Hypertensive encephalopathy

Gregory Youngnam Chang MD (Dr. Chang of the Barrow Neurologic Institute has no relevant financial relationships to disclose.)
Zachary N London MD, editor. (Dr. London of the University of Michigan has no relevant financial relationships to disclose.)
Originally released June 9, 1999; last updated May 8, 2012; expires May 8, 2015
Notice: This article has expired and is therefore not available for CME credit.

This article includes discussion of hypertensive encephalopathy, hypertensive crisis, hypertensive emergency, hypertensive urgency, occipital-parietal encephalopathy syndrome, reversible posterior leukoencephalopathy syndrome, and RPLS. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

Although clinical presentation of hypertensive encephalopathy can be nonspecific when accompanied by posterior occipital edematous lesions on MRI, the diagnosis should be considered. Prompt blood pressure lowering results in clinical resolution and normalization of MRI findings. It is important to remember that rarely hypertensive encephalopathy may present with primary brainstem edema with or without occipital involvement. This so-called “brainstem hypertensive encephalopathy” may not respond to simple blood pressure lowering, and surgical intervention may be life-saving.

Historical note and terminology

The term “hypertensive encephalopathy” was introduced by Oppenheimer and Fishberg (Oppenheimer and Fishberg 1928). They described essential clinical characteristics of acute malignant hypertension. Ten years prior, Volhard was the first to separate clearly acute hypertension-induced neurologic dysfunction from a uremic state and introduced the term “pseudouremia” to refer to hypertensive encephalopathy (Volhard 1918).

Although the association of eclampsia and elevated blood pressure has been known since the turn of the century, it was not until 1935 that Volhard suggested “eclamptic uremia” in a woman who had identical clinical and pathologic changes and the same underlying pathophysiology as hypertensive encephalopathy (Volhard 1935). This has been further confirmed by modern neuroimaging techniques (Schwartz et al 1992). Recognition of this association of cerebral edema and eclampsia led to the first effective surgical treatment of craniotomy and dural incision in 1911 (Zangemeister 1911). Subsequently, less drastic measures of venesection and repeated spinal taps were used to relieve the effects of cerebral edema.

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