Gastrointestinal symptoms in type-1 diabetes: Is it all about brain plasticity?

• Published in: European journal of pain 2011-03, Vol.15 (3), p.249-257
• Main Authors: Frøkjær, Jens Brøndum, Egsgaard, Line Lindhardt, Graversen, Carina, Søfteland, Eirik, Dimcevski, Georg, Blauenfeldt, Rolf Ankerlund, Drewes, Asbjørn Mohr
• Format: Article
• Language: English
• Subjects: Adult; Analysis of Variance; Anesthesia & Perioperative Care; Autonomic Nervous System Diseases - diagnosis; Autonomic Nervous System Diseases - physiopathology; Autonomic neuropathy; Blood Glucose; Brain - physiopathology; Diabetes; Diabetes Mellitus, Type 1 - physiopathology; Diabetic Neuropathies - diagnosis; Diabetic Neuropathies - physiopathology; Electric Stimulation; Electroencephalography; Esophagus - physiopathology; Evoked brain potentials; Evoked Potentials - physiology; Experimental pain; Female; Gastrointestinal Diseases - diagnosis; Gastrointestinal Diseases - physiopathology; Humans; Male; Middle Aged; Oesophagus; Pain - physiopathology; Pain Medicine
• ISSN: 1090-3801; 1532-2149
• DOI: 10.1016/j.ejpain.2010.08.004

Abstract Background and aims Autonomic neuropathy seems to play a central role in the development of gastrointestinal symptoms in diabetes. In order to explore the neuronal mechanisms behind the symptoms we evaluated the brain processing of painful visceral stimuli. Methods Evoked brain potentials were recorded to assess the response to painful oesophageal electrical stimuli in 15 healthy volunteers and 14 type-1 diabetes patients with autonomic neuropathy and related gastrointestinal symptoms. Source reconstruction analysis (fixed Multiple Signal Classification (MUSIC) algorithm) was applied to estimate the location of the evoked electrical activity in the brain. Results The patients had increased oesophageal sensory thresholds compared to the controls ( P = 0.004). The latencies of the evoked brain potentials at vertex (Cz) were increased ( P = 0.007) and amplitudes reduced ( P = 0.011) in diabetics. Compared with controls the patients had a posterior shift of the electrical sources in the anterior cingulate cortex at 54 ms, and additional sources close to the posterior insula at 95 ms and in medial frontal gyrus at 184 ms. Conclusions There is evidence of altered central processing to visceral stimulation, and both peripheral and central mechanisms seem involved. Central neuronal reorganisation may contribute to our understanding of the gastrointestinal symptoms in patients with diabetic autonomic neuropathy and this may guide development and evaluation of new treatment modalities.