• Yuebing Li, Devang Gor, Debra Walicki, Donna Jenny, David Jones, Peter Barbour, and John Castaldo.
• Division of Neurology, Department of Medicine, Lehigh Valley Health Network, Allentown, Pennsylvania 18103, USA.
• J Stroke Cerebrovasc Dis. 2012 Nov 1;21(8):873-82.

BackgroundControversy still exists over the etiology and pathophysiology of reversible posterior leukoencephalopathy syndrome (RPLS). This large single-center case series aims to describe the clinical and imaging features of RPLS in an attempt to deduce the etiology of the disorder and the mechanisms of brain injury.MethodsA retrospective chart and imaging review was conducted on 59 cases of RPLS in 55 patients.ResultsFive RPLS imaging patterns were observed: posterior predominant (n = 40), anterior predominant (n = 7), diffuse lesion (n = 7), basal ganglia predominant (n = 3), and brainstem/cerebellum predominant patterns (n = 2). RPLS resulted in permanent neurologic deficits in 14 patients and death in 4 patients. Hypertension was seen in 57 (97%) cases, and mean arterial blood pressure exceeded 140 mm Hg in 30 (51%) cases. Follow-up magnetic resonance imaging scans revealed a significant worsening of vasogenic edema in 2 cases, both with persistent hypertension. Magnetic resonance imaging scans revealed areas of ischemia in 14 cases, all within or at areas closely adjacent to vasogenic edema. Diffuse vasculopathy was seen in 8 cases. There was a lack of correlation between the presence of vasculopathy and the degree of vasogenic edema (P = .62), but a correlation was suggested between ischemia and vasculopathy (P = .02).ConclusionsThis study strongly suggests that hypertension-induced vasodilation rather than vasoconstriction-mediated hypoxia is likely the major mechanism responsible for the development of vasogenic edema, and that vasoconstriction may contribute to the development of ischemia in RPLS.Copyright © 2012 National Stroke Association. Published by Elsevier Inc. All rights reserved.

49 keywords...

hide…