讨慢性酒精中毒性周围神经病患者神经电生理变化特点.方法 35例酒精中毒性周围神经病患者与35例正常人行肌电图检测后进行统计学分析.结果 观察组的正中神经、尺神经、腓总神经和腓浅神经的神经传导速度(NCV)明显低于对照组.结论 神经电生理检测是本病早期诊断与周围神经受损评价的敏感指标.     

慢性正己烷中毒的神经电生理表现

目的分析慢性正己烷中毒的神经电生理表现。方法应用常规肌电图技术对２２例慢性正己烷中毒患者进行肌电图、神经传导速度检测。结果慢性正己烷中毒患者电生理检查异常率为５５％,感觉神经传导速度减慢为９％,运动神经传导速度减慢为４３％,远端潜伏期延长为２８％。结论慢性正己烷中毒以损害运动神经远端为主,神经损害与接触正己烷时间有关。     

血浆同型半胱氨酸和胱抑素C与糖尿病周围神经病变的相关性研究

目的 探讨同型半胱氨酸（Hcy）和胱抑素C（Cys-C）与糖尿病周围神经病变（DPN）的相关性. 方法 选取2009年1月至2013年10月于我院就诊的T2DM患者248例,根据2010年版《中国2型糖尿病防治指南》诊断标准将对象分为亚临床糖尿病神经病变组（SDPN组）80例、糖尿病神经病变组（DPN组）52例和单纯T2DM组（T2DM组）116例.检测各组Hcy、Cys-C、FPG、HbA1 c、TG及TC等水平. 结果 3组年龄、性别比、BMI、FPG、TG、TC、HDL-C和LDL-C、SBP、DBP及血清肌酐（Scr）比较差异无统计学意义（P＞0.05）.与T2DM组比较,SDPN组和DPN组病程、Hcy和Cys-C升高（P＜0.05或P＜0.01）,且DPN组Hcy高于SDPN组（P＜0.05）.SDPN组和DPN组正中神经运动神经传导速度（MCV）和感觉神经传导速度（SCV）、腓总神经MCV和SCV较T2DM组降低（P＜0.05或P＜0.01）;DPN组正中神经MCV和SCV、腓总神经MCV和SCV较SDPN组低（P＜0.05或P＜0.01）.SDPN组和DPN组正中神经F波潜伏期和腓总神经H反射潜伏期较T2DM组升高（P＜0.05或P＜0.01）;DPN组正中神经F波潜伏期,腓总神经H反射潜伏期较SDPN组高（P＜0.05或P＜0.01）.Logistic回归分析显示,Hcy、Cys-C、病程、SBP和HbA1c是DPN的独立影响因素. 结论 SDPN和DPN患者神经反射潜伏期延长,MCV和SCV减慢,且血浆Hcy与肌电图各参数相关,提示血浆Hcy与神经传导异常相关,说明血浆Hey可作为DPN的预测因子与危险因素.这两类患者Cys-C浓度升高,且与Hcy水平相关,提示Cys-C可能与Hcy共同作用,加重DPN.     

交感神经皮肤反应与神经传导测定对糖尿病周围神经病变的诊断价值

[摘要]目的 分析比较交感神经皮肤反应与神经传导速度对糖尿病周围神经病变的诊断价值。方法 选取本院2014年1月-2015年12月门诊收治的43例2型糖尿病患者和43例健康体检者,同时行神经电图检测,包括感觉神经传导速度、运动神经传导速度和交感神经皮肤反应,并对结果进行记录和统计学分析。结果 糖尿病组的正中神经、尺神经、腓总神经、胫神经的运动神经传导速度和正中神经、尺神经、腓肠神经、腓浅神经的感觉神经传导速度均明显低于健康组（P＜0.01）;健康组上下肢的起始潜伏期均明显少于糖尿病组（P＜0.01）,但糖尿病组上下肢的波幅与健康组相比较,差异均无统计学意义（P＞0.05）;糖尿病组患者的下肢的神经传导速度的异常率（34.84%）明显高于上肢（18.85%）,两者差异存统计学意义（χ2=16.97,P＜0.01）;上肢的交感神经皮肤反应异常率（35.24%）低于下肢（55.74%）,差异存统计学意义（χ2=10.33,P＜0.01）;神经传导速度和交感神经皮肤反应总异常率分别为25.58%、45.49％,交感神经皮肤反应的总异常率显著高于神经传导速度,差异存统计学意义（χ2=39.96,P＜0.01）。 结论 神经传导速度和交感神经皮肤反应作为糖尿病自主神经及周围神经病变诊断的重要指标,可为糖尿病周围神经病的早期诊断提供重要依据,且交感神经皮肤反应对糖尿病周围神经病早期诊断的敏感性更高。     

