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The pattern and time course of somatosensory changes in the human UVB sunburn model reveal the presence of peripheral and central sensitization

Gustorff, Burkharda; Sycha, Thomasb; Lieba-Samal, Dorisa; Rolke, Romanc,d; Treede, Rolf-Detlefe; Magerl, Waltere,*

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doi: 10.1016/j.pain.2012.12.020
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Summary Ultraviolet B irradiation induces generalized hyperalgesia to all pain modalities primarily on the basis of multiple mechanisms of peripheral sensitization, but also involves central sensitization (secondary hyperalgesia and dynamic mechanical allodynia).

The ultraviolet B (UVB) sunburn model was characterized with a comprehensive battery of quantitative sensory testing (QST). Primary hyperalgesia in UVB-irradiated skin and secondary hyperalgesia in adjacent nonirradiated skin were studied in 22 healthy subjects 24 h after irradiation with UVB at 3-fold minimal erythema dose of a skin area 5 cm in diameter at the thigh and compared to mirror-image contralateral control areas. The time course of hyperalgesia over 96 h was studied in a subgroup of 12 subjects. Within the sunburn area, cold hyperesthesia (P = .01), profound generalized hyperalgesia to heat (P < .001), cold (P < .05), pinprick and pressure (P < .001), and mild dynamic mechanical allodynia (P < .001) were present. The finding of cold hyperalgesia and cold hyperesthesia is new in this model. The sunburn was surrounded by large areas of pinprick hyperalgesia (mean ± SEM, 218 ± 32 cm2) and a small rim of dynamic mechanical allodynia but no other sensory changes. Although of smaller magnitude, secondary hyperalgesia and dynamic mechanical allodynia adjacent to the UVB-irradiated area were statistically highly significant. Primary and secondary hyperalgesia developed in parallel within hours, peaked after 24–32 h, and lasted for more than 96 h. These data reveal that the UVB sunburn model activates a broad spectrum of peripheral and central sensitization mechanisms and hence is a useful human surrogate model to be used as a screening tool for target engagement in phases 1 and 2a of drug development.

Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.

aVienna Human Pain Research Group, Department of Anaesthesia, General Intensive Care Medicine and Pain Control, Medical University of Vienna, Währinger Gürtel 18-20, 1090 Vienna, Austria

bVienna Human Pain Research Group, Department of Neurology, Medical University of Vienna, Währinger Gürtel 18-20, 1090 Vienna, Austria

cDepartment of Neurology, University Hospital, Johannes Gutenberg-University, Langenbeckstrasse 1, D-55099 Mainz, Germany

dDepartment of Palliative Medicine, University Hospital Bonn, Sigmund-Freud-Str. 25, D-53127 Bonn, Germany

eDepartment of Neurophysiology, Center of Biomedicine and Medical Technology Mannheim (CBTM), Medical Faculty Mannheim, Ruprecht-Karls-University Heidelberg, Ludolf-Krehl-Strasse 13-17, D-68167 Mannheim, Germany

*Corresponding author.

E-mail address:walter.magerl@medma.uni-heidelberg.de

Article history: Received 3 April 2012; Received in revised form 14 November 2012; Accepted 20 December 2012.

© 2013 Lippincott Williams & Wilkins, Inc.
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