The journal of pain : official journal of the American Pain Society
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Mild knee pain is a common symptom in later life. Despite this fact, there are few data on the impact of it worsening or how individuals alter their appraisals and behavior when it becomes severe. We sought to describe the changes that accompany a substantial deterioration in characteristic knee pain. A nested case-control analysis of existing cohort data identified 57 adults aged over 50 years experiencing progression from mild to severe characteristic pain intensity 18 months later and compared them, before and after this transition, with 228 controls whose knee pain did not progress. Worsening knee pain was accompanied by a marked increase in pain frequency and extent, functional limitation, depressive symptoms, catastrophising, praying and hoping, and use of oral and topical analgesia. Most individuals consulted a general practitioner either during or after this episode. Although relatively rare, substantial deterioration in knee pain has a major impact on those affected. Timely presentation to primary care, addressing potentially unhelpful appraisals and coping strategies, reinforcing core nonpharmacological management, and future research to identify triggering events for substantial deterioration and loss of adequate pain control should be part of an agenda to improve care for this important minority of older adults with knee pain. ⋯ This article describes what happens when the common symptom of mild knee pain in later life becomes significantly worse. The results may help clinicians understand the health impact, changes in patient appraisal and coping, and treatments that typically accompany this change in symptoms.
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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
Effects of intramuscular anesthesia on the expression of primary and referred pain induced by intramuscular injection of hypertonic saline.
Intramuscular injection of hypertonic saline produces pain in the belly of the injected muscle (primary pain) and, often, pain that projects distally (referred pain). While it is known that referred pain can be induced during complete sensory block of the distal site, there is little evidence as to whether the perception of referred pain depends on ongoing input from the primary stimulus. We assessed whether blocking the noxious input following the induction of pain blocks the primary but not the referred pain. A cannula was inserted into the tibialis anterior muscle in 15 subjects (8 male, 7 female). In a quasi-random crossover design conducted over 2 experimental sessions, each subject received a bolus intramuscular injection of .5 mL of 5% hypertonic saline, followed 90 seconds later by either: A) A second bolus injection or; B) An injection of 2 mL lignocaine through the same cannula. Protocol A was followed 60 seconds later by either a sham injection or an injection of lignocaine, while protocol B was followed 60 seconds later by either a sham injection or an injection of hypertonic saline. Subjects mapped the areas of primary and referred pain, and rated the intensities at these sites every 30 seconds until the cessation of pain. In all subjects, the area and intensity of primary pain rapidly disappeared within 7.5 minutes of intramuscular lignocaine injection (P < .02 relative to the nonanesthesia condition). With the exception of 2 subjects, in whom the referred pain continued in the absence of primary pain, the referred pain declined in parallel with local pain: the mean total pain intensity declined by 74% in both regions. We conclude that the maintenance of referred muscle pain usually depends on ongoing noxious inputs from the site of primary muscle pain. ⋯ Referred pain is a significant clinical problem, and commonly occurs with pain originating in muscle but not from skin. It is important to know the primary source of the pain so that treatment can be directed to this site rather to the site of referral.
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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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Bodily representations of the primary somatosensory (SI) cortex are constantly modified according to sensory input. Increased input due to training as well as loss of input due to deafferentation are reflected as changes in the extent of cortical representations. Recent studies in complex regional pain syndrome (CRPS) patients have indicated that the chronic pain itself is associated with cortical reorganization. However, it is unclear whether the observed reorganization is specific for CRPS or if it can be detected also in other types of chronic pain. We therefore searched for signs of cortical reorganization in a group of 8 patients who suffered from chronic pain associated with herpes simplex virus infections. The pain was widespread but restricted to unilateral side of the body and included the upper limb. We recorded neuromagnetic responses to tactile stimulation of fingers of both hands in patients and in a group of healthy, matched control subjects. In the patients, the distance between the thumb (D1) and little finger (D5) representations in SI cortex was statistically significantly smaller in the hemisphere contralateral to painful side than in the hemisphere contralateral to healthy side. In the control subjects, the D1-D5 distance was the same in both hemispheres. ⋯ The present results indicate that cortical reorganization occurs in chronic neuropathic pain patients even without peripheral nerve damage. It is possible that cortical reorganization is related to chronic pain, regardless of its etiology. Causality between reorganization and chronic pain should be examined further to develop therapeutic approaches for chronic pain.