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Subcutaneous Botulinum toxin type A reduces capsaicin-induced trigeminal pain and vasomotor reactions in human skin

Gazerani, Parisaa,b; Pedersen, Natalia Spicinac; Staahl, Camillaa,c; Drewes, Asbjørn Mohra,c; Arendt-Nielsen, Larsa,*

doi: 10.1016/j.pain.2008.10.005

The present human study aimed at investigating the effect of subcutaneous administration of Botulinum toxin type A (BoNT/A) on capsaicin-induced trigeminal pain, neurogenic inflammation and experimentally induced cutaneous pain modalities. Fourteen healthy males (26.3 ± 2.6 years) were included in this double-blind and placebo-controlled trial. The subjects received subcutaneous BoNT/A (22.5 U) and isotonic saline in the mirror sides of their forehead. Pain and neurogenic inflammation was induced by four intradermal injections of capsaicin (100 μg/μL) (before, and days 1, 3 and 7 after treatments). The capsaicin-induced pain intensity, pain area, the area of secondary hyperalgesia, the area of visible flare and vasomotor reactions were recorded together with cutaneous heat, electrical and pressure pain thresholds. BoNT/A reduced the capsaicin-induced trigeminal pain intensity compared to saline (F = 37.9, P < 0.001). The perceived pain area was smaller for the BoNT/A-treated side compared to saline (F = 7.8, P < 0.05). BoNT/A reduced the capsaicin-induced secondary hyperalgesia (F = 5.3, P < 0.05) and flare area (F = 10.3, P < 0.01) compared to saline. BoNT/A reduced blood flow (F1,26 = 109.5, P < 0.001) and skin temperature (F1,26 = 63.1, P < 0.001) at the capsaicin injection sites compared to saline and its suppressive effect was maximal at days 3 and 7 (P < 0.05, post hoc test). BoNT/A elevated cutaneous heat pain thresholds (F = 17.1, P < 0.001) compared to saline; however, no alteration was recorded for electrical or pressure pain thresholds (P > 0.05). Findings from the present study suggest that BoNT/A appears to preferentially target Cfibers and probably TRPV1-receptors, block neurotransmitter release and subsequently reduce pain, neurogenic inflammation and cutaneous heat pain threshold.

aCenter for Sensory-Motor Interactions (SMI), Department of Health Sciences and Technology, Aalborg University, Fredrik Bajers Vej 7 D-3, DK-9220 Aalborg, Denmark

bFaculty of Pharmaceutical Sciences, The University of British Columbia, Vancouver, Canada

cCenter for Visceral Biomechanics and Pain, Department of Gastroenterology, Aalborg University Hospital, Denmark

*Corresponding author. Tel.: +45 9940 8830; fax: +45 9815 4008.

E-mail:; E-mail:

Submitted March 4, 2008; revised October 9, 2008; accepted October 14, 2008.

© 2009 Lippincott Williams & Wilkins, Inc.
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