The journal of pain : official journal of the American Pain Society
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Facilitated pain mechanisms and impaired pain inhibition are often found in chronic pain patients. This study compared clinical pain profiles, pain sensitivity, as well as pronociceptive and antinociceptive mechanisms in patients with localized low back pain (n = 18), localized neck pain (n = 17), low back and radiating leg pain (n = 18), or neck and radiating arm pain (n = 17). It was hypothesized that patients with radiating pain had facilitated pain mechanisms and impaired pain inhibition compared with localized pain patients. ⋯ Temporal summation of pain was increased in patients with radiating back pain compared with localized back pain (P < .03). Patients with radiating arm pain or localized low back pain demonstrated hyperalgesia to heat and pressure in nonpainful body areas (P < .05), as well as well as a facilitated clinical pain profile compared with patients with localized neck pain (P = .03). Patients with radiating pain patterns demonstrated facilitated temporal summation suggesting differences in the underlying pain mechanisms between patients with localized back pain and radiating pain.
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Psychosocial factors that protect against negative outcomes for individuals with chronic pain have received increased attention in recent years. Pain resilience, or the ability to maintain behavioral engagement and regulate emotions as well as cognitions despite prolonged or intense pain, is one such factor. A measure of pain-specific resilience, the Pain Resilience Scale, was previously identified as a better predictor of acute pain tolerance than general resilience. ⋯ A confirmatory factor analysis confirmed the 2-factor structure of the Pain Resilience Scale previously observed among respondents without chronic pain, although one item from each subscale was dropped in the final version. For this chronic pain sample, structural equation modeling showed that pain resilience contributes unique variance to a model including pain acceptance and pain self-efficacy in predicting quality of life and pain intensity. Further, pain resilience was a better fit in this model than general resilience, strengthening the argument for assessing pain resilience over general resilience.
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Cancer-induced bone pain (CIBP) remains a major challenge in advanced cancer patients because of our lack of understanding of its mechanisms. Previous studies have shown the vital role of γ-aminobutyric acid B receptors (GABABRs) in regulating nociception and various neuropathic pain models have shown diminished activity of GABABRs. However, the role of spinal GABABRs in CIBP remains largely unknown. ⋯ Our behavioral results show that acute as well as chronic intrathecal treatment with baclofen, a GABABR agonist, significantly attenuated CIBP-induced mechanical allodynia and ambulatory pain. The expression levels of GABABRs were significantly decreased in a time-dependent manner and colocalized mostly with neurons and a minority with astrocytes and microglia. Chronic treatment with baclofen restored the expression of GABABRs and markedly inhibited the activation of cyclic adenosine monophosphate (cAMP)-dependent protein kinase and the cAMP-response element-binding protein signaling pathway.
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The number of studies on trigeminal nerve injury using animal models remains limited. A rodent model of trigeminal neuropathic pain was first developed in 1994, in which chronic constriction injury (CCI) is induced by ligation of the infraorbital nerve (IoN). This animal model has served as a major tool to study trigeminal neuropathic pain. Unfortunately, the surgical procedure in this model is complicated and far more difficult than ligation of peripheral nerves (eg, sciatic nerve). The aim of this study was to improve on the current surgical procedure of IoN ligation to induce trigeminal neuropathic pain in rats. We show that the IoN can be readily accessed through a small facial incision. CCI can be induced by ligation of a segment at the distal IoN (dIoN). This dIoN-CCI procedure is simple, minimally invasive, and time-saving. Our data show that the dIoN-CCI procedure consistently induced acute as well as chronic nociceptive behaviors in rats. Daily gabapentin treatment attenuated mechanical allodynia and reduced face-grooming episodes in dIoN-CCI rats. ⋯ The orofacial pain caused by trigeminal nerve damage is severe and perhaps more debilitating than other types of neuropathic pain. However, studies on trigeminal neuropathic pain remain limited. This is largely because of the lack of proper animal models because of the complexity of the existing surgical procedures required to induce trigeminal nerve injury. Our improved dIoN-CCI model is likely to make it more accessible to study the cellular and molecular mechanisms of neuropathic pain caused by trigeminal nerve damage.