刺五加离子导入治疗糖尿病周围神经病变30例疗效观察

为观察刺五加离子导入治疗糖尿病周围神经病变的临床疗效，用该法对31例糖尿病周围神经病变患者(治疗组)进行治疗，并与29例经常规糖尿病治疗者(对照组)进行对比。结果显示，治疗组各临床症状好转率，特别是肢体疼痛、足背动脉波动减弱、肢体皮肤色泽变浅及体位性低血压好转率明显高于对照组，两组比较有显著性差异(P＜0．01)；治疗组正中神经、尺神经和腓总神经的感觉神经传导速度(SCV)、运动末端潜伏期(MLP)较同组治疗前和对照组治疗后均明显改善，组间比较有显著性差异(P均＜0．01)。提示刺五加离子导入疗法可在一定程度上促进受损神经组织的修复和再生，改善神经髓鞘功能，降低糖尿病周围神经病变的致残率．     

神经传导速度在糖尿病无症状性周围神经病中的应用价值

目的：探讨神经传导速度（NCV）在糖尿病（DM）无症状性周围神经病变患者中的应用价值。方法：选择DM伴周围神经病变患者（有症状组）25例及无周围神经病变症状患者（无症状组）30例,分别测定双侧正中神经、尺神经、胫神经及腓总神经运动传导速度（MCV）和双侧正中神经、尺神经、胫神经及腓浅神经感觉传导速度（SCV）,并对30例无神经系统症状的患者用空腹血测糖化血红蛋白（HbAlc）,3个月后复查神经传导速度和HbAlc。结果：NCV能及早发现有周围神经损害亚临床糖尿病周围神经病变（DPN）患者,NCV的异常率与血糖升高关系密切,动态观察NCV对了解疾病预后很重要。     

中药熏洗配合针灸治疗糖尿病周围神经病变的效果

目的探讨中药熏洗联合针灸治疗糖尿病周围神经病变的效果。方法择取该院2012年3月—2014年5月糖尿病周围神经病变患者114例,将其按照数字法随机分组,分别为对照组和观察组,每组57例,其中对照组患者采取常规西药治疗,观察组患者采取中药熏洗联合针灸治疗,比较两组糖尿病周围神经病变患者治疗前后的正中神经和腓总神经的神经传导速度,并比较两组患者的治疗效果。结果两组糖尿病周围神经病变患者治疗前的正中神经和腓总神经的神经传导速度对比,数据差异无统计学意义(P0.05),经过治疗后,两组患者正中神经和腓总神经的神经传导速度数据均优于治疗前,观察组患者数据优于对照组患者(P0.05),两组患者治疗效果对比,观察组患者治疗总有效率显著高于对照组患者(P0.05)。结论在对糖尿病周围神经病变患者的治疗中,采取中药熏洗联合针灸治疗能够改善其正中神经和腓总神经的神经传导速度,提高治疗效果。     

交感神经皮肤反应与神经传导速度对糖尿病周围神经病变的诊断价值

目的:分析交感神经皮肤反应(SSR)与神经传导速度(NCV)对糖尿病周围神经病变(DPN)的诊断价值。方法:选取43例2型糖尿病患者和43例健康体检者,同时行神经电图检测,包括感觉神经传导速度(SCV)、运动神经传导速度(MCV)和交感神经皮肤反应(SSR),并进行统计学分析。结果:糖尿病组的正中神经、尺神经、腓总神经、胫神经的MCV和正中神经、尺神经、腓肠神经、腓浅神经的SCV均明显低于健康组(均P0.01);健康组上下肢的起始潜伏期均明显短于糖尿病组(均P0.01),但糖尿病组上下肢的波幅与健康组比较,差异有统计学意义(P0.01);糖尿病组患者下肢NCV和SSR的异常率均明显高于上肢(34.8%vs 18.9%,55.7%vs 35.2%,均P0.01);SSR总异常率显著高于NCV(45.5%vs 24.2%,P0.01)。结论:NCV和SSR可为DPN的早期诊断提供重要依据,且SSR敏感性更高。     

