200例2型糖尿病患者神经传导速度检测分析

目的:探讨2型糖尿病(DM)患者周围神经病变的客观神经电生理特点。方法:分别对200例DM患者,其中有周围神经损害临床表现组(DM-I)100例和无周围神经损害临床表现组(DM-Ⅱ)100例,与50例正常成人进行运动神经传导速度(MCV)、感觉神经传导速度(SCV)、复合肌肉动作电位(CMAP)、感觉神经动作电位(SNAP)进行测定。结果:两组患者所测的MCV、SCV、CMAP、SNAP与正常对照组比较有显著差异,而DM-I组与DM-II所测的MCV、SCW、CMAP、SNAP比较亦有显著差异,下肢神经的4个参数总异常率高于上肢。结论:(1)神经传导速度的检测有助于糖尿病周围神经病的早期诊断。(2)DM并发周围神经损害在临床症状出现之前已有神经传导速度的改变。(3)下肢神经的总异常率高于上肢。     

Amplitude of sensory nerve action potential in early stage diabetic peripheral neuropathy： an analysis of 500 cases

Early diagnosis of diabetic peripheral neuropathy is important for the successful treatment of diabetes mellitus. In the present study, we recruited 500 diabetic patients from the Fourth Affiliated Hospital of Kunming Medical University in China from June 2008 to September 2013：221 cases showed symptoms of peripheral neuropathy （symptomatic group） and 279 cases had no symptoms of peripheral impairment （asymptomatic group）. One hundred healthy control subjects were also recruited. Nerve conduction studies revealed that distal motor latency was longer, sensory nerve conduction velocity was slower, and sensory nerve action potential and amplitude of compound muscle action potential were significantly lower in the median, ulnar, posterior tibial and common peroneal nerve in the diabetic groups compared with control subjects. Moreover, the alterations were more obvious in patients with symptoms of peripheral neuropathy. Of the 500 diabetic patients, neural conduction abnormalities were detected in 358 cases （71.6%）, among which impairment of the common peroneal nerve was most prominent. Sensory nerve abnormality was more obvious than motor nerve abnormality in the diabetic groups. The amplitude of sensory nerve action potential was the most sensitive measure of peripheral neuropathy. Our results reveal that varying degrees of nerve conduction changes are present in the early, asymptomatic stage of diabetic peripheral neuropathy.     

Therapeutic Effects of Aldose Reductase Inhibitor on Experimental Diabetic Neuropathy through Synthesis/Secretion of Nerve Growth Factor

We investigated alterations in nerve growth factor (NGF) and ciliary neurotrophic factor (CNTF) contents during treatment with epalrestat, an aldose reductase inhibitor (ARI), on streptozotocin (STZ)-induced diabetic neuropathy in rats. Diabetic rats showed a statistically significant reduction in H-wave-related sensory nerve conduction velocity (HSNCV) and in NGF content in sciatic nerves during the experiment of 8 weeks. No reduction in the CNTF content in sciatic nerves was seen in the diabetic rats. The epalrestat treatment, which started 4 weeks after STZ injection, resulted in a significantly greater NGF content and faster HSNCV than those in untreated diabetic rats. But no statistically significant alterations of motor nerve conduction velocity (MNCV) or CNTF content were seen during the treatment. ARI showed the stimulating effect for NGF synthesis/secretion in rat Schwann cell culturein vitro.These findings suggest that decreased levels of NGF in diabetic sciatic nerves may be involved in the pathogenesis of diabetic neuropathy in these rats and further show that epalrestat treatment can be useful for the treatment of diabetic neuropathy through NGF-induction in Schwann cells and/or inhibition of the polyol pathway.     

Comparison of short-term effects of insulin and essential fatty acids on the slowed nerve conduction of streptozotocin diabetes in rats.

