The journal of pain : official journal of the American Pain Society
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Prescription of opioids for nonmalignant musculoskeletal pain has increased substantially in recent years, but there is little information on the incidence of, or factors associated with, such prescription for work-related back pain. In a prospective cohort study (N = 1,067), we examined associations between worker sociodemographic and other characteristics and opioid prescription within six weeks of the first medical visit for workers' compensation claims for work loss due to back injury. We examined administrative, pharmacy, and worker-reported data. In bivariate logistic regression models, Hispanics were less likely than non-Hispanic whites to receive opioid prescriptions, and very high body mass index, daily tobacco use, greater pain and physical disability, pain radiating below the knee, injury severity categorizations (from medical records) of major sprain and radiculopathy, and worse mental health were associated with opioid prescription. Adjusting for demographics, pain intensity, and physical disability, opiate prescription was significantly associated with daily tobacco use, pain radiating below the knee, and injury severity categories (major sprain and radiculopathy). Knowledge of worker characteristics associated with early opioid prescription may be useful in future studies of the role of early pain treatment in influencing subsequent course of pain and disability among workers with back injuries. ⋯ Little is known about patient characteristics that may influence physicians' decisions concerning prescription of opioids for acute back pain. Not surprisingly, workers with more severe back injuries are more likely to be prescribed opioids, but reasons for prescription disparities based on ethnicity and tobacco use warrant further study.
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This high-resolution electroencephalography (EEG) study tested the hypothesis that the suppression of rolandic alpha power before predictable painful stimulation affects the subject's subsequent evaluation of pain intensity, as a reflection of the influence of expectancy processes on painful stimulus processing. High-resolution EEG data were recorded (126 channels) from 10 healthy adult volunteers during the expectancy of a painful CO(2)-laser stimulation at the right wrist. Surface laplacian estimation enhanced the EEG spatial information content over 6 scalp regions of interest (left frontal, right frontal, left central, right central, left parietal, and right parietal areas). Spectral power was computed for 3 alpha sub-bands with reference to the individual alpha frequency peak (about 5-7 Hz for alpha 1, 7-9 Hz for alpha 2, and 9-11 Hz for alpha 3). The suppression of the alpha power before the painful stimulation [as reflected by the event-related desynchronization (ERD)] indexed the anticipatory cortical processes. Results showed maximum (negative) correlations between the alpha 2 and alpha 3 ERD amplitude at the left central area and the subjective evaluation of pain intensity (P < .001). The stronger the anticipatory alpha 2 and alpha 3 ERD, the higher the subjective evaluation of pain intensity. For alpha 3, that correlation was confirmed even when the effect of habituation across the recording session was taken into account. These results suggest that the anticipatory suppression of the alpha rhythms over the contralateral primary sensorimotor cortex predicts subsequent subjects' evaluation of pain intensity, in line with its crucial role for the discrimination of that intensity. ⋯ This electroencephalographic study showed that anticipatory activation/deactivation of sensorimotor cortex roughly predicts subjective evaluation of pain. This motivates further investigation on possible implications for the understanding of central chronic pain. Chronic pain patients might exaggerate the anticipatory activation of sensorimotor cortex to negligible pain stimuli.
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This report describes a study of how patients view their pain medications. Two hundred and twenty patients with chronic pain completed a set of 78 items regarding beliefs and concerns about pain medication, a brief measure of medication use, and measures of depression and disability. Item and scale analyses resulted in a 47-item measure, the Pain Medication Attitude Questionnaire (PMAQ), that assesses 7 areas of patient concern: addiction, perceived need, unfavorable scrutiny by others, adverse side effects, tolerance, mistrust in the prescribing doctor, and withdrawal. These seven scales had excellent internal consistency and predictable relations with the measures of medication use, depression, and disability supporting their validity. Correlation analyses highlighted relatively strong associations between concerns about medication and measures of emotional distress and disability, suggesting that these concerns may add significantly to the burden of chronic pain. We suggest that concerns about medication use warrant further study and may deserve clinical attention. ⋯ All medication use by chronic pain sufferers is essentially a pattern of patient behavior over time. As such, it appears to be multiply-determined, by beliefs, emotions, bodily sensations, and the social, cultural, and personal learning history that give these experiences their meaning and functions.
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Non-N-methyl-D-aspartate (non-NMDA) glutamate receptor antagonists modify multiple pain transmission pathways and are of particular interest in analgesic development because of their capacity to interfere with evoked pain. Evoked pain is a problem for postoperative patients and is characteristic of the plantar incision model for postoperative pain. The purpose of this study was to assess the efficacy of a non-NMDA receptor antagonist LY293558 on mechanical hyperalgesia after plantar incision in the rat. Parenteral, intrathecal, or intraplantar administration of LY293558 was tested against the mechanical hyperalgesia that characterizes the model. Sprague-Dawley rats were assigned to 1 of 3 groups. LY293558 or vehicle was administered intraperitoneally, intrathecally, or intraplantarly. The hind paw withdrawal threshold to punctate stimulation by using von Frey filaments and response frequency to a nonpunctate stimulus directly to the wound were measured. Motor tests after administration of LY293558 were also examined in rats that did not undergo incision. The greatest dose of parenterally administered LY293558 (34 micromol/kg) decreased the responses to mechanical stimuli after plantar incision. Rotorod performance was decreased at these same times. Intrathecal injection of LY293558 (0.5 and 2.0 nmol) produced inhibition of mechanical sensitivity and produced lower extremity motor side effects. Repeated intrathecal administration produced sustained anesthesia for 24 hours but had no analgesic effect the next day. Local administration did not decrease response after incision. LY293558 was most effective for evoked pain when administered intrathecally. ⋯ Control of evoked pain after surgery is inadequate but is linked to perioperative outcome. These data suggest that non-NMDA receptor antagonists like LY293558 will be most effective for evoked pain in postoperative patients if administered spinally.
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Spinal glial activation and consequent interleukin-1 (IL-1) release are implicated in pain facilitation induced by inflammation/damage to skin and peripheral nerves. It is unclear whether pain facilitation induced at deep tissue sites also depends on these. We investigated whether spinal IL-1 and/or glial activation mediates bilateral allodynia induced by repeated unilateral intramuscular injections of acidic saline to rats. Given the prominent role of spinal IL-1 in various bilateral pain models, we predicted that intrathecal IL-1 receptor antagonist (IL-1ra) would suppress bilateral allodynia in this model as well. Surprisingly, neither single nor repeated intrathecal injections of IL-1ra affected allodynia, measured by the von Frey test, induced by prior intramuscular acidic saline compared with vehicle-injected controls. In addition, we tested the effect of 2 additional intrathecal manipulations that are broadly efficacious in suppressing glially mediated pain facilitation: (1) a glial metabolic inhibitor (fluorocitrate) and (2) the anti-inflammatory cytokine, interleukin-10 (IL-10). Like IL-1ra, fluorocitrate and IL-10 each failed to reverse allodynia. Finally, we observed no significant activation of glial cells, as assessed by immunohistochemistry of glial activation markers, in the lumbar spinal cord in response to intramuscular acidic saline. Taken together, the present data suggest that acidic saline-induced bilateral allodynia is created independently of glial activation. ⋯ From converging lines of evidence, the current studies suggest that persistent bilateral allodynia induced by repeated intramuscular acidic saline is not mediated by spinal IL-1 and/or spinal glial activation. As such, this might represent the first evidence for pain facilitation occurring in the absence of glial involvement.