Ⅱ型糖尿病周围神经病变患者的神经传导速度与空腹血糖和糖基化血红蛋白(HbA_1)的关系

通过36例非胰岛素依赖型糖尿病(NIDDM)患者的神经传导速度与空腹血糖、HbA_1的关系研究,发现所有患者正中、尺、腓神经运动神经传导速度(MNCV)都显著减慢,正中、尺神经感觉神经潜伏期(SNI)延长,H反射时间延长,血糖与各条神经MNCV呈负相关,而与H反射时间呈正相关,但与各神经SNI无关。HbA_1与各神经MNCV呈负相关,与各神经SNI呈正相关。     

红花黄色素联合腺苷钴胺治疗糖尿病周围神经病变效果观察

目的 探讨注射用红花黄色素联合腺苷钴胺治疗糖尿病周围神经病变（DPN）的临床疗效.方法 将227例DPN患者随机分为治疗组（1 10例）和对照组（1 17例）.治疗组采用红花黄色素联合腺苷钴胺治疗,对照组采用腺苷钴胺常规治疗.分别于治疗前、治疗后1周行肌电图检测症状明显一侧肢体腓总神经和正中神经的感觉传导速度（SNCV）和运动传导速度（MNCV）,观察自觉神经症状改善情况并评定疗效.结果 两组治疗后腓总神经及正中神经SNCV、MNCV均较治疗前显著改善（P均＜0.05）.治疗组治疗后正中神经SNCV及腓总神经MNCV高于对照组（P均＜0.05）.治疗组总有效率高于对照组（P＜0.05）.结论 红花黄色素联合腺苷钴胺治疗DPN疗效确切.     

Nerve conduction abnormalities in untreated maturity-onset diabetes: relation to levels of fasting plasma glucose and glycosylated hemoglobin.

The role of metabolic abnormalities in the development of diabetic neuropathy is controversial. To investigate the influence of hyperglycemia on nerve conduction, we studied 20 untreated maturity-onset diabetic patients and 23 normal control subjects of similar age. Nerve conduction velocity of motor (median, peroneal, and tibial) and sensory (median and sural) nerves in diabetic patients was significantly slowed and H-reflex latency time prolonged. Levels of fasting plasma glucose in diabetic subjects were correlated with slowed motor conduction velocity of the median, peroneal, and tibial nerves but not with sensory nerve conduction velocities. Levels of glycosylated hemoglobin, an index of long-term glycemia, were correlated with slowing of peroneal motor conduction velocity in diabetic patients. These associations could not be explained by patient age or duration of diabetes. These findings suggest that the degree of hyperglycemia of untreated maturity-onset diabetes contributes to the motor nerve conduction abnormalities in this disease.     

The electrophysiological findings of subclinical neuropathy in patients with recently diagnosed type 1 diabetes mellitus

