Diabetic neuropathy differs between type 1 and type 2 diabetes Insights from magnetic resonance neurography

Abstract

Objective: To visualize and quantify differences of microstructural nerve damage in distal symmetric diabetic neuropathy (DPN) between type 1 diabetes (T1D) and type 2 diabetes (T2D), and to detect correlations between neuropathic symptoms and serological risk factors.

Methods: 3T magnetic resonance neurography of the sciatic nerve was performed in 120 patients (T1D n=35; T2D n=85) with either DPN (n=84) or no DPN (NDPN; n=36). Results were subsequently correlated with clinical, serological, and electrophysiological patient data.

Results: T2-weighted (T2w) hyperintense lesions correlated negatively with tibial compound motor action potential (r=-0.58; p<0.0001) and peroneal nerve conduction (r=0.51; p=0.0002), and positively with neuropathy disability (NDS; r=-0.54; p<0.0001) and severity score (NSS; r=0.52; p<0.0001), and HbA1c levels (r=0.23; p=0.014). T2w-hypointense lesions correlated positively with NDS, NSS (r=0.28; p=0.002; r=0.36; p<0.0001), and serum triglycerides (r=0.34; p=0.0003), and negatively with serum HDL (r=-0.48; p<0.0001). For DPN in T1D, elevated values of T2w-hyperintense lesions (19.67%±4.13 vs. 12.49%±1.23; p=0.027) and HbA1c (8.74%±0.29 vs. 7.11%±0.16; p<0.0001) were found when compared to T2D. For DPN in T2D, elevated T2w-hypointense lesions (23.41mm³±2.69 vs. 11.43mm³±1.74; p=0.046), triglycerides (220.70mg/dl±23.70 vs. 106.60mg/dl±14.51; p<0.0001), and lower serum HDL (51.29mg/dl±3.02 vs. 70.79mg/dl±4.65; p<0.0001) were found when compared to T1D.

Interpretation: The predominant type of nerve lesions in DPN differs between T1D and T2D. Correlations found between lesion type and serological parameters indicate that predominant nerve lesions in T1D are associated with poor glycemic control and loss of nerve conduction, whereas predominant lesions in T2D are associated with changes in lipid metabolism. These findings may be helpful for future studies on the underlying pathophysiological pathways and possible treatments for DPN in T1D and T2D. This article is protected by copyright. All rights reserved.

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