The journal of pain : official journal of the American Pain Society
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A controlled experimental study was performed to examine the efficacy of the endogenous pain inhibitory systems and whether this (mal)functioning is associated with symptom increases following exercise in patients with chronic whiplash-associated disorders (WAD). In addition, 2 types of exercise were compared. Twenty-two women with chronic WAD and 22 healthy controls performed a submaximal and a self-paced, physiologically limited exercise test on a cycle ergometer with cardiorespiratory monitoring on 2 separate occasions. Pain pressure thresholds (PPT), health status, and activity levels were assessed in response to the 2 exercise bouts. In chronic WAD, PPT decreased following submaximal exercise, whereas they increased in healthy subjects. The same effect was established in response to the self-paced, physiologically limited exercise, with exception of the PPT at the calf which increased. A worsening of the chronic WAD symptom complex was reported post-exercise. Fewer symptoms were reported in response to the self-paced, physiologically limited exercise. These observations suggest abnormal central pain processing during exercise in patients with chronic WAD. Submaximal exercise triggers post-exertional malaise, while a self-paced and physiologically limited exercise will trigger less severe symptoms, and therefore seems more appropriate for chronic WAD patients. ⋯ The results from this exercise study suggest impaired endogenous pain inhibition during exercise in people with chronic WAD. This finding highlights the fact that one should be cautious when evaluating and recommending exercise in people with chronic WAD, and that the use of more individual, targeted exercise therapies is recommended.
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We demonstrate and evaluate a method for modeling acute pain resolution in individual patients over 6 days following an emergency department visit for an acutely painful condition. Five hundred and thirteen patients presenting with acutely painful conditions provided 11-point numerical ratings of pain intensity at discharge from an emergency department and daily thereafter for a total of 6 days. Latent growth curve modeling with a linear fit yielded measures of initial pain intensity (intercept) and rate of pain resolution (slope) for each individual patient. The linear fits provided good approximations of individual pain trajectories. The average patient had intercept of 6.57 with a slope of -.61. On Day 4, 54.6% of patients reported a pain level equal to or greater than 4. Classification of individual patients by slope revealed that 79% of the sample had the expected negative slope for acute pain resolution while 21% had flat or positive slopes, indicating lack of pain resolution or worsening of pain over time following discharge. The standard errors of measurement for the acute pain trajectories were markedly smaller than those for conventional pain ratings, indicating that the trajectory approach to pain measurement improves measurement precision. ⋯ The acute pain trajectory provides more information than conventional pain measurement and increases measurement precision. It provides a means of determining the efficacy of acute pain management in the emergency department. The rate of pain resolution is a potentially valuable outcome measure for controlled clinical trials.
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Taking opioids with other central nervous system (CNS) depressants can increase risk of oversedation and respiratory depression. We used telephone survey and electronic health care data to assess the prevalence of, and risk factors for, concurrent use of alcohol and/or sedatives among 1,848 integrated care plan members who were prescribed chronic opioid therapy (COT) for chronic noncancer pain. Concurrent sedative use was defined by receiving sedatives for 45+ days of the 90 days preceding the interview; concurrent alcohol use was defined by consuming 2+ drinks within 2 hours of taking an opioid in the prior 2 weeks. Some analyses were stratified by substance use disorder (SUD) history (alcohol or drug). Among subjects with no SUD history, 29% concurrently used sedatives versus 39% of those with an SUD history. Rates of concurrent alcohol use were similar (12 to 13%) in the 2 substance use disorder strata. Predictors of concurrent sedative use included SUD history, female gender, depression, and taking opioids at higher doses and for more than 1 pain condition. Male gender was the only predictor of concurrent alcohol use. Concurrent use of CNS depressants was common among this sample of COT users regardless of substance use disorder status. ⋯ Risks associated with concurrent use of CNS depressants are not restricted to COT users who abuse those substances. And, the increased risk of concurrently using CNS depressants is not restricted to opioid users with a prior SUD history. COT requires close monitoring, regardless of substance use disorder history.
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Paclitaxel often induces persistent painful neuropathy as its most common treatment-limiting side effect. Little is known concerning the underlying mechanisms. Given the prominent role of glial cells in many types of neuropathic pain, we investigated here the morphological and functional changes of spinal astrocytes and microglia in a rat model of paclitaxel-induced neuropathy. Immunohistochemistry, western blotting, and real-time polymerase chain reaction were performed with samples from 109 rats up to 28 days after paclitaxel treatment. Paclitaxel (2 mg/kg, i.p.) induced a rapid and persistent activation of spinal astrocytes assessed using glial fibrillary acidic protein, but not apparent activation of microglia assessed using OX42, Iba-1, and phosphorylated p38. In the context of astocyte activation, there was a significant downregulation of glial glutamate transporters GLAST and GLT-1 in spinal dorsal horn. The activation of spinal astrocytes by paclitaxel was not associated with expression of pro-inflammatory cytokines including tumor necrosis factor-α, interleukin-1β, or interleukin-6 in spinal dorsal horn. Systemic treatment with minocycline (50 mg/kg, i.p.) prevented activation of astrocytes and downregulation of glial glutamate transporters in spinal dorsal horn induced by paclitaxel. These data suggest the involvement of spinal astrocytes but not microglia in the pathogenesis of paclitaxel-induced neuropathy. ⋯ Spinal astrocytes and/or glial glutamate transporters could be new therapeutic targets for paclitaxel-induced painful neuropathy.