Pain
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Comparative Study
Inflammation-induced decrease in voluntary wheel running in mice: a nonreflexive test for evaluating inflammatory pain and analgesia.
Inflammatory pain impacts adversely on the quality of life of patients, often resulting in motor disabilities. Therefore, we studied the effect of peripheral inflammation induced by intraplantar administration of complete Freund's adjuvant (CFA) in mice on a particular form of voluntary locomotion, wheel running, as an index of mobility impairment produced by pain. The distance traveled over 1 hour of free access to activity wheels decreased significantly in response to hind paw inflammation, peaking 24 hours after CFA administration. ⋯ The CFA-induced decrease in voluntary wheel running was dose-dependently reversed by subcutaneous administration of antiinflammatory and analgesic drugs, including naproxen (10-80 mg/kg), ibuprofen (2.5-20mg/kg), diclofenac (1.25-10mg/kg), celecoxib (2.5-20mg/kg), prednisolone (0.62-5mg/kg), and morphine (0.06-0.5mg/kg), all at much lower doses than reported in most rodent models. Furthermore, the doses that induced recovery in voluntary wheel running did not reduce CFA-induced mechanical allodynia, indicating a greater sensitivity of the former as a surrogate measure of inflammatory pain. We conclude that monitoring changes in voluntary wheel running in mice during peripheral inflammation is a simple, observer-independent objective measure of functional changes produced by inflammation, likely more aligned to the global level of pain than reflexive measures, and much more sensitive to analgesic drug effects.
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Comparative Study
Is treatment of postherpetic neuralgia in the community consistent with evidence-based recommendations?
Few studies have examined the extent to which treatment of patients with neuropathic pain in the community is consistent with evidence-based treatment recommendations. U. S. health care claims were used to identify patients who received a diagnosis of postherpetic neuralgia (PHN). ⋯ There was a wide range of initial treatment durations, but the means and medians suggest that patients and clinicians often decide to change the initial treatment within 2 months, either by discontinuing it, replacing it with a new medication, or adding a new medication. Although there were generally shorter treatment durations with opioid analgesics and tramadol, these medications were more frequently used in beginning treatment than the other treatments. The results suggest that a considerable number of patients with PHN in the community are not receiving evidence-based treatment.
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This report examines day-to-day variability in rheumatology patients' ratings of pain and related quality-of-life variables as well as predictors of that variability. Data from 2 studies were used. The hypothesis was that greater psychological distress (i.e., depression and anxiety) and poorer coping appraisals (i.e., higher pain catastrophizing and lower self-efficacy) are associated with more variability. ⋯ Anxiety was not significantly associated with day-to-day variability. The results of these studies suggest that individual differences in the magnitude of symptom fluctuation may play a vital role in understanding patients' adjustment to pain. Future research will be needed to examine the clinical utility of measuring variability in patients' pain and well-being, and to understand whether reducing variability may be an important treatment target.
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Osteoarthritis (OA) is a chronic condition characterized by pain during joint movement. Additionally, patients with advanced disease experience pain at rest (ie, ongoing pain) that is generally resistant to nonsteroidal antiinflammatory drugs. Injection of monosodium iodoacetate (MIA) into the intraarticular space of the rodent knee is a well-established model of OA that elicits weight-bearing asymmetry and referred tactile and thermal hypersensitivity. ⋯ Additionally, systemic or intraarticular HC030031, a TRPA1 antagonist, failed to block high-dose MIA-induced weight asymmetry or ongoing pain. Our studies suggest that a high dose of intraarticular MIA induces ongoing pain originating from the site of injury that is dependent on afferent fiber activity but apparently independent of TRPV1 or TRPA1 activation. Identification of mechanisms driving ongoing pain may enable development of improved treatments for patients with severe OA pain and diminish the need for joint replacement surgery.