title: Posterior leukoencephalopathy without severe hypertension: utility of diffusion-weighted MRI.
abstract: OBJECTIVE
  Standard MRI confirms the diagnosis of posterior leukoencephalopathy syndrome (PLES), recently associated with an increasing number of medical conditions. In PLES, T2-weighted MRI demonstrates hyperintensity spreading out from posterior brain regions; the pathophysiology remains mysterious. In the acute setting, diffusion-weighted imaging (DWI), but not standard MR imaging, can distinguish ischemic injury from those conditions known to cause vasogenic brain edema. DWI is potentially valuable in understanding the pathophysiology of PLES and in diagnosing patients who do not have previously known risk factors.
  
  
  METHODS
  Serial CT and MRI studies (including DWI, apparent diffusion coefficient [ADC] maps, and, in one instance, perfusion-weighted imaging) were performed in three female patients with a neurologic syndrome consistent with PLES while hospitalized for treatment of other conditions.
  
  
  RESULTS
  None of the patients had previously described risk factors for PLES; all had only mild elevations in blood pressure. MRI showed large, abnormal, T2 hyperintense regions in the posterior cerebrum with corresponding hyperintensity on ADC maps-signal characteristics predominantly consistent with vasogenic edema. There were also smaller patchy posterior cortical regions with decreased ADC and bright DWI consistent with infarction in one, and dramatic conversion of a large region to an ischemic pattern in another.
  
  
  CONCLUSIONS
  ADC maps and DWI can successfully differentiate PLES from early cerebral ischemia, thus playing a pivotal role in treatment decisions. PLES is associated with a wider variety of conditions than has been previously reported and is not always reversible. Hyperintense DWI signal in patients with the syndrome likely marks a tissue stage of permanent brain injury.
authors.affiliation: Stroke Service of the Neurology Department, Massachusetts General Hospital and Harvard Medical School, Boston 02114, USA.
authors.forename: H
authors.initials: H
authors.lastname: Ay
authors.forename: F S
authors.initials: FS
authors.lastname: Buonanno
authors.forename: P W
authors.initials: PW
authors.lastname: Schaefer
authors.forename: D A
authors.initials: DA
authors.lastname: Le
authors.forename: B
authors.initials: B
authors.lastname: Wang
authors.forename: R G
authors.initials: RG
authors.lastname: Gonzalez
authors.forename: W J
authors.initials: WJ
authors.lastname: Koroshetz
mesh_terms: D000328:Adult; D000368:Aged; D001794:Blood Pressure; D001921:Brain / Q000000981:diagnostic imaging / Q000473:pathology*; D001927:Brain Diseases / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology*; D002540:Cerebral Cortex / Q000000981:diagnostic imaging / Q000473:pathology; D005260:Female; D006801:Humans; D006973:Hypertension; D008279:Magnetic Resonance Imaging / Q000379:methods*; D008875:Middle Aged; D014057:Tomography, X-Ray Computed