The Clinical journal of pain
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The aims of this study were to (1) identify behaviors that occur in noncommunicative nursing home residents that are perceived by nurses to be indicators of pain, (2) determine factors affecting the differentiation of pain behaviors from similar behaviors due to other causes, and (3) assess nurses' perceptions of the prevalence and importance of specific indicators of pain as well as barriers to the detection of pain in this population. ⋯ The study of pain among the noncommunicative elderly and, in particular, the development of a tool that can be used to assess their pain may greatly improve the quality of life of the estimated 20% to 35% of nursing home residents who cannot adequately express their needs.
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The assumption that individuals are capable of accurately recalling past painful experiences has been a fundamental tenet of a number of cognitive-behavioral theories of pain, including the gate control theory. However, there has been very little research on the topic in the past, and the results have often been contradictory. A general conclusion that can be drawn is that memory for pain is variable, and there is need to identify what factors contribute to this variability in memory for pain. The current study examined the relation of catastrophizing to the recall of persistent pain associated with rheumatoid arthritis. ⋯ Participants who scored higher on catastrophizing demonstrated better accuracy in the recall of general pain intensity and pattern over a 30-day diary period. The results of the study are discussed in terms of future studies as well as their potential clinical importance.
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The efficacy of the anticonvulsant drug carbamazepine in the management of trigeminal neuralgia is evidenced in several controlled trials, and the numbers needed to treat to obtain one patient with at least 50% pain relief (NNT) is 1.7. Single small trials have shown that baclofen alone provides pain relief (NNT = 1.4) and that lamotrigine has an additional effect in patients with insufficient relief using carbamazepine or phenytoin (NNT = 2.1). Uncontrolled observations and clinical practice indicate that phenytoin, clonazepam, sodium valproate, gabapentin, and lidocaine will also relieve trigeminal neuralgia. ⋯ Acute exacerbation has successfully been treated with intravenous loading with phenytoin or lidocaine, but again these procedures have not been tested in controlled trials. In conclusion, carbamazepine is the mainstay of pharmacotherapy of trigeminal neuralgia, and secondary drug choices are baclofen, lamotrigine, oxcarbazepine, phenytoin, gabapentin, and sodium valproate. Controlled trials testing the effect of some of these drugs, new drugs, and drug combinations are needed.
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There are no satisfactory animal models of trigeminal neuralgia, and it is difficult to obtain essential data from patients. However, trigeminal neuralgia presents with such idiosyncratic signs and symptoms, and responds to so distinctive a set of therapeutic modalities, that scientific deduction can be used to generate likely hypotheses. The ignition hypothesis of trigeminal neuralgia is based on recent advances in the understanding of abnormal electrical behavior in injured sensory neurons, and new histopathologic observations of biopsy specimens from patients with trigeminal neuralgia who are undergoing microvascular decompression surgery. ⋯ The hyperexcitable afferents, in turn, give rise to pain paroxysms as a result of synchronized afterdischarge activity. The ignition hypothesis accounts for the major positive and negative signs and symptoms of trigeminal neuralgia, for its pathogenesis, and for the efficacy of treatment modalities. Proof, however, awaits the availability of key experimental data that can only be obtained from patients with trigeminal neuralgia.