To assess the prevalence of subclinical neuropathy within the first year of type 1 diabetes mellitus, 30 patients and 14 healthy subjects have been studied prospectively. The patients whose diabetes duration was longer than 1 year have been excluded from the study. Control group consisted of healthy volunteers. Subjective neuropathy symptoms, neurological examination, and electrophysiological findings were evaluated. All patients were clinically asymptomatic. At least two abnormal independent neurophysiological nerve parameters, which were required as the criterion of the peripheral nervous system subclinical involvement, were found as in 96.6% of diabetic patients in the first years. The percentages of abnormal electrophysiological parameters in different motor and sensory nerves were 86.7% in sural nerve, 83.3% in peroneal motor nerve, 73.3% in posterior tibial motor nerve, 66.7% in median motor nerve, 63.3% in ulnar motor nerve, 60% in median sensory nerve, and 46.7% in ulnar sensory nerve. While distal motor latency, F conduction time, and minimum F latency were the most frequent abnormal parameters in the upper extremity electrophysiological study; conduction velocity, minimum and mean F latencies, F conduction time were the most frequent abnormal parameters in the lower extremity. In all sensory nerve conduction studies, the most frequent abnormal parameter was the onset latency. In the autonomic sympathetic nerve electrophysiological study, plantar SSR latency was found significantly longer than the control group. In the lower extremity generally somatic motor fibres, sensory large fibres and sympathetic autonomic nerve fibres were found to be more affected. There is a correlation between HbA1c levels and nerve conduction velocity in posterior tibial and peroneal nerves. However, upper extremity nerve conduction dysfunction was not correlated with HbA1c value. Neither the duration of disease nor the age of the subject correlated with the nerve dysfunction.     

Pulse pressure is independently associated with sensorimotor peripheral neuropathy in patients with type 2 diabetes

OBJECTIVES: The mechanisms responsible for the onset and progression of sensorimotor peripheral neuropathy (SMPN) in type 2 diabetes remain largely unknown. Although a link between hypertension and SMPN has been observed, it is not clear which blood pressure (BP) component (i.e. systolic, SBP; diastolic, DBP; or pulse pressure, PP) is primarily involved. We sought to determine the relationship between BP components and parameters of nerve function in type 2 diabetes. DESIGN: Cross-sectional study. SETTING: Academic medical centre. SUBJECTS: A total of 55 consecutive ambulatory patients with type 2 diabetes (age 62.6 +/-8.0 years, mean +/- SD). INTERVENTIONS: Measurement of clinic BP and 10 neurophysiological parameters: motor nerve conduction velocity (NCV; median, ulnar, posterior tibial and peroneal nerve), sensory amplitude (AMP) and latency (LAT; median, ulnar and sural nerve). RESULTS: Univariate analysis showed that age, diabetes duration, SBP and PP were negatively correlated with nerve function. Regression analysis showed that, after correcting for age, duration of diabetes, glycated haemoglobin, body mass index, microalbuminuria and SBP, PP was independently and negatively associated with NCV (median, P =0.011; ulnar, P = 0.001; peroneal, P = 0.006 and posterior tibial, P = 0.005) and signal AMP (ulnar, P = 0.027; sural, P = 0.055), and positively associated with signal LAT (median, P = 0.083; sural, P = 0.021). SBP was negatively associated with signal AMP (median, P = 0.012) and positively associated with LAT (ulnar, P = 0.018). By contrast, DBP failed to show any significant correlation with nerve function. CONCLUSIONS: The PP is strongly associated with neurophysiological parameters of nerve function in patients with type 2 diabetes. This relationship is independent of traditional risk factors and other BP components.     

Neurophysiological study of the effect of combined kidney and pancreas transplantation on diabetic neuropathy: a 2-year follow-up evaluation

Previous study have reported a significant improvement of peripheral neuropathy following combined pancreas and kidney transplantation attributed to improvement of blood glucose control by some authors and to elimination of uraemia by others. To asses the specific role of uraemia and hyperglycaemia in neuropathy, 16 diabetic uraemic patients with combined pancreas and kidney transplantation were compared to 9 diabetic patients with a renal graft only. Neurophysiological studies of peripheral neuropathy included ulnar and deep peroneal nerve motor conduction velocity, median and sural nerve sensory conduction velocity were performed at baseline and 1 and 2 years after transplantation. One year after transplantation mean nerve conduction velocity significantly improved in both groups. However, changes were statistically significant in the kidney-pancreas group only. At the 2 year follow-up nerve conduction velocity had increased further in the pancreas-kidney group only. These data suggest that improvement of nerve conduction velocity following pancreas and kidney transplantation is predominantly due to the long-term euglycaemic state.     