Early effects of insulin and essential fatty acids on nerve conduction were studied. Insulin-dependent diabetes was induced in rats using streptozocin (65 mg/kg, i.p.); control rats were treated with buffer. Five weeks later, diabetic rats were divided into 5 groups. Two groups were given oral essential fatty acids (75% linoleic and 9% gamma-linolenic acids) for a further 3 and 5 days, respectively. Two other groups received subcutaneous insulin for a further 3 or 5 days. A group of diabetic rats were left without further treatment. Motor nerve conduction velocity was measured terminally in all rats by stimulating the sciatic nerve and recording EMGs in the gastrocnemius muscle under urethane anaesthesia. Sensory nerve conduction velocity was measured by stimulating and recording from the saphenous nerve trunk. Diabetic rats had significantly slowed motor and sensory nerve conduction velocities after 5 weeks (16.7%, P less than 0.001). Three days treatment with either insulin or fatty acids corrected the slowed motor nerve conduction velocity to a normal level. Conduction velocity in myelinated sensory nerves was still 10% slower in diabetic rats treated with insulin for 3 days (P less than 0.01). It was above the control level by 11% in diabetic rats treated with fatty acids for the same period (P less than 0.01). Conduction velocities in both sensory and motor nerves were normal in diabetic rats treated with either insulin or fatty acids for 5 days. It was concluded that both insulin and essential fatty acids had early effects on nerve conduction in diabetic rats. The speed of their actions, and the magnitudes of responses were different in sensory and motor nerves.     

Effect of 4-methylcatechol on sciatic nerve growth factor level and motor nerve conduction velocity in experimental diabetic neuropathic process in rats.

This study examined the effects of 4-methylcatechol (4-MC), a nonamine catechol compound, on the neuropathic process of streptozotocin (STZ)-induced diabetic rats. 4-MC is one of the potent stimulators of nerve growth factor (NGF) synthesis at the cellular level and in cultured sciatic nerve segments of rats. Diabetic rats showed a statistically significant fall in sciatic motor nerve conduction velocity (MNCV) and a significantly reduced NGF content in the sciatic nerve (38.5 +/- 2.8% of control, P less than 0.01) during the experimental period of 4 weeks. 4-MC treatment of the diabetic rats for 4 weeks starting from the STZ injection elevated the NGF content (140% of untreated diabetic rats, P less than 0.05) and prevented the reduction in MNCV, but no effect on high blood glucose levels was seen. These findings suggest that decreased NGF levels in the sciatic nerve of the experimental diabetic rat may be involved in the development of the diabetic neuropathic process and that 4-MC, which can elevate endogenous NGF levels in vivo, may compensate for the inhibitory effect of STZ on the NGF level in progressive diabetic neuropathy.     

糖尿病周围神经病病情分级与电生理的相关性

目的探讨糖尿病周围神经病病情分级与电生理的相关性。方法依据糖尿病性周围神经病的诊断标准确定入选对象;依据糖尿病周围神经病病情分级对入选对象进行临床分级;应用丹麦产DANTEC CANTATA型肌电图仪,进行运动神经和感觉神经传导功能检查。结果腓肠神经、正中神经诱发感觉动作电位波幅(SNAP)和腓总神经复合肌肉动作电位波幅(CMAP)随病情分级的升高而明显减低(P<0.05);腓肠神经、正中神经感觉传导速度(SCV)和腓总神经、正中神经运动传导速度(MCV)3级与1、2两级比较显著减慢(P<0.05)。结论神经电生理改变,尤其感觉神经电生理改变,易此作为糖尿病周围神经病情程度评定的指标。     

Autonomic and electrophysiological studies in patients with signs or symptoms of diabetic neuropathy

