Pain
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The analgesic effectiveness and safety of oral tramadol were compared with standard analgesics using a meta-analysis of individual patient data from randomised controlled trials in patients with moderate or severe pain after surgery or dental extraction. Calculation of %maxTOTPAR from individual patient data, and the use of > 50%maxTOTPAR defined clinically acceptable pain relief. Number-needed-to-treat (NNT) for one patient to have > 50%maxTOTPAR compared with placebo was used to examine the effectiveness of different single oral doses of tramadol and comparator drugs. ⋯ There was a dose response with tramadol, tending towards higher incidences at higher doses. Single-patient meta-analysis using more than half pain relief provides a sensitive description of the analgesic properties of a drug, and NNT calculations allow comparisons to be made with standard analgesics. Absolute ranking of analgesic performance should be done separately for postsurgical and dental pain.
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The aim of this study was to examine whether mean data from categorical pain intensity and visual analogue scales for both pain intensity and relief could be used reliably to derive dichotomous outcome measures for meta-analysis. Individual patient data from randomised controlled trials of single-dose analgesics in acute postoperative pain were used. The methods used were as follows: data from 132 treatments with over 4700 patients were used to calculate mean %maxSPID (categorical pain intensity), %maxVAS-SPID (visual analogue pain intensity) and %maxVAS-TOTPAR (visual analogue pain relief); these were used to derive relationships with the number of patients who achieved at least 50% pain relief (%maxTOTPAR). ⋯ Reports of randomised trials of analgesics frequently describe results of studies in the form of mean derived indices, rather than using discontinuous events, such as number of proportion of patients obtaining at least 50% pain relief. Because mean data inadequately describe information with a non-normal distribution, combining such mean data in systematic reviews may compromise the results. Showing that dichotomous data can reliably be derived from mean SPID, VAS-SPID and VAS-TOTPAR as well as TOTPAR data in previously published acute pain studies makes much more information accessible for meta-analysis.
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The mechanical allodynia and edema related to a subcutaneous carrageenin injection are increased by a conditioning carrageenin injection 7 days before (Guilbaud et al., 1992). In the present study, the possibility of preventing this by bupivacaine infiltration was tested. In the first part of the experiment, the time course of a carrageenin induced inflammation of the right hind paw was assessed in animals receiving local anesthetic injection (0.2 ml of bupivacaine 0.5% solution with epinephrine) either 5 min before (BUPI PRE group) or 60 min after (BUPI POST group) the carrageenin injection (0.2 ml of 1% solution). ⋯ In contrast, the increase in allodynia and edema was less intense in the BUPI PRE group than in the other groups (P < 0.0001 and P < 0.02 respectively). Bupivacaine injections had no effect on allodynia and edema related to a second contra-lateral carrageenin injection. These results suggest that bupivacaine infiltration, when administered before the first conditioning injection of carrageenin, can prevent the reinforcement of mechanical allodynia and edema related to a second ipsilateral injection of carrageenin 7 days later.
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The opioid antagonist, naloxone, produces equivocal effects on the magnitude of nociceptive responses in several animal models of persistent pain, including the formalin test. Hindpaw injection of dilute formalin produces not only inflammation but also phasic (Phase 1) and persistent (Phase 2) behavioral and cardiovascular nociceptive responses in the rat. ⋯ Although the 100 mg/kg per h dose significantly decreased these responses, it also produced muscle rigidity and profound bradycardia. We conclude that endogenous opioids do not significantly modulate the nociceptive processing induced by subcutaneous formalin.
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Randomized Controlled Trial Clinical Trial
Effect of adrenergic receptor activation on post-herpetic neuralgia pain and sensory disturbances.
Patients with acute herpes zoster, and to a lesser extent post-herpetic neuralgia (PHN), have been reported to respond to local anesthetic blockade of the sympathetic nervous system. In animal models of nerve injury, local injection of adrenergic agonists after nerve injury, but not before, excites nociceptors. In some patients with chronic neuropathic pain, local application of norepinephrine evokes pain. ⋯ After injection of the adrenergic agonist into PHN skin, both overall PHN pain and allodynia severity were significantly greater than after saline injection, peaking at 10-15 min post-injection. Even when PHN has been present for years, adrenergic receptor stimulation in PHN skin increases pain, most likely through direct activation of C-nociceptors in the painful skin. Increased allodynia is most likely mediated centrally and driven by the increase in C-nociceptor input.