This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Web of Science (7) Citing Articles via Google Scholar Google Scholar Articles by Sycha, T. Articles by Auff, E. Search for Related Content PubMed PubMed Citation Articles by Sycha, T. Articles by Auff, E.

---

PAIN MEDICINE

A Lack of Antinociceptive or Antiinflammatory Effect of Botulinum Toxin A in an Inflammatory Human Pain Model

Thomas Sycha, MD^*, Doris Samal, MD, Boris Chizh, MD, PhD^||, Stephan Lehr, PhD, Burkhard Gustorff, MD, Peter Schnider, MD, and Eduard Auff, MD^*

Departments of *Neurology, Anesthesia and General Intensive Care Medicine, and Institute for Medical Computersciences, Medical University of Vienna; Department of Neurology, Landeskrankenhaus Grimmenstein-Hochegg, Austria; and ||GlaxoSmithKline, Addenbrooke’s Centre for Clinical Investigation, Cambridge, England

Address correspondence and reprint requests to Thomas Sycha, MD, Department of Neurology, Medical University of Vienna, Währinger-Gürtel 18-20, A-1090 Vienna, Austria. Address e-mail to thomas.sycha{at}meduniwien.ac.at.

Several in vitro and in vivo investigations have shown that botulinum toxin A (BoNT/A) can inhibit the release of substance P and excitatory amino acids. Recently, a marked antinociceptive effect of BoNT/A and inhibition of glutamate release was observed in an animal pain model with inflammatory sensitization. In the present study, we tested the antiinflammatory and antihyperalgetic effect of BoNT/A in a well-characterized human inflammatory pain model. Using a randomized, double-blind, paired study design, we compared the effects of 100 mouse units of BoNT/A versus pure saline. Thermal and mechanical pain testings and superficial skin blood flow measurements were performed at baseline, at 48 h (in normal skin), and at 72 h (in inflamed skin) thereafter. Ultraviolet B irradiation resulted in a local inflammation with significant primary and secondary hyperalgesia. However, despite the evidence of efficacy on sudomotor function, BoNT/A had no effect on pain measures in either normal or inflamed skin. Signs of inflammation and primary and secondary hyperalgesia were found to be unaffected by BoNT. We have confirmed that BoNT/A has no direct effect on acute, noninflammatory pain. Furthermore, despite highly promising data from animal research, we have not observed antiinflammatory or antinociceptive effects of BoNT/A in human inflammatory pain.