Clinical utility of dorsal sural nerve conduction studies

A technique of testing sensory nerve conduction of the dorsal sural nerve in the foot was used in 38 normal subjects and 70 patients with peripheral neuropathies. The normal dorsal sural sensory nerve action potential (SNAP) had a mean amplitude of 8.9 microV (range 5-15 microV), mean latency to negative peak of 4.0 ms (range 3.2-4.7 ms), and mean conduction velocity of 34.8 m/s (range 30-44 m/s). Optimal placement of the recording electrodes to obtain a maximal nerve action potential was proximal to digits 4 and 5. Cooling to below 25 degrees C prolonged the latency but did not decrease the SNAP amplitude. Among the patients with peripheral neuropathy, dorsal sural SNAP was absent in 68 (97%), whereas only 54 (77%) showed abnormalities of sural sensory conduction. The diagnostic sensitivity of sensory nerve conduction studies in peripheral neuropathies may be significantly improved by the use of this technique for evaluating the action potential of the dorsal sural nerve.     

A comparison of sural nerve conduction studies in patients with impaired oral glucose tolerance test

OBJECTIVE: Monitoring of the sural nerve is a sensitive method for detection of neuropathies. We examined different methods of studying sural nerve conduction in a group of patients with impaired glucose tolerance (IGT) in the same study. MATERIALS AND METHODS: Several parameters of sural nerve were investigated in 20 patients. First, sensory nerve conduction studies of the sural nerve were performed on the distal-leg and the proximal-leg segments. Second, dorsal sural nerve studies were conducted. Third, the sural/radial sensory nerve action potential (SNAP) amplitude ratios were calculated. The results were compared with those obtained from 21 healthy controls. RESULTS: Abnormal results revealing peripheral neuropathy were found in only one patient and dorsal sural SNAP was absent in another patient (5%). Although the results of nerve conduction studies were within normal ranges except the patient with peripheral neuropathy, the lower extremity nerves and especially sural nerves have been found to be more affected and the parameters revealed large differences between groups (P < 0.05). Only dorsal sural nerve latency related to fasting blood glucose level in patients (<0.05). DISCUSSION AND CONCLUSIONS: Sural nerve studies should be of value to determine neuropathy in IGT patients. This study supported the idea that IGT is a transitional state before diabetes and also the importance of the dorsal sural nerve latencies for early detection of neuropathy.     

Dorsal sural nerve conduction study in vitamin B(12) deficiency with megaloblastic anemia

Peripheral neuropathy is frequently observed in B(12) deficiency. In spite of this, there is little knowledge about peripheral neuropathy in B(12) deficiency because the severity of clinical involvement of the central nervous system clearly outweighs signs and symptoms due to peripheral nervous system involvement. We primarily investigated peripheral neuropathy with dorsal sural conduction study, which is a new method for detection of early peripheral neuropathy, in B(12) deficiency with megaloblastic anemia. Conventional nerve conduction studies and tibial sensory-evoked potential (SEP) recording were also performed. Twenty-eight B(12)-deficient patients (15 male, 13 female, mean age 65.8 years) with megaloblastic anemia and 18 age- and sex-matched controls were included in the study. Although dorsal sural sensory nerve action potentials (SNAPs) were not recorded in 15 (54%) of 28 patients, only 9 (32%) of them were found to have polyneuropathy by conventional conduction studies. Furthermore, patients with dorsal sural SNAP had mean lower amplitude, mean longer latency, and slower velocity response when compared with controls. Twenty patients (71%) were diagnosed as having myelopathy by the combination of tibial SEP and neurological findings. Two patients whose dorsal sural SNAPs were not recorded had normal tibial SEP responses; therefore, these patients were considered to have isolated peripheral neuropathy. As a result, we conclude that dorsal sural nerve conduction study is a reliable method for detection of early peripheral neuropathy in B(12) deficiency.     

Superficial radial sensory nerve potentials in immune-mediated and diabetic neuropathies.

