Pain
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Multicenter Study Clinical Trial
Possible selves in chronic pain: self-pain enmeshment, adjustment and acceptance.
The aim of this study was to test whether enmeshment of self and pain predicted adjustment (depression and acceptance) in a chronic pain population. 89 chronic pain patients completed standardized self-report measures of depression and acceptance and generated characteristics describing their current actual self, hoped-for self and feared-for self, and made judgments about the degree to which their future possible selves (hoped-for and feared-for) were dependent on the absence or presence of pain, i.e. enmeshed with pain. Hierarchical multiple regression analyses showed that after accounting for the influence of demographics (age, gender), pain characteristics and the degree of role interference attributable to pain, the proportion of hoped-for self characteristics that could be achieved even with the presence of pain predicted the magnitude of depression and acceptance scores. The findings are discussed with reference to the enmeshment hypothesis and theories of self-discrepancy, self-regulation and hopelessness.
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Activated glial cells (microglia and astroglia) in the spinal cord play a major role in mediating enhanced pain states by releasing proinflammatory cytokines and other substances thought to facilitate pain transmission. In the present study, we report that intrathecal administration of minocycline, a selective inhibitor of microglial cell activation, inhibits low threshold mechanical allodynia, as measured by the von Frey test, in two models of pain facilitation. In a rat model of neuropathic pain induced by sciatic nerve inflammation (sciatic inflammatory neuropathy, SIN), minocycline delayed the induction of allodynia in both acute and persistent paradigms. ⋯ In a model of spinal immune activation by intrathecal HIV-1 gp120, we show that the anti-allodynic effects of minocycline are associated with decreased microglial activation, attenuated mRNA expression of interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), IL-1beta-converting enzyme, TNF-alpha-converting enzyme, IL-1 receptor antagonist and IL-10 in lumbar dorsal spinal cord, and reduced IL-1beta and TNF-alpha levels in the CSF. In contrast, no significant effects of minocycline were observed on gp120-induced IL-6 and cyclooxygenase-2 expression in spinal cord or CSF IL-6 levels. Taken together these data highlight the importance of microglial activation in the development of exaggerated pain states.
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Comment Letter Comparative Study
Comment on: Gilron I, Orr E, Tu D, O'Neill JP, Zamora JE, Bell AC. A placebo-controlled randomized clinical trial of perioperative administration of gabapentin, rofecoxib and their combination for spontaneous and movement-evoked pain after abdominal hysterectomy. Pain 113 (2005) 191-200.
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Comparative Study
Effects of amitriptyline and gabapentin on bilateral hyperalgesia observed in an animal model of unilateral axotomy.
Nociceptive responses in an animal model of peripheral nerve injury were studied. The left common sciatic nerve was exposed, tightly ligated at two locations and transected between the ligatures. A bilateral decrease in the nociceptive threshold to mechanical stimulation was observed within 3 h after the operation. ⋯ Similar bilateral hyperalgesia was observed when axotomy was performed using silk thread instead of chromic gut. When this axotomy model was applied to mice, the nociceptive thresholds in both paws immediately showed a significant decrease in the same manner as in rats. The bilateral and systemic hyperalgesia observed in this axotomy model, which resembles the clinical features of chronic neuropathic pain, suggests the involvement of the central nervous system in the maintenance of the chronic pain state.