Thirty-five patients with symptoms or signs of diabetic neuropathy were tested for autonomic neuropathy by measuring heart rate and blood pressure changes during an orthostatic tilt test, a single deep breath and the Valsalva manoeuvre and these results were related to electrophysiological measurements made on the common peroneal and sural nerves. The sural sensory action potential (SAP) was more strongly correlated with these tests of autonomic function (particularly with the brake index of the orthostatic tilt test (P less than 0.001) and the fall in systolic blood pressure 1 min after tilt (P less than 0.001], than the common peroneal nerve compound motor action potential, its minimum F wave latency or nerve conduction velocities. Patients with a detectable sural SAP had significantly higher brake indices than those with absent sural SAPs. Significant correlations were also obtained with the common peroneal motor nerve conduction velocity (MNCV) and autonomic tests and patients with MNCV less than and greater than 38 m/sec showed significant differences in many autonomic tests. The sural SAP amplitude, being less susceptible to factors that influence nerve conduction velocity, may be useful in identifying patients with an autonomic neuropathy.     

Vitamin D and Nerve Conduction In Pediatric Type-1 Diabetes Mellitus

IntroductionThe aim of this study is to investigate a possible association between vitamin D deficiency and diabetic peripheral neuropathy in pediatric patients with type 1 diabetes mellitus.Materials-methodsTwenty-nine patients with type 1 diabetes mellitus and 19 healthy controls were included to the study. All individuals were evaluated for diabetic peripheral neuropathy with nerve conduction studies. Complete blood cell count, biochemical investigations, serum vitamin D levels, hemoglobin A1c levels were recorded.ResultsNo statistically significant differences between the diabetes and control groups in terms of gender, age, body weight, height, body mass index, systolic and diastolic blood pressures, laboratory investigations, serum vitamin D levels and nerve conduction studies was found. Patients with diabetes were grouped as patients with normal serum vitamin D levels and patients with vitamin D deficiency. Sensory nerve action potential of sural nerve and motor peroneal nerve velocity were statistically significantly lower in diabetic patients with vitamin D deficiency compared to diabetic patients with normal vitamin D levels (p 0.009 and 0.005 respectively).ConclusionOur results suggested that hypovitaminosis D might lead to development of neuropathic changes particularly on the lower limb nerves even in the early stages of the disease. It should be kept in mind that patients with hypovitaminosis D should be elaborately examined and closely followed up for the development of diabetic neuropathic changes, even if glucose control is achieved.     

Diabetes mellitus exacerbates motor and sensory impairment in CMT1A

Abstract Charcot‐Marie‐Tooth disease type 1A (CMT1A) is caused by a duplication of PMP22 on chromosome 17 and is the most commonly inherited demyelinating neuropathy. Diabetes frequently causes predominantly sensory neuropathy. Whether diabetes exacerbates CMT1A is unknown. We identified 10 patients with CMT1A and diabetes and compared their impairment with 48 age‐matched control patients with CMT1A alone. Comparisons were made with the Charcot‐Marie‐Tooth disease (CMT) neuropathy score (CMTNS) and by electrophysiology. The CMTNS was significantly higher in patients with diabetes (20.25 ± 2.35) compared with controls (15.19 ± 0.69; p = 0.01). Values were particularly higher for motor signs and symptoms. Seven of the 10 diabetic patients had CMTNS >20 (severe CMT), while only 7 of the 48 age‐matched controls had scores >20. There was a trend for CMT1A patients with diabetes to have low compound muscle action potentials and sensory nerve action potentials, although nerve conduction velocities were not slower in diabetic patients compared with controls. Diabetes was associated with more severe motor and sensory impairment in patients with CMT1A.     