OBJECTIVE: The pattern of abnormal median-normal sural sensory nerve action potential (SNAP) is frequently found in acute/chronic inflammatory demyelinating polyneuropathy (AIDP/CIDP), whereas sural/radial SNAP amplitude ratio is sensitive to detect dying-back degeneration. To investigate whether radial SNAP and its amplitude ratio to median or sural SNAP provide additional particular patterns of sensory nerve involvement. METHODS: Superficial radial, median, and sural SNAPs were recorded in 63 normal subjects and in 132 patients with AIDP/CIDP (n = 22), diabetic neuropathy (n = 83), or other axonal polyneuropathy (n = 27). Median/radial and sural/radial amplitude ratios were examined. RESULTS: In normal subjects, median/radial ratio was 0.96 +/- 0.05 (mean +/- SEM), and sural/radial ratio was 0.50 +/- 0.03. Compared with normal controls, the median/radial ratio was lower in patients with AIDP/CIDP (0.64 +/- 0.11; P < 0.001) or diabetic neuropathy (0.75 +/- 0.04; P = 0.08), but similar in those with other neuropathy (0.94 +/- 0.10). The sural/radial ratio was higher in the AIDP/CIDP group (0.71 +/- 0.08; P = 0.10), and lower in the diabetic (0.36 +/- 0.03; P < 0.001) and other axonal neuropathy groups (0.40 +/- 0.07; P = 0.08). CONCLUSIONS: AIDP/CIDP is associated with a reduced median/radial ratio and increased sural/radial ratio, probably reflecting demyelination predominant in the distal nerve terminals. Diabetic neuropathy is characterized by decreases in both median/radial and sural/radial ratios, presumably due to coexistence of carpal tunnel pathology and dying-back degeneration. SIGNIFICANCE: Comparison of multiple SNAP amplitudes provides information about characteristic distribution patterns of sensory nerve involvement in peripheral neuropathies.     

Dorsal ulnar cutaneous nerve conduction: reference values

We investigated the reference values of the dorsal ulnar cutaneous nerve (DUC) sensory nerve conduction (SNC) in 66 healthy individuals. Measurements were processed using stimulating electrodes positioned between the ulnar bone and the flexor carpi ulnaris muscle, 11-13 cm proximal to the active electrode recording. Superficial recording electrodes were placed on the fourth intermetacarpal space. The mean sensory conduction velocity (SCV) in males was 63.7 - 0.16 x age +/- 3.36 m/s and in females was 57.7 +/- 3.37 m/s. The mean sensory nerve action potential (SNAP) amplitude in males was 19.5 +/- 10.7 microV and in females was 24.6 +/- 5.8 microV. The mean SNAP duration was 0.96 +/- 0.13 ms. No significant differences regarding the DUC-SCV, distal latency, and SNAP duration or amplitude were found between both sides of the same subject. The amplitude of the SNAP was higher in females than males. The effects of age on DUC-SCV were distinct for each gender.     

Medial plantar and dorsal sural nerve conduction studies increase the sensitivity in the detection of neuropathy in diabetic patients.

OBJECTIVE: Clinical utility of nerve conduction studies (NCS) of the medial plantar and dorsal sural nerves in the early detection of polyneuropathy have already been shown separately. However, at present, there is no data about the combined assessment of these two nerves in distal sensory neuropathy. In the present study, we aimed to evaluate the medial plantar and dorsal sural NCS in a group of diabetic patients with distal sensory neuropathy (DSN) and in healthy controls. METHODS: Thirty healthy and 30 diabetic adult patients were included. In all subjects, peripheral motor and sensory NCS were performed bilaterally with surface electrodes on the lower limbs including medial plantar and dorsal sural nerves. In addition, motor and sensory nerves were studied unilaterally on the upper limb. RESULTS: In all patients, nerve action potential (NAP) amplitudes of sural and superficial peroneal nerves were within normal ranges, but in the patient group mean value was significantly lower than in the controls. Among clinically defined 30 DSN patients, medial plantar NAP amplitude was abnormal in 18 (60%) and dorsal sural nerve amplitude was abnormal in 13 (40%) of the patients bilaterally. Additionally, the onset NCV of the dorsal sural nerve was significantly slower in patients than controls (P=0.038). Evaluation of both of these nerves increased the sensitivity up to 70% in the detection of neuropathy. CONCLUSIONS: Bilateral NCS assessment of both of the medial plantar and dorsal sural nerves together increases the rate of diagnosis of diabetic distal sensory neuropathy compared to assessment of either of these nerves. SIGNIFICANCE: Assessment of medial plantar in addition to dorsal sural NCS together increases the sensitivity in the detection of neuropathy and allows earlier diagnosis, especially when routine NCS are normal.     

