Abstract

We report on a 42-year-old female patient who presented with high arterial blood pressure of 245/150 mmHg and hypertensive brainstem encephalopathy that involved the brainstem and extensive supratentorial deep gray and white matter. The lesions were nearly completely resolved several days after stabilization of the arterial blood pressure. Normal diffusion-weighted imaging findings and high apparent diffusion coefficient values suggested that the main pathomechanism was vasogenic edema owing to severe hypertension. On the basis of a literature review, the absolute value of blood pressure or whether the patient can control his/her blood pressure seems not to be associated with the degree of the lesions evident on magnetic resonance imaging. It remains to be determined if the acceleration rate and the duration of elevated arterial blood pressure might play a key role in the development of the hypertensive encephalopathy pattern.

Highlights

  • On the second day after admission (46 hours after symptom onset), a brain MRI examination was conducted

  • Discussion ly We present a female patient with untreated hypertension who developed HBE involving the n entire cerebellum and the deep supratentorial o regions

  • She presented with drowsiness, vertigo, and ataxia without accome panying motor weakness or visual disturbs ances

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Summary

Republic of Korea

Normalization of blood pressure.[4,23] symmetrical lesions described here were not Our patient had extensive high-intensity the typical MRI abnormality correlated with simple thromboembolic stroke signals in the brainstem and cerebellum, as observed in cases of HE is hyperintensity in because of the lack of major brainstem signs, well as in the subcortical deep white and gray the white matter in the parieto-occipital areas the absence of acute ischemic findings on ini- matter in T2-weighted and FLAIR images. Mild acceleration of - hypertension might affect small-caliber artern ies (distal pial branches), such as in the pario eto-occipital area as in a report of the influence of mild acceleration of hypertension on

HBE plus extensive supratentorial deep lesions
An unusual case of hypertensive
Reversible posterior leukoencephalopathy
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