Botulinum Toxin for the Treatment of Neuropathic Pain

Abstract

Botulinum toxin (BoNT) has been used as a treatment for excessive muscle stiffness, spasticity, and dystonia. BoNT for approximately 40 years, and has recently been used to treat various types of neuropathic pain. The mechanism by which BoNT acts on neuropathic pain involves inhibiting the release of inflammatory mediators and peripheral neurotransmitters from sensory nerves. Recent journals have demonstrated that BoNT is effective for neuropathic pain, such as postherpetic neuralgia, trigeminal neuralgia, and peripheral neuralgia. The purpose of this review is to summarize the experimental and clinical evidence of the mechanism by which BoNT acts on various types of neuropathic pain and describe why BoNT can be applied as treatment. The PubMed database was searched from 1988 to May 2017. Recent studies have demonstrated that BoNT injections are effective treatments for post-herpetic neuralgia, diabetic neuropathy, trigeminal neuralgia, and intractable neuropathic pain, such as poststroke pain and spinal cord injury.

Keywords: botulinum toxin; neuropathic pain; neuropathic pain treatment.

Figure 1

(A) Noxious stimuli cause inflammation through the release of neuropeptides and inflammatory mediators, which can cause peripheral sensitization. This action also occurs in DRG, dorsal horn of spinal cord and can lead to central sensitization. Botulinum toxin (BoNT) inhibits the release of pain mediators in peripheral nerve terminal, DRG, and spinal cord neuron, thereby reducing the inflammatory response and preventing the development of peripheral and central sensitization. Symbols; SP, substance P; CGRP, calcitonin gene related protein; DRG, dorsal root ganglion; (B) The hyperexcitability and spontaneous action potential mediated by the Na channel in peripheral sensory neuron contribute to the pathophysiology of neuropathic pain. BoNT can control neuropathic pain by blocking the Na channel; (C) Some of the BoNT appear to retrograde transport along the axons. SNAP-25 is cleaved in the dorsal horn of the spinal cord and central nuclei after a small amount of BoNT is administered to the periphery, thereby boosting the retrograde transport of BoNT.