Botulinum toxin (BoNT) is used to treat excessive muscle stiffness, spasticity, and dystonia. BoNT has been used for over four decades to treat different types of neuropathic pain. The treatment mechanism is based on the inhibition and the release of inflammatory mediators and peripheral neurotransmitters that originate from the sensory nerves (Park & Park, 2017). Generally, BoNT has been widely used to treat neuropathic pain, and it is effective in dealing with posttherpetic neuralgia, trigeminal neuralgia, and peripheral neuralgia.
Additionally, the toxin has been used to treat excessive muscle stiffness, spasticity, and dystonia. BoNT is easily absorbed in the neuromuscular junction and the parasympathetic axon. Again, the toxin is easily absorbed from the junction and axon to the motor neural terminal since it responds accordingly to the presence of acetylcholine (Park & Park, 2017). Administering BoNT locally has significant impacts on neuropathic pain. Therefore, the toxin is effective in facilitating muscle relaxation based on analgesic effects that are independent of muscle movements. The toxin acts through the dissociation of the duration that muscles take to relax and it minimizes the duration of pain relief.
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The BoNT’s structure contains a protein group consisting of anaerobic bacteria, Clostridium botulinum that exists in roughly 40 subtypes. The most commonly used drugs in pain management are BoNT-A, which has a molecular weight of 900,000, and its structure depicts a double-chain protein (Park & Park, 2017). Generally, the toxin can bind acceptors at the nerve end and facilitate the breakdown of a peptide bond. It then binds to ganglioside receptors to improve the structure of the cell membrane.
BoNT toxin is effective in reducing inflammation in the case of acute injury. Exposure to BoNT reduces the action of neurotransmitters that cause chronic inflammation and acute injury; hence, leading to anti-inflammatory effects on the body. BoNT also reduces local inflammation around nerve terminals. The toxin is effective in reducing edema without causing any significant localized muscle weakness. Further, BoNT can deactivate sodium channels by stimulating several cellular functions in patients experiencing severe pain (Park & Park, 2017). For instance, it stimulates transmission, secretion, contraction, and sensation to ensure a neuronal excitable membrane with distinct features other than those of anesthetics, tetrodotoxin, and antiepileptic drugs.
BoNT is used in managing pain in post-surgical neuralgia. The BoNT is efficacious in managing post-herpetic neuralgia and post-traumatic neuralgia. Specifically, the BoNT can reduce burning sensation, allodynic brush sensitivity, and improve QOL when used in pain management among post-surgical neuralgia (Park & Park, 2017). The toxin can as well be used to manage pain in cancer patients, especially those treated with radiotherapy and surgery. Also, the toxin in managing pain in patients with occipital neuralgia. It can lessen sharp/shooting pain and prevent inflammation when the patients experience dull/aching pain.
However, carpal tunnel syndrome is ineffective in managing carpal tunnel syndrome since it is insignificant in pain relief, especially in electrophysiological changes. It does not effectively relieve pain through electrophysiological changes. BoNT also causes irreversible adverse effects in patients suffering from severe pain. For instance, BoNT-A leads to muscle weakness, dysphagia, flu-like symptoms, and pain during swallowing (Park & Park, 2017). Therefore, the toxin cannot be used to manage other pain conditions, such as cerebral palsy, which is usually linked to a hematoma, lower limb weakness, pain, and bilateral ptosis. In this regard, the toxin causes minor complications like antibody formation and other immune-related problems when used to manage pain in neuropathic patients.
Reference
Park, J. & Park, H. J. (2017). Botulinum toxin for the treatment of neuropathic pain. Toxins , 9(9), 260. Multidisciplinary Digital Publishing Institute (MDPI). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5618193/
