Pain
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Clinical Trial
Sensitivity of patients with painful temporomandibular disorders to experimentally evoked pain.
Temporomandibular disorders (TMD) represent a group of chronic painful conditions involving the muscles of mastication and the temporomandibular joint. We determined whether patients with painful TMD are more sensitive to noxious stimuli than age-matched control subjects. Fifty-two TMD patients (16 with muscle pain and 36 with combined muscle and joint pain) and 23 age-matched and gender-matched volunteers participated. ⋯ Furthermore, the submaximal effort tourniquet procedure, which is capable of altering acute orofacial pain (Sigurdsson and Maixner, 1994) did not produce a consistent reduction in orofacial pain associated with TMD. We concluded that TMD patients are more sensitive to noxious stimuli than pain-free controls. These findings provide additional evidence that TMD is a psychophysiological disorder of the central nervous system which modulates emotional, physiological and neuroendocrine responses to emotional and physical stressors.
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This study, performed in freely moving rats, evaluates the effects of the two most prescribed analgesics, aspirin and acetaminophen, on carrageenin inflammation and the associated c-Fos expression in the rat lumbar spinal cord. Maximal dorsal horn c-Fos expression is observed 3 h after carrageenin (6 mg/150 microliters of saline), with Fos-like (Fos-LI) neurones being predominantly located in laminae I-II and V-VI (41 +/- 3% and 39 +/- 5% of the total number of Fos-LI neurones per section for the control group, respectively) of the dorsal horn. Pretreatment with aspirin (75 or 150 mg/kg, i.v.) reduced the number of Fos-LI neurones induced by carrageenin-inflammation (28 +/- 2% and 45 +/- 1% reduction, respectively; P < 0.001 for both). ⋯ Our results suggest that the effects of both drugs are mainly due to peripheral site of action without rejecting an additional central site of action of systemic non-steroidal anti-inflammatory drugs (NSAIDs) and acetaminophen. In addition, our results suggest that the approach we used could be a useful tool to evaluate systematically and quantitatively the effects of NSAIDs. Finally, the effects obtained with the low dose of acetaminophen question the classical view of textbooks claiming that such a compound had no anti-inflammatory effect and are in agreement with previous observations in humans.
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Randomized Controlled Trial Comparative Study Clinical Trial
Increased pressure pain sensibility in fibromyalgia patients is located deep to the skin but not restricted to muscle tissue.
This study was aimed at comparing pressure pain sensibility in different tissues in fibromyalgia patients. Pressure pain thresholds (PPTs) were assessed in 16 fibromyalgia (FM) patients bilaterally at the bony part of epicondylus lateralis humeri, at the belly of m. extensor carpi ulnaris and at m. brachioradialis where the radial nerve branches pass underneath. Following a double-blind design, either a local anesthetic cream (EMLA) or a control cream was applied to the skin and PPTs were reassessed. ⋯ The PPTs over the bony and the 'pure' muscle sites did not differ. Application of EMLA, compared to control cream, did not change PPTs over any area examined. The results demonstrated that pressure-induced pain sensibility in FM patients is not most pronounced in muscle tissue and does not depend on increased skin sensibility.
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Meta Analysis
Efficacy of epidural steroid injections for low-back pain and sciatica: a systematic review of randomized clinical trials.
The purpose of the study was to assess the efficacy of epidural steroid injections for low-back pain. Data was obtained using computer-aided search of published randomized clinical trials and assessment of the methods of the studies. Twelve randomized clinical trials evaluating epidural steroid injections were identified. ⋯ The efficacy of epidural steroid injections has not been established. The benefits of epidural steroid injections, if any, seem to be of short duration only. Future research efforts are warranted, but more attention should be paid to the methods of the trials.
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It has recently become accepted that the activated immune system communicates to brain via release of pro-inflammatory cytokines. This review examines the possibility that pro-inflammatory cytokines (interleukins and/or tumor necrosis factor) mediate a variety of commonly studied hyperalgesic states. ⋯ Lastly, we will examine the potential roles that both pro-inflammatory cytokines and the neural circuits that they activate may play in the hyperalgesic states produced by irritants, inflammatory agents, and nerve damage. The possibility is raised that apparently diverse hyperalgesic states may converge in the central nervous system and activate similar or identical neural circuitry.