A closer look to botulinum neurotoxin type A-induced analgesia

Abstract

Chronic pain indicates a type of pain that lasts over time and is accompanied by diagnostic and therapeutic difficulties. It follows that treatment failures are common and patients roam from doctor to doctor in search of an effective care program. So there is an urgent need for long-acting and effective therapeutics to alleviate symptoms of the varied forms of chronic pain. During the past few years, a good success has been achieved with a derivative of a neurotoxin. It has been shown that administration of this toxin can block the release of neurotransmitters and pain mediators. Botulinum neurotoxin type A (BoNT/A) is well known as a treatment for neuromuscular conditions such as dystonia and spasticity. However, the clinical application for BoNT/A has continued to expand. Its analgesic effect has been used in clinical practice with satisfactory results. This review provides an introduction of a hypothesis for the mechanism by which BoNT/A eases chronic pain. It also summarizes the clinical therapeutic effects of BoNT/A in different types of chronic pain and its potential prospects.

Keywords: Analgesia; BoNT/A; BoNTs; Botulinum neurotoxin type A; Botulinum neurotoxins; CCBs; CCI; CGRP; CNS; CPRS; Calcitonin gene-related peptide; Calcium channel blockers; Central nervous system; Chronic constriction injury; Chronic pain; Complex regional pain syndrome; GABA; Gamma-aminobutyric acid; HC; Heavy chain; LC; Light chain; MFPS; Myofascal pain syndrome; RA; Rheumatoid arthritis; SNAP; SNARE; SP; Soluble N-ethyl maleimide-sensitive fusion protein attachment protein receptor; Substance P; Synaptosomal associated protein; Synaptosomal associated protein of 25 kDa; TCAs; TN; TRPV; Transient receptor potential vanilloid; Tricyclic antidepressants; Trigeminal neuralgia; VAS; Visual analogue scale.