The journal of pain : official journal of the American Pain Society
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Neonatal pain experiences have been associated with altered processing and perception of pain in later life, but findings tend to vary among studies. We have compared experimental pain tolerance and subjective health complaints in a population-based cohort of adolescents born extremely preterm to that of matched term controls. Subjects performed a standardized cold pressor task (hand in ice water) and completed validated questionnaires regarding current subjective health complaints, including pain issues. Thirty-one (89%) of 35 eligible preterm subjects (mean gestational age 26.8 weeks) and 28 (80%) term controls participated in this follow-up study at mean age 17.8 years. Ten (32%) subjects born preterm versus 17 (61%) born at term reached the ceiling time of 180 seconds immersion time in the ice water, a hazard ratio for early withdrawal of 2.05 (95% confidence interval, 1.72 to 2.44), with males explaining most of the difference. For subjects born preterm, the risk of early withdrawal decreased significantly with more days of mechanical ventilation, more pain events, and more doses of morphine during the newborn period. Subjective pain ratings during the cold pressor task as well as health-related complaints and pain issues reported in the questionnaires were similar in the preterm and term groups. ⋯ Despite reduced tolerance to experimental pain, subjects born preterm scored their pain experiences similarly to those of term controls. Surprisingly, preterm subjects exposed to most painful and invasive neonatal experiences and also to most doses of morphine had a pain response at follow-up most closely resembling that of the control group.
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The aim of this study was to investigate the psychometric properties of an abbreviated version of the Tampa Scale for Kinesiophobia (TSK) in a clinical sample of patients with chronic pain. Chronic pain patients (n = 276) seeking treatment at an interdisciplinary treatment center completed self-report questionnaires including the TSK-13, and 2 tests of physical functioning. Four competing models of the TSK were tested using confirmatory factor analysis. Internal consistency was assessed, as were discriminant evidence of construct validity and concurrent criterion-related validity. Incremental validity was assessed with hierarchical multiple regressions controlling for pain severity. The analyses indicated that an 11-item, 2-factor structure best fit the data. The first factor, somatic focus, consisted of 5 items, while the second factor, activity avoidance, was comprised of 6 items. The TSK-11 scales demonstrated acceptable levels of internal consistency, as well as evidence of discriminant, concurrent criterion-related, and incremental validity. Somatic focus uniquely predicted perceived disability while activity avoidance uniquely predicted actual physical performance, controlling for pain severity. The 2-factor structure of the TSK-11 was found to be a brief, reliable, and valid measure of fear of movement/(re)injury for chronic pain patients. We recommend that the TSK-11 be used in future research and in clinical settings. ⋯ In this study, confirmatory factor analysis identified the 2-factor TSK-11 as the best fitting model of TSK factor structure. The TSK-11 is a brief, reliable, and valid measure of fear of movement/(re)injury for chronic pain patients.
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Telomere length, considered a measure of biological aging, is linked to morbidity and mortality. Psychosocial factors associated with shortened telomeres are also common in chronic pain; yet, little is known about telomere length in pain populations. Leukocyte telomere length was evaluated in 66 women with fibromyalgia and 22 healthy female controls. Participants completed questionnaires and a subgroup of fibromyalgia patients underwent quantitative sensory testing (QST; n = 12) and neuroimaging (n = 12). Telomere length was measured using the quantitative polymerase chain reaction method. Although patients had shorter telomere length than controls, the difference was not statistically significant. However, higher levels of pain within fibromyalgia were associated with shorter telomere length (P = .039). When pain and depression were combined, patients categorized as high-pain/high-depression had an age-adjusted telomere length 265 base pairs shorter than those with low-pain/low-depression (P = .043), a difference consistent with approximately 6 years of chronological aging. In the subset tested, telomere length was also related to pain threshold and pain sensitivity, as well as gray matter volume, such that patients with shorter telomeres were more sensitive to evoked pain and had less gray matter in brain regions associated with pain processing (eg, primary somatosensory cortex). These preliminary data support a relationship between pain and telomere length. ⋯ Our findings support a link between premature cellular aging and chronic pain. These preliminary data imply that chronic pain is a more serious condition than has typically been recognized in terms of bodily aging.
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Estimates of geographic variation among states and counties in the prevalence of opioid prescribing are developed using data from a large (135 million) representative national sample of opioid prescriptions dispensed during 2008 by 37,000 retail pharmacies. Statistical analyses are used to estimate the extent to which county variation is explained by characteristics of resident populations, their healthcare utilization, proxy measures of morbidity, availability of healthcare resources, and prescription monitoring laws. Geographic variation in prevalence of prescribed opioids is large, greater than the variation observed for other healthcare services. Counties having the highest prescribing rates for opioids were disproportionately located in Appalachia and in southern and western states. The number of available physicians was by far the strongest predictor of amounts prescribed, but only one-third of county variation is explained by the combination of all measured factors. Wide variation in prescribing opioids reflects weak consensus regarding the appropriate use of opioids for treating pain, especially chronic noncancer pain. Patients' demands for treatment have increased, more potent opioids have become available, an epidemic of abuse has emerged, and calls for increased government regulation are growing. Greater guidance, education, and training in opioid prescribing are needed for clinicians to support appropriate prescribing practices. ⋯ Wide geographic variation that does not reflect differences in the prevalence of injuries, surgeries, or conditions requiring analgesics raises questions about opioid prescribing practices. Low prescription rates may indicate undertreatment, while high rates may indicate overprescribing and insufficient attention to risks of misuse.
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The preprotachykinin A gene (ppt-A) codes for Substance P (SP), supports nociceptive sensitization, and modulates inflammatory responses after incision. Repeated opioid use produces paradoxical pain sensitization-termed opioid-induced hyperalgesia (OIH) -which can exacerbate pain after incision. Here the contribution of SP to peri-incisional nociceptive sensitization and nociceptive mediator production after opioid treatment was examined utilizing ppt-A knockout (-/-) mice and the neurokinin (NK1) receptor antagonist LY303870. Less mechanical allodynia was observed in ppt-A(-/-) mice compared to wild types (wt) after morphine treatment both before and after incision. Moreover, LY303870 administered with morphine reduced incisional hyperalgesia in wt mice. Incision after saline or escalating morphine treatment upregulated skin IL-1β, IL-6, G-CSF and MIP-1α levels in ppt-A(-/-) and wt mice similarly. However, chronic morphine treatment greatly exacerbated increases in skin nerve growth factor levels after incision, an effect entirely dependent upon intact SP signaling. Additionally, SP dependent upregulation of prodynorphin, NMDA1 and NK1 receptor expression in spinal cord was seen after morphine treatment and incision. A similar pattern was seen for 5-HT3 receptor expression in tissue from dorsal root ganglia. Therefore, SP may work at both central and peripheral sites to enhance nociceptive sensitization after morphine treatment and incision. ⋯ These studies show that SP signaling modulates enhanced nerve growth factor production and changes in neuronal gene expression seen after incision in mice previously exposed to morphine.