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Background
the pathophysiological mechanism of pain symptomsdiabetic peripheral neuropathy (DPN) is not clearThis may be relevant to some MRI signs, but there is no studypurpose
this study aims to evaluate the correlation between neurostructure, neuropathy load and spatial distribution and pain in patients with DPNmaterials and methods
This study included patients with type I or type 2 diabetesAll subjects performed 3T MR neuroimaging, mainly using T2-lipid sequence to image the sciatic nerveAt the same time, patients are tested for clinical and electrophysiological physiologyFor intergroup comparisons, the analysis is made using variance analysis and Kruskal-Wallis testingThe correlation coefficient is calculated using Spearman correlation analysisresults131 subjects were included in this study, with 45 cases of type 1 and 86 cases of type 2 diabetes, and 64, 37 and 30 cases of pain, pain, pain and non-DPN, respectivelyThe lesion volume of the pain DPN group (15.2% s 1.6) accounted for 100 percent of the total nerve volume than the painless DPN group (10.4% to 1.7, P .03) and the non-DPN group (8.3% s 1.7; P .001) The number and extent of neuroT2 abnormally high signallesions is associated with a score of neurofunctional disorders (r s 0.37; 95% CI: 0.21, 0.52; r s 0.37; 95% CI: 0.20, 0.52), neuropathy symptoms score (r s 0.41; 95% CI: 0.25, 0.55; r 0.34; 95% CI: 0.17, 0.49) has a positive correlation; the number and degree of abnormally high signal lesions of the nerve T2 has a significant negative correlation with the tibia nerve conduction velo (r .23; 95% CI: -0.44, -0.01; s r -0.37; 95% CI: -0.55, -05.55 The area of the neural cross-section is positively correlated with the neurodysfunction score (r s 0.23; 95% CI: 0.03, 0.36), and negative correlation with the tibia nerve conduction rate (r -0.24; 95% CI: -0.45, -0.01) conclusions
this study shows that the number and degree of abnormally high signallesions of neuropathy around pain diabetes is more significant than that of patients with peripheral neuropathy with painless diabetes This suggests that near-end damage in nerve cellulose is associated with the progression of neuropathic sensory symptoms around diabetes