Peripheral neuropathy associated with; plasma cell dyscrasia: a clinical and electrophysiological follow-up study

Thirteen patients with polyneuropathy associated with plasma cell dyscrasia had serial electrophysiological studies. Five patients with monoclonal IgG had motor and/or sensory symptoms of which 4 correlated with slow motor and sensory nerve conduction. The 4 patients with monoclonal IgM reactive with myelin-associated glycoprotein (MAG), had predominantly motor symptoms, demyelination in the nerve biopsy and slow motor and sensory nerve conduction. Four patients with monoclonal IgM without anti-MAG activity had mainly sensory symptoms, axonal neuropathy on nerve pathology and slow or absent sensory nerve conduction. After treatment with plasmapheresis and chemotherapy 9 patients improved clinically and 4 were unchanged. Criteria for electrophysiologic improvement were presence of sensory or motor responses that were absent before treatment, conduction velocity increased by more than 10 m/s and increase of amplitude by more than 100%. Electrophysiological studies showed improvement in 7, were unchanged in 4, and worse in 2. Sensory velocities in ulnar and sural nerves were significantly improved following treatment (P less than 0.002) and the same trend was noted for the sensory velocity in the median nerve (P less than 0.19). We conclude that nerve conduction studies in combination with clinical examinations are useful in documenting the effects of treatment in these neuropathies.     

138例糖尿病患者神经电图分析

目的探讨2型糖尿病患者周围神经病变(DPN)的神经电生理特点及其与病程的关系。方法连续记录138例血糖控制良好的糖尿病患者神经电图(包括感觉神经传导速度SCV和运动神经传导速度MCV)的检测结果,并根据糖尿病病程将其分组进行比较。结果共检测周围神经1669条,异常神经313条(18.75%),下肢异常率(132/530,24.9%)明显高于上肢(59/517,11.4%)(P<0.0001),感觉神经(122/622,19.6%)与运动神经(191/1047,18.2%)受累无差异(P=0.5665);糖尿病病程10年以上者运动、感觉神经异常率(24.3%,33%)明显高于病程小于10年组(14.2%,14%)(P<0.001)。病程大于10年组神经传导速度均较病程小于10年组减慢,正中神经、胫后神经运动传导速度和尺神经、腓肠神经感觉传导速度有统计学意义(P<0.05);除尺神经外所查运动神经近远端复合肌肉动作电位波幅(CAMP)病程≥10年组均明显低于病程<10年组。结论尽管受检时血糖控制良好,但依然有周围神经电生理异常变化。2型糖尿病患者下肢神经传导异常率高于上肢,尤以运动神经明显。病程是糖尿病周围神经损害的危险因素,随着病程增加神经传导异常率和损伤严重程度增高。     

Clinical utility of dorsal sural nerve conduction studies in healthy and diabetic children.

OBJECTIVE: Monitoring of the dorsal sural sensory nerve action potential (SNAP) is a sensitive method for detection of peripheral neuropathies. We tried to determine the normal dorsal sural nerve conduction values of the childhood population and assessed the clinical utility of this method in diabetic children who have no clinical sign of peripheral neuropathy. METHODS: In the study, 36 healthy and 27 diabetic children were included. In all subjects peripheral motor and sensory nerve studies were performed on the upper and lower limbs including dorsal sural nerve conduction studies. RESULTS: The dorsal sural SNAP mean amplitude was 8.24+/-3.08 microV, mean latency was 2.47+/-0.48 ms, mean sensory conduction velocity was 41.63+/-5.43 m/s in healthy children. Dorsal sural SNAPs were absent bilaterally in one diabetic patient. In the other 26 diabetic patients, the mean dorsal sural nerve distal latency was longer (2.93+/-0.63 ms, P = 0.004), mean SCV was slower than in healthy subjects (36.68+/-7.66 m/s, P = 0.005). However, dorsal sural nerve amplitude was not different between the groups. A dorsal sural nerve latency of more than 2.9 ms had a sensitivity of 50% and a specificity of 75%. A dorsal sural nerve velocity of less than 36 m/s had a sensitivity of 54% and a specificity of 92%. CONCLUSIONS: We designated the reference values of the dorsal sural nerve in healthy children. In addition, our findings suggest that dorsal sural nerve conduction studies may have value to determine neuropathy in the early stages in children with diabetes. SIGNIFICANCE: The dorsal sural nerve conduction studies in diabetic children may have value to determine the neuropathy in its early stages.     

