The journal of pain : official journal of the American Pain Society
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In this descriptive study of chronic pain in a community sample of 292 women who had separated from their abusive partners on average 20 months previously, more than one-third experienced high disability pain as measured by Von Korff's Chronic Pain Grade. Beyond the usual pain locations associated with abuse, 43.2% reported swollen/painful joints. More interference in daily life was attributed to joint pain than to back, head, stomach, pelvic or bowel pain. Women with high disability pain were more likely to have experienced child abuse, adult sexual assault, more severe spousal abuse, lifetime abuse-related injuries, symptoms of depression and post-traumatic stress disorder, lifetime suicide attempts, difficulty sleeping, and unemployment. High disability pain also was associated with visits to a family doctor and psychiatrist and use of medication in more than prescribed dosages. Less than 25% of women with high disability pain were taking opioids, or prescription nonsteroidal anti-inflammatory medications. Interestingly, high disability pain was not related to smoking, use of street drugs, potential for alcohol dependence, age, income, or education. The findings add to knowledge of severity and patterns of chronic pain in abused women and support the need for further multivariate analysis of the relationships among abuse experiences, mental health, and chronic pain severity to better inform decisions regarding diagnosis and treatment. ⋯ Understanding patterns of chronic pain in abuse survivors and their associations with abuse history, mental health symptoms, health service use, and medication is important for clinical assessment and intervention. Chronic pain persisted long after leaving abusive partners and extended beyond usual locations (back, headache, pelvic, gastrointestinal) to include swollen/painful joints.
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Central nervous system lesions cause peripheral dysfunctions currently attributed to central cell death that compromises function of intact peripheral nerves. Injecting quisqualate (QUIS) into the rat spinal cord models spinal cord injury (SCI) and causes at-level scratching and self-injury. Such overgrooming was interpreted to model pain until patients with self-injurious scratching after SCI reported itch motivated scratching that was painless because of sensory loss. Because self-injurious scratching is difficult to explain by central mechanisms alone, we hypothesized that QUIS injections damage peripheral axons of at-level afferents. QUIS was injected into thoracic spinal cords of 18 Long-Evans rats. Animals were killed 3 days after overgrooming began or 14 days after injection. Spinal cord lesions were localized and DRG-immunolabeled for ATF-3. At-level and control skin samples were PGP9.5-immunabeled to quantify axons. Eighty-four percent of QUIS rats overgroomed. Skin in these regions had lost two-thirds of epidermal innervation as compared with controls (P < .001). Rats that overgroomed had 47% less axon-length than nongrooming rats (P = .006). The presence of ATF-3 immunolabeled neurons within diagnosis-related groups of QUIS rats indicated death of afferent cell bodies. Overgrooming after QUIS injections may not be due entirely to central changes. As in humans, self-injurious neuropathic scratching appeared to require loss of protective pain sensations in addition to peripheral denervation. ⋯ This study suggests that intramedullary injection of quisqualic acid in rats causes death of at-level peripheral as well as central neurons. Self-injurious dermatomal scratching that develops in spinal-injured rats may reflect neuropathic itch and loss of protective pain sensations.
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Stress-induced hyperalgesia (SIH), a common clinical observation associated with multiple painful diseases including functional urinary disorders, presently has no mechanistic explanation. Using a footshock treatment, a classic stressor, to magnify physiological responses in a model of urinary bladder pain, we examined one potential group of mediators of SIH, the corticotropin-releasing factor (CRF)-related neuropeptides. Exposure to a footshock treatment produced bladder hypersensitivity in female Sprague-Dawley rats, manifested as significantly more vigorous visceromotor responses (VMRs) to urinary bladder distension (UBD) compared with rats that were exposed to a non-footshock treatment. This bladder hypersensitivity was significantly attenuated by blocking spinal CRF(2) receptors but not CRF(1) receptors. Furthermore, spinal administration of urocortin 2, a CRF(2) receptor agonist, augmented UBD-evoked VMRs in a way similar to what was observed after exposure to Footshock, an effect significantly attenuated by pretreatment with spinal aSVG30, a CRF(2) receptor antagonist. Surprisingly, neither spinal administration of CRF nor the CRF(1) receptor antagonist antalarmin had an effect on bladder nociceptive responses. The results of the present study not only provide further support for a role of stress in the exacerbation of bladder pain but also implicate spinal urocortins and their endogenous receptor, the CRF(2) receptor, as potential mediators of this effect. ⋯ This study presents evidence that spinal urocortins and CRF(2) receptors are involved in stress-induced hypersensitivity related to the urinary bladder. This provides a basis for investigating how urocortins mediate SIH, ultimately leading to more effective treatment options for patients with painful bladder syndromes as well as stress-exacerbated chronic pain.