LAUSR

http://dx.doi.org/10.1590/0100-3984.2017.0188 Pantelis Kraniotis1,a, Aikaterini Solomou1,b 1. University General Hospital of Patras, Patras, Greece. a. https://orcid.com/0000-0001-9149-1586; b. https://orcid.com/0000-0002-8501-1192. Correspondence: Pantelis Kraniotis, MD. University General Hospital of Patras. Hippokratous av., Patras 265 00, Greece. Email: [email protected]. Received 16 October 2017. Accepted after revision 27 November 2017. in the central nervous system is the result of a combination of disruption of the blood-brain barrier, high vascularity, and contrast leakage into the lymphatic system. After one week, infarcts show parenchymal enhancement, due to breakdown of the bloodbrain barrier. New imaging techniques, such as DWI and perfusionweighted imaging, have increased the accuracy of the diagnosis of acute cerebral ischemia, although there are some cases in which it cannot be distinguished from other entities. In addition, because of pseudonormalization, subacute infarcts may not show restricted diffusion on DWI. FLAIR is highly sensitive for the detection of ischemic lesions. Although it is considered to be heavily T2-weighted, rendering cerebrospinal fluid as dark, it also shows mild contrast enhancement on T1WI, which is responsible for the increased conspicuity of gadolinium enhancement. Pathologic conditions that present contrast enhancement on T1WI usually show marked enhancement on contrast-enhanced FLAIR. This is exactly what occurred in the case presented here, in which DWI pseudonormalization did not help reveal the subacute cortical infarct. When a subacute cortical infarct is suspected, delayed contrast-enhanced FLAIR imaging is the best choice for demonstrating the lesion and for differentiating it from an older lesion with gliosis.