Neuroplastic alterations in brain responses to painful visceral stimulations reflects individual neuropathic symptoms in diabetes mellitus patients.

Background/aims Abnormal visceral sensory function in diabetes mellitus (DM) leads to neuronal changes in the enteric, peripheral and/or central nervous system (CNS). To explore the role of diabetic autonomic neuropathy (DAN) in patients with long-standing DM, we investigated psychophysical responses and neuronal activity recorded as evoked brain potentials (EPs) and dipolar source modelling. Methods Fifteen healthy volunteers and 14 type-1 DM patients with DAN were assessed with a symptom score index characterizing upper GI abnormalities. Multi-channel (62) electroencephalography was recorded during painful electrical stimulation of the lower oesophagus. Brain activity to painful stimulations was modelled by use of Brain Electrical Source Analysis (BESA). Results Diabetic patients had higher stimulus intensities to evoke painful sensation (P<0.001), longer latencies of N2 and P2 components (both P<0.001), lower amplitudes of P1-N2 and N2-P2 complexes (P<0.001; P = 0.02). Inverse modelling of brain sources showed deeper bilateral insular dipolar source localization (P = 0.002). Symptom score index was negatively correlated to the depth of insular activity (P = 0.004) and positively correlated to insular dipole strength (P = 0.03). Conclusion DM patients show neuroplastic changes in the central nervous system. The role of abnormal insular processing may explain the development and persistence of upper GI-symptoms related to DAN. This enhanced understanding of DAN may have clinical and therapeutical implications.