Pain
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Neuropathic pain or persistent dysesthesias may be initiated by mechanical, chemical, or ischemic damage to peripheral sensory nerves. In animal models of neuropathic pain, transection or constrictive injury to peripheral nerves produces ectopic discharges originating at both injury sites and related dorsal root ganglia (DRG), and, consequently, hyperexcitability in associated dorsal horn (DH) neurons of the spinal cord. Since ectopic discharges are inhibited by agents that block voltage-sensitive Na+ channels, it has been postulated that accumulation of Na+ channels in the membrane at nerve injury sites may contribute to, or be responsible for, the development of ectopic neuronal activity (ENA). ⋯ Inhibition of ENA in neuromas and DRG did not recover within 10 min after 100 or 300 microg/kg TTX. By comparison, the ED50 value for the initial decrease of HR was 17.9 (15.0-21.5) microg/kg, and partial recovery occurred within approximately 3 min. These data support the hypothesis that Na+ channel accumulation contributes to the generation of ectopic discharges in neuromas and DRG, and suggest that TTX-sensitive Na+ channels located at the nerve injury site and DRG play an important role in the genesis of neuropathic pain.
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Randomized Controlled Trial Clinical Trial
The visual analogue pain intensity scale: what is moderate pain in millimetres?
One way to ensure adequate sensitivity for analgesic trials is to test the intervention on patients who have established pain of moderate to severe intensity. The usual criterion is at least moderate pain on a categorical pain intensity scale. When visual analogue scales (VAS) are the only pain measure in trials we need to know what point on a VAS represents moderate pain, so that these trials can be included in meta-analysis when baseline pain of at least moderate intensity is an inclusion criterion. ⋯ For those reporting severe pain 85% scored over 54 mm with a mean score of 75 mm. There was no difference between the corresponding VAS scores of men and women. Our results indicate that if a patient records a baseline VAS score in excess of 30 mm they would probably have recorded at least moderate pain on a 4-point categorical scale.
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Randomized Controlled Trial Clinical Trial
Loss of analgesic effect of morphine due to coadministration of rifampin.
Methadone withdrawal symptoms have been reported in drug addicts treated with the tuberculostatic rifampin. Whereas this interaction can be explained by induction of phase I drug metabolism (CYP3A4), knowledge about induction of phase II metabolism (e.g., UDP-glucuronosyltransferases = UGTs) and its influence on drug effects in man, however, is very limited. The potent analgesic morphine is metabolized by more than one UGT to the active metabolite morphine-6-glucuronide and to morphine-3-glucuronide, which is devoid of analgesic activity. ⋯ Moreover, during treatment with rifampin a proportional reduction of AUCs of morphine-3-glucuronide (P < or = 0.01), morphine-6-glucuronide (P < or = 0.05) and morphine was observed. Since urinary recoveries of both morphine-3-glucuronide and morphine-6-glucuronide were also reduced during administration of rifampin, there is no evidence for a contribution of UGT induction to the observed interaction. In summary, a major drug interaction was observed between morphine and rifampin, which could not be attributed to induction of UGTs, but resulted in a complete loss of analgesic effects of the opioid.
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Randomized Controlled Trial Clinical Trial
Ketamine, an NMDA receptor antagonist, suppresses spatial and temporal properties of burn-induced secondary hyperalgesia in man: a double-blind, cross-over comparison with morphine and placebo.
Effects of morphine and ketamine (NMDA receptor antagonist) on temporally summated pain ('wind-up-like pain') and spatial aspects of secondary hyperalgesia were investigated in 12 healthy volunteers. Hyperalgesia was produced by a local 1 degree burn injury covering 12.5 cm2 on the medial surface of the calf. Primary hyperalgesia was determined by measuring heat pain detection threshold (HPDT) within the site of injury. ⋯ Morphine did not significantly change the size of the area of secondary hyperalgesia and did not affect 'wind-up-like pain'. Ketamine or morphine did not change thermal detection thresholds. We conclude that spatial and temporal mechanisms, underlying secondary hyperalgesia, are mediated by glutamatergic transmission via NMDA receptors.
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Comparative Study Clinical Trial Controlled Clinical Trial
Differences in patients' and family caregivers' perceptions of the pain experience influence patient and caregiver outcomes.
The purposes of this study were to determine if there were differences in pain intensity scores, pain duration scores, mood states, and quality of life of oncology outpatients whose pain intensity scores were congruent with their family caregivers compared to patients whose pain intensity scores were non-congruent and to determine if there were differences in mood states, health status, and caregiver strain between family caregivers whose pain intensity scores were congruent with their family members and those family caregivers whose pain intensity scores were non-congruent. A total of 78 patient-caregiver dyads participated in the study. Patients completed a Demographic Questionnaire, a Cancer Pain Questionnaire, the Profile of Mood States, and the Multidimensional Quality of Life Scale-Cancer 2. ⋯ Patients in the non-congruent dyads (i.e. difference of >10 on the VAS score) had significantly more mood disturbance and a poorer quality of life than patients in the congruent dyads. Family caregivers in the non-congruent dyads had significantly higher caregiver strain score than caregivers in the congruent dyads. These findings suggest that differences in the perception of the pain experience between patients and their family caregivers is associated with deleterious outcomes for the patient and their family caregivers.