Neurogenic pulmonary edema (NPE) is an underdiagnosed clinical entity. Its pathophysiology is multifactorial but largely unknown. We report two cases of NPE and review the literature on NPE cases reported since 1990. A 21-year-old man had a seizure episode following cranioplasty. He became increasingly dyspneic, and clinical and laboratory signs of respiratory failure were evident. Chest radiography and computed tomography showed bilateral diffuse infiltrates. After supportive measures were taken, complete respiratory recovery occurred in 72 hours. A 52-year-old woman had several seizure episodes following subarachnoid hemorrhage due to a cavernoma. She became increasingly dyspneic upon arrival at the hospital. After tracheostomy and oxygen support were established, chest radiography showed bilateral diffuse infiltrates. Respiratory recovery was excellent, and the patient was eupneic with normal results of chest radiography 48 hours later. Fourteen reports (21 cases) were found. Thirteen patients were female, and the mean age of the patients was 31.6 years. The most frequent underlying factor was subarachnoid hemorrhage (42.9%). Symptom onset occurred <4 hours after the neurologic event in 71.4% of cases. One third of the patients presented with pink frothy sputum. Chest radiography showed bilateral diffuse infiltrates in 90.5% of cases. Supportive measures included oxygen support and vasoactive drugs. Recovery was usually very rapid: 52.4% of patients recovered in <72 hours. Almost 10% of patients died of NPE. Our two cases had clinical and laboratory features in common with most NPE cases. Physicians should remember NPE when neurologic patients suddenly become dyspneic. The mortality rate is high, but surviving patients usually recover very quickly.

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OBJECTIVES:1) To correlate the methylation status of the O6-methylguanine-DNA-methyltransferase (MGMT) promoter to its gene and protein expression levels in glioblastoma and 2) to determine the most reliable method for using MGMT to predict the response to adjuvant therapy in patients with glioblastoma.BACKGROUND:The MGMT gene is epigenetically silenced by promoter hypermethylation in gliomas, and this modification has emerged as a relevant predictor of therapeutic response.METHODS:Fifty-one cases of glioblastoma were analyzed for MGMT promoter methylation by methylation-specific PCR and pyrosequencing, gene expression by real time polymerase chain reaction, and protein expression by immunohistochemistry.RESULTS:MGMT promoter methylation was found in 43.1% of glioblastoma by methylation-specific PCR and 38.8% by pyrosequencing. A low level of MGMT gene expression was correlated with positive MGMT promoter methylation (p = 0.001). However, no correlation was found between promoter methylation and MGMT protein expression (p = 0.297). The mean survival time of glioblastoma patients submitted to adjuvant therapy was significantly higher among patients with MGMT promoter methylation (log rank = 0.025 by methylation-specific PCR and 0.004 by pyrosequencing), and methylation was an independent predictive factor that was associated with improved prognosis by multivariate analysis.DISCUSSION AND CONCLUSION:MGMT promoter methylation status was a more reliable predictor of susceptibility to adjuvant therapy and prognosis of glioblastoma than were MGMT protein or gene expression levels. Methylation-specific polymerase chain reaction and pyrosequencing methods were both sensitive methods for determining MGMT promoter methylation status using DNA extracted from frozen tissue.