[Case of reversible posterior leukoencephalopathy syndrome after discontinuation of antihypertensive therapy].

A 36-year-old man who was poorly compliant with his antihypertensive medication regimen was admitted to our hospital because he had nausea and an altered mental status. His disorientation increased on admission. His blood pressure was 219/156 mmHg. No focal neurologic deficits were detected, but a cranial computed tomography (CT) performed on admission revealed a low-density area in the brainstem region. Subsequent cranial T2-weighted and fluid-attenuated inversion-recovery (FLAIR) magnetic resonance imaging (MRI) performed on the same day revealed high-intensity areas in the brainstem, bilateral cerebellar hemisphere, bilateral occipito-temporal subcortical white matter, right thalamus, and the right basal ganglia region. Diffusion-weighted MRI revealed that the edema was of vasogenic origin and was not indicative of ischemia/infarction. Biochemical testing revealed a blood urea nitrogen level of 35.7 mg/dL, a serum creatinine level of 3.27 mg/dL, proteinurea (4.6 g/24 hours), and a glomerular filtration rate of 47. 6 mL/min/1.83 m2. These findings suggested a diagnosis of chronic kidney disease (CKD). The patient was diagnosed with hypertensive encephalopathy, and treatment with intravenous diltiazem was initiated. The clinical symptoms resolved 3 days after admission, and the abnormal findings in CT and MRI demonstrated completely resolved 44 days after admission. This was a rare case of reversible posterior leukoencephalopathy syndrome (RPLS) that was caused by severe hypertension and was aggravated by discontinuation of antihypertensive therapy. RPLS was caused by vasogenic edema because of sudden elevations in systemic blood pressure which exceed the autoregulatory capacity of the brain vasculature.