Pain
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Randomized Controlled Trial Clinical Trial
Clinical precision of myofascial trigger point location in the trapezius muscle.
Myofascial trigger points (TrPs) have been clinically described as discrete areas of muscle tenderness presenting in taut bands of skeletal muscle. Using well-defined clinical criteria, prior investigations have demonstrated interrater reliability in the diagnosis of TrPs within a given muscle. No reports exist, however, with respect to the precision with which experienced clinicians can determine the anatomic locations of TrPs within a muscle. ⋯ The algometer responses associated with TrP estimates varied inversely with respect to the clinical group's reliability in identify the TrP locations. To summarize, for the trapezius muscle, this study demonstrates that two trained examiners can reliably localize latent TrPs with a precision that essentially approaches the physical dimensions of the clinician's own fingertips. Finally, it should be recognized that the ability to precisely document TrP location appears critical to the success of future studies that may be designed to investigate the etiology and pathogenesis of this commonly diagnosed clinical disorder.
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Based on bed-side neurological testing, it has recently been shown that 33% of chronic complex regional pain syndrome (CRPS) type I patients exhibit sensory impairments, which extend past the painful area of the affected limb in a hemisensory distribution (Pain, 80 (1999) 95). In the present study, the clinically observed changes in touch and temperature sensations on the side of the body ipsilateral to the affected limb were investigated quantitatively. Neurophysiological and psychological examinations were conducted to detect changes in the peripheral and central nervous system as well as psychopathological abnormalities. ⋯ For all methods applied, there was no statistically significant difference in the incidence of pathological results between patients with generalized and patients with spatially restricted sensory abnormalities. Psychological examination using the structured clinical interview on DSM-IV (SKID) demonstrated a high frequency of affective and anxiety disorders, however, without significant differences between both groups. We conclude that hemisensory impairment in patients with CRPS Type I is probably related to functional disturbances in processing of noxious events in the thalamus and may be a clinical correlate of subcortical brain plasticity in chronic pain.
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Previous studies in our laboratory have demonstrated that cannabinoids administered intravenously attenuate the duration of nocifensive behavior and block the development of hyperalgesia produced by intraplantar injection of capsaicin. In the present study, we extended these observations and determined whether cannabinoids attenuate capsaicin-evoked pain and hyperalgesia through spinal and peripheral mechanisms, and whether the antihyperalgesia was receptor mediated. Separate groups of rats were pretreated 7 min before capsaicin with an intrathecal injection of vehicle or the cannabinoid receptor agonist WIN 55,212-2 at doses of 0.1, 1.0 or 10 microg in 10 microl. ⋯ SR141716A (100 microg) co-injected with WIN 55,212-2 (30 microg) partially attenuated the effects of WIN 55,212-2 on hyperalgesia to heat. Intraplantar injection of the highest dose of WIN 55,212-2 did not interfere with the development of hyperalgesia following capsaicin injection into the contralateral paw. These data show that cannabinoids possess antihyperalgesic properties at doses that alone do not produce antinociception, and are capable of acting at both spinal and peripheral sites.
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Partial sciatic nerve injury causes neuropathic pain associated with behavioral changes such as spontaneous pain, hyperalgesia and allodynia. Both central and peripheral sensitization of pain pathways are likely to be involved in these alterations. Nerve injury induced plastic changes in the dorsal horn, where the second relay nociceptive neurons are located, may contribute to the central sensitization process. ⋯ Using immunocytochemistry, we found that 3 weeks following PSNL, the number of phosphorylated (p) CREB-IR cells was significantly increased in the injured side dorsal horn of rats, particularly in the superficial laminae. Interestingly, the majority of pCREB-IR cells expressed protein kinase Cgamma, an enzyme shown to be involved in the development of neuropathic pain in PSNL model. Taken together, these results suggest that increased CREB phosphorylation induced by PSNL may be one of the key molecular events leading to synaptic alterations and persistent pain in the PSNL model of neuropathic pain.
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Clinical Trial Controlled Clinical Trial
Osteoarthritis and its association with muscle hyperalgesia: an experimental controlled study.
Hypertonic saline effectively excites muscle nociceptors. Muscle hyperalgesia was assessed in osteoarthritis (OA) by intramuscular infusion of 0.5 ml hypertonic saline (6%) into the tibialis anterior muscle in humans. Patients (n=14) with OA in the lower extremities were compared with an equal number of age- and sex-matched healthy controls. ⋯ OA patients had increased pain intensity VAS after the infusion in the right leg compared with controls (P<0.05). Referred and radiating pain areas at 2 min post-infusion increased in OA patients and not in controls as compared with the local pain areas (P<0.05). It is concluded that muscle hyperalgesia and extended pain areas might be due to central sensitization caused by painful osteoarthritis.