SUMMARY:Posterior reversible encephalopathy syndrome (PRES) is a neurotoxic state coupled with a unique CT or MR imaging appearance. Recognized in the setting of a number of complex conditions (preeclampsia/eclampsia, allogeneic bone marrow transplantation, organ transplantation, autoimmune disease and high dose chemotherapy) the imaging, clinical and laboratory features of this toxic state are becoming better elucidated. This review summarizes the basic and advanced imaging features of PRES, along with pertinent features of the clinical and laboratory presentation and available histopathology. Many common imaging/clinical/laboratory observations are present among these patients, despite the perception of widely different associated clinical conditions.

SUMMARY:Posterior reversible encephalopathy syndrome (PRES) is a neurotoxic state accompanied by a unique brain imaging pattern typically associated with a number of complex clinical conditions including: preeclampsia/eclampsia, allogeneic bone marrow transplantation, solid organ transplantation, autoimmune diseases and high dose cancer chemotherapy. The mechanism behind the developing vasogenic edema and CT or MR imaging appearance of PRES is not known. Two theories have historically been proposed: 1) Severe hypertension leads to failed auto-regulation, subsequent hyperperfusion, with endothelial injury/vasogenic edema and; 2) vasoconstriction and hypoperfusion leads to brain ischemia and subsequent vasogenic edema. The strengths/weaknesses of these hypotheses are reviewed in a translational fashion including supporting evidence and current available imaging/clinical data related to the conditions that develop PRES. While the hypertension/hyperperfusion theory has been most popular, the conditions associated with PRES have a similar immune challenge present and develop a similar state of T-cell/endothelial cell activation that may be the basis of leukocyte trafficking and systemic/cerebral vasoconstriction. These systemic features along with current vascular and perfusion imaging features in PRES appear to render strong support for the older theory of vasoconstriction coupled with hypoperfusion as the mechanism.T he mechanism of posterior reversible encephalopathy syndrome (PRES) is not known. Two opposing hypotheses are commonly cited, but the issue is controversial: 1) The current more popular theory suggests that severe hypertension exceeds the limits of autoregulation, leading to breakthrough brain edema; 2) the earlier original theory suggests that hypertension leads to cerebral autoregulatory vasoconstriction, ischemia, and subsequent brain edema. The issues surrounding these theories are reviewed to summarize the potential values of each mechanism. Current Popular Theory: Hypertension, Failed Autoregulation, HyperperfusionSevere hypertension with failed autoregulation, injury to the capillary bed, and hyperperfusion remains the most popular theory for the brain edema that develops in PRES. [1][2][3][4] This concept is naturally intuitive, due to the frequent presence of hypertension at toxicity, and was originally embraced as the cause of eclampsia, historically labeled as a "hypertensive disorder of pregnancy." The hypertension/hyperperfusion theory is primarily based on blood pressure exceeding the autoregulation limits of the brain. AutoregulationAutoregulation is an intrinsic function of the vasculature of the brain, designed to maintain a stable blood flow in the face of fluctuating blood pressure. 5,6 Under normal circumstances, brain vessels possess intrinsic vascular tone.7 With autoregulation, vasodilation occurs as blood pressure drops and vasoconstriction occurs as blood pressure increases. [5][6][7] This function is regulated by the endothelium with release of relaxing factors (endothelium-de...

BACKGROUND AND PURPOSE:Although the term posterior reversible encephalopathy syndrome (PRES) was popularized because of the typical presence of vasogenic edema in the parietal and occipital lobes, other regions of the brain are also frequently affected. We evaluated lesion distribution with CT and MR in a large cohort of patients who experienced PRES to comprehensively assess the imaging patterns identified.

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BACKGROUND AND PURPOSE:The cause of posterior reversible encephalopathy syndrome (PRES) is unknown. Two primary hypotheses exist: 1) hypertension exceeding auto-regulatory limits leading to forced hyper-perfusion and 2) vasoconstriction and hypo-perfusion leading to ischemia with resultant edema. The purpose of this study was to evaluate the catheter angiography (CA), MR angiography (MRA), and MR perfusion (MRP) features in PRES in order to render further insight into its mechanism of origin.

BACKGROUND AND PURPOSE:Posterior reversible encephalopathy syndrome (PRES) is known to occur after solid organ transplantation (SOT), potentially associated with cyclosporine and tacrolimus. In this study, we assess the frequency and clinical and imaging characteristics of PRES after SOT.

BACKGROUND CONTEXT: The North American Spine Society's (NASS) Evidence Based Clinical Guideline for the Diagnosis and Treatment of Low Back Pain features evidence-based recommendations for diagnosing and treating adult patients with nonspecific low back pain. The guideline is intended to reflect contemporary treatment concepts for nonspecific low back pain as reflected in the highest quality clinical literature available on this subject as of February 2016. PURPOSE: The purpose of the guideline is to provide an evidence-based educational tool to assist spine specialists when making clinical decisions for adult patients with nonspecific low back pain. This article provides a brief summary of the evidence-based guideline recommendations for diagnosing and treating patients with this condition. STUDY DESIGN: This is a guideline summary review. METHODS: This guideline is the product of the Low Back Pain Work Group of NASS' Evidence-Based Clinical Guideline Development Committee. The methods used to develop this guideline are detailed in the complete guideline and technical report available on the NASS website. In brief, a multidisciplinary work group of spine care specialists convened to identify clinical questions to address in the guideline. The literature search strategy was developed in consultation with medical librarians. Upon completion of the systematic literature search, evidence relevant to the clinical questions posed in the guideline was reviewed. Work group members utilized NASS evidentiary table templates to summarize study conclusions, identify study strengths and weaknesses, and assign levels of evidence. Work group members participated in webcasts and in-person rate expert opinion when necessary. The draft guideline was submitted to an internal and external peer review process and ultimately approved by the NASS Board of Directors. RESULTS: Eighty-two clinical questions were addressed, and the answers are summarized in this article. The respective recommendations were graded according to the levels of evidence of the supporting literature. CONCLUSIONS: The evidence-based clinical guideline has been created using techniques of evidence-based medicine and best available evidence to aid practitioners in the diagnosis and treatment of adult patients with nonspecific low back pain. The entire guideline document, including the evidentiary tables, literature search parameters, literature attrition flowchart, suggestions for future research, and all of the references,

In a retrospective review, 3 (3.8%) of 78 patients developed recurrent posterior reversible encephalopathy syndrome. Underlying clinical conditions included sickle cell disease, antibody-positive autoimmune disease, and allogeneic bone marrow transplantation. Infection (bacterial/viral) was suspected or documented in both episodes in all 3 patients. Evidence of endothelial injury (schistocyte formation and increased lactate dehydrogenase) was documented in all patients, and multiple organ dysfunction syndrome developed during the hospital course of all admissions.