Continuum of sensory profiles in diabetes mellitus patients with and without neuropathy and pain

Raputova J, Rajdova A, Vollert J, Srotova I, Rebhorn C, Üçeyler N, Birklein F, Sommer C, Vlckova E, Bednarik J.

Eur J Pain. 2022 Sep 7. doi: 10.1002/ejp.2034. Epub ahead of print. PMID: 36069121.


13 Sep 2022

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Background: Quantitative sensory testing (QST) assesses the functional integrity of small and large nerve fibre afferents and central somatosensory pathways; QST was assumed to provide insight into the mechanisms of neuropathy. We analysed QST profiles and phenotypes in diabetes mellitus patients to study whether these could differentiate patients with and without pain and neuropathy.

Methods: A standardised QST protocol was performed and 'loss and gain of function' abnormalities were analysed in four groups of subjects: diabetic patients with painful (pDSPN; n=220) and non-painful distal symmetric polyneuropathy (nDSPN; n=219), diabetic patients without neuropathy (DM; n=23), and healthy non-diabetic subjects (n=37). Based on the QST findings, diabetic subjects were further stratified into four predefined prototypic phenotypes: sensory loss (SL), thermal hyperalgesia (TH), mechanical hyperalgesia (MH), and healthy individuals.

Results: Patients in the pDSPN group showed the greatest hyposensitivity ('loss of function'), and DM patients showed the lowest, with statistically significant increases in thermal, thermal pain, mechanical, and mechanical pain sensory thresholds. Accordingly, the frequency of the SL phenotype was significantly higher in the pDSPN subgroup (41.8%), than expected (p<0.0042). The proportion of 'gain of function' abnormalities was low in both pDSPN and nDSPN patients without significant differences.

Conclusions: There is a continuum in the sensory profiles of diabetic patients, with a more pronounced sensory loss in pDSPN group probably reflecting somatosensory nerve fibre degeneration. An analysis of 'gain of function' abnormalities (allodynia, hyperalgesia) did not offer a key to understanding the pathophysiology of spontaneous diabetic peripheral neuropathic pain.

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