RESUMO
BACKGROUND: Changes in nitric oxide (NO) production in the dorsal root ganglia (DRG) may contribute to allodynia after nerve injury. It is known that the histochemistry of NADPH-diaphorase (NADPH-d) is known to be not always coincident with NOS. This study was conducted to investigate the relationship between nNOS and NADPH-d expression in the DRG in a spinal nerve injury model of neuropathic pain, and to elucidate role that NO plays in neuropathic pain. METHODS: nNOS immunohistochemistry and/or NADHP-d histochemistry were conducted in the DRG of a spinal nerve transection model of neuropathic pain, and the pain behavior was then measured by a von Frey filament test of the hindpaws of wild type and nNOS knock-out mice. RESULTS: nNOS immunoreactive neurons and NADPH-d stained neurons were not always identical. Additionally NADPH-d increased, but nNOS did not increase significantly in the DRG after spinal nerve transection. Neuropathic pain behavior increased in the hindpaw of nNOS(-/-) mice after spinal nerve transection, but was lower than that of wild type mice after spinal nerve transection. CONCLUSIONS: nNOS immunoreactive neurons and NADPH-d stained neurons were not always identical in the DRG, and a novel NADPH-d positive source may be involved in neuropathic pain after spinal nerve transection. Changes in nNOS expression in the DRG were not the primary cause of neuropathic pain behavior in a spinal nerve transection model of neuropathic pain.
RESUMO
Cauda equina syndrome is a well-known but rare complication of spinal anesthesia. An 80-year-old man was scheduled for both herniorrhaphy. Spinal anesthesia was performed at the L3-4 interspinous space with 0.5% hyperbaric bupivacaine 12 mg. Eight hours after anesthesia, the patient complained bilateral sensorimotor deficits of the lower extremities and peroneal region. Urinary and fecal incontinence were also observed. MRI and myelography showed severe central spinal stenosis at L3-4 and L4-5. EMG showed cauda equina syndrome. Seven weeks after the procedure, left decompressive subtotal laminectomy L2-L5 was done. The patient still complains the neuropathic pain in the both lower extremities and ambulates using a walker. The local anesthetic was injected into thecal sac between maximum stenoses, and it is likely that there was poor upward spread leading to maldistribution of local anesthetic and resultant local anesthetic toxicity.
RESUMO
BACKGROUND: A priming dose of rocuronium can shorten the onset time of neuromuscular blockade. The purpose of this study was to evaluate the effect of priming with rocuronium on the onset time and intubation conditions during tracheal intubation with low-dose rocuronium (0.35 mg/kg) and to compare results with those for rocuronium 0.45 mg/kg. METHODS: One hundred twenty four patients were randomly allocated to three groups. Following induction of anesthesia, groups I and III received normal saline while group II received a priming dose of rocuronium (0.05 mg/kg). Three minutes after priming, groups I, II and III received, respectively, 0.45 mg/kg, 0.3 mg/kg and 0.35 mg/kg rocuronium. Intubation was performed 2 minutes after the administration of an intubating dose and intubation conditions were evaluated. Neuromuscular blockade was assessed by accelerography. RESULTS: The proportion of cases having optimal intubation conditions in group I was higher than in groups II and III. There was no significant difference in the onset times among groups. Neuromuscular blockade at 60, 90 and 120 seconds after an intubating dose was similar among all groups except at 60 sec. Maximal blockade for group I was deep compared to groups II and III. CONCLUSIONS: Rocuronium 0.35 mg/kg does not provide satisfactory intubation conditions. There are no effects on onset time and intubation conditions due to priming during tracheal intubation with rocuronium 0.35 mg/kg.
