{"title":"Transient cortical blindness due to hypertensive encephalopathy. Magnetic resonance imaging correlation.","authors":"T R Marra, M Shah, M A Mikus","doi":"10.3109/01658109309037000","DOIUrl":null,"url":null,"abstract":"<p><p>Striking reversible signal intense magnetic resonance imaging (MRI) lesions were observed in the occipital cortex of a 16-year-old girl who presented with an attack of transient cortical blindness as the initial manifestation of hypertensive encephalopathy (HTE). The lesions were seen to best advantage on T2-weighted imaging and were not visible on computed tomography (CT). It is proposed that such occipital lobe MRI lesions likely reflect extravasation of fluid and proteins across the blood brain barrier, damaged as a consequence of cerebral autoregulation failure.</p>","PeriodicalId":77200,"journal":{"name":"Journal of clinical neuro-ophthalmology","volume":"13 1","pages":"35-7"},"PeriodicalIF":0.0000,"publicationDate":"1993-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/01658109309037000","citationCount":"9","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of clinical neuro-ophthalmology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3109/01658109309037000","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 9
Abstract
Striking reversible signal intense magnetic resonance imaging (MRI) lesions were observed in the occipital cortex of a 16-year-old girl who presented with an attack of transient cortical blindness as the initial manifestation of hypertensive encephalopathy (HTE). The lesions were seen to best advantage on T2-weighted imaging and were not visible on computed tomography (CT). It is proposed that such occipital lobe MRI lesions likely reflect extravasation of fluid and proteins across the blood brain barrier, damaged as a consequence of cerebral autoregulation failure.