210-OR: Cerebral Morphometric Alterations in Painless and Painful Diabetic Peripheral Neuropathy

Abstract

Aims: Neuroimaging studies have found structural alterations in brain regions involved in the somatomotor system in diabetic peripheral neuropathy (DPN) and painful-DPN (pDPN). However, most of these studies have had small cohorts of subjects, without consideration of pDPN phenotypes. Here we present the largest DPN neuroimaging study, which examines differences in brain morphology in DPN and phenotypes of painful-DPN. Methods: 229 participants were enrolled, 177 with diabetes (46 no-DPN, 56 painless-DPN and 75 pDPN; 25 irritable [IR] and 50 non-irritable [NIR] phenotype), and 52 healthy volunteers underwent detailed clinical, neurophysiological and quantitative sensory testing (DFNS) assessments, and 3-dimensional T1-weighted brain MRI (3.0T, Phillips). Brain volumetry was performed using Freesurfer. Results: At the post-central gyrus, in comparison with HV (1.92mm±0.11) and NoDPN (1.90mm±0.14), there was a significantly reduced cortical thickness in DPN (1.85mm±0.14), in pDPN (1.87mm±0.12) cortical thickness was reduced compared with HV. At the precentral gyrus, both DPN (2.29mm±0.16) and pDPN (2.28mm±0.16) had significantly reduced cortical thickness compared with HV (2.37mm±0.14) and NoDPN (2.36mm±0.13). At the insula, compared with HV (2.93mm±0.15) the cortical thickness was reduced in DPN (2.85mm±0.18) and pDPN (2.84mm±0.17). The cortical thickness at the pre and postcentral gyrus, and insula correlated with measures of nerve conduction. Moreover, the mean anterior cingulate cortical (ACC) thickness was significantly reduced in the IR- (2.40mm±0.23) compared to NIR-pDPN (2.58mm±0.20; p=0.003). Conclusions: Key somatomotor brain regions have a reduced cortical thickness in patients with DPN and pDPN, which correlate with neurophysiological measures suggestive of an ascending axonopathy. Moreover, the cortical thickness at the ACC differentiated IR and NIR, suggesting neuroplasticity in this region may play a role determining clinical phenotypes in pDPN. Disclosure G. P. Sloan: None. D. Selvarajah: None. K. Teh: None. P. Shillo: None. I. D. Wilkinson: None. S. Tesfaye: Advisory Panel; Self; Angellini, Bayer AG, Eva Pharma, Wörwag Pharma, Speaker’s Bureau; Self; Abbott, AstraZeneca, Grunenthal Group, MSD Corporation, Novo Nordisk, Pfizer Inc.