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Aims/introduction: A gold standard in the diagnosis of diabetic polyneuropathy (DPN) is a nerve conduction study. However, as a nerve conduction study requires expensive equipment and well-trained technicians, it is largely avoided when diagnosing DPN in clinical settings. Here, we validated a novel diagnostic method for DPN using a point-of-care nerve conduction device as an alternative way of diagnosis using a standard electromyography system., Materials and Methods: We used a multiple regression analysis to examine associations of nerve conduction parameters obtained from the device, DPNCheck™, with the severity of DPN categorized by the Baba classification among 375 participants with type 2 diabetes. A nerve conduction study using a conventional electromyography system was implemented to differentiate the severity in the Baba classification. The diagnostic properties of the device were evaluated using a receiver operating characteristic curve., Results: A multiple regression model to predict the severity of DPN was generated using sural nerve conduction data obtained from the device as follows: the severity of DPN = 2.046 + 0.509 × ln(age [years]) - 0.033 × (nerve conduction velocity [m/s]) - 0.622 × ln(amplitude of sensory nerve action potential [µV]), r = 0.649. Using a cut-off value of 1.3065 in the model, moderate-to-severe DPN was effectively diagnosed (area under the receiver operating characteristic curve 0.871, sensitivity 70.1%, specificity 87.7%, positive predictive value 83.0%, negative predictive value 77.3%, positive likelihood ratio 5.67, negative likelihood ratio 0.34)., Conclusions: Nerve conduction parameters in the sural nerve acquired by the handheld device successfully predict the severity of DPN., (© 2020 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd.)

Mild palmar digital neuropathy may be underestimated because selective nerve conduction studies (NCS) of the palmar digital nerve are challenging. We herein report two cases of palmar digital neuropathy. We performed sensory NCS in each finger using the standard approach. Both cases showed a decrease in the amplitude of sensory nerve action potential (SNAP) in the localized finger. Furthermore, the sensory nerve inching test identified the lesion site. When performing NCS in patients with finger sensory impairment, we recommend recording the SNAP in each finger using standard NCS at the wrist, as well as sensory nerve inching testing.

Aims/introduction: Diabetic polyneuropathy is one of the most frequent diabetic complications, and impairs patients' quality of life. We evaluated the efficacy and safety of ranirestat (40 mg/day) in patients with diabetic polyneuropathy., Materials and Methods: This was a multicenter, placebo-controlled, randomized double-blind, parallel-group, phase III study in which 557 patients were randomly assigned to either the ranirestat or placebo group and assessed for 52 weeks. The co-primary end-points were the changes in tibial motor nerve conduction velocity and total modified Toronto Clinical Neuropathy Score as a measure of clinical symptoms., Results: There was a significant increase in tibial motor nerve conduction velocity in the ranirestat group compared with the placebo group. The difference between groups in the change at last observation was 0.52 m/s (P = 0.021). Increases in nerve conduction velocity in the ranirestat group were found not only in the tibial motor nerves, but also in the median motor nerves, proximal median sensory nerves and distal median sensory nerves. No significant differences in modified Toronto Clinical Neuropathy Score or safety parameters were found between the two groups., Conclusions: Ranirestat (40 mg/day) was well tolerated and improved nerve conduction velocity. Regarding symptoms and signs, no detectable benefits over the placebo were observed in the ranirestat group during the 52 weeks of treatment., (© 2018 The Authors Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd.)

Aims/introduction: Despite being the most common complication of diabetes, the pattern of clinical development of diabetic neuropathy is not well-known. In the present study, we retrospectively examined sequential changes in nerve conduction studies (NCS) for 4 years to characterize the way neuropathic changes develop in patients with type 2 diabetes., Materials and Methods: We randomly selected 158 patients with type 2 diabetes who newly visited Naka Memorial Clinic, Ibaraki, Japan, and underwent serial 4-year NCS. Records of clinical profile, signs and symptoms of neuropathy, and NCS data from median and tibial nerves were extracted to determine the progression of neuropathy. NCS data were represented by motor nerve conduction velocities, amplitudes of compound muscle action potentials (CMAPs) and minimal latencies of F-wave., Results: The prevalence of clinical neuropathy in 158 cases was 30% at baseline and 29% at the end of the study, with improvement of glycated hemoglobin (8.6-6.9%). Over 4 years, there were no changes of the signs and symptoms of neuropathy. Motor nerve conduction velocities were slightly improved or consistent at the fourth year compared with those at the beginning (+1.5% in median nerve, P < 0.05; +0.8%, not significant in the tibial nerve). The extent of the glycated hemoglobin correction correlated with the improvement of motor nerve conduction velocity. In contrast, CMAPs of both median and tibial nerves were decreased (-11.6%, P < 0.01; -3.7%, P < 0.05, respectively). For the decrease in CMAPs, no specific risk factors were identified by logistic regression analysis., Conclusions: The present study showed progressive decline of CMAPs despite improved glycemic controls or the lack of NCV slowing in patients with early type 2 diabetes., (© 2016 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd.)

Diabetic nerve exhibits morphological vulnerability to ischemia and reperfusion, in contrast to its physiological resistance to ischemic conduction failure (RICF). To examine the sequence of ischemic conduction failure after reperfusion in diabetic nerve, we measured sciatic-tibial nerve conduction before and during 30-180 min of ischemia and after reperfusion for up to 1 week in streptozocin (STZ)-induced diabetic rats. RICF in diabetic rats was confirmed during ischemia. After reperfusion, control nerves showed an immediate recovery in amplitude of compound muscle action potential (CMAP) following ischemia for 120 min or less, and delayed recovery after 150 min of ischemia. In contrast, recovery in diabetic nerves was delayed even after 1 h of ischemia. Ischemia for 75 min in diabetic nerve resulted in either delayed or no recovery of the CMAP upon reperfusion. Following ischemia for 90 or 120 min, axonal degeneration was observed in diabetic nerve. Thus, severe ischemia for 60 or 75 min causes prolonged ischemic conduction failure in diabetic nerve, compared with 150 min in control nerve. In conclusion, diabetic nerve shows delayed recovery of ischemic conduction failure after brief ischemia, compared to controls, suggesting that patients with diabetic neuropathy have a worse prognosis when faced with nerve ischemia., (Muscle Nerve, 2006.)

We reported an electrophysiological severity classification for diabetic polyneuropathy (DPN) using a nerve conduction study (NCS). This new classification system combines of the amplitude and velocity of NCS and classifies DPN into five stages. Stage 0 is the mildest stage, while Stage IV is the most severe. Here, we clarified the association of this classification system with small fiber abnormalities. We measured intra-epidermal nerve fiber densities (IENFD) and pain threshold using intra-epidermal electrical stimulation (IES) to evaluate the function of small fibers. We recruited 65 patients with diabetes, and performed NCS, skin biopsy and pain threshold using IES. The mean IENFD observed in the skin biopsies were 8.27 n/mm in Stage 0, 7.79 n/mm in Stage I, 4.49 n/mm in Stage II, 2.85 n/mm in Stage III, and 0 n/mm in Stage IV. The mean pain thresholds were 0.05 mA in Stage 0, 0.11 mA in Stage I, 0.08 mA in Stage II, 0.27 mA in Stage III, and 0.59 mA in Stage IV. In summary, the abnormalities of IENFD and pain threshold correlated with electrophysiological severity. The present results indicate that the large fiber dysfunction in DPN progresses in parallel with the small fiber abnormalities. [ABSTRACT FROM AUTHOR]