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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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.
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Our aim was to describe the referred pain patterns and size of areas of trigger points (TrPs) in the masticatory and neck-shoulder muscles of women with myofascial temporomandibular disorders (TMD). Twenty-five women with myofascial TMD and 25 healthy matched women participated. Bilateral temporalis, deep masseter, superficial masseter, sternocleidomastoid, upper trapezius and suboccipital muscles were examined for TrPs by an assessor blinded to the subjects' condition. TrPs were identified with manual palpation and categorized into active and latent according to proposed criteria. The referred pain areas were drawn on anatomical maps, digitalized, and measured. The occurrence of active (P < .001) and latent TrPs (P = .04) were different between groups. In all muscles, there were significantly more active and latent TrP in patients than controls (P < .001). Significant differences in referred pain areas between groups (P < .001) and muscles (P < .001) were found: the referred pain areas were larger in patients (P < .001), and the referred pain area elicited by suboccipital TrPs was greater than the referred pain from other TrPs (P < .001). Referred pain areas from neck TrPs were greater than the pain areas from masticatory muscle TrPs (P < .01). Referred pain areas of masticatory TrPs were not different (P > .703). The local and referred pain elicited from active TrPs in the masticatory and neck-shoulder muscles shared similar pain pattern as spontaneous TMD, which supports the concept of peripheral and central sensitization mechanisms in myofascial TMD. ⋯ The current study showed the existence of multiple active muscle TrPs in the masticatory and neck-shoulder muscles in women with myofascial TMD pain. The local and referred pain elicited from active TrPs reproduced pain complaints in these patients. Further, referred pain areas were larger in TMD pain patients than in healthy controls. The results are also in accordance with the notion of peripheral and central sensitization mechanisms in patients with myofascial TMD.