Neuropathic pain refers to pain caused by a lesion or disease of the somatosensory nervous system. Diabetic neuropathy, postherpetic neuralgia, radiculopathy pain, trigeminal neuralgia and complex regional pain syndrome are all neuropathic pain syndromes.

Local administration of botulinum neurotoxin (BoNT)) has proven significant effects on the treatment of neuropathic pain. Abnormal muscle contractions contribute to chronic pain. Botulinum neurotoxin serotype A (BoNT-A) is well known to have an effect on inhibition of muscle contraction and this may partially explain its effect on chronic pain. In preclinical models, BoNT-A was found to effectively block the release of several pain-related neurotransmitters, including norepinephrine, substance P, glutamate and calcitonin gene-related peptide, from afferent nerve terminals and dorsal root ganglia. These pain-related neurotransmitters can stimulate depolarization of C fibers, which are responsible for propagation of chronic pain. BoNT-A also decreases local inflammation around the nerve terminal.

This chapter offers clinical description and pictorial illustration for injection of BoNT for the particular conditions of diabetic neuropathy, postherpetic neuralgia and trigeminal neuralgia.

Introduction

Botulinum neurotoxin (BoNT) has been used effectively to alleviate pain in many pain disorders and has been proven to be a good choice for treatment of neuropathic pain. There have been no major side effects, only minor local infection. Randomized controlled studies and open-label studies indicate BoNT is beneficial in diabetic neuropathic pain, trigeminal neuralgia and postherpetic neuralgia (Piovesan et al., 2005; Ranoux et al., 2008; Yuan et al., 2009; Xiao et al., 2010). This chapter discusses the putative mechanisms of BoNT action and injection methodology for these three conditions.

Peripheral and central sensitization processes are involved in the pathophysiology of neuropathic pain (Baron, 2006; Pace et al., 2006). Abnormal muscle contraction, released substance P and calcitonin gene-related peptide also play significant roles in hyperalgesia of neuropathic pain. An ideal therapy for neuropathic pain should block these pain-inducing pathways as completely as possible. Muscle paralytic mechanisms, vasodilatation, pain-related neurotransmitter blockage, peripheral inflammatory pain inhibition and the inhibition of central pain perception contribute to the effectiveness of BoNT for neuropathic pain (Ranoux et al., 2008; Yuan et al., 2009; Neumeister et al., 2009).