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Parkinsonism Relat Disord. 2011 Nov;17 Suppl 1:S28-33. doi: 10.1016/j.parkreldis.2011.06.013.

Updates on the antinociceptive mechanism hypothesis of botulinum toxin A.

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1
Discovery Research, Biological Sciences, Allergan, 2525 Dupont Drive, Irvine, CA 92612-1599, USA. Aoki_Roger@Allergan.com

Abstract

Botulinum toxin A has been traditionally viewed as a motor nerve specific treatment. However, clinical uses for botulinum toxin A have continued to expand, with increased use in conditions implicating sensory pain nerve dysfunction. Chronic pain is associated with excess pain fiber activity. When the site of this excess activity resides in the peripheral portion of the pain pathway, a condition of peripheral sensitization can establish. During this state, excess pain signaling reaches the central nervous system, which can then lead to a condition of central sensitization, manifesting as the symptoms associated with chronic pain (i.e. burning, electric pain, lowered pain threshold to normal stimuli, etc). Experimentally, botulinum toxin type A has been shown to reduce neuropeptides and neurotransmitter release from treated cells or nerve endings and to attenuate nociception in both neuropathic and non-neuropathic pain models. This review summarizes the literature to update the hypothesis for the mechanism by which botulinum toxin type A can modulate chronic pain.

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