Pain
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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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In the present study, Brandtstädter's (1992) distinction between assimilation and accommodation as two fundamental means of coping is applied to the field of chronic pain. Assimilative coping involves active attempts (e.g. instrumental activities, self-corrective actions, compensatory measures) to alter unsatisfactory life circumstances and situational constraints in accordance with personal preferences. Conversely, accommodative coping (e.g. downgrading of aspirations, positive reappraisal, self-enhancing comparisons) is directed towards a revision of self-evaluative and personal goal standards in accordance with perceived deficits and losses. ⋯ Most important, the ability to flexibly adjust personal goals attenuated the negative impact of the pain experience (pain intensity, pain-related disability) on psychological well-being (depression). Furthermore, pain-related coping strategies led to a reduction of disability only when accompanied by a high degree of flexible goal adjustment. The theoretical and clinical implications of these findings for coping research and the treatment of chronic pain patients are discussed.
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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.
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N-Methyl-D-aspartate (NMDA) receptor antagonists have been repeatedly shown to attenuate the development of opiate tolerance and dependence in rodents. In the present experiments, continuous subcutaneous infusion of either MK-801 (0.01 mg/kg/h but not 0.005 mg/kg/h) or DM (0.133, 0.67 and 1.33 mg/kg/h) reliably prolonged the antinociceptive effect of continuous subcutaneous infusion of morphine sulfate (2.0 mg/kg/h), indicating attenuation of the development of morphine tolerance. Furthermore, this prolonged antinociception was completely reversible by naloxone (10 mg/kg, i.p.). ⋯ The effects of MK-801 on all withdrawal symptoms were confounded, however, by the appearance of flaccidity following naloxone administration to rats having received MK-801 and morphine. These results extend previous observations by showing that the prolonged antinociception observed following co-administration of morphine and an NMDA antagonist is completely naloxone-reversible, supporting the notion that this antinociception reflects prolongation of an opioid receptor-mediated effect. The different profiles of side effects associated with MK-801 and DM, however, suggest that (1) attenuation of naloxone-precipitated withdrawal symptoms by MK-801 may be an artifact of toxicity, and (2) DM may prove clinically useful for the prevention of morphine tolerance, given its lack of observable side effects when administered concurrently with morphine to rodents.
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Two established phenomena contribute to the generation of post-injury pain hypersensitivity: peripheral sensitization, an increase in transduction sensitivity of high threshold A delta and C-fibre nociceptors, and central sensitization, an increase in excitability of neurones in the spinal cord triggered exclusively by C-fibre inputs. We now describe a novel phenomenon: progressive tactile hypersensitivity, which contributes to a cumulative allodynia during inflammation. Behavioural measurements in conscious intact animals showed that repeated light touch stimuli delivered at 5-min intervals to an inflamed paw, established 48 h earlier by an intra-plantar injection of complete Freund's adjuvant (CFA), resulted in a progressive reduction in the mechanical withdrawal threshold by more than 75%, from its already hypersensitive basal level. ⋯ Progressive hypersensitivity, measured here as a progressive tactile allodynia after inflammation in either intact or decerebrate-spinal rats, with its gradual build-up and contribution from A beta fibres, is very different from the central sensitization induced by C-fibre stimulation which is characterised by a peak increase in excitability soon after the conditioning input followed by a steady decrement to baseline levels. Progressive hypersensitivity is likely to be the consequence of an alteration in the function and phenotype of afferents innervating inflamed tissue and the pattern of excitation they produce in spinal neurones. The phenomenon may have an important role in the development of inflammatory pain and hypersensitivity.