The journal of pain : official journal of the American Pain Society
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Evaluating pain in verbal children in the hospital setting is done primarily through serial assessments of pain intensity using single-item measures. However, little remains known about intensity scales' relative responsiveness and uniqueness from negative affect in this clinical setting. In the present study, a total of 411 assessments using 3 common pediatric pain intensity measures (the Faces Pain Scale-Revised, a verbally presented numeric rating scale, and a visual analog scale) were obtained over a period of 3 days from 29 children ages 9 to 18 years following a relatively standardized surgical procedure. Hierarchical linear models were used to compare the 3 scales on responsiveness over postoperative recovery time, invariance across baseline variables (age, sex, and baseline mood), and distinctiveness from changes in negative affect. Results showed that all 3 pain-intensity measures were highly interrelated, varied similarly with age and baseline state anxiety, and were comparably related to contemporaneous changes in affect. However, patients tended to rate pain intensity higher on the Numerical Rating Scale, and only this scale failed to reflect a decreasing trend in pain scores with elapsed surgical recovery time. Potential implications for clinical practice are discussed. ⋯ This article presents data comparing the responsiveness over time and association with negative affect of 3 single-item pediatric pain-intensity scales commonly used in hospital settings. The results can help inform the selection of self-report measures when serially evaluating pain and treatment response in hospitalized children.
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Research has largely ignored the systematic examination of physicians' attitudes towards providing care for patients with chronic noncancer pain. The objective of this study was to identify barriers and facilitators to opioid treatment of chronic noncancer pain patients by office-based medical providers. We used a qualitative study design using individual and group interviews. Participants were 23 office-based physicians in New England. Interviews were audiotaped, transcribed, and systematically coded by a multidisciplinary team using the constant comparative method. Physician barriers included absence of objective or physiological measures of pain; lack of expertise in the treatment of chronic pain and coexisting disorders, including addiction; lack of interest in pain management; patients' aberrant behaviors; and physicians' attitudes toward prescribing opioid analgesics. Physician facilitators included promoting continuity of patient care and the use of opioid agreements. Physicians' perceptions of patient-related barriers included lack of physician responsiveness to patients' pain reports, negative attitudes toward opioid analgesics, concerns about cost, and patients' low motivation for pain treatment. Perceived logistical barriers included lack of appropriate pain management and addiction referral options, limited information regarding diagnostic workup, limited insurance coverage for pain management services, limited ancillary support for physicians, and insufficient time. Addressing these barriers to pain treatment will be crucial to improving pain management service delivery. ⋯ This article demonstrates that perceived barriers to treating patients with chronic noncancer pain are common among office-based physicians. Addressing these barriers in physician training and in existing office-based programs might benefit both noncancer chronic pain patients and their medical providers.
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Because fibromyalgia (FM) patients frequently report activity-dependent deep tissue pains, impulse input from painful body regions may be relevant for their musculoskeletal complaints. In addition, peripheral impulse input may induce and maintain thermal and mechanical hyperalgesia of FM patients. If so, activity and rest may alternately enhance and diminish intensity of FM pain. However, the effects of exercise on pain are ambiguous in studies of FM. Whereas exercise-only studies demonstrated increased pain and hyperalgesia during and after physical activity, some exercise studies that included rest periods resulted in decreased FM pain and increased function. To further clarify these effects, we examined the effects of alternating exercise with rest on clinical pain and thermal/mechanical hyperalgesia of 34 FM patients and 36 age-matched healthy controls (NC). Using an ergometer, all subjects performed arm exercise to exhaustion twice alternating with 15-minute rest periods. Although strenuous muscle activity was reported as painful by most FM subjects, overall clinical pain consistently decreased during the rest periods. Additionally, FM subjects' pain sensitivity to mechanical pressure decreased after each exercise and rest session. ⋯ FM is a pain-amplification syndrome that depends at least in part on peripheral tissue impulse input. Whereas muscle activity increased overall pain, short rest periods produced analgesic effects.
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The endocannabinoids anandamide and 2-arachidonoylglycerol are predominantly regulated by the respective catabolic enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL). Inhibition of these enzymes elevates endocannabinoid levels and attenuates neuropathic pain. In the present study, CB₁ and CB₂ receptor-deficient mice were subjected to chronic constriction injury (CCI) of the sciatic nerve to examine the relative contribution of each receptor for the anti-allodynic effects of the FAAH inhibitor, PF-3845, and the MAGL inhibitor, JZL184. CCI caused marked hypersensitivity to mechanical and cold stimuli, which was not altered by deletion of either the CB₁ or CB₂ receptor, but was attenuated by gabapentin, as well as by each enzyme inhibitor. Whereas PF-3845 lacked anti-allodynic efficacy in both knockout lines, JZL184 did not produce anti-allodynic effects in CB₁ (-/-) mice, but retained its anti-allodynic effects in CB₂ (-/-) mice. These data indicate that FAAH and MAGL inhibitors reduce nerve injury-related hyperalgesic states through distinct cannabinoid receptor mechanisms of action. In conclusion, although endogenous cannabinoids do not appear to play a tonic role in long-term expression of neuropathic pain states, both FAAH and MAGL represent potential therapeutic targets for the development of pharmacological agents to treat chronic pain resulting from nerve injury. ⋯ This article presents data addressing the cannabinoid receptor mechanisms underlying the anti-allodynic actions of endocannabinoid catabolic enzyme inhibitors in the mouse sciatic nerve ligation model. Fatty acid amide hydrolase and monoacylglycerol lipase inhibitors reduced allodynia through distinct cannabinoid receptor mechanisms. These enzymes offer potential targets to treat neuropathic pain.
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The aim of the study is to test if sustained nociceptive mechanical stimulation (SNMS) of latent myofascial trigger points (MTrPs) induces widespread mechanical hyperalgesia. SNMS was obtained by inserting and retaining an intramuscular electromyographic (EMG) needle within a latent MTrP or a nonMTrP in the finger extensor muscle for 8 minutes in 12 healthy subjects. Pain intensity (VAS) and referred pain area induced by SNMS were recorded. Pressure pain threshold (PPT) was measured immediately before and after, and 10-, 20-, and 30-minutes after SNMS at the midpoint of the contralateral tibialis anterior muscle. Surface and intramuscular EMG during SNMS were recorded. When compared to nonMTrPs, maximal VAS and the area under VAS curve (VASauc) were significantly higher and larger during SNMS of latent MTrPs (both, P < .05); there was a significant decrease in PPT 10 minutes, 20 minutes, and 30 minutes postSNMS of latent MTrPs (all, P < .05). Muscle cramps following SNMS of latent MTrPs were positively associated with VASauc (r = .72, P = .009) and referred pain area (r = .60, P = .03). Painful stimulation of latent MTrPs can initiate widespread central sensitization. Muscle cramps contribute to the induction of local and referred pain. ⋯ This study shows that MTrPs are one of the important peripheral pain generators and initiators for central sensitization. Therapeutic methods for decreasing the sensitivity and motor-unit excitability of MTrPs may prevent the development of muscle cramps and thus decrease local and referred pain.