The Clinical journal of pain
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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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Randomized Controlled Trial Clinical Trial
Effects of a controlled exercise trial on pain in nursing home residents.
To report preliminary data relevant to the effects of an exercise and toileting intervention on pain among incontinent nursing home (NH) residents. ⋯ No significant changes in pain reports were attributable to exercise despite significant improvements in physical performance. In fact, there was a tendency for pain reports to increase with exercise. These preliminary findings suggest that exercise alone may be ineffective for pain management among incontinent NH residents. Care providers should consider that exercise to improve physical function may increase pain symptoms, requiring preemptive analgesia, other pain control strategies, or modified exercise techniques for this frail segment of the NH population.
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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.
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The seven botulinum neurotoxin serotypes share less than 50% sequence homology and are immunologically distinct. The neurotoxins inhibit release of the neurotransmitter acetylcholine from the axon terminals of motor neurons, preganglionic sympathetic and parasympathetic neurons, and postganglionic parasympathetic nerves by a multi-step mechanism that differs slightly, but significantly, for each serotype. ⋯ The resulting muscle paralysis has provided the basis for therapeutic use of botulinum toxin types A and B in a variety of focal dystonias. The safety of the botulinum toxins, when administered focally, has permitted their widespread use in a number of other painful conditions.
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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.