Supplemental Oxygen Concentration and Increased Signal Intensity of Cerebrospinal Fluid on FLAIR MR Images

Abstract

From: Flavio T. Braga, MD,* Antonio J. da Rocha, MD, PhD,* and Ricardo B. Fonseca, MD Department of Radiology, Santa Casa de Misericordia de Sao Paulo, Sao Paulo, Brazil* Department of Radiology, Vanderbilt University Medical Center 1161 21st Avenue South, MCN CCC-1118, Nashville, TN 37232-2675 e-mail: ricardo.fonseca@vanderbilt.edu Editor: We read with great interest the article by Dr Frigon and colleagues (1) in the October 2004 issue of Radiology,“Supplemental Oxygen Causes Increased Signal Intensity in Subarachnoid Cerebrospinal Fluid on Brain FLAIR MR Images Obtained in Children during General Anesthesia.” This article deals with a subject that is part of our line of research. The increase in signal intensity (SI) in the cerebrospinal fluid (CSF) on fluid-attenuated inversion-recovery (FLAIR) magnetic resonance (MR) images that results from inspired oxygen levels has been shown in the literature (2–4). As indicated by the authors, awareness of this phenomenon is important to avoid diagnostic mistakes. The article fulfills its objective of showing a relationship between a high fraction of inspired oxygen (FIO2) and an elevation in the CSF SI on FLAIR images. However, one methodologic issue deserves further analysis. As the study was performed, it is not possible to categorically determine whether the persistence of high SI in the CSF in some patients after inhaling 30% O2 is due to propofol or an insufficient amount of time between image acquisitions to allow for equilibrium of the blood and CSF O2 tension. We believe, however, that the persistent high SI is due to the order in which the sequences were performed. Had the authors chosen to acquire the images with 30% FIO2 first before acquiring images with 100% FIO2, high SI would not occur with 30% FIO2, and it would be certain that propofol was not responsible for CSF hyperintensity on FLAIR images. After observing high SI in the CSF of anesthetized patients, Fillipi et al (2) proposed propofol as the culprit. However, a meticulous study by Deliganis et al (3) showed that O2 causes the increase in SI in the CSF. Our study did not show any change in the CSF SI with different anesthetic drugs, including propofol (4). We believe that it is essential to control the FIO2 in patients who are anesthetized during brain MR imaging, especially in patients suspected of having meningeal disease, be it inflammatory or neoplastic. Specifically, if the FIO2 is kept below 50%, there should be no artifactual increase in the SI of the CSF on FLAIR images (4) and, therefore, increased SI in the CSF can be interpreted as pathologic. On the other hand, we have used increased FIO2 to perform a type of noninvasive MR cisternography, with good results in the identification and characterization of small cystic lesions in the subarachnoid space (5). Finally, we congratulate Dr Frigon and colleagues for furthering the knowledge on the relationship between oxygen and increased SI in the CSF on FLAIR MR images.