Botulinum Toxin for the Treatment of Neuropathic Pain.

Junghyun Park,Hue Jung Park

doi:10.3390/toxins9090260

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.

Highlights

Botulinum toxin (BoNT) has been used for decades in the treatment of diseases, such as dystonia or seizures, and cosmetic treatments
We investigate the mechanism of BoNT in neuropathic pain by examining the effects of the drug for intractable neuropathic pains, such as postherpetic neuralgia, diabetic neuropathy, complex regional pain syndrome, trigeminal neuralgia, phantom limb pain, spinal cord injury-induced neuropathic pain, and central poststroke pain
Before beginning BoNT therapy, patients with neuropathic pain require a careful assessment of functional limitations, goals, and expected outcomes

Summary

Introduction

Botulinum toxin (BoNT) has been used for decades in the treatment of diseases, such as dystonia or seizures, and cosmetic treatments. BoNT is useful in conditions such as strabismus because it causes long lasting but reversible paralysis via the administration of small amounts locally [1,2]. As BoNT purification technology develops, the range of use of this drug has been expanded, and the number of Food and Drug Administration (FDA)-approval diseases has increased. Common to these applications is the fact that BoNT is absorbed from the neuromuscular junction or parasympathetic axon terminal to the motor neuron terminal because the toxin is responsible for the release of acetylcholine. Numerous reports suggest that local administration of BoNT has a significant effect on neuropathic pain

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