Table of Contents Author Guidelines Submit a Manuscript
BioMed Research International
Volume 2013, Article ID 610727, 11 pages
Clinical Study

Cerebral Activation during Von Frey Filament Stimulation in Subjects with Endothelin-1-Induced Mechanical Hyperalgesia: A Functional MRI Study

1Multidisciplinary Pain Center, Antwerp University Hospital and University of Antwerp, Wilrijkstraat 10, 2650 Edegem, Belgium
2Laboratory for Pain Research, University of Antwerp, Wilrijk, Belgium
3Department of Radiology, Antwerp University Hospital and University of Antwerp, Edegem, Belgium

Received 30 June 2013; Accepted 14 August 2013

Academic Editor: Gjumrakch Aliev

Copyright © 2013 Guy H. Hans et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Endothelin-1 (ET-1) is an endogenously expressed potent peptide vasoconstrictor. There is growing evidence that ET-1 plays a role in the pain signaling system and triggers overt nociception in humans. The underlying neuronal pathways are still a matter of great debate. In the present study, we applied an intradermal ET-1 sensitization model to induce mechanical hyperalgesia in healthy subjects. Functional magnetic resonance imaging (fMRI) was used to tease out the cortical regions associated with the processing of ET-1-induced punctate hyperalgesia, as compared to a nonnoxious mechanical stimulation of the contralateral arm. Von Frey hair testing revealed the presence of increased responsiveness to punctate stimulation in all subjects. Activational patterns between nonpainful control stimulation and hyperalgesic stimulation were compared. Two major observations were made: (1) all cortical areas that showed activation during the control stimulation were also present during hyperalgesic stimulation, but in addition, some areas showed bilateral activation only during hyperalgesic stimulation, and (2) some brain areas showed significantly higher signal changes during hyperalgesic stimulation. Our findings suggest that injection of ET-1 leads to a state of punctate hyperalgesia, which in turn causes the activation of multiple brain regions. This indicates that ET-1 activates an extended neuronal pathway.