Hypertensive Encephalopathy with Reversible Brainstem Edema
A 36-year-old male with idiopathic hypertension (duration >6 yrs) was admitted to our hospital for abrupt-onset headache, right facial palsy, dysarthria, and right hemiparesis that had developed three hours earlier. Two weeks prior to admission, he stopped his antihypertensive medication. BP recorded at the time of presentation was 230/160 mm Hg.\nLaboratory studies were within normal range and ophthalmologic evaluation was unremarkable. Specifically, no papilledema was evident. Routine chest X-ray and echocardiogram suggested severe concentric left ventricular hypertrophy, later confirmed by transthoracic echocardiography. Emergency computed tomographic (CT) scan of the brain revealed small amount (7 cc) of intracranial hemorrhage involving the left basal ganglia, and there was relative hypodensity of the brainstem (). CT angiography demonstrated no cerebral vascular abnormalities, including vertebrobasilar circulation. Brain MRI showed diffuse high-signal intensities on T2-weighted images and fluid-attenuated inversion recovery images without gadolinium enhancement in the pons and midbrain. No high signal intensities in diffusion-weighted images (DWI) and high signal intensities in apparent diffusion coefficient (ADC) images, implying that the changes were not due to cerebral infarction (). There were also no abnormal findings other than the small amount of hemorrhage in basal ganglia, which was confirmed already in CT ().\nBased on these findings, a diagnosis of acute hypertensive encephalopathy with intracranial hemorrhage was made. We immediately initiated intravenous antihypertensive therapy. Ten days later, systolic and diastolic pressures were successfully stabilized. Follow-up MRI (including DWI) on Day 16 of hospitalization revealed complete resolution of prior imaging aberrations involving the brainstem ().