Abstract
Botulinum neurotoxin (BoNT), derived from Clostridium botulinum, has been used therapeutically for focal dystonia, spasticity, and chronic migraine. Its spectrum as a potential treatment for neuropathic pain has grown. Recent opinions on the mechanism behind the antinociceptive effects of BoNT suggest that it inhibits the release of peripheral neurotransmitters and inflammatory mediators from sensory nerves. There is some evidence showing the axonal transport of BoNT, but it remains controversial. The aim of this review is to summarize the experimental and clinical evidence of the antinociceptive effects, mechanisms, and therapeutic applications of BoNT for neuropathic pain conditions, including postherpetic neuralgia, complex regional pain syndrome, and trigeminal neuralgia. The PubMed and OvidSP databases were searched from 1966 to May 2015. We assessed levels of evidence according to the American Academy of Neurology guidelines. Recent studies have suggested that BoNT injection is an effective treatment for postherpetic neuralgia and is likely efficient for trigeminal neuralgia and post-traumatic neuralgia. BoNT could also be effective as a treatment for diabetic neuropathy. It has not been proven to be an effective treatment for occipital neuralgia or complex regional pain syndrome.
Highlights
Botulinum neurotoxin (BoNT), derived from Clostridium botulinum, has been used worldwide for cosmetic therapeutic purposes and for the treatment of neurologic disorders, such as dystonia or spasticity [1,2]
The results of this study suggest that BoNT/B can be taken up by the peripheral terminal and be transported to the ipsilateral dorsal root ganglia (DRG) to cleave vesicle-associated membrane protein (VAMP)
To investigate the antinociceptive effects of BoNT, we assessed levels of evidence from clinical and experimental studies according to the American Academy of Neurology guidelines
Summary
Botulinum neurotoxin (BoNT), derived from Clostridium botulinum, has been used worldwide for cosmetic therapeutic purposes and for the treatment of neurologic disorders, such as dystonia or spasticity [1,2]. BoNT has seven antigenically different serotypes (A–G) [4], and its main mechanism is the inhibition of acetylcholine (Ach) neurotransmitter release at presynaptic nerve terminals, which results in a reduction of muscle fiber activity [2,4,5]. BoNT inhibits the exocytosis of Ach from cholinergic nerve endings by endocytosing into the presynaptic membranes of neuromuscular junctions and cleaving proteins that are essential for Ach exocytosis [6]. These proteins are required for the docking of Ach-containing vesicles to presynaptic membranes. In addition to the impairment of SNARE-mediated synaptic vesicle fusion to nerve terminals, this study demonstrated that BoNT/A selectively inhibits C- but not Aδ-menigeal nociceptors. Additional references were found by reviewing individual references from the articles, which were searched using PubMed
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