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。     

Technique for studying conduction in the lateral cutaneous nerve of calf

We describe a novel technique for assessing conduction in the lateral cutaneous nerve of the calf (LCNC), a branch of the common peroneal nerve, based on a study of 32 healthy subjects. Both antidromic and orthodromic techniques were used in each of the 64 limbs to obtain a sensory nerve action potential (SNAP) of the LCNC over a distance of 12 cm. In 60 limbs (93.7%) a SNAP was obtainable with either the antidromic or orthodromic technique. In 21 limbs (32. 8%), the SNAP was obtained both antidromically and orthodromically. In 33 limbs (51.6%), the SNAP was obtained only antidromically, and in 6 (9.4%), only orthodromically. In four limbs, the response was unobtainable. Mean antidromic onset latency was 2.1 ms +/- SD 0.3, peak latency was 2.6 ms +/- SD 0.4, amplitude (without averaging) was 4.3 microV +/- SD 2.5, and conduction velocity was 60 m/s +/- SD 10. Mean orthodromic onset latency was 2.3 ms +/- SD 0.3, peak latency was 2.7 ms +/- SD 0.3, amplitude was 5.0 microV +/- SD 2.2, and conduction velocity was 52 m/s +/- SD 5. Utilization of this technique allows for more detailed localization of common peroneal nerve injury based on whether it is proximal or distal to the origin of the LCNC.     

Sensory nerve action potentials in the evaluation of diabetic polyneuropathy]

In order to clarify the suitability of sensory nerve action potential(SNAP) in the evaluation of diabetic polyneuropathy, we studied measurements of SNAPs in the median, ulnar and sural nerves. Subjects were 253 patients with non-insulin dependent diabetes mellitus; 167 men and 86 women, aged 58.2 +/- 12.8(mean +/- SD) years old. Their diabetic history was 10.2 +/- 8.6 years. SNAPs were recorded antidromically from index finger, little finger and lateral to the Achilles tendon, respectively. Twenty-eight patients, in whom any one of the SNAPs couldn't be obtained, were already excluded from this study. The polyneuropathy index (PNI) was calculated from 12 indices concerning to the velocity or long distance latency in motor nerve conduction studies of 4 nerves. The PNI is known to be an excellent index to express the degree of diabetic polyneuropathy. Amplitude and conduction velocity in each nerve was 28.6 +/- 15.6 microV and 46.2 +/- 7.4 m/sec in the median nerve, 26.7 +/- 15.8 microV and 47.0 +/- 6.5 m/sec in the ulnar nerve, 13.1 +/- 6.5 microV and 43.1 +/- 6.0 m/sec in the sural nerve, respectively. The coefficient of correlation of the measurements between median and ulnar nerves was larger than other assortment of nerves. The coefficient of correlation of each measurement with PNI was around 0.40 in the amplitude and around 0.55 in the conduction velocity. Nevertheless, the mean value of the 3 nerves had a higher coefficient of correlation with PNI; 0.48 in the amplitude and 0.60 in the conduction velocity. SNAP measurements of a single nerve are often largely affected by the inter-individual differences, inter-nerve differences or measuring errors. But the mean value of the 3 nerves will be better in exploring the degree of diabetic polyneuropathy. Evaluation of diabetic polyneuropathy by SNAPs will be best achieved by using the mean value of these 3 nerves.     

The medial plantar and medial peroneal cutaneous nerve conduction studies for diabetic polyneuropathy

Objective of this study was to determine which nerve conduction is more sensitive electrophysiologically in the diagnosis of polyneuropathy in diabetics by evaluating the sensory conduction in medial plantar nerve and medial peroneal (dorsal) cutaneous nerves. Additionally to investigate the relation between Neuropathy Symptom Score (NSS) and Neuropathy Disability Score (NDS) values used in the diagnosis of these conduction studies. Forty patients with diagnosis diabetic neuropathy were included into this study. In diabetic polyneuropathic patient group, both medial plantar and medial dorsal cutaneous nerve sensory action potential were not bilaterally obtained in 19 patients (47.5%). Sensitivity and specificity of medial dorsal cutaneous nerve and medial plantar nerve sensory conduction abnormalities in diagnosis of diabetic polyneuropathy were higher compared to sural nerve conduction abnormalities. This study showed that both medial plantar and medial dorsal cutaneous nerve conduction study performed bilaterally was a highly sensitive and specific method in diagnosis of diabetic neuropathy.     

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.     

Peripheral nerve function during hyperglycemic clamping in healthy subjects

The influence of hyperglycemia with physiological hyperinsulinemia on peripheral nerve function was studied in 10 non-diabetic subjects. Blood glucose concentration was raised from 3.8 +/- 0.2 mmol/l (mean +/- SEM) to 17.1 +/- 1.4 mmol/l (mean +/- SEM) within 15 min and kept at this level for 120 min by intravenous glucose infusion. Sensory and motor nerve conduction velocity, and distal motor latency in the ulnar nerve were determined before, immediately after induction of hyperglycemia, and again after 120 min of hyperglycemia. Mean sensory nerve conduction velocity increased from 57.7 m/s to 59.5 m/s (P less than 0.005) immediately after induction of hyperglycemia, and after 120 min of hyperglycemia mean sensory nerve conduction velocity was 59.6 m/s (P less than 0.05). An insignificant increase was seen in motor nerve conduction velocity during hyperglycemia. Mean distal motor latency decreased from 3.1 ms to 3.0 ms (P less than 0.025) immediately after induction of hyperglycemia, and after 120 min of hyperglycemia distal motor latency was 2.9 ms (P less than 0.05). We conclude that short term hyperglycemia with physiological hyperinsulinemia seems to increase sensory nerve conduction velocity and decrease motor latency.     

