Neurologia medico-chirurgica
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Neurol. Med. Chir. (Tokyo) · Jan 2000
Case ReportsTransvenous embolization of carotid-cavernous sinus fistula associated with a primitive trigeminal artery--case report.
A 58-year-old female presented with right conjunctival chemosis and right abducens nerve paresis. Cerebral angiography demonstrated a right carotid-cavernous sinus fistula associated with persistent primitive trigeminal artery. ⋯ Follow-up angiography performed 14 days after the embolization revealed complete disappearance of the carotid-cavernous sinus fistula due to thrombosis, which was presumably accelerated by the coils. Transvenous coil embolization should be considered as an alternative treatment for high-flow carotid-cavernous sinus fistula, but only if transarterial balloon embolization is not successful or unavailable.
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Neurol. Med. Chir. (Tokyo) · Jan 2000
Changes in local cerebral blood flow, glucose utilization, and mitochondrial function following traumatic brain injury in rats.
The pathophysiology of secondary brain damage following experimental traumatic brain injury was investigated by measuring local cerebral blood flow (lCBF), local cerebral glucose utilization (lCGU), and activity of succinate dehydrogenase (SDH), which is a mitochondrial enzyme of the tricarboxylic acid cycle, in the rat brain after moderate lateral fluid percussion injury. Measurements used autoradiography for lCBF and lCGU with [14C]iodoantipyrine and [14C]2-deoxyglucose, respectively. Regional SDH activity was determined using quantitative imaging of formazan produced from 2,3,5-triphenyl tetrazolium chloride by SDH. lCBF decreased at 1 hour after injury and was significantly lower than the preinjury level in almost all regions of both hemispheres at 6 and 24 hours, and remained low at 2 weeks. lCGU increased 1 hour after injury but was significantly decreased at 6 and 24 hours, and at 2 weeks in most regions of both hemispheres. ⋯ Necrosis in the injured cortex and reduction of the number of neurons in the ipsilateral hippocampus were observed 2 weeks after injury. The present study showed that a decrease in lCBF and mitochondrial dysfunction occur with glucose hypermetabolism around 1 hour after lateral fluid percussion injury, and that lCBF, lCGU, and mitochondrial function all deteriorate after 6 hours. This suggests that lCBF and cellular metabolism may change dynamically during the several hours following traumatic brain injury, and afterwards neuronal damage may result in an irreversible change in the areas with depressed glucose hypermetabolism in the early period after injury in combination with mitochondrial dysfunction.