The journal of pain : official journal of the American Pain Society
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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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The present study examined the hyponociceptive effect of swimming exercise in a chemical behavioral model of nociception and the mechanisms involved in this effect. Male mice were submitted to swimming sessions (30 min/d for 5 days). Twenty-four hours after the last session, we noticed that swimming exercise decreased the number of abdominal constriction responses caused by acetic acid compared with the nonexercised group. The hyponociception caused by exercise in the acetic acid test was significantly attenuated by intraperitoneal (i.p.) pretreatment of mice with naloxone (a nonselective opioid receptor antagonist, 1 mg/kg), ρ-chlorophenylalanine methyl ester (PCPA, an inhibitor of serotonin synthesis, 100 mg/kg once a day for 4 consecutive days), and by bilateral adrenalectomy. Collectively, the present results provide experimental evidences indicating for the first time that high-intensity extended swimming exercise reduces pain-related behavior in mice. The mechanisms involve an interaction with opioid and serotonin systems. Furthermore, endogenous opioids released by adrenal glands probably are involved in this effect. ⋯ Our results indicate that high-intensity extended exercise endogenously controls acute pain by activation of opioidergic and serotonergic pathways. Furthermore, these results support the use of exercise as a nonpharmacological approach for the management of acute 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.
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The protein kinase mammalian target of rapamycin (mTOR) regulates mRNA translation and is inhibited by rapamycin. Signaling pathways involving mTOR are implicated in physiological and pathophysiological processes. We determined the spinal effects of the rapamycin analogue cell cycle inhibitor (CCI)-779 on neuronal responses and behavioral hypersensitivity in a model of persistent neuropathic pain. We also assessed the anatomical distribution of spinal mTOR signaling pathways. Specifically, we ligated rat spinal nerves L5 and L6 to produce a model of neuropathic pain. After confirming neuropathy with behavioral testing, we obtained in vivo single-unit extracellular stimulus-evoked recordings from deep dorsal horn spinal neurons. We applied CCI-779 spinally in electrophysiological and behavioral studies and assessed its effects accordingly. We also used immunohistochemistry to probe for mTOR signaling pathways in dorsal root ganglia (DRG) and the spinal cord. We found that spinally administered CCI-779 rapidly attenuated calibrated mechanically but not thermally evoked neuronal responses and mechanically evoked behavioral responses. Immunohistochemistry showed presence of mTOR signaling pathways in nociceptive-specific C-fiber DRG and in neurons of inner lamina II of the spinal cord. We conclude that alterations in the activity of spinal mTOR signaling pathways are crucial to the full establishment of spinal neuronal plasticity and behavioral hypersensitivity associated with nerve injury. ⋯ This study is consistent with growing evidence implicating mTOR signaling pathways as important modulators of persistent pain, providing novel insights into the molecular mechanisms of pain maintenance and potential for novel approaches into treating chronic pain.
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The central nucleus of the amygdala (CeA) is involved in processing and regulation of pain. We determined whether amygdaloid corticotropin-releasing factor (CRF) contributes to pain modulation in the neuropathic rat. Emotional aspect of pain was assessed by an aversive place-conditioning test and sensory aspect of pain by determining monofilament-induced limb-withdrawal threshold. CRF₆₋₃₃ (an inhibitor of CRF-binding protein) or CRF₉₋₄₁, a nonselective CRF receptor antagonist, was microinjected to the left or right CeA or a control site in rats with spared nerve injury (SNI) or sham operation of the left hind limb. In SNI animals, CRF₆₋₃₃ in the left or right CeA, but not in a control site, attenuated emotional painlike behavior and increased sensory pain. In sham controls, CRF₆₋₃₃ in the right but not left CeA increased sensory aspect of pain, without influence on place-avoidance behavior. The effects induced by CRF₆₋₃₃ were reversed by CRF₉₋₄₁. The results indicate that endogenous CRF in the CeA, through action on CRF receptors, may differentially influence emotional and sensory aspects of pain in neuropathy. While the right CeA had a dominant role in modulation of pain-related responses in sham controls, left as well as right CeA contributed to pain modulation in neuropathic animals. ⋯ An increase in free endogenous corticotropin-releasing factor in the central nucleus of the amygdala was accompanied by increased cutaneous hypersensitivity and decreased emotional painlike behavior in neuropathic animals. This finding indicates that CRF in the amygdala may have differential effects on sensory and emotional aspects of neuropathic pain.