The journal of pain : official journal of the American Pain Society
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Low back pain (LBP) patients show reorganized trunk muscle activity but if similar changes are manifest in recurrent LBP (R-LBP) patients during asymptomatic periods remains unknown. In 26 healthy and 27 currently asymptomatic R-LBP participants electromyographic activity (EMG) was recorded from trunk and gluteal muscles during series of stepping up and down on a step bench before and during experimentally intramuscular induced unilateral and bilateral LBP. Pain intensity was assessed using numeric rating scale (NRS) scores. ⋯ In both groups, bilateral compared with unilateral experimental NRS scores were higher (P < .001) and patients compared with controls reported higher NRS scores during both pain conditions (P < .04). In patients, unilateral pain decreased ΔRMS-EMG in the Iliocostalis muscle and bilateral pain decreased ΔRMS-EMG in all back and gluteal muscles during step tasks (P < .05) compared with controls. In controls, bilateral versus unilateral experimental pain induced increased step task duration and trunk RMS-EMG whereas both pain conditions decreased step task duration and trunk RMS-EMG in R-LBP patients compared with controls (P < .05).
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Ketamine has been widely used as an analgesic and produces dissociative anesthetic effects. The antinociceptive effects of ketamine have been studied, but the involvement of endocannabinoids in these effects has not yet been investigated. In this study, we evaluated the involvement of the endocannabinoid system in the peripheral antinociceptive effects induced by ketamine. ⋯ Additionally, the administration of the endocannabinoid metabolizing enzyme inhibitor (.5 µg per paw) or an AEA reuptake inhibitor, (5Z,8Z,11Z,14Z)N(4Hydroxy2methylphenyl)5,8,11,14 eicosatetraenamide (2.5 µg per paw) significantly enhanced low-dose ketamine-induced peripheral antinociception. AEA paw levels were increased only after ketamine administration to prostaglandin E2-injected paws. These data suggest that ketamine, in the presence of a nociceptive stimulus, induces a selective release of AEA levels and subsequent CB1 cannabinoid activation at the peripheral level.