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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Trigeminal nerve damage often leads to chronic pain syndromes including trigeminal neuralgia, a severely debilitating chronic orofacial pain syndrome. Options for treatment of neuropathic pain are limited in effectiveness and new approaches based on a better understanding of the underlying pathologies are required. Partial ligation has been shown to effectively mimic many of the qualities of human neuropathic pain syndromes. We have devised a mouse model of trigeminal neuralgia using a partial infraorbital nerve ligation (pIONL) that induces persistent pain behaviors and morphological changes in the brainstem. We found that the pIONL effectively induced mechanical allodynia lasting for more than 3 weeks. Cell proliferation (bromodeoxyuridine), activation of astrocytes and microglia in the ipsilateral caudal medulla, and persistent satellite cell reaction in the ipsilateral ganglion were observed. Neurochemical markers calcitonin gene-related peptide, substance P were decreased in medullary dorsal horn ipsilateral to the injury side, whereas substance P receptor NK1 expression was increased after 8 days. Nerve injury marker ATF3 was markedly increased in ipsilateral trigeminal ganglion neurons at 8 days after pIONL. The data indicate that partial trigeminal injury in mice produces many persistent anatomical changes in neuropathic pain, as well as mechanical allodynia. ⋯ This study describes the development of a new mouse model of trigeminal neuropathic pain. Our goal is to devise better treatments of trigeminal pain, and this will be facilitated by characterization of the underlying cellular and molecular neuropathological mechanisms in genetically designed mice.
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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.