The journal of pain : official journal of the American Pain Society
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Comparative Study
Metoclopramide versus hydromorphone for the emergency department treatment of migraine headache.
We conducted a retrospective cohort study to compare the effects of metoclopramide versus hydromorphone for the initial emergency department treatment of migraine headache at an urban teaching hospital. The primary outcome measure was the mean difference in the subjects' self-reported pain scores before and after the administration of the initial medication treatment. We also estimated crude and adjusted relative risks (using Poisson multivariate regression modeling) to assess and control potential confounding by age, gender, race, and pain score before initial medication. Two hundred subjects were included, with 51 (25.5%) receiving intravenous or intramuscular hydromorphone, 95 (47.5%) receiving intravenous metoclopramide, and 54 (27.0%) receiving 1 of several other medications. Using a standardized pain scale of 0 to 10, mean pain score reductions were 2.3 points for hydromorphone, 3.7 points for metoclopramide, and 2.8 points for all other medications combined (P < .001). When comparing metoclopramide versus hydromorphone, the crude relative risk for pain reduction of 3 or more points was 1.76 (95% CI, 1.12-2.75, P = .01), and the adjusted relative risk was 1.60 (95% CI, 0.84-3.03, P = .15). Metoclopramide also resulted in less use of rescue medications, faster times to discharge, and no difference in the frequency of adverse reactions. ⋯ Metoclopramide appears to be an effective initial medical treatment for migraine headaches in the emergency department setting, but its pharmacologic mechanism remains incompletely understood. A double-blinded, randomized, controlled trial comparing standard dosages of hydromorphone versus metoclopramide will be needed to definitively determine which medication is more effective.
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The objective of this article is to provide an overview of the natural history and treatment of herpes zoster, with a focus on pain management. Herpes zoster has the highest incidence of all neurological diseases, occurring annually in approximately 1 million people in the United States. A basic feature of herpes zoster is a marked increase in incidence with aging and with diseases and drugs that impair cellular immunity. Herpes zoster begins with reactivation of varicella zoster virus in dorsal root or cranial nerve ganglia, which is often accompanied by a prodrome of dermatomal pain or abnormal sensations. Varicella zoster virus spreads in the affected primary afferent nerve to the skin and produces a characteristic dermatomal maculopapular and vesicular rash and pain. Herpes zoster acute pain lowers quality of life and interferes with activities of daily living. Antiviral therapy and scheduled analgesics form the pharmacotherapeutic foundation for herpes zoster acute pain reduction. If moderate to severe herpes zoster pain is not adequately relieved by antiviral agents in combination with oral analgesic medications, then corticosteroids, anticonvulsants (eg, gabapentin or pregabalin), tricyclic antidepressants (eg, nortriptyline or desipramine), or neural blockade can be considered. ⋯ This article presents information on the clinical features and treatment of herpes zoster. This information will help clinicians diagnose and manage herpes zoster pain.
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The heat pain threshold was assessed in 32 healthy participants after a mild burn on the dorsal surface of each hand, after injection of an opioid antagonist (80 microg naloxone) or vehicle alone (0.2 mL saline) into the burnt skin of 1 hand, and after repeated painful immersion of this hand in cold water for up to 180 seconds. We hypothesized that sensitivity to heat would decrease at the burn-injured site after the immersions, due to local release of opioids into the burnt skin. Naloxone augmented cold-induced pain during the immersions in participants who tolerated the longest immersions, implying that release of endogenous opioids suppressed cold-pain. After the immersions, sensitivity to heat decreased at the burn-injured site in the immersed hand, but naloxone did not block this effect. Instead, naloxone altered sensitivity to heat in unburnt skin, implying that thermal hyperalgesia at sites of burn injury masked the modulatory effects of opioids. In particular, naloxone blocked a decrease in sensitivity to heat at an unburnt site on the contralateral hand of participants who tolerated the longest immersions, consistent with central or systemic opioid release. Naloxone reduced sensitivity to heat at unburnt sites in participants who tolerated medium-length immersions, suggesting that an increase in systemic or central opioid activity evoked thermal hyperalgesia in this group. In addition, in a small group of participants who tolerated only brief immersions, naloxone blocked decreases in sensitivity to heat at an unburnt site in the immersed hand. These findings suggest that repeated painful immersions trigger local opioid release in participants who tolerate only brief immersions, and elicit central or systemic opioid release in participants who tolerate longer immersions. ⋯ This article demonstrates that repeated immersion of the hand in painfully cold water increases opioid activity and that the increase in opioid activity exerts multiple opposing effects on sensitivity to heat. Individual differences in the response to opioids might contribute to individual differences in pain tolerance.
