Abstract
Botulinum neurotoxin is widely used for the treatment of central and peripherical neurological conditions. Initially used to treat strabismus, over the years its use has been expanded also to spasticity and other neurological disorders. This review summarizes the evidence from the published literature regarding its effect on neuropathic pain. Almost all investigations were performed using onabotulinum toxin type A (BoNT/A). Most studies provided positive results, even though toxin formulation, dose, dilution, injection techniques, and sites are heterogeneous across studies. Future larger, high-quality, specifically designed clinical trials are warranted to confirm botulinum neurotoxin efficacy in neuropathic pain.
Highlights
Neuropathic pain (NP) is a pain caused by a lesion or a disease affecting the somatosensory nervous system and encompasses common neurological pain syndromes such as trigeminal neuralgia (TN), postherpetic neuralgia (PHN), diabetic neuropathic pain (DN), and postsurgical neuralgia.NP is caused by pathological changes involving the peripheral and the central nervous system (CNS)
Among the numerous pharmacological studies on botulinum toxin (BoNT) for NP treatment in adults, we identified 22 randomized controlled trials (RCT), 20 case reports (CR), and 10 open label (OL) studies including a total of 1,543 patients
Eighteen studies focused on the effect of botulinum toxin in TN, nine in traumatic, compressive and post-surgical causes of NP, six in PHN, five in complex regional pain syndrome (CRPS), four in post-stroke pain (PSP), four in spinal cord injury (SCI), three in painful diabetic neuropathy (PDN), two in occipital neuralgia, two in phantom limb pain (PLP), two in neurogenic thoracic outlet syndrome (NTOS), and four in chronic pelvic pain syndrome (CPPS)
Summary
NP is caused by pathological changes involving the peripheral (nerves, plexus, roots, and sensitive ganglia) and the central nervous system (CNS). The pathologies responsible for tissue specific symptoms of NP comprise viral infections (e.g., herpes simplex, varicella zoster, and human immunodeficiency virus), metabolic disorders with mitochondrial dysfunctions (e.g., diabetes), stroke, mechanical injuries to the CNS or peripheral nerves [1, 2], and toxic effects, above all anti-neoplastic compounds (e.g., oxaliplatin, vincristine) [3]. Nociceptor activation is one of the most relevant NP peripheral mechanism, causing abnormal neuronal hyperexcitability, hyperalgesia, and allodynia [4,5,6]. The glutamate pathway mediates basic responses to nociceptive stimuli and contributes to the spinal dorsal horn hyperexcitability, manifesting with synaptic plasticity, and long-term potentiation [6,7,8]
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