Botulinum toxin A (
BoNT/A) has been used therapeutically to treat muscular hypercontractions and sudomotor hyperactivity. There is increasing evidence that
BoNT/A might also have
analgesic properties, in particular in
headache. In the present investigation we tested the often cited hypothesis that
BoNT/A-induced
analgesia can be attributed to inhibition of
neuropeptide release from nociceptive nerve fibers. In 15 healthy volunteers
BoNT/A (5, 10, 20 mouse units
BOTOX) or saline (contralateral side) was injected intracutaneously on the volar forearm. On day zero, the day of injection, no further tests were performed. We repeatedly elicited
pain,
mechanical hyperalgesia and neurogenic flare by
transcutaneous electrical stimulation simultaneously on the
BoNT/A and saline treated side on day 1, 2, 3, 7 and 14 after injection. Before each session, sweating and local
anhidrosis was assessed by
iodine starch staining.
BoNT/A suppressed sweating as early as from the second day after injection (p < 0.001). The size of electrically induced flare was smaller on the
BoNT/A treated arm (
BoNT/A side: 21.46 cm(2) +/- 3.58, saline side 24.80 +/- 3.46, p < 0.005) and
BoNT/A reduced electrically-induced
pain by about 10 % (p < 0.001). However,
hyperalgesia to pin-prick and
allodynia after electrical stimulation were unchanged. In conclusion our results indicate that peripheral
neuropeptide release is attenuated by
BoNT/A. In contrast, the
analgesic effect of
BoNT/A was very limited. Therefore we assume that other than
neuropeptide mechanisms must be important for
BoNT/A induced
pain relief in clinical
pain syndromes.