Hypertensive encephalopathy

Catherine Albin MD (

Dr. Albin of Partners Neurology, Brigham & Women’s Hospital and Massachusetts General Hospital has no relevant financial relationships to disclose.

Sashank Prasad MD (Dr. Prasad of Brigham and Women's Hospital in Boston, Massachusetts, has no relevant financial relationships to disclose.)
Douglas J Lanska MD FAAN MS MSPH, editor. (

Dr. Lanska of the University of Wisconsin School of Medicine and Public Health, the Medical College of Wisconsin, and IM Sechenov First Moscow State Medical University has no relevant financial relationships to disclose.

Originally released June 9, 1999; last updated April 30, 2018; expires April 30, 2021

This article includes discussion of hypertensive encephalopathy, posterior reversible encephalopathy syndrome, PRES, reversible posterior leukoencephalopathy syndrome, and RPLS. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.


Clinical manifestations of hypertensive encephalopathy are often nonspecific and include altered mental status, headache, vision changes, and seizures. The pathophysiology of hypertensive encephalopathy can be regarded as failure of cerebral autoregulation from a sudden elevation of blood pressure that results in endothelial injury and vasogenic edema. Radiographically, hypertensive encephalopathy most commonly presents with evidence of posterior-predominant T2-hyperintense lesions without pathologic contrast enhancement. Although classically these changes are noted in the parietal and occipital lobes, edematous changes can also be found in the deep gray matter, brainstem, or cerebellum or even anteriorly. Clinical symptoms and radiographic findings are most often reversible with prompt blood pressure management. In the case of posterior reversible leukoencephalopathy that is triggered by an offending medication, it is critical to identify and withdraw that agent as well.

Historical note and terminology

Volhard was the first to distinguish hypertension-induced neurologic dysfunction from a uremic state and introduced the term “pseudouremia” to refer to hypertensive encephalopathy (Volhard 1918). Ten years later, the term “hypertensive encephalopathy” was introduced by Oppenheimer and Fishberg (Oppenheimer and Fishberg 1928). With the advent of modern neuroimaging techniques in the 1980s, Rail and Perkins published a case series of patients with the clinical syndrome of hypertensive encephalopathy that also demonstrated hypodensity in the posterior white matter on computerized tomography (Rail and Perkin 1980). Several years later, Hauser and colleagues demonstrated that magnetic resonance imaging was even more sensitive for demonstrating increased T2 signal in the posterior white matter and occipital lobes (Hauser et al 1988). These radiographic findings in hypertensive encephalopathy, posterior reversible encephalopathy syndrome, and reversible posterior leukoencephalopathy syndrome supported the concept that the syndrome results from fluid and protein extravasation across the blood-brain barrier, owing to failure of cerebral autoregulation.

In 1996, Hinchey and colleagues published a series of patients who presented with headaches, vomiting, confusion, seizures, cortical blindness, and other visual abnormalities arising from various etiologies--eclampsia, acute hypertension, renal failure, or treatment with certain immunosuppressants. MRI imaging in all cases demonstrated posterior leukoencephalopathy without infarction that resolved after cessation of the purportedly triggering medication, delivery, or control of blood pressure. Immunosuppressant or chemotherapeutic agents that have come to be associated with this syndrome including cyclosporine, tacrolimus, sirolimus, cisplatin, interferon alpha, bevacizumab, CHOP (cyclophosphamide, doxorubicin, vincristine, prednisone), and sorafenib. Hinchey and colleagues named this entity reversible posterior leukoencephalopathy syndrome, which was meant to capture the diverse etiologies resulting in an overlapping cineradiographic syndrome that also included hypertensive encephalopathy. Their article sparked controversy in the literature, prompting others to point out that such patients were at risk of hemorrhage and ischemia, and, thus, the syndrome was not necessarily “reversible.” Moreover, many reported cases emphasized that the findings are not strictly “posterior”; such authors suggested “hyperperfusion syndrome” as an alternate name (Schwartz 1996).

To address some of the inaccuracies conveyed by the name reversible posterior leukoencephalopathy syndrome, the term posterior reversible encephalopathy syndrome was later coined in the radiology literature in 2000 (Casey et al 2000). Posterior reversible leukoencephalopathy has become the more widely accepted term to describe the syndrome described in this article (Vaughn et al 2008).

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