A 14-year-old male patient developed severe right limb pain after traumatic sciatic nerve injury. His pain was diagnosed as neuropathic pain (complex regional pain syndrome, type II). He did not respond to any conventional therapy for limb pain including non-steroidal antiinflammatory drugs, antidepressants, anticonvulsants, continuous epidural administration of local anesthetics and psychotherapy. Following continuous epidural administration of a very low dose of ketamine, an N-methyl-D-aspartic acid (NMDA) receptor antagonist, 25 microg/kg per h for 10 days, complete pain relief was obtained without any side-effects. There has been no recurrence of pain for 8 months after discontinuation of epidural ketamine. The symptoms related to dysfunction of the sympathetic nervous system still remained after complete pain relief. We discuss pain mechanisms, pain relief and the use of ketamine in this case.

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Although an acute selective inhibition of neuronal NOS decreases sevoflurane MAC and cerebellar cGMP concentrations in mice, there was a dissociation between the two parameters during long-term neuronal NOS inhibition. There may be cGMP-independent compensatory mechanisms that mediate nociception when NOS is chronically inhibited.

The formalin test is an animal model of persistent pain. Although biphasic behavioral responses to formalin injection have been well described, the significance of the biphasic time course of the pain behaviors has not been established. To explore the significance of the behavioral responses to the formalin injection, we measured and analyzed cortical electroencephalogram (EEG) during the formalin tests in rats. Formalin was injected subcutaneously in the hindpaw of freely moving rats, and behavioral responses were visually counted and recorded. Results were compared with a control group which received saline injection. Neocortical EEG was recorded from implanted dural surface electrodes and analyzed using a Fast Fourier Transformation. Formalin produced biphasic pain behaviors with a transient pause between two phases. Cortical EEG recordings showed a biphasic change; a vigilant pattern (a low amplitude high frequency activity) followed by a non-vigilant pattern (a high amplitude low frequency activity), showing a good correlation with apparent arousal states of rats. Observed discrepancies between pain behaviors and EEG-measured vigilance stages included (1) a vigilant EEG pattern persisted during the transient pause of pain behavior, and (2) pain behaviors persisted even after non-vigilant EEG pattern became dominant. The results of the current study showed that there are temporal discrepancies between the pain behaviors and EEG-measured vigilance during the formalin test in rats. The temporal relationship between the 'pain' behaviors and nociception per se may not be as solid as believed.

We report a Japanese woman who survived severe 5fluorouracil (5-FU) toxicity after receiving 5Ј-deoxy-5fluoro-uridine (5ЈDFUR) for the treatment of breast cancer (pt2n1m1); the toxicity was due to decreased dihydropyrimidine dehydrogenase (DPD) activity. Pharmacokinetic investigation showed very high and prolonged plasma 5-FU concentrations after termination of the oral administration of 5ЈDFUR. The DPD activity in all plasma samples was below 30 pmol/min per mg protein. Her urinary thymine and uracil levels were high, and the ratios of urinary dihydrothymine/thymine and dihydrouracil/uracil were very low compared with the ratios in healthy people. These findings suggest that determination of urinary pyrimidine and dihydropyrimidine levels would be an appropriate urinary screening sytem that may be useful for evaluating DPD activity before 5-FU treatment is initiated.