The Clinical journal of pain
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Understanding the pathophysiology of a pain syndrome is helpful in selecting appropriate treatment strategies. Nociceptive pain is related to damage to tissues due to thermal, chemical, mechanical, or other types of irritants. Neuropathic pain results from injury to the peripheral or central nervous system. ⋯ A clear benefit of botulinum toxin therapy for treatment of neuropathic pain disorders is that it often relieves pain symptoms. Although the precise mechanism of pain relief is not completely understood, the injection of botulinum toxin may reduce various substances that sensitize nociceptors. As a result, botulinum toxin types A and B are now being actively studied in nociceptive and neuropathic pain disorders to better define their roles as analgesics.
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Botulinum toxin is approved for the treatment of muscle overactivity associated with several disorders, such as dystonias. However, control of muscle spasm often results in pain relief as well. Effective relief of pain associated with myofascial pain syndrome provides a model for the use of botulinum toxin to relieve pain associated with other types of soft-tissue syndromes, such as fibromyalgia. ⋯ Several studies have demonstrated the efficacy of botulinum toxin types A and B in treating several neuropathic pain disorders. Proper patient selection, injection technique, and dosing are critical to obtaining the best outcomes in managing pain with botulinum toxin. Additional study is needed to better characterize its use for the treatment of pain.
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Botulinum toxin has been shown to effectively treat several types of pain associated with neurologic disorders. It has recently been evaluated for the treatment of various types of headaches. In studies of migraine headache, chronic daily headache (more than 15 days of headache per month), tension-type headache, and post-whiplash headache, patients have reported decreased pain after treatment with botulinum toxin type A. ⋯ It may also provide peripheral and central neurogenic effects and reduce inflammation. Large, rigorously controlled trials of botulinum toxin are needed to better characterize its effects on various types of headaches and its role as a therapeutic agent. Current data suggest that botulinum toxin is safe and does not produce systemic effects associated with other types of headache treatments.
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This article reviews the current status of dermatological uses for botulinum toxin type A (Botox), recently approved in the United States for treatment of glabellar wrinkles, and type B (Myobloc), approved for cervical dystonia. The respective formulations of Botox and Myobloc are described, and injection techniques and special considerations for administration in the treatment of dermatologic conditions are also discussed. ⋯ Although direct comparisons between botulinum toxins for dermatologic applications are complicated by the lack of functional equivalence of the standard potency assays, appropriate dosing strategies for obtaining satisfactory clinical results using type B are being established, which will add to the experience already gained with type A. The diffusion characteristics of type B appear to show different and potentially advantageous clinical profiles in the treatment of crows' feet and hyperhidrosis compared with type A.
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The therapeutic effects of botulinum toxin are principally, if not exclusively, derived from an alteration in the release of acetylcholine (ACh) at pre-synaptic neurons. The rationale for how these effects could be beneficial in conditions characterized by excessive muscle contraction is clear, but the hypotheses regarding botulinum toxin-induced effects on pain are highly speculative. We explore five possible mechanisms by which botulinum toxin could directly or indirectly alter pain, including: 1) changes in the sensitivity and response patterns of group III and IV muscle nociceptors, 2) diminished activity in the gamma-motor neurons and consequent changes in muscle spindle afferents, 3) alterations in cholinergic control of vascular and autonomic functions, including neurogenic inflammation, 4) induced neuroplastic changes in the processing of afferent somatosensory activity at multiple levels of the neuroaxis, and 5) direct non-cholinergic effects on pain afferents.