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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Chronic low back pain is the second most common illness reported by patients in the United States and accounts for substantial morbidity and health-care resource utilization. Many back and spine stressors can contribute to tissue injury, resulting in acute or chronic pain. In response to injury, biochemical processes that cause inflammation and nerve sensitization increase pain levels and contribute to a cycle of reactivity that further heightens patients' sensitivity to pain stimuli. ⋯ Preliminary evaluations have shown that this treatment is safe and has the advantage of providing local relief directly to the site of injury or pain, without causing systemic side effects. Initial data from small trials also suggest that botulinum toxin is effective, alleviating back pain in selected patients. On the basis of these promising results, additional study in larger trials is warranted.
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The aim of this study was to examine childhood traumatic experiences and dissociative characteristics in women with chronic headache and low back pain. ⋯ There were no significant differences between the headache and low back pain groups in terms of prevalence of history of neglect; abuse; or sexual, physical, and emotional abuse separately. In addition, no significant differences were found between the groups with respect to the Dissociative Experiences Scale scores. However, analysis of the SDQ scores showed that the neglect rate in the two groups differed significantly. According to our findings, the neglect rate was higher in the headache group, thus warranting further research to investigate the sensitivity of the SDQ for neglect.
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Whiplash-associated disorders (WADs) occur as a result of trauma and are often due to motor vehicle accidents and sports injuries. Cervical injury is attributed to rapid extension followed by neck flexion. The exact pathophysiology of WAD is uncertain but probably involves some degree of aberrant muscle spasms and may produce a wide range of symptoms. ⋯ In addition, recent preliminary data from a small trial showed that type B toxin (Myobloc) produced almost immediate pain relief for most patients with post-whiplash headache. Although botulinum toxin has not been evaluated in large long-term trials, these initial data are promising and suggest a role for this agent in the treatment of WAD. Additional study is needed to identify the subset of patients with WAD who are most likely to respond to treatment with botulinum toxin.
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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.