The Clinical journal of pain
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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.
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Pharmacoeconomic analysis is increasingly being used to assist decision makers in getting the biggest "bang for the buck" within cost-constrained health care budgets. The tools and techniques of this science, however, have scarcely been applied to neuropathic pain. ⋯ Pharmacoeconomic analysis of neuropathic pain treatments can play an influential role in formulary committee deliberations, treatment algorithms, and decision making in the clinical setting. By describing the fundamental concepts and key challenges in this field, it is hoped that this article will represent a useful first step toward a pharmacoeconomic model of neuropathic pain.
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Randomized Controlled Trial Clinical Trial
Postdelivery of alfentanil and ketamine has no effect on intradermal capsaicin-induced pain and hyperalgesia.
The predelivery of intravenous alfentanil (a mu opioid agonist) and ketamine (an -methyl d-aspartate antagonist) has recently been shown to decrease the secondary hyperalgesia induced by intradermal capsaicin. The focus of this study was to determine the effects of the postdelivery of intravenous alfentanil and ketamine on intradermal capsaicin-induced secondary hyperalgesia. ⋯ Consistent with animal studies on preemptive analgesia, this study demonstrates that alfentanil and ketamine have a differential effect when delivered before and after a painful stimulus. Because of the differential effect seen, future studies on the pharmacology of human experimental pain should evaluate both predrug and postdrug delivery.
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This article reviews the prevalence, risk factors, natural history, and impact on quality of life of painful diabetic neuropathy (PDN) and postherpetic neuralgia (PHN). ⋯ Both conditions are common complications of their underlying disorders and can profoundly diminish the quality of life of affected persons.
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Botulinum toxin has dramatically improved the treatment of a variety of neurologic disorders. Two botulinum toxin preparations are commercially available in the United States: type A (Botox) and type B (Myobloc). ⋯ This mechanism enables botulinum toxin to alleviate symptoms of focal dystonias (which are characterized by excessive muscle contraction), and it may also, along with other theoretical mechanisms, be responsible for pain relief. Studies conducted in patients with cervical dystonia have shown that botulinum toxin effectively reduces pain associated with this disorder, suggesting that this agent may be effective in alleviating other painful syndromes.