糖尿病周围神经病电生理特点及与血糖水平的关系

目的研究糖尿病周围神经病的神经电生理特点以及与血糖水平的关系。方法分析2013年3月~2014年3月于本院神经内科住院的108例糖尿病周围神经病患者,测定其正中、尺、胫、腓总神经的运动传导速度(MCV)和复合肌肉动作电位波幅(CMAP),以及正中、尺、腓肠神经、腓浅神经的感觉传导速度(SCV)和感觉神经动作电位波幅(SNAP),比较上、下肢和运动、感觉神经异常情况,分析糖化血红蛋白(HbA1C)、餐后2 h血糖对神经传导速度(NCV)的影响。结果糖尿病患者下肢运动神经病变重于上肢,且差异明显(P<0.05)。感觉神经损害重于运动神经,且差异明显(P     

Spontaneous diabetes mellitus in a rhesus monkey: neurophysiological studies

Peripheral neuropathy is a common complication of human diabetes, but its occurrence in spontaneously diabetic monkeys is unknown. Four months after developing diabetes, a 22-year-old female rhesus monkey had nerve conduction studies which were compared with control data obtained from 9 nondiabetic rhesus monkeys. In the diabetic monkey, median and ulnar sensory action potential amplitudes and the median motor distal latency differed from controls by more than two standard deviations. Conduction velocities in the diabetic monkey were less than the mean values in controls, although none were beyond two standard deviations of control means. These electrophysiologic abnormalities are similar to those described in human diabetes and suggest that the spontaneously diabetic monkey peripheral nervous system may be a suitable model of experimental diabetic neuropathy.     

2型糖尿病周围神经病变与C肽水平的相关性研究

目的探讨C肽的生物学活性与2型糖尿病周围神经病变的相关关系,为临床C肽与胰岛素联合应用治疗2型糖尿病并发症提供更多的理论支持。方法回顾性分析98例2型糖尿病患者的神经传导速度与空腹C肽水平的关联性(因不同的神经传导速度不同,特以右侧腓肠神经感觉支为例)。结果相关分析显示:神经传导速度与体重指数,C肽呈正相关,与病程、糖化血红蛋白呈负相关。随着C肽水平的下降,2型糖尿病周围神经病变的分期逐渐加重。结论 C肽对神经具有保护性作用,推测其具有剂量依赖性,外源性C肽应用可能成为2型糖尿病周围神经病变的一种新的治疗手段。     

H反射对糖尿病神经根病的诊断作用

目的 探讨糖尿病神经根病变的存在及H反射对糖尿病神经根病的诊断作用。方法 应用经典的H反射和周围神经传导检测方法对正常对照组30例及糖尿病组42例进行对比研究。结果 糖尿病组神经传导速度较正常组减慢，异常率为66，7％，感觉神经传导速度异常率高于运动神经传导速度。H反射的异常率为85，7％。结论 H反射较常规周围神经传导速度检测具有更高的诊断敏感性，与远端神经病变相比较糖尿病近段神经病具有相当高的患病频率。     

Near nerve local insulin prevents conduction slowing in experimental diabetes

Insulin may have direct effects on axons through its actions on insulin receptors or through cross occupancy of insulin-like growth factor-1 receptors. We tested the hypothesis that insulin itself influences conduction of myelinated fibers independent of hyperglycemia in experimental diabetes. Low dose intermittent (0.2 units thrice weekly) Toronto (regular) insulin was injected at the sciatic notch and knee near the left sciatic nerve of rats rendered diabetic with citrate buffered streptozotocin or nondiabetic rats given citrate only. Identical volumes of normal saline were injected near the contralateral right sciatic nerve. The diabetic rats developed hyperglycemia, elevated glycosylated hemoglobin levels and had slowing of right (saline treated) sciatic tibial motor and caudal sensory conduction velocity. In contrast, local insulin treatment on the left side prevented conduction slowing, unilaterally increasing conduction velocity. In nondiabetic rats, conduction velocities were slightly higher on the insulin treated side, but the influence of insulin was less robust than in diabetics. The insulin treated sural branches of the sciatic nerves in diabetics had a higher percentage of small (≤9.0 μm diameter) myelinated fibers than the saline treated nerves. Local insulin has a trophic influence on myelinated fibers that is prominent in diabetic nerves and is independent of hyperglycemia.     

