Pain
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Case Reports
A case of uncommon withdrawal symptoms after a short period of spinal morphine administration.
A 54-year-old female with chronic failed back surgery syndrome and pain in the back and the right leg was treated by chronic spinal morphine administration by an external pump. After a positive test instillation over a 3-week period the spinal catheter was removed. Within 24 h the patient developed fever, leucocytosis, impaired sense of smell and allodynia and hyperpathia in all 4 limbs. ⋯ Good pain relief could be obtained with the daily instillation of 5 mg morphine intrathecally. Fever, leucocytosis, impaired sense of smell, allodynia and hyperpathia in the limbs reappeared a few weeks later. Evaluation showed catheter migration out of the spinal canal.
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We asked 78 chronic low back pain patients to report on their usual pain intensity, and on the lifestyle changes caused by their pain, on a horizontally-oriented visual analogue scale (VAS). Also, the usual and the current pain intensities were examined on a vertical VAS. Statistical analysis showed normal distribution of data in the measurement of usual pain on the horizontal VAS, but no homogeneous distribution on the vertical VAS. ⋯ Also, there was no reduction of the failure rate by giving additional oral explanations in the use of the scale to the patient. Owing to a negative influence in distribution of rates and an increase in the failure rate, complex questions should be avoided. A short written introduction to the scale is sufficient, and oral explanations are not essential.
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This study determines the effects of dexamethasone versus co-administered dexamethasone and diclofenac, on carrageenan-evoked spinal c-Fos expression and peripheral oedema in the freely moving rat. Drugs were administered intravenously 25 min before intraplantar injection of carrageenan (6 mg/150 microliters of saline). Three hours later the number of spinal c-Fos-LI neurones and peripheral oedema were assessed. ⋯ The attenuation by co-administered dexamethasone and diclofenac, of both c-Fos expression and the peripheral oedema, was significantly greater than the effect of dexamethasone alone (P < 0.001 for both) and diclofenac alone (P < 0.001 for both). Our study illustrates enhanced attenuating effects of co-administered dexamethasone and diclofenac on both inflammatory oedema and the associated spinal expression of c-Fos, an indicator of nociceptive transmission at the spinal level. The apparent interactions between the mechanisms of action of NSAIDs and steroids suggest that co-therapy may produce beneficial inflammatory and pain relief in the absence of excessive side effects.
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Many aspects of bilateral presentation or recurrence of reflex sympathetic dystrophy (RSD) are unknown. For this reason 1183 consecutive patients with RSD were analyzed. In 10 patients RSD started in symmetrical limbs. ⋯ Reflex sympathetic dystrophy may recur in the same or in another limb, although only in a minority of patients. Recurrences occur especially in younger patients and in the symmetrical limb. Diagnosis of a recurrence is difficult, for often the recurrence is spontaneous and presents with few signs and symptoms.
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Supraspinal opioid analgesia is mediated in part by connections between the periaqueductal gray (PAG) and rostral ventromedial medulla (RVM). Morphine analgesia elicited from the PAG is respectively decreased by selective serotonergic and opioid receptor antagonists administered into the RVM, and increased by RVM neurotensin antagonists. Since glutamate and excitatory amino acid (EAA) receptors are also active in the RVM, the present study evaluated whether either competitive (AP7) or non-competitive (MK-801) N-methyl-D-aspartate (NMDA) antagonists or a kainate/AMPA (CNQX) antagonist microinjected into the RVM altered morphine (2.5 micrograms) analgesia elicited from the PAG as measured by the tail-flick and jump tests. ⋯ In contrast, small but significant reductions in mesencephalic morphine analgesia occurred on the jump test following CNQX (0.5 microgram, 2.2 nmol) in the RVM. NMDA antagonists did not markedly alter either basal nociceptive thresholds following RVM administration, or mesencephalic morphine analgesia following administration into medullary placements lateral or dorsal to the RVM. These data implicate EAA and particularly NMDA receptors in the RVM in modulating the transmission of opioid pain-inhibitory signals from the PAG.