Symmetry and temporal variability of neurography]

The aims of the present study are to document side-to-side differences and temporal variability, between two trials (T1 and T2 at a time interval of 3 months) of nerve conduction measurements collected from 30 healthy subjects (mean age 22 +/- 2 years). METHODS: The protocol at T1 consisted of motor nerve conduction studies of median, ulnar, peroneal and tibial nerves bilaterally, with measurement of (a) motor response size (amplitude and area); (b) terminal latency; (c) minimal, mean and maximal F-wave latency; (d) motor conduction velocity; and (e) F-wave occurrence. T1 also involved sensory nerve conduction studies of median, ulnar, radial, lateral and medial cutaneous, sural and superficial peroneal nerves bilaterally, with measurement of sensory potential size (amplitude and area) and computation of sensory conduction velocity. The protocol at T2 consisted of identical measurements from the dominant side. RESULTS AND CONCLUSION: There was a negative relationship between the variability of parameters evaluating nervous conduction and the length of the nerve segment under study. Thus, the smallest side-to-side and temporal variabilities are measured for minimal F-wave latencies (on average 2-3%). The limits of symmetry and temporal variability are particularly useful for diagnosis of unilateral peripheral neuropathy or neurophysiological follow-up of patients with neuropathy, when the variability of the parameter under study is weak and when there is a high correlation between values recorded on the left and on the right or at T1 and T2. This was the case for motor response size of tibial and ulnar nerves, sensory potential size of radial nerve and minimal F-wave latencies from each studied motor nerve.     

Sural sensory action potential identifies diabetic peripheral neuropathy responders to therapy

Identifying patients with diabetic peripheral neuropathy (DPN) amenable to therapy is a challenge. To determine whether the amplitude of the sural sensory nerve action potential (sural SNAP) reflects the severity of DPN, an analysis was performed on 205 patients with DPN, identified by an abnormal vibration detection threshold (VDT), who were enrolled in a multinational clinical trial investigating ruboxistaurin (RBX) mesylate. Nerve conduction velocity and response amplitude and latency were measured and compared. VDT was significantly lower in those with preserved sural SNAPs (n = 128) than in those in whom they were absent (n = 77; 21.5 vs. 22.7 JND units, P = 0.002). Thus, preserved sural SNAP denoted less severe DPN. Logistic regression analyses evaluating baseline characteristics, HbA(1c), and baseline symptom scores identified only DPN duration as a factor that might contribute to the presence of sural SNAP (P = 0.004; OR = 0.896). For patients with abnormal VDT, preserved sural SNAP identifies a patient population with less severe DPN who may respond to therapeutic intervention in clinical trials.     

Delayed somatosensory conduction in acute painful neuropathy of diabetes

We examined the peripheral–central sensory conduction by using somatosensory evoked potential (SEP) in a 48 year old diabetic patient with acute painful neuropathy. The sural, ulnar and median sensory nerve conduction and SEP elicited by wrist stimulation showed no abnormalities, nevertheless, the tibial nerve SEP revealed absent spinal N19 and a remarkable delay of the cortical arrival time. These findings suggest involvement of the dorsal roots or the dorsal column in the acute painful neuropathy of diabetes.     

Peripheral nerve function during hyperglycemic clamping in insulin-dependent diabetic patients

