title: Spectrum and potential pathogenesis of reversible posterior leukoencephalopathy syndrome.
abstract: BACKGROUND
  Controversy 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.
  
  
  METHODS
  A retrospective chart and imaging review was conducted on 59 cases of RPLS in 55 patients.
  
  
  RESULTS
  Five 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).
  
  
  CONCLUSIONS
  This 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.
authors.affiliation: Division of Neurology, Department of Medicine, Lehigh Valley Health Network, Allentown, Pennsylvania 18103, USA.
authors.forename: Yuebing
authors.initials: Y
authors.lastname: Li
authors.forename: Devang
authors.initials: D
authors.lastname: Gor
authors.forename: Debra
authors.initials: D
authors.lastname: Walicki
authors.forename: Donna
authors.initials: D
authors.lastname: Jenny
authors.forename: David
authors.initials: D
authors.lastname: Jones
authors.forename: Peter
authors.initials: P
authors.lastname: Barbour
authors.forename: John
authors.initials: J
authors.lastname: Castaldo
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000970:Antineoplastic Agents / Q000009:adverse effects; D062186:Arterial Pressure; D001921:Brain / Q000473:pathology; D001929:Brain Edema / Q000145:classification / Q000175:diagnosis* / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D002545:Brain Ischemia / Q000175:diagnosis / Q000209:etiology; D002533:Cerebral Angiography / Q000379:methods; D038524:Diffusion Magnetic Resonance Imaging; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology; D007166:Immunosuppressive Agents / Q000009:adverse effects; D018810:Magnetic Resonance Angiography; D008297:Male; D008875:Middle Aged; D010414:Pennsylvania; D054038:Posterior Leukoencephalopathy Syndrome / Q000145:classification / Q000175:diagnosis* / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D011237:Predictive Value of Tests; D011379:Prognosis; D012189:Retrospective Studies; D012307:Risk Factors; D013997:Time Factors; D014057:Tomography, X-Ray Computed; D017585:Ultrasonography, Doppler, Transcranial; D014661:Vasoconstriction; D014664:Vasodilation; D055815:Young Adult
chemical_list: D000970:Antineoplastic Agents; D007166:Immunosuppressive Agents