Cerebral excitability is abnormal in patients with painful chronic pancreatitis
Article first published online: 16 APR 2012
© 2012 European Federation of International Association for the Study of Pain Chapters
European Journal of Pain
Volume 17, Issue 1, pages 46–54, January 2013
How to Cite
Olesen, S.S., Hansen, T.M., Graversen, C., Valeriani, M. and Drewes, A.M. (2013), Cerebral excitability is abnormal in patients with painful chronic pancreatitis. European Journal of Pain, 17: 46–54. doi: 10.1002/j.1532-2149.2012.00155.x
This research was supported by Karen Elise Jensen's Foundation, Hertha Christensen's Foundation, and Christenson-Ceson's Family Foundation.
Conflict of interest
The authors have no conflicts of interest.
- Issue published online: 11 DEC 2012
- Article first published online: 16 APR 2012
- Manuscript Accepted: 26 MAR 2012
- Karen Elise Jensen's Foundation
- Hertha Christensen's Foundation
- Christenson-Ceson's Family Foundation
We investigated whether patients with painful chronic pancreatitis (CP) present abnormalities in the cerebral response to experimental pain stimuli.
Contact heat-evoked potentials (CHEPS) were recorded in 15 patients with CP and in 15 healthy volunteers during repetitive stimulation of the upper abdominal region (pancreatic ‘viscerotome’) and the right forearm (heterologous area). Three sequences of painful stimuli were applied at each site. Subjective pain scores were assessed by a visual analogue scale. Habituation was calculated as the relative change in CHEPS amplitudes between the first and the third stimulation sequence.
As expected pain scores decreased in healthy volunteers during successive stimulations at both sites (i.e., habituation), while in the CP group, they remained unchanged. The cerebral response consisted of an early-latency, low-amplitude response (N1, contralateral temporal region) followed by a late, high-amplitude, negative–positive complex (N2/P2, vertex). During successive stimulation of the pancreatic area, N2/P2 amplitude increased 25% in CP patients, while they decreased 20% in healthy volunteers (p = 0.006). After stimulation of the forearm, N2/P2 amplitudes increased 3% in CP patients compared to a decrease of 20% in healthy volunteers (p = 0.06).
Taken together, CP patients had an abnormal cerebral response to repetitive thermal stimuli. This was most prominent after stimulation of the upper abdominal area. As this area share spinal innervation with the pancreatic gland, these findings likely mirror distinctive abnormalities in cerebral pain processing.