Pain
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Cannabinoid receptor agonists diminish responses to painful stimuli. Extensive evidence implicates the CB(1) receptor in the production of antinociception. However, the capacity of CB(2) receptors, which are located outside the central nervous system (CNS), to produce antinociception is not known. ⋯ AM1241 did not produce the CNS cannabinoid effects of hypothermia, catalepsy, inhibition of activity or impaired ambulation, while this tetrad of effects was produced by the mixed CB(1)/CB(2) receptor agonist WIN55,212-2. Peripheral antinociception without CNS effects is consistent with the peripheral distribution of CB(2) receptors. CB(2) receptor agonists may have promise clinically for the treatment of pain without CNS cannabinoid side effects.
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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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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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The Faces Pain Scale (FPS; Bieri et al., Pain 41 (1990) 139) is a self-report measure used to assess the intensity of children's pain. Three studies were carried out to revise the original scale and validate the adapted version. In the first phase, the FPS was revised from its original seven faces to six, while maintaining its desirable psychometric properties, in order to make it compatible in scoring with other self-rating and observational scales which use a common metric (0-5 or 0-10). ⋯ There were no significant differences between the means on the FPS-R and either of the analogue scales. The FPS-R is shown to be appropriate for use in assessment of the intensity of children's acute pain from age 4 or 5 onward. It has the advantage of being suitable for use with the most widely used metric for scoring (0-10), and conforms closely to a linear interval scale.