Elevated von Willebrand factor antigen predicts deterioration in diabetic peripheral nerve function

Summary We have studied the temporal relationship of plasma von Willebrand Factor (vWF), a marker of endothelial damage, with the development of complications in 63 young diabetic patients (56 of whom were insulin-dependent) who took part in a prospective study. Results are presented from baseline to follow-up. In the group as a whole, no significant changes were found in any autonomic function tests, temperature discrimination threshold or nerve conduction velocities. Median motor and peroneal latency were significantly increased, while median motor, peroneal motor and sural sensory potentials were significantly decreased at follow-up compared with baseline (p<0.001). There was a significant fall in mean plasma vWF antigen and ristocetin co-factor activity in the entire group. Within the group, we identified eight patients whose peroneal motor and sural sensory conduction velocities had decreased by over 2 ms^–1. In these patients (Group A), baseline vWF antigen and activity were significantly higher than in the rest of the patients (Group B), (p=0.04) and vWF antigen was still significantly higher after 3 years (p=0.02). There were no differences between the groups in incidence of retinopathy, urinary albumin excretion rate or macrovascular disease. To assess the influence of glycaemic control on vWF, we first compared a matched group (C) of diabetic patients with similar HbA₁ to that of group A, but with normal nerve conduction velocities: vWF was still significantly higher in group A compared with group C (p=0.02). Furthermore, hierarchical regression showed that vWF predicted deteriorating nerve function independently of glycaemic control or the type of diabetes. Endothelial dysfunction may be associated with development of peripheral neuropathy in young diabetic patients.Abbreviations Standardized regression coefficient - B unstandardized regression coefficient - IQR inter-quartile ranges - MMCV median motor nerve conduction velocity - MSCV median sensory nerve conduction velocity - PMCV peroneal motor nerve conduction velocity - SSCV sural sensory nerve conduction velocity - UAER urinary albumin excretion rate - vWF von Willebrand factor - vWFact von Willebrand factor activity - vWFag von Willebrand factor antigen - IDDM insulin-dependent diabetes mellitus - NIDDM non-insulin-dependent diabetes mellitus     

Presence of carpal tunnel syndrome in diabetics: Effect of age,sex, diabetes duration and polyneuropathy

Summary Common thought is that diabetic neuropathy is a predisposing factor to entrapment syndromes. Carpal tunnel syndrome (CTS) is the most frequent entrapment neuropathy; females and old people are most frequently affected (Comi et al., 1978). Prevalence of CTS in diabetics and associated risk factors were studied in 401 patients (208 males and 193 females) with insulin-dependent and non-insulin-dependent diabetes using electrophysiological techniques. Median nerve sensory and motor conduction velocity, ulnar and peroneal nerve motor conduction velocity and sural nerve sensory conduction velocity were investigated in all patients. Diagnostic criteria for CTS were the presence of delayed median nerve sensory conduction velocity in the palm-wrist tract and of increased distal motor latency. Polyneuropathy was defined by slowing-down of conduction velocity in two or more nerves. Forty-five patients (11.2%), 36 females and 9 males, showed CTS. One-hundred-sixty-eight patients (41.8%), 74 females and 94 males, were suffering from peripheral neuropathy. The strongest risk factors for CTS, in order of importance, were: female sex, older age and presence of neuropathy. Polyneuropathy but not CTS was related to duration of diabetes.     

Subclinical nerve dysfunction in children and adolescents with IDDM

Summary The purpose of this study was to investigate whether young insulin-dependent diabetic patients still develop peripheral nerve dysfunction when using modern multiple insulin injection therapy and to elucidate if this correlated with various disease parameters. Seventy-five patients, 7 to 20 years old with a duration of diabetes of more than 3 years, and 128 age-matched healthy control subjects underwent bilateral studies of median, peroneal, and sural nerves. Presence of diabetes lowered motor conduction velocity (p<0.0001), sensory conduction velocity (p<0.0001) and sensory nerve action potential (p<0.05) in all examined nerves. The mean change in conduction velocity induced by diabetes was –4.8 m/s in the peroneal nerve, –3.3 m/s in the median motor nerve, –2.6 m/s in the sural nerve and –2.4 m/s in the median sensory nerve. Fifty-seven percent of the patients had abnormal conduction (values outside 95% predictive interval) which was seen most often in the motor nerves, especially in the peroneal nerve (41%) followed by the median nerve (24%). In multiple regression analysis, long-term poor metabolic control and increased body length correlated with nerve dysfunction identified in most examined parameters. Three patients had signs or symptoms suggestive of neuropathy. It is concluded that despite modern multiple insulin injection therapy, with reasonably good metabolic control, nerve dysfunction is still common in children and adolescents with insulin-dependent diabetes mellitus. Risk factors are increased height and long-term poor metabolic control.Abbreviations IDDM Insulin-dependent diabetes mellitus - MIT multiple insulin injection therapy - MCV motor nerve conduction velocity - CMAP compound muscle action potential - DML distal motor latency - SCV sensory nerve conduction velocity - SNAP sensory nerve action potential     