Prevalence of subclinical neuropathy in diabetic patients: assessment by study of conduction velocity distribution within motor and sensory nerve fibres

Nerve conduction velocity distribution (CVD) study is a newly-developed electrodiagnostic method for detecting alterations in the composition of nerve fibres according to their conduction velocity. The presence of subclinical neuropathy was evaluated in 138 diabetic patients by CVD study of four motor nerves (external popliteal and ulnar nerves bilaterally) and two sensory nerves (median nerve bilaterally), and the data obtained were compared with standard electrophysiological parameters in the same nerve segments. CVD studies revealed an altered distribution pattern in 106 of 129 evaluable patients for motor nerves (82%) and in 67 of 115 evaluable patients for sensory nerves (58%), while standard examination gave abnormal findings in 92 of 137 patients (67%) and in 33 of 118 patients (11%), respectively. Of the patients adequately evaluated by both techniques, 21 of 129 patients (16%) revealed altered CVD data unaccompanied by slowing of maximum nerve conduction velocity, and 37 patients of 101 (37%) showed similar findings for sensory nerves. Subclinical alterations of motor and sensory nerve CVD were not significantly related to age or to metabolic control expressed as glycated haemoglobin levels; a significantly longer duration of disease was found in patients with motor and mixed subclinical neuropathy with respect to non-neuropathic patients. The CVD study allowed us to detect subclinical abnormalities of motor and sensory nerve fibres; often this is a more sensitive method than the standard electrodiagnostic study. This method can be very useful as a diagnostic tool and in research in the study of the progression of diabetic neuropathy. Received: 21 March 1997 Received in revised form: 8 September 1997 Accepted: 7 October 1997     

Conduction velocity study in type 1 diabetic patients

The role of metabolic abnormalities in the development of diabetic neuropathy is controversial. To investigate the peripheral nerve function and the influence of hyperglycemia on nerve conduction in insulin-dependent diabetes, a one-year neurophysiological study was carried out in 30 type 1 diabetic patients ranging in age from 2-16 years. During the 12-month follow-up period the glycosylated hemoglobin determination, motor conduction velocity of the peroneal nerve and the motor and sensory conduction of the tibial nerve were assessed 3 times, at the beginning of the study and every 6 months thereafter. The sensory latency was found significantly delayed in these patients as compared with the controls. The degree of sensory conduction slowing correlated well with the glycosylated hemoglobin concentrations and improved with the reduction in hyperglycemia.     

实验性2型糖尿病大鼠模型及其周围神经病变特点

目的:制备发病过程类似人类2型糖尿病的大鼠模型,并观察其周围神经病变特点。方法:用高糖高脂饲料喂养Wistar大鼠诱发胰岛素抵抗,然后用亚致病剂量的链脲菌素(STZ)腹腔注射,诱发高血糖。在不同的时间观察其肌电图和周围神经的病理改变。结果:此方法制备的2型糖尿病大鼠周围神经病变特点有:1、坐骨神经运动传导速度降低。动作电位的波幅降低;2、腓肠神经有髓神经纤维的数目、有髓神经纤维的总截面积和纤维密度较正常对照组减少。结论:Wistar大鼠用高糖高脂饮食结合小剂量STZ注射可成功制备2型糖尿病大鼠模型,并具有典型的周围神经病变特点,是研究2型糖尿病及其慢性并发症的理想模型。