Case report
An unusual case of hypertensive encephalopathy

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Summary

This case report describes a 59-year-old male who presented with headaches, seizures and hypertension followed by coma. Initial magnetic resonance imaging showed T2 hyperintensities typical of Hypertensive Encephalopathy (HE), the follow up scans showed diffusion-weighted imaging (DWI) hyperintensities which is a rare finding in HE. DWI hyperintensities are typically suggestive of areas of cytotoxic damage, and the presence of these changes makes this case unusual, since the pathogenesis of HE is usually due to vasogenic oedema rather than cytotoxic damage of the brain tissue.

Introduction

The radiological findings in Hypertensive Encephalopathy (HE) are variable. Magnetic resonance neuroimaging shows a characteristic posterior leukoencephalopathy that predominantly affects the white matter of the parieto-occipital regions.[1], [2] These changes are best seen in the T2 weighted images. Studies with DWI imaging show that the leukoencephalopathy is primarily due to vasogenic rather than cytotoxic oedema.[3], [4] The likely pathogenesis of vasogenic oedema is thought to be hypertensive cerebrovascular endothelial dysfunction, disruption of the blood–brain barrier with increased permeability, cerebral oedema and microhaemorrhage formation.3 There have been case reports of patients with HE who had hyperintensities in DWI images.[5], [6] It is not clear as to the underlying pathogenesis of these changes, but autoregulatory vasoconstriction leading to hypoperfusion could be a possible mechanism.7 It is not clear whether HE patients with DWI changes have a poorer prognosis.5 We report a patient with HE due to renal artery stenosis who had DWI changes in addition to typical MRI changes of HE, who went on to have complete clinical recovery.

Section snippets

Case report

Our patient was a 59-year-old man admitted to Geelong hospital with a 6-week history of headaches, nausea and vomiting. On the day of admission, he was found confused and brought to emergency department. On presentation, he was disoriented in time and place, GCS score was 14, and he was moving all limbs symmetrically. The blood pressure was raised at 250/90, pulse 80 sinus rhythm, and afebrile. Neurological examination did not reveal any focal deficits, in particular no neck stiffness.

Discussion

In the patient we have reported the diagnosis of hypertensive encephalopathy is supported by clinical presentation, fluctuating high blood pressure readings in a man who was normotensive previously and reversible changes on radiological investigations. The patient’s hypertension was corrected by angioplasty of the left renal artery stenosis.

Hypertensive encephalopathy has been described with fluctuating blood pressures,9 and tends to be less prominent in previously hypertensive individuals,

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