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This study aimed to determine if electromyographic (EMG) diagnostic evaluation can predict functional outcome in patients undergoing transforaminal lumbar spine epidural injections. In this retrospective study, functional outcome by Oswestry Disability Index (ODI) and verbal rating scale (VRS) for current pain severity was evaluated in 39 patients undergoing lumbar transforaminal epidural spinal injections (ESI). Subjects with low back pain (mean age, 60 +/- 12.5 years) were evaluated for functional improvement post EMG and ESI. Of 39 patients tested with EMG before injection, 18 patients were positive for radiculopathy and 21 had a normal or negative examination. The patients were followed postinjection on average of 10.8 (SD +/- 3.9) weeks. Pretreatment ODI scores were not significantly different between groups showing positive (72.3 SD +/- 12.7) and negative (65.9 SD +/- 18.6, P > .05) EMG findings. There was significantly greater improvement of ODI for EMG positive radiculopathy (7.11 SD +/- 9.5) compared with negative EMG (3.2 SD +/- 17.4, P < .05). Positive radiculopathy subjects complained of more pain by VRS before ESI than subjects with negative EMG findings, 8.1 SD +/- 1.0 and 7.3 SD +/- 0.8, respectively, which was not significant (P > .05). VRS mean improvement was not significantly different in the positive EMG group (1.8 SD +/- 1.2) compared with a negative EMG (1.2 SD +/- 1.2, P > .05). ⋯ The results appear to show that patients undergoing transforaminal ESI, who have a positive radiculopathy by EMG before injection, will have significant improvement in functional outcome by ODI but not with current pain intensity by VRS. This study suggests the importance and diagnostic value of ordering electromyography studies for lumbar radiculopathy evaluation, which may lead to prediction of outcome with lumbar transforaminal epidural spinal procedures. Furthermore, the current study highlights the difficulty of pain evaluation outcome by VRS.
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Opiate analgesic tolerance is defined as a need for higher doses of opiates to maintain pain relief after prolonged opiate exposure. Though changes in the opioid receptor undoubtedly occur during conditions of opiate tolerance, there is increasing evidence that opiate analgesic tolerance is also caused by pronociceptive adaptations in the spinal cord. We have previously observed increased glutamate release in the spinal cord dorsal horn of neonatal rats made tolerant to the opiate morphine. In this study, we investigate whether spinal substance P (SP) and its receptor, the neurokinin 1 (NK1) receptor, are also modulated by prolonged morphine exposure. Immunocytochemical studies show decreased SP- and NK1-immunoreactivity in the dorsal horn of morphine-treated rats, whereas SP mRNA in the dorsal root ganglia is not changed. Electrophysiological studies show that SP fails to activate the NK1 receptor in the morphine-treated rat. Taken together, the data indicate that chronic morphine treatment in the neonatal rat is characterized by a loss of SP effects on the NK1 receptor in lamina I of the neonatal spinal cord dorsal horn. The results are discussed in terms of compensatory spinal cord processes that may contribute to opiate analgesic tolerance. ⋯ This article describes anatomical and physiological changes that occur in the spinal cord dorsal horn of neonatal rats after chronic morphine treatment. These changes may represent an additional compensatory process of morphine tolerance and may represent an additional therapeutic target for the retention and restoration of pain relief with prolonged morphine treatment.