4.3 Article

Slowed EEG rhythmicity in patients with chronic pancreatitis: evidence of abnormal cerebral pain processing?

Journal

EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY
Volume 23, Issue 5, Pages 418-424

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MEG.0b013e3283457b09

Keywords

biomarker; chronic pain; chronic pancreatitis; electroencephalography (EEG); neuropathic pain; pain; spectral analysis

Funding

  1. Karen Elise Jensen Foundation
  2. Spar Nord Foundation
  3. Obelske Family Foundation
  4. Heinrich Kopp's Grant

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Background and aim Intractable pain usually dominates the clinical presentation of chronic pancreatitis (CP). Slowing of electroencephalogram (EEG) rhythmicity has been associated with abnormal cortical pain processing in other chronic pain disorders. The aim of this study was to investigate the spectral distribution of EEG rhythmicity in patients with CP. Patients and methods Thirty-one patients with painful CP (mean age 52 years, 19 male) and 15 healthy volunteers (mean age 49, nine male) were included. A multichannel EEG was recorded from 62 surface electrodes. Amplitude strengths of the resting EEG were retrieved based on wavelet frequency analysis and summarized in frequency bands with corresponding topographic mapping. Results Patients with CP had slowed EEG rhythmicity compared with healthy volunteers. This was evident as increased activity in the lower frequency bands delta (1-3.5 Hz) (P=0.05), theta (3.5-7.5 Hz) (P<0.001) and alpha (7.5-13.5 Hz) (P<0.001). Due to normalization a reciprocal relationship was observed for the high frequency band beta (13.5-32 Hz). In a sub-analysis, delta band activity was modified by diabetes, opioid treatment and alcohol aetiology of CP. However, no effect modification was seen for the theta or alpha bands. Differences in theta activity were located over centro-frontal brain regions, whereas differences in delta, alpha and beta band activity were located in frontal regions. Conclusion Slowed EEG rhythmicity was evident in patients with CP. This possibly mirrors abnormal central pain processing and may serve as a clinically useful biomarker of abnormal central pain processing. Eur J Gastroenterol Hepatol 23: 418-424 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.

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