IDF21-0671 Identification of neurophysiological abnormalities in nerve in patients with type 1 diabetes

Abstract

Background: The progression of neuropathy is a continuum from subclinical neuropathy detectable with electrophysiological tests to clinically evident one recognizable on neurological examination. Although there has been considerable research of peripheral neuropathy in type 1 diabetes, still there is controversy regarding the pattern of nerve involvement in diabetic neuropathy. Detection of the pattern of nerve involvement can help to establish a protocol for screening of diabetic peripheral neuropathy (DPN) in its subclinical stage. Aim: The aim of this study was to describe the pattern of nerve involvement in type 1 diabetic patients with subclinical neuropathy using nerve conduction studies. Method: 65 patients with type 1 diabetes, ages from 18 to 55 years, and 34 controls without diabetes matched to the patient group were included into the study. All patients and controls underwent a standard neurological examination (NSS and NDS (the variant used in Belarus) score) and bilateral nerve conduction study (NCS) of the sensory and motor lower limb nerves using NeuroSoft machine. Interpretation of the results was based on the following normal reference ranges: n. Peroneus superficialis A> 10μV, v> 45 m/s; n Suralis A> 5 μV, v> 45 m / s; n Peroneus profundus A> 3mV, v> 40 m/s; n Tibialis A> 3.5mV, v> 40m/s. Data was analysed using IBM SPSS statistics v 20.0. Results: Clinically evident DPN was detected in 14 patients with type 1 diabetes from 65 examined. The use of NCS allowed to identify the subclinical stage of polyneuropathy (abnormalities in at least two of the electrophysiological parameters) additionally in 35 patients who had no symptoms and clinical signs of DPN. In all the patients of the control group, the NCS parameters were in the reference range. Regarding abnormal NCS parameters in patients with subclinical diabetic neuropathy (conduction velocity vs. amplitude of the compound action potential), amplitudes reduction for the n. Peroneus superficialis and n. Peroneus profundus predominated. Median of the amplitude for n. Peroneus superficialis in patients with subclinical diabetic polyneuropathy was 7.22 [5.25; 8.54] μV vs. 12.4 [10.57; 16.2] μV in the control group, p <0.001; for n. Peroneus profundus 2.21 [1.68; 2.68]mV vs. 3.15 [3.04; 3.42]mV in the control group, p <0.001. Significant differences in the amplitudes for n.Suralis and n.Tibialis has not been identified. Nerve conduction velocity (NCV) in both groups – in patients with the subclinical diabetic polyneuropathy and the control group – was within the reference range. However, the medians of NCV for n. Suralis and n. Tibialis were significantly lower in the group of patients with neuropathy compared with the controls – 47.08 [44.35; 50.13]m/s vs. 51.3 [47.6; 59.05]m/s, p = 0.025 and 44.8 [42.15; 48.2]m/s vs. 49.35 [48.30; 53.45]m/s, p = 0.004, respectively. Conclusion: In patients with type 1 diabetes with a subclinical stage of diabetic polyneuropathy the most frequent neurophysiological abnormalities were reduced amplitudes (the axonal damage) for sensory and motor fibers of n. Peroneus.