Key result
Participants with painless diabetic peripheral neuropathy had a significantly lower thalamic NAA:Cr ratio (1.55) compared to healthy volunteers and other diabetes subgroups (ANOVA p < 0.001), suggesting thalamic neuronal dysfunction occurs in established painless-DPN but is preserved in painful-DPN.
Why the study?
To determine neuronal function in the thalamus and primary somatosensory cortex across different subgroups of diabetic peripheral neuropathy, including subclinical- and painful-DPN.
Cross-Sectional (n=130)
Single-blind
No
p-value: p=<0.001
Preservation of thalamic neuronal function may be a prerequisite for neuropathic pain in diabetic peripheral neuropathy.
Thalamic NAA:Cr reduction may distinguish painless DPN phenotypes; leaves open central mechanisms and requires prospective validation before clinical use.
Introduction: In this study, we used proton Magnetic Resonance Spectroscopy (1H-MRS) to determine the neuronal function in the thalamus and primary somatosensory (S1) cortex in different subgroups of DPN, including subclinical- and painful-DPN. Method: One-hundred and ten people with type 1 diabetes [20 without DPN (no-DPN); 30 with subclinical-DPN; 30 with painful-DPN; and 30 with painless-DPN] and 20 healthy volunteers, all of whom were right-handed men, were recruited and underwent detailed clinical and neurophysiological assessments. Participants underwent Magnetic Resonance Imaging at 1.5 Tesla with two 1H-MRS spectra obtained from 8 ml cubic volume voxels: one placed within left thalamus to encompass the ventro-posterior lateral sub-nucleus and another within the S1 cortex. Results: < 0.001]. There were no significant group differences in S1 cortical neurometabolites. Conclusion: In this largest cerebral MRS study in DPN, thalamic neuronal dysfunction was found in advanced painless-DPN with preservation of function in subclinical- and painful-DPN. Furthermore, there was a preservation of neuronal function within the S1 cortex in all subgroups of DPN. Therefore, there may be a proximo-distal gradient to central nervous system alterations in painless-DPN, with thalamic neuronal dysfunction occurring only in established DPN. Moreover, these results further highlight the manifestation of cerebral alterations between painful- and painless-DPN whereby preservation of thalamic function may be a prerequisite for neuropathic pain in DPN.
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Gandhi et al. (2023) conducted a cross-sectional in Diabetic Peripheral Neuropathy (n=130). Painless diabetic peripheral neuropathy vs. Healthy volunteers and other diabetes subgroups (no-DPN, subclinical-DPN, painful-DPN) was evaluated on Thalamic NAA:Cr ratio (p=<0.001). Participants with painless diabetic peripheral neuropathy had a significantly lower thalamic NAA:Cr ratio (1.55) compared to healthy volunteers and other diabetes subgroups (ANOVA p < 0.001), suggesting thalamic neuronal dysfunction occurs in established painless-DPN but is preserved in painful-DPN.
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