The journal of pain : official journal of the American Pain Society
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Pain is often undetected in older people with dementia partly due to a deterioration of cognitive functioning. Observational scales enable the measurement of pain by registering physiological changes, facial expressions, or behaviors. Previous research showed that the Pain Assessment Checklist for Seniors with Limited Ability to Communicate (PACSLAC) is especially useful to measure pain in older people with dementia. PACSLAC was recently translated into Dutch and refined, thus forming PACSLAC-D. The current study uses a different approach to refining PACSLAC by (1) selecting items on the basis of ratings of nursing personnel and (2) applying confirmatory robust maximum likelihood factor analysis and (3) item response theory to investigate the psychometric properties of the selected items. Of the items that nursing personnel frequently registered, 18 valid and reliable items remained. Fourteen of these 18 items were also selected for PACSLAC-D, which confirms that these items are valid and reliable indicators of pain in older people with dementia. Confirmatory factor analysis showed that a 3-factor model is most adequate to describe the data. Differential item functioning analyses indicated that 2 items were biased. Ultimately, a refined version of PACSLAC was created that nursing personnel with different educational backgrounds might use to assess pain in older people with varying degrees of dementia. ⋯ This article describes the selection of items of PACSLAC on the basis of ratings of nursing personnel. By comparing this item selection with the items selected for PACSLAC-D, one can confirm that certain items are sound indicators of pain, whereas others need some attention (eg, through the training of raters).
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A single gene deletion causes lack of leptin and obesity in B6.V-Lep(ob) (obese; ob) mice compared with wild-type C57BL/6J (B6) mice. This study compared the phenotype of nociception and supraspinal antinociception in obese and B6 mice by testing 2 hypotheses: (1) microinjection of cholinomimetics or an adenosine receptor agonist, but not morphine, into the pontine reticular formation (PRF) is antinociceptive in B6 but not obese mice, and (2) leptin replacement in obese mice attenuates differences in nociceptive responses between obese and B6 mice. Adult male mice (n = 22) were implanted with microinjection guide tubes aimed for the PRF. The PRF was injected with neostigmine, carbachol, nicotine, N(6)-p-sulfophenyladenosine (SPA), morphine, or saline (control), and latency to paw withdrawal (PWL) from a thermal stimulus was recorded. B6 and ob mice did not differ in PWL after saline microinjection into the PRF. Neostigmine, carbachol, and SPA caused PWL to increase significantly in B6 but not obese mice. An additional 15 obese mice were implanted with osmotic pumps that delivered leptin for 7 days. Leptin replacement in obese mice restored the analgesic effect of PRF neostigmine to the level displayed by B6 mice. The results show for the first time that leptin significantly alters supraspinal cholinergic antinociception. ⋯ This study specifies a brain region (the pontine reticular formation), cholinergic neurotransmission, and a protein (leptin) modulating thermal nociception. The results are relevant for efforts to understand the association between obesity, disordered sleep, and hyperalgesia.
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Randomized Controlled Trial Multicenter Study
Lacosamide in painful diabetic neuropathy: an 18-week double-blind placebo-controlled trial.
The efficacy and tolerability of oral lacosamide (200, 400, and 600 mg/day) was evaluated in patients with painful diabetic neuropathy in a double-blind, randomized, placebo-controlled trial. The primary target dose to be confirmed was lacosamide 400 mg/day. Efficacy was assessed by changes in pain scale scores from baseline, with changes over the last 4 weeks of the 12-week maintenance period regarded as the primary endpoint. Endpoint reductions in mean pain score were higher with all doses of lacosamide, reaching the level of significance with 400 mg/day (P = .05). Over the treatment period (titration + maintenance), pain relief was significantly higher than placebo with lacosamide 400 (P = .02) and 600 mg/day (P = .03). Lacosamide had an early-onset effect with significant reductions over placebo during the titration period. Nonparametric and mixed-model analysis approaches gave similar results, supporting significant efficacy at 400 mg/day. Secondary criteria such as Patient's Global Impression of Change, responder rates, and pain-free days provided additional support. Adverse events included dizziness, nausea, and headache. Incidence of cognitive and behavioral adverse events was low. This trial suggests that lacosamide has beneficial effects and may be a suitable treatment option for patients with diabetic neuropathic pain. ⋯ This study presents efficacy and safety results of a phase 3, double-blind, placebo-controlled trial of the anticonvulsant drug lacosamide in patients with painful diabetic neuropathy. Lacosamide treatment at a dose of 400 mg/day reduced diabetic neuropathic pain with a favorable safety and tolerability profile that may be suitable for patients with diabetes.
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Fibromyalgia (FM) is a chronic pain condition marked by centrally mediated augmentation of pain and sensory processes. Skepticism has marked the history of this condition, but more recent study has identified neurobiological underpinnings supporting many of the symptoms associated with this condition. Early research in FM had unprecedented latitude within the rheumatology community to borrow heavily from theory and methods being applied in chronic pain research more generally. These insights facilitated rapid advances in FM research, not the least of which was the abandonment of a peripheral focus in favor of studying central mechanisms associated with central augmentation. Currently, rapid-paced discovery is taking place in FM genetics, patient assessment, new therapeutic targets, and novel methods of treatment delivery. Such insights are not likely to be limited in application just to FM and could have relevance to the broader field of pain research as well. ⋯ This manuscript reviews the history of FM and its diagnosis, evidence supporting central augmentation of pain in FM, potential mechanisms of central augmentation, current approaches to integrated care of FM, and areas of active collaboration between FM research and other chronic pain conditions.
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Cross-sectional studies have suggested a relationship between respiratory disorders, incontinence, gastrointestinal symptoms, and back pain. However, longitudinal data are lacking. This study aimed to evaluate whether these disorders increase risk for the development of back pain. A total of 2943 younger, 2298 mid-age, and 2258 older women from the Australian Longitudinal Study on Women's Health who reported no back pain during the preceding 12 months were followed for 4, 2, and 3 years, respectively. Crude and adjusted associations between the development of back pain and changes in the presence of incontinence, breathing difficulty, and gastrointestinal symptoms were assessed with logistic regression. Women with preexisting incontinence (prevalence ratios [PR]: 1.26 to 1.46) and gastrointestinal symptoms (PR: 1.24 to 1.44) and women who developed breathing problems (PR: 1.63 to 2.11) were more likely to develop back pain than women without such problems. Menstrual pain and allergy were also associated with back pain development. Consistent with predictions from physiological data, this study provides novel evidence that the presence and/or development of incontinence, respiratory problems, and gastrointestinal symptoms are associated with the development of back pain. This highlights the importance of comorbidities and suggests opportunities for future preventative interventions. ⋯ This study demonstrates that women with incontinence, respiratory disorders, and gastrointestinal symptoms have increased risk for the development of back pain. Evidence of compromised control of the spine in people with incontinence and respiratory disorders and the potential for viscerosomatic hyperalgesia in people with gastrointestinal symptoms may provide physiological explanations for these findings.