Peripheral and autonomic nerve function in 259 diabetic patients with peripheral neuropathy treated with ponalrestat (an aldose reductase inhibitor) or placebo for 18 months. United Kingdom/Scandinavian Ponalrestat Trial.

The potential of the aldose reductase inhibitor ponalrestat (600 mg daily) to ameliorate diabetic neuropathy was evaluated in 259 diabetes mellitus patients with peripheral neuropathy (defined by abnormal vibration perception threshold and abnormal peroneal motor conduction velocity) in a double-blind placebo-controlled clinical trial running for 18 months. Overall, no beneficial effect of ponalrestat on vibration perception thresholds, nerve conduction velocities, and nerve action potential amplitudes was detected. Because vibration perception thresholds and conduction velocities in median, peroneal, and sural nerves did not deteriorate in the placebo group, the potential of ponalrestat to prevent the expected deterioration in peripheral nerve function that occurs with an increased duration of diabetes was not tested. Patients with an abnormal heart rate reaction to standing (abnormal 30:15 ratio; n = 84) on ponalrestat did not deteriorate in this autonomic nerve function test as shown in those on placebo. In conclusion, ponalrestat did not improve peripheral nerve function in diabetes mellitus patients with signs of peripheral neuropathy, although it did ameliorate a deterioration in autonomic nerve function in diabetic patients with signs of autonomic neuropathy.     

Lower extremity nerve function in patients with lower extremity ischemia

BACKGROUND: We determined whether lower extremity ischemia, as measured by the ankle brachial index (ABI), is associated with impaired lower extremity nerve function. METHODS: Participants included 478 persons with peripheral arterial disease (PAD) identified from noninvasive vascular laboratories and 292 persons without PAD identified from a general medicine practice and noninvasive vascular laboratories. Peripheral arterial disease was defined as an ABI lower than 0.90 (mild PAD: ABI, 0.70 to <0.90; moderate PAD: ABI, 0.50 to <0.70; and severe PAD: ABI, <0.50). The ABI and electrophysiologic measures of the peroneal, sural, and ulnar nerves were obtained. RESULTS: Among 546 participants without diabetes, PAD participants had significantly impaired peripheral nerve function in the upper and lower extremities compared with non-PAD participants. After adjusting for age, sex, race, smoking, height, body mass index, recruitment source, alcohol use, disk disease, spinal stenosis, cardiac disease, and cerebrovascular disease, these associations were not statistically significant. After adjusting for confounders among nondiabetic participants, those with severe PAD (ABI, <0.50) had poorer peroneal nerve conduction velocity (NCV) compared with participants without PAD (42.6 vs 44.8 m/s; P = .003) and poorer peroneal NCV compared with participants with mild PAD (42.6 vs 45.0 m/s; P = .001) or moderate PAD (42.6 vs 44.1 m/s; P = .03). Among 224 participants with diabetes, after adjusting for confounders, PAD was associated with poorer peroneal NCV (40.8 vs 43.5 m/s; P = .01), sural nerve amplitude (3.1 vs 4.8 muV; P = .045), and ulnar NCV (47.6 vs 50.2 m/s; P = .03) compared with those without PAD. CONCLUSIONS: Our findings suggest that leg ischemia impairs peroneal nerve function. This association is less strong in patients with diabetes, perhaps because of the overriding influence of diabetes on peripheral nerve function. Clinicians should consider screening for PAD in patients with idiopathic peroneal nerve dysfunction. Peripheral arterial disease-associated nerve dysfunction may contribute to PAD-associated functional impairment.