Pain
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Osteoarthritis (OA) is a debilitating and painful disease, the incidence of which increases with advancing age. One of the confounding aspects of OA is that there is a disconnect between the severity of joint degeneration and the intensity of pain reported. This study examined the relationship between age, joint nociception, and joint pathology in an animal model of naturally occurring OA. ⋯ Micro-CT and histopathological determination of OA positively correlated with age; however, there was no significant correlation between the severity of joint degeneration and nociception. In the Dunkin Hartley model of inveterate OA, the level of joint pathology correlates well with increasing age. This study also provides the first objective evidence that there is no correlation between joint nociception and articular damage, thereby corroborating the clinical observation that pain is a poor predictor of OA severity.
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The current study examined the Photograph Series of Daily Activities (PHODA) Scale in a sample of chronic low back pain patients with high and low levels of kinesiophobia (pain-related fear). Thirty-three participants completed a modified version of the PHODA (PHODA-M) that obtained ratings of both anticipated pain and harm. Participants' responses on the PHODA-M were compared to predicted and experienced pain and harm ratings collected during a graded-difficulty reaching task. ⋯ In comparison to low fear participants, high fear participants showed larger correlations between pain expectancies for movements depicted in the PHODA and their ratings of predicted and experienced pain on each movement comprising the reaching task. Additionally, high fear participants showed larger associations between the perceived harmfulness of PHODA activities and predicted and experienced harm ratings in response to the reaching task. Implications for the findings are discussed.
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Direct application of cannabinoids to the medullary dorsal horn (MDH) inhibits lamina V nociceptive neurons. The present study compared the effect of the cannabinoid receptor agonist, WIN 55,212-2 (WIN-2) on the activity of lamina I and lamina V MDH neurons using extracellular single unit recording in anesthetized rats. Activity evoked by a contact thermode was measured before and after local application of WIN-2 (0.5-2.0 microg/microl) to the brainstem. ⋯ In separate experiments, the effect of intrathecal administration of WIN-2 to the MDH on head withdrawal latencies elicited by fast and slow heat ramps applied to the whisker pad was assessed in lightly anesthetized rats. Head withdrawal latencies elicited by slow but not by fast heat stimulation were increased by WIN-2. Taken together, these results emphasize the importance of lamina I neurons in the control of a nociceptive heat-evoked reflex.
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Ionotropic gamma-aminobutyric acid (GABA(A)) receptors control the relay of nociceptive signals at several levels of the neuraxis. Experiments with systemically applied benzodiazepines, which enhance the action of GABA at these receptors, have suggested both anti- and pronociceptive effects. The interpretation of such experiments has been notoriously difficult because of confounding sedation. ⋯ The relative contributions of these subunits were alpha2 approximately alpha3>alpha5, and thus very similar to those found for intrathecal diazepam (0.09 mg/kg). Accordingly, SL-651498 (10mg/kg, p.o.), an "anxioselective" benzodiazepine site agonist with preferential activity at alpha2/alpha3 subunits, significantly reduced formalin-induced flinching in wild-type mice. We conclude that systemic diazepam exerts a genuine antihyperalgesic effect, which depends on spinal GABA(A) receptors containing alpha2 and/or alpha3 subunits.