Four‐year sequential nerve conduction changes since first visit in Japanese patients with early type 2 diabetes. Issue 3 (9th December 2016)

• Record Type: Journal Article
• Authors: Kobori, Mariko; Yagihashi, Soroku; Shiina, Norie; Shiozawa, Nana; Haginoya, Akiko; Ojima, Misato; Douguchi, Satako; Tamasawa, Atsuko; Saitou, Miyoko; Baba, Masayuki; Osonoi, Takeshi
• Is Part Of: Journal of diabetes investigation. Volume 8:Issue 3(2017)
• Page Start: 369
• Page End: 376
• Publication Date: 2016-12-09
• Subjects: Diabetic neuropathy -- Natural history -- Nerve conduction; Diabetes -- Periodicals; Diabetes -- Research -- Periodicals; Diabetes Mellitus -- Periodicals; 616.462005
• DOI: 10.1111/jdi.12583
• Languages: English
• ISSNs: 2040-1116

Abstract

Abstract : In Japanese patients with early type 2 diabetes, progression of neuropathy is slow, not detected by motor nerve conduction delay, but only detectable marginal decrease in compound muscle action potentials. Abstract: 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.