The journal of pain : official journal of the American Pain Society
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Fear of injury has been posited as crucial in pain-related anxiety and in the development of chronic pain; however, research has only measured fear of injury indirectly through other constructs (eg, fear of illness and fear of movement). The current study tested fear of injury as an independent contributor to pain-related anxiety and impairment. Patients (n = 78; 37% women) in a work-hardening treatment program for chronic low back pain completed self-report measures of pain-related anxiety, anxiety sensitivity, fear of injury, current pain, and impairment. Behavioral measures of impairment included lifting capacity, treatment outcomes, and days absent from treatment. Structural equation modeling tested the role of fear of injury within contemporary theory. Fit for the theoretical model was excellent and superior to an alternative model. Variance accounted for in pain-related anxiety by fear of injury, anxiety sensitivity, and current pain was 64%, while pain-related anxiety and current pain predicted 49% of variance in latent impairment. Fear of injury directly predicted pain-related anxiety (β = .42) and indirectly predicted impairment through pain-related anxiety (β = .19). Fear of injury may warrant theoretical and clinical consideration as an important contributor to pain-related anxiety and impairment; however, research is needed to explore how it may be causally related with other constructs. ⋯ Fear of injury directly predicts pain-related anxiety and indirectly predicts self-reported and behavioral impairment. Fear of injury may warrant inclusion in contemporary theories of chronic pain. Clinicians may benefit from considering the construct in interventions for chronic pain.
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Dispositional optimism has been shown to beneficially influence various experimental and clinical pain experiences. One possibility that may account for decreased pain sensitivity among individuals who report greater dispositional optimism is less use of maladaptive coping strategies such as pain catastrophizing, a negative cognitive/affective response to pain. An association between dispositional optimism and conditioned pain modulation, a measure of endogenous pain inhibition, has previously been reported. However, it remains to be determined whether dispositional optimism is also associated with temporal summation (TS), a measure of endogenous pain facilitation. The current study examined whether pain catastrophizing mediated the association between dispositional optimism and TS among 140 older, community-dwelling adults with symptomatic knee osteoarthritis. Individuals completed measures of dispositional optimism and pain catastrophizing. TS was then assessed using a tailored heat pain stimulus on the forearm. Greater dispositional optimism was significantly related to lower levels of pain catastrophizing and TS. Bootstrapped confidence intervals revealed that less pain catastrophizing was a significant mediator of the relation between greater dispositional optimism and diminished TS. These findings support the primary role of personality characteristics such as dispositional optimism in the modulation of pain outcomes by abatement of endogenous pain facilitation and less use of catastrophizing. ⋯ Results from this study further support the body of evidence that attests to the beneficial effects of positive personality traits on pain sensitivity and pain processing. Further, this study identified diminished pain catastrophizing as an important mechanism explaining the inverse relation between dispositional optimism and endogenous pain facilitation.
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Spinal glial cells contribute to the development of many types of inflammatory and neuropathic pain. Here the contribution of spinal astrocytes and astrocyte gap junctions to oxaliplatin-induced mechanical hypersensitivity was explored. The expression of glial fibrillary acidic protein (GFAP) in spinal dorsal horn was significantly increased at day 7 but recovered at day 14 after oxaliplatin treatment, suggesting a transient activation of spinal astrocytes by chemotherapy. Astrocyte-specific gap junction protein connexin 43 (Cx43) was significantly increased in dorsal horn at both day 7 and day 14 following chemotherapy, but neuronal (connexin 36 [Cx36]) and oligodendrocyte (connexin 32 [Cx32]) gap junction proteins did not show any change. Blockade of astrocyte gap junction with carbenoxolone (CBX) prevented oxaliplatin-induced mechanical hypersensitivity in a dose-dependent manner and the increase of spinal GFAP expression, but had no effect once the mechanical hypersensitivity induced by oxaliplatin had fully developed. These results suggest that oxaliplatin chemotherapy induces the activation of spinal astrocytes and this is accompanied by increased expression of astrocyte-astrocyte gap junction connections via Cx43. These alterations in spinal astrocytes appear to contribute to the induction but not the maintenance of oxaliplatin-induced mechanical hypersensitivity. Combined, these results suggest that targeting spinal astrocyte/astrocyte-specific gap junction could be a new therapeutic strategy to prevent oxaliplatin-induced neuropathy. ⋯ Spinal astrocytes but not microglia were recently shown to be recruited in paclitaxel-related chemoneuropathy. Here, spinal astrocyte gap junctions are shown to play an important role in the induction of oxaliplatin neuropathy.
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The aim of this study was to determine whether pregabalin affects nociceptive behavior and central sensitization in a trigeminal neuropathic pain model. A partial infraorbital nerve transection (p-IONX) or sham operation was performed in adult male rats. Nociceptive withdrawal thresholds were tested with von Frey filaments applied to the bilateral vibrissal pads pre- and postoperatively. On postoperative day 7, the behavioral assessment was conducted before and at 30, 60, 120, and 180 minutes after and 24 hours after pregabalin (.1, 1, 10, 100 mg/kg intraperitoneally) or saline injection. The effects of pregabalin or saline were also examined on the mechanoreceptive field and response properties of nociceptive neurons recorded in the medullary dorsal horn at postoperative days 7 to 10. Reduced withdrawal thresholds reflecting bilateral mechanical allodynia were observed in p-IONX rats until postoperative day 28, but not in sham-operated rats. At postoperative day 7, pregabalin significantly and dose-dependently reversed the reduced mechanical withdrawal thresholds in p-IONX rats. Pregabalin also attenuated central sensitization of the neurons, as reflected in reversal of their reduced activation threshold, increased responses to pinch/pressure, and enhanced stimulus-response function. This study provides the first documentation that pregabalin attenuates the mechanical allodynia and central sensitization that characterize this trigeminal neuropathic pain model, and supports its clinical use for treating craniofacial neuropathic pain. ⋯ Trigeminal nerve injury in rats produced facial mechanical hypersensitivity and trigeminal central sensitization of medullary dorsal horn neurons that were markedly attenuated by systemically administered pregabalin, suggesting its potential clinical utility for orofacial neuropathic pain.
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Pain is common after sexual assault (SA), but etiology of pain symptoms after SA is unknown. Preclinical studies suggest that the release of endogenous opioids during stress produces delayed-onset hyperalgesia. In human studies, individuals with ≥1 G allele at the μ-opioid receptor functional single nucleotide polymorphism A118G have been shown to have a reduced response to opioids. We hypothesized that if opioid-mediated hyperalgesia contributes to pain after SA, women SA survivors with 1 or more G alleles at A118G would experience reduced postassault pain. Among 52 European American women SA survivors presenting for care within 48 hours of SA, those with a G allele (12/52, 23%) experienced less severe pain (F[1,39] = 11.55, P = .002) and a reduced extent of pain (F[1,41] = 11.01, P = .002) during the 6 weeks after SA. These associations between the presence of 1 or more G alleles and reduced pain severity and reduced pain extent after SA remained significant in multivariable models controlling for age, income, education, reported pain prior to assault, and pain at the time of initial evaluation. ⋯ These results suggest that endogenous opioid-mediated hyperalgesia may contribute to pain symptoms after sexual assault. Further studies examining mechanisms mediating the development of pain after sexual assault, and the potential influence of opioid-mediated hyperalgesia, are needed.