Clinical and Radiological Analysis of Reversible Posterior Leukoencephalopathy Syndrome in Children / 소아과

clinical and radiologic findings that mainly involve the white/gray matter of the parieto-occipital lobes. The purpose of this study was to determine its clinical and radiological characteristics. METHODS: A total of 15 pateints were involved in the study. Their medical records and radiological features of brain MRI were retrospectively reviewed and analyzed. RESULTS: Fifteen pateints were involved. (9 males and 5 females). The patients' ages ranged from 2-20 years (mean age:10 years). The brain MRI revealed fairly symmetric areas of increased T2 signal involving both white and gray matter of parieto-occipital regions. The condition seemed to be associated with cyclosporin A and steroid therapy or a variety of other conditions in which blood pressure rises acutely. CONCLUSION: Reversible posterior leukoencephalopathy syndrome is a complicated neurological condition, but a better understanding of this complex syndrome may obviate unnecessary investigations and lead to prompt and appropriate management of the associated problems.

Effect of Hypoxia-ischemia on c-fos Expression in the Neonatal Rat Brain

PURPOSE: Brain damage resulting from a combination of hypoxia and ischemia in the newborn infant remains a major cause of perinatal death, cerebral palsy, mental retardation and epilepsy. Metabolic stress, including ischemia, hypoxia and seizures, induces the expression of a variety of stress proteins including nuclear proto-oncogene c-fos. The induction of c-fos can be considered a biomarker of events resulting from ischemia-hypoxia. However, it has been suggested that the mechanism for c-fos activation in the fetal brain is not mature prior to postnatal day 13-21. This study was undertaken to determine the induction of c-fos in neonatal rat brain by hypoxia-ischemia and the regions of brain most vulnerable to hypoxia-ischemia. MEHTODS: Ten-day-old postnatal rat pups, subjected to unilateral carotid artery dissection combined with 2-hour hypoxia, were killed at 2 hours and 6 hours after hypoxia-ischemia, and their brains were examined by immunohistochemistry. RESULTS: Hypoxia-ischemia induced prominent expression of c-fos in the cingulate cortex and hippocampus in the postnatal rats 2 hours after the insult. CONCLUSION: Hypoxia-ischemia results in increased c-fos expression in 10-day-old rat pups. The results of this experiment also demonstrate that the neonatal rat hippocampus and cortex are the most sensitive brain regions to the induction of c-fos following hypoxia-ischemia.

Effect of Hypoxia-ischemia on c-fos Expression in the Neonatal Rat Brain

PURPOSE: Brain damage resulting from a combination of hypoxia and ischemia in the newborn infant remains a major cause of perinatal death, cerebral palsy, mental retardation and epilepsy. Metabolic stress, including ischemia, hypoxia and seizures, induces the expression of a variety of stress proteins including nuclear proto-oncogene c-fos. The induction of c-fos can be considered a biomarker of events resulting from ischemia-hypoxia. However, it has been suggested that the mechanism for c-fos activation in the fetal brain is not mature prior to postnatal day 13-21. This study was undertaken to determine the induction of c-fos in neonatal rat brain by hypoxia-ischemia and the regions of brain most vulnerable to hypoxia-ischemia. MEHTODS: Ten-day-old postnatal rat pups, subjected to unilateral carotid artery dissection combined with 2-hour hypoxia, were killed at 2 hours and 6 hours after hypoxia-ischemia, and their brains were examined by immunohistochemistry. RESULTS: Hypoxia-ischemia induced prominent expression of c-fos in the cingulate cortex and hippocampus in the postnatal rats 2 hours after the insult. CONCLUSION: Hypoxia-ischemia results in increased c-fos expression in 10-day-old rat pups. The results of this experiment also demonstrate that the neonatal rat hippocampus and cortex are the most sensitive brain regions to the induction of c-fos following hypoxia-ischemia.