The journal of pain : official journal of the American Pain Society
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Comparative Study
Sex differences in thermal pain sensitivity and sympathetic reactivity for two strains of rat.
Human females are more sensitive than males to brief nociceptive stimuli such as heat and cold. However, a more pronounced peripheral vasoconstriction by females than by males during prolonged nociceptive stimulation predicts that females would be more sensitive to prolonged cold but not heat stimulation. We tested this possibility with reflex (lick/guard) and operant escape and preference tests of sensitivity to prolonged stimulation of Long-Evans and Sprague-Dawley rats. Escape responses to cold stimulation revealed a greater sensitivity of females. In contrast, males were more sensitive to nociceptive heat stimulation. An operant preference test of relative sensitivity to cold or heat stimulation confirmed these results. Cold was more aversive than heat for females, but heat was more aversive than cold for males. Recordings of skin temperature during nociceptive heat stimulation were consistent with the results of operant testing. A reduction in skin temperature (peripheral vasoconstriction) during nociceptive stimulation should increase cold sensitivity as observed for females relative to males. Lick/guard testing did not confirm the results of operant testing. Lick/guard (L/G) responding to nociceptive heat stimulation was greater for females than for males. Female escape responses to heat were more variable than males, but L/G responding of males to the same stimulus was more variable than for females. ⋯ A variety of chronic pain conditions are more prevalent for females, and psychological stress (with attendant sympathetic activation) is implicated in development and maintenance of these conditions. Therefore, understanding relationships between gender differences in pain sensitivity and sympathetic activation could shed light on mechanisms for some varieties of chronic pain.
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Meta Analysis
Acupuncture for tension-type headache: a meta-analysis of randomized, controlled trials.
We investigated the efficacy and safety of acupuncture for the treatment of tension-type headache by conducting a systematic review and meta-analysis of randomized, controlled trials. The Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, CINAHL, and PsycINFO were searched from inception through August 2007. No search or language restrictions were applied. Eight randomized, controlled trials met our inclusion criteria. Pooled data from 5 studies were used for the meta-analysis. Our primary outcome was headache days per month. We assessed data from 2 time points: During treatment and at long-term follow-up (20-25 weeks). The weighted mean difference (WMD) between acupuncture and sham groups was used to determine effect size, and a validated scale was used to assess the methodological quality of included studies. During treatment, the acupuncture group averaged 8.95 headache days per month compared with 10.5 in the sham group (WMD, -2.93 [95% CI, -7.49 to 1.64]; 5 trials). At long-term follow-up, the acupuncture group reported an average of 8.21 headache days per month compared with 9.54 in the sham group (WMD, -1.83[95% CI, -3.01 to -0.64]; 4 trials). The most common adverse events reported were bruising, headache exacerbation, and dizziness. ⋯ This meta-analysis suggests that acupuncture compared with sham for tension-type headache has limited efficacy for the reduction of headache frequency. There exists a lack of standardization of acupuncture point selection and treatment course among randomized, controlled trials. More research is needed to investigate the treatment of specific tension-type headache subtypes.
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Randomized Controlled Trial
Massage reduces pain perception and hyperalgesia in experimental muscle pain: a randomized, controlled trial.
Massage is a common conservative intervention used to treat myalgia. Although subjective reports have supported the premise that massage decreases pain, few studies have systematically investigated the dose response characteristics of massage relative to a control group. The purpose of this study was to perform a double-blinded, randomized controlled trial of the effects of massage on mechanical hyperalgesia (pressure pain thresholds, PPT) and perceived pain using delayed onset muscle soreness (DOMS) as an endogenous model of myalgia. Participants were randomly assigned to a no-treatment control, superficial touch, or deep-tissue massage group. Eccentric wrist extension exercises were performed at visit 1 to induce DOMS 48 hours later at visit 2. Pain, assessed using visual analog scales (VAS), and PPTs were measured at baseline, after exercise, before treatment, and after treatment. Deep massage decreased pain (48.4% DOMS reversal) during muscle stretch. Mechanical hyperalgesia was reduced (27.5% reversal) after both the deep massage and superficial touch groups relative to control (increased hyperalgesia by 38.4%). Resting pain did not vary between treatment groups. ⋯ This randomized, controlled trial suggests that massage is capable of reducing myalgia symptoms by approximately 25% to 50%, varying with assessment technique. Thus, potential analgesia may depend on the pain assessment used. This information may assist clinicians in determining conservative treatment options for patients with myalgia.
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The objective of this study was to assess the impact of persistent inflammation on spinal gamma-aminobutyric acid-A (GABA-A) receptor-mediated modulation of evoked nociceptive behavior in the adult rat. Nocifensive threshold was assessed with von Frey filaments applied to the dorsal surface of the hind paw. The GABA-A receptor agonist muscimol, the antagonist gabazine, the benzodiazepine receptor agonist midazolam, and antagonists PK11195 and flumazenil were administered spinally in the presence and absence of complete Freund's adjuvant (CFA)-induced inflammation. In naive rats, muscimol increased and gabazine decreased nociceptive threshold. After CFA, the effects of these compounds were reversed: Low doses of muscimol exacerbated the inflammation-induced decrease in nociceptive threshold and gabazine increased nociceptive threshold. Midazolam increased nociceptive threshold both in the presence and absence of inflammation. Flumazenil but not PK11195 blocked the analgesic effects of midazolam. These findings indicate that inflammation-induced changes in GABA-A signaling are complex and are likely to involve several distinct mechanisms. Rectifying the changes in GABA-A signaling may provide effective relief from hypersensitivity observed in the presence of inflammation. ⋯ An inflammation-induced shift in spinal GABA-A receptor signaling from inhibition to excitation appears to underlie inflammatory pain and hypersensitivity. Use of GABA-A receptor selective general anesthetics in association with therapeutic interventions may be contraindicated. More importantly, rectifying the changes in GABA-A signaling may provide effective relief from inflammatory hypersensitivity.