The influence of hyperglycemia on peripheral nerve function was studied in 9 patients with long-term insulin-dependent diabetes. Blood glucose concentration was raised 13.5 +/- 0.5 mmol/l (mean +/- SEM) within 15 min and kept approximately 15 mmol/l over basal level for 120 min by intravenous glucose infusion. Hyperglycemia was accompanied by increased plasma osmolality. Sensory and motor nerve conduction and distal motor latency in the ulnar nerve were determined before, immediately after induction of hyperglycemia, and again after 120 min hyperglycemia. Distal (5th finger - wrist) and proximal (wrist - elbow) sensory nerve conduction showed an insignificant increase as hyperglycemia was induced. During hyperglycemia mean distal sensory conduction decreased from 53.1 m/s to 50.4 m/s (P less than 0.05) and mean proximal sensory conduction decreased from 56.0 m/s to 54.2 m/s (P less than 0.01). A mean of distal and proximal sensory conduction increased (53.5 m/s vs 54.6 m/s) (P less than 0.05) as hyperglycemia was induced and decreased (54.6 m/s vs 52.3 m/s) (P less than 0.01) during clamping. Motor nerve conduction decreased insignificantly throughout the study. Mean distal motor latency decreased from 3.1 ms to 2.8 ms (P less than 0.005) immediately after induction of hyperglycemia. During hyperglycemia it increased from 2.8 ms to 3.1 ms (P less than 0.001). We conclude that acute induction of hyperglycemia in long-term diabetics seems to increase sensory conduction and decrease distal motor latency, while 120 min hyperglycemia seems to decrease sensory conduction and increase distal motor latency.(ABSTRACT TRUNCATED AT 250 WORDS)     

Study on the latency difference between compound muscle and sensory nerve action potentials]

In motor nerve conduction studies compound muscle action potentials (CMAPs) appear later than sensory nerve action potentials (SNAPs). This time lag originates from the conduction delay at the distal motor axon, neuromuscular transmission time and muscle action potential induction time. To investigate the latency difference between CMAPs and SNAPs we studied 46 healthy individuals, 46 patients with diabetes mellitus and 33 patients with carpal tunnel syndrome, using the lumbrical and interossei recording method. In this method the recording active electrode was placed on the 2nd lumbrical muscle and the reference electrode on the proximal palmar aspect of the index finger. Supramaximal stimulation was given to the median or ulnar nerve trunk at 9-cm proximal to the recording active electrode. The CMAP from the 2nd lumbrical muscle (L) and the SNAP from the digital nerve (N) were recorded after median nerve stimulation, and the CMAP from the 2nd interossei muscles (I) was recorded after ulnar nerve stimulation. The residual latency, which is arbitrary defined as the latency difference (L-N) in this study, was 1.38 +/- 0.15 (mean +/- SD) msec in healthy individuals. About 1 msec of the residual latency is regarded as the time for neuromuscular transmission and the time to evoke muscle activities. Thus, the conduction delay at the distal motor axon was calculated as about 0.4 msec in healthy individuals. The residual latency was relatively constant in 29 diabetic patients without conduction delay across the carpal tunnel, which was defined by the latency difference (L-I) < or = 0.4 msec. Their sensory nerve conduction velocities (calculated from N latency) were always above 40 m/sec. On the other hand in diabetic patients with conduction delay across the carpal tunnel, which was defined by the latency difference (L-I) > 0.4 msec, the residual latency gradually increased as the sensory nerve conduction velocity decreased. Their sensory nerve conduction velocities were mostly less than 40 m/sec. The similar relationship was observed in patients with carpal tunnel syndrome without diabetes mellitus. We consider that the diabetic neuropathy alone doesn't cause the increase of the residual latency. Instead, severe conduction delay across the carpal tunnel decreases the N velocity and increases the residual latency. We can also regard the relationship between the latency difference (L-N) and N velocity as being in inverse proportion. Perhaps the increase of the residual latency was simply caused by the proportional decrease in the conduction velocity at the distal motor axon, not by the special mechanism concerning to the carpal tunnel syndrome. This paper presented the electrophysiological changes seen in the distal segment secondary to the proximal entrapment.     

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     

F-wave latency,the most sensitive nerve conduction parameter in patients with diabetes mellitus

In this study we examined the diagnostic sensitivity of minimal F-wave latency, F-wave persistence, motor nerve conduction velocity (MCV), and amplitude of the compound motor action potential (CMAP) of the median, ulnar, tibial, and peroneal nerves, and of sensory conduction velocity (SCV) and sensory nerve action potential (SNAP) amplitude of the sural nerve in 82 diabetic patients. For the median, ulnar, and tibial nerves the Z scores of the minimal F-wave latency were significantly larger than those of the MCV, and for all four motor nerves the Z scores of the minimal F-wave latency were significantly larger than those of the amplitude of the CMAP. The Z scores of the peroneal minimal F-wave latency exceeded those of peroneal MCV, sural SCV, and sural SNAP. F-wave persistence did not differ significantly from the reference values. In conclusion, minimal F-wave latency is the most sensitive measure for detection of nerve pathology and should be considered in electrophysiological studies of diabetic patients. © 1997 John Wiley & Sons, Inc. Muscle Nerve 20: 1296–1302, 1997     

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。