Posterior Reversible Encephalopathy Syndrome (PRES)

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Identifier PRES_Lee
Title Posterior Reversible Encephalopathy Syndrome (PRES)
Creator Andrew G. Lee, MD; Zane Foster
Affiliation (AGL) Chairman, Department of Ophthalmology, The Methodist Hospital, Houston, Texas; Professor of Ophthalmology, Weill Cornell Medicine, New York City, New York; (ZF) Class of 2020, Baylor College of Medicine, Houston, Texas
Subject Pathology; Encephalopathy; Neuroimaging
Description Dr. Lee lectures medical students on posterior reversible encephalopathy syndrome.
Transcript (Reversible Posterior Leukoencephalopathy Syndrome) "Posterior Reversible Encephalopathy Syndrome: it doesn't have to be encephalopathy, does not have to be reversible, and it does not have to be posterior to be PRES. However, we're going to talk about the classic version: posterior reversible encephalopathy syndrome. The way that this comes to me as a neuro-ophthalmologist is PRES can affect occipital lobes. It can be unilateral, or it can be bilateral. So; that means it can produce a homonymous hemianopsia or cortical blindness. There are many causes of PRES. The most common ones are elevation of blood pressure, malignant hypertension, hypertensive urgencies and hypertensive emergencies, and in pregnancy, eclampsia. But also medications can cause it, including immunosuppressive therapies like tacrolimus. There are other causes too, but these are the most common. It is reversible because the type of edema that we see on MRI scan. That edema is seen on T2 is vasogenic edema in PRES rather than cytotoxic edema as in stroke, so all of these mechanisms - hypertension, eclampsia, and immunosuppressive agents - have a common mechanism of breakdown of the blood-brain barrier. And when you have breakdown of the blood-brain barrier, more water can come out of the blood vessel and we call that type of edema "Vaso-" (from the vessel) "-genic" (genesis). So vasogenic edema is the type of edema that is associated with breakdown of the blood-brain barrier, and PRES. And the way we can see that on imaging is even though both vasogenic edema from the vessel and cytotoxic edema ("cyto-", cell, "toxic", death or illness) cytotoxic edema and vasogenic edema both produce increased T2 signal, in this case the occipital lobe. But the DWI - the diffusion-weighted imaging - can help us establish whether we are dealing with restricted diffusion from cytotoxic edema, or just increased amounts of water from vasogenic edema from breakdown of blood brain barrier. So in patients with cytotoxic edema, the cells swell up and that restricts the movement of the water and that restricted diffusion is seen as hyperintensity on DWI and associated hypointensity on ADC. So it'll be bright on DWI and dark on ADC. If it's restricted diffusion of water in cytotoxic edema and that might be irreversible. In contrast, if it's just vasoedema, either the DWI is normal or both the DWI and the ADC are both hyper intense and that's just T2 shine through. So if it just shines through all the sequences: bright on T2, bright on DWI and bright on ADC, that is more suggested that it is vasogenic edema, and in the great clinical setting of hypertension, eclampsia or meds, that's more likely to be a posterior reversible encephalopathy syndrome.
Date 2019-03
Language eng
Format video/mp4
Type Image/MovingImage
Collection Neuro-Ophthalmology Virtual Education Library: Andrew G. Lee Collection: https://novel.utah.edu/Lee/
Publisher North American Neuro-Ophthalmology Society
Holding Institution Spencer S. Eccles Health Sciences Library, University of Utah, 10 N 1900 E SLC, UT 84112-5890
Rights Management Copyright 2019. For further information regarding the rights to this collection, please visit: https://NOVEL.utah.edu/about/copyright
ARK ark:/87278/s6kq2f4z
Setname ehsl_novel_lee
ID 1403731
Reference URL https://collections.lib.utah.edu/ark:/87278/s6kq2f4z
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