Pain
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This study examined the relative predictive validities of several measures of pain intensity. Forty chronic pain patients completed 6-14 days worth of hourly pain ratings, which were averaged to obtain a measure of actual average pain intensity. These patients then made ratings, on 101-point numerical rating scales, of worst, least, and usual pain during the previous 2 wks, and of their current pain. ⋯ Of all possible composites of usual, least, worst, and current pain ratings, the arithmetic mean of least and usual pain had the strongest relationship to actual average pain. The inclusion of ratings of most pain or current pain in any composite score actually weakened the relationship between the composite score and actual average pain intensity. These results suggest that, when clinicians or researchers wish to assess average pain among chronic pain patients, but cannot obtain multiple measures of pain over time, the most valid measure would be the arithmetic mean of patient-recalled least and usual pain.
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Clinical Trial Controlled Clinical Trial
The effect of ketamine on phantom pain: a central neuropathic disorder maintained by peripheral input.
Hyperactivity of N-methyl D-aspartate (NMDA) receptors may be one of the factors in the maintenance of persistent stump and phantom limb pain. Ketamine (bolus at 0.1 mg/kg/5 min followed by an infusion of 7 micrograms/kg/min) was administered intravenously to 11 patients with established stump and phantom limb pain in a double-blind saline-controlled study. All 11 patients responded with a decrease in the rating of stump and phantom limb pain assessed by visual analogue scale (VAS) and McGill Pain Questionnaire (MPQ). ⋯ Side effects were observed in nine patients. The results support the notion that stump and phantom pain are generated by activity in afferent fibres activated by mechanical but not by thermal stimuli and that the NMDA receptor is involved in the maintenance of postamputation pain states. NMDA receptor antagonists may have a potential in the treatment of stump and phantom limb pain.
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Withdrawal responses to heat and mechanical stimuli applied to the plantar surface of the rat hindpaw were measured before and after an intraplantar injection of capsaicin. In separate groups of rats, capsaicin doses of 1, 10 and 30 micrograms, and the vehicle were given into the center of the plantar surface in a volume of 10 microliters. Withdrawal latency evoked by radiant heat and the frequency of withdrawal evoked by mechanical stimuli (von Frey monofilaments) were obtained from both hindpaws before and after injection. ⋯ Injection of the vehicle did not significantly alter withdrawal responses to heat or mechanical stimuli. These studies demonstrate that intraplantar injection of capsaicin in rats produces hyperalgesia to heat and mechanical stimuli. This model should be useful for correlative behavioral, physiological and pharmacological studies of underlying mechanisms of capsaicin-evoked hyperalgesia.
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Experimental pain can elevate vibrotactile threshold, a phenomenon attributed in the literature to the operation of a 'touch gate.' It is not known, however, whether clinical pain produces similar effects. To explore this possibility, we measured vibrotactile threshold in patients with temporomandibular disorders (TMD) whose pain had a prominent myalgic component. Two-interval forced-choice tracking was used to determine threshold for a 25-Hz vibratory stimulus presented on the cheek. ⋯ These findings are consistent with the idea of a touch gate, and suggest the usefulness of further research in this area with clinical pain populations. The effects of an adapting stimulus (25 Hz, 20 dB SL) were also studied, and found to produce parallel elevations in vibrotactile threshold in the TMD and pain-free groups. This result indicates that at least some adaptation occurs at a higher (subsequent) level of somatosensory information processing than does the touch gating implied by the unadapted thresholds.
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This study examined possible psychological differences between Reflex Sympathetic Dystrophy (RSD) and non-RSD chronic pain patients. Unlike the few previous studies in this area, this study controlled statistically for age and pain duration differences across diagnostic groups, and included a non-RSD limb pain control group. Subjects were a consecutive series of 34 RSD, 50 non-RSD limb pain (Limb), and 165 low back pain (LBP) patients presenting for treatment at the Rush Pain Center. ⋯ These results provide partial support for clinical assumptions that RSD patients are more psychologically dysfunctional than other chronic pain patients. However, these conclusions do not generalize across all comparison groups. The fact that RSD and non-RSD limb pain patients were quite similar on nearly all measures suggests that sympathetic mediation of pain is not the source of these psychological differences.