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  • Updated 11.05.2021
  • Released 06.09.1999
  • Expires For CME 11.05.2024

Hypertensive encephalopathy

Introduction

Overview

Hypertensive encephalopathy is a syndrome in which altered mental status, headache, vision changes, and/or seizures accompany elevated blood pressure. Failure of cerebral autoregulation from a sudden elevation of blood pressure 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. Thus, hypertensive encephalopathy shares many clinical and radiographic features with posterior reversible encephalopathy syndrome (PRES). 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.

Key points

Hypertensive encephalopathy results from endothelial dysfunction triggered by a sudden and sustained rise in blood pressure; the degree of elevation may be moderate, especially in patients without a prior history of hypertension.

Clinically, pathophysiologically, and radiographically, hypertensive encephalopathy shares many features of posterior reversible encephalopathy syndrome (PRES) and may be thought of as a subtype of this syndrome.

Clinically, manifestations include headache, altered mental status, visual disturbances, and seizures.

T2-weighted magnetic resonance imaging most commonly reveals posterior and white-matter-predominant vasogenic edema that does not respect the posterior cerebral artery territory boundary; this can be helpful in confirming the diagnosis and excluding mimics of hypertensive encephalopathy such as ischemic stroke.

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 (49). Ten years later, the term hypertensive encephalopathy was introduced by Oppenheimer and Fishberg (38). 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 (39). 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 (23). 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. Hinchey and colleagues named this entity reversible posterior leukoencephalopathy syndrome, which was meant to capture the diverse etiologies resulting in an overlapping radiographic syndrome that also included hypertensive encephalopathy (26).

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 (PRES) was later coined in the radiology literature in 2000 (05). PRES has now been described as a result of a plethora of etiologies, but hypertension continues to be chief among them.

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