Peripheral and central nervous contribution to gastrointestinal symptoms in diabetic patients with autonomic neuropathy. (12th December 2012)

• Record Type: Journal Article
• Authors: Brock, C.; Graversen, C.; Frøkjær, J.B.; Søfteland, E.; Valeriani, M.; Drewes, A.M.
• Is Part Of: European journal of pain. Volume 17:Number 6(2013)
• Page Start: 820
• Page End: 831
• Publication Date: 2012-12-12
• Subjects: Pain -- Periodicals; Pain -- Treatment -- Periodicals; Pain -- Physiological aspects -- Periodicals; 616.0472
• DOI: 10.1002/j.1532-2149.2012.00254.x
• Languages: English
• ISSNs: 1090-3801

Abstract

<abstract abstract-type="main"> <title>Abstract</title> <sec id="ejp254-sec-0001" sec-type="section"> <title>Background & Aims</title> <p>Long‐term diabetes mellitus (DM) has been associated with neuronal changes in the enteric, peripheral and/or central nervous system. Moreover, abnormal visceral sensation and gastrointestinal (GI) symptoms are seen in up to 75% of patients. 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 and dipolar source modelling.</p> </sec> <sec id="ejp254-sec-0002" sec-type="section"> <title>Methods</title> <p>Fifteen healthy volunteers and 14 type‐1 DM patients with DAN were assessed with a symptom score index characterizing upper GI abnormalities. Multichannel (62) electroencephalography was recorded during painful electrical stimulation of the lower oesophagus. Brain activity to painful stimulations was modelled using Brain Electrical Source Analysis (<sc>besa</sc>).</p> </sec> <sec id="ejp254-sec-0003" sec-type="section"> <title>Results</title> <p>Diabetic patients had higher stimulus intensities to evoke painful sensation (<italic>p</italic> ≤ 0.001), longer latencies of N2 and P2 components (both <italic>p</italic> ≤ 0.001), and lower amplitudes of P1‐N2 and N2‐P2 complexes (<italic>p</italic> ≤ 0.001; <italic>p</italic> = 0.02). Inverse modelling of brain sources showed deeper bilateral insular dipolar source localization (<italic>p</italic> = 0.002). Symptom score index was negatively correlated with the depth of insular activity (<italic>p</italic> = 0.004) and positively correlated with insular dipole strength (<italic>p</italic> = 0.03).</p> </sec> <sec id="ejp254-sec-0004" sec-type="section"> <title>Conclusion</title> <p>DM patients show peripheral and central neuroplastic changes. Moreover, the role of abnormal insular processing may explain the appearance and persistence of GI symptoms related to DAN. This enhanced understanding of DAN may have future clinical and therapeutical implications.</p> </sec> </abstract>