Altered resting state EEG in chronic pancreatitis patients: toward a marker for chronic pain
Authors De Vries M, Wilder-Smith O, Jongsma M, Van den Broeke E, Arns M, Van Goor H, Van Rijn C
Received 4 July 2013
Accepted for publication 13 August 2013
Published 25 November 2013 Volume 2013:6 Pages 815—824
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 4
Marjan de Vries,1 Oliver HG Wilder-Smith,2 Marijtje LA Jongsma,3 Emanuel N van den Broeke,1 Martijn Arns,5,6 Harry van Goor,1 Clementina M van Rijn4
1Department of Surgery, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands; 2Department of Anesthesiology, Pain and Palliative Care, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands; 3Behavioral Science Institute, Radboud University Nijmegen, Nijmegen, The Netherlands; 4Donders Institute for Brain, Cognition and Behavior, Radboud University Nijmegen, Nijmegen, The Netherlands; 5Research Institute Brainclinics Nijmegen, Nijmegen, The Netherlands; 6Department of Experimental Psychology, Utrecht University, Utrecht, The Netherlands
Objectives: Electroencephalography (EEG) may be a promising source of physiological biomarkers accompanying chronic pain. Several studies in patients with chronic neuropathic pain have reported alterations in central pain processing, manifested as slowed EEG rhythmicity and increased EEG power in the brain's resting state. We aimed to investigate novel potential markers of chronic pain in the resting state EEG of patients with chronic pancreatitis.
Participants: Resting state EEG data from 16 patients with persistent abdominal pain due to chronic pancreatitis (CP) were compared to data from healthy controls matched for age, sex and education.
Methods: The peak alpha frequency (PAF) and power amplitude in the alpha band (7.5–13 Hz) were compared between groups in four regions of interest (frontal, central, parietal, and occipital) and were correlated with pain duration.
Results: The average PAF was lowered in CP patients compared with that in healthy controls, observed as a statistically significant between-group effect (mean 9.9 versus 9.5 Hz; P=0.049). Exploratory post hoc analysis of average PAF per region of interest revealed a significant difference, particularly in the parietal and occipital regions. In addition, we observed a significant correlation between pain duration and PAF and showed increased shifts in PAF with longer pain durations. No significant group differences were found in peak power amplitudes.
Conclusion: CP pain is associated with alterations in spontaneous brain activity, observed as a shift toward lower PAF. This shift correlates with the duration of pain, which demonstrates that PAF has the potential to be a clinically feasible biomarker for chronic pain. These findings could be helpful for assisting diagnosis, establishing optimal treatment, and studying efficacy of new therapeutic agents in chronic pain patients.
Keywords: chronic pain, neuropathic pain, chronic pancreatitis, electroencephalography, EEG, alpha oscillations, peak frequency
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