title: Changes in background blood-brain barrier integrity between lacunar and cortical ischemic stroke subtypes.
abstract: OBJECTIVE
  Lacunar stroke is associated with endothelial dysfunction and histologically with intrinsic cerebral microvascular disease of unknown cause. Endothelial dysfunction could impair blood-brain barrier integrity. We assessed background blood-brain barrier leakage in patients with lacunar ischemic stroke compared with cortical stroke controls.
  
  
  METHODS
  We recruited patients with lacunar or mild cortical ischemic stroke and assessed generalized cerebral blood-brain barrier leak with MRI and intravenous gadolinium at least 1 month after stroke. We used detailed image processing to compare signal change before and for 30 minutes postcontrast throughout gray matter, white matter, and cerebrospinal fluid with summary analyses and general linear modeling.
  
  
  RESULTS
  Among 48 patients (29 lacunar, 19 cortical), postcontrast enhancement was significantly higher in cerebrospinal fluid (P=0.04, Mann-Whitney U), and nonsignificantly higher in white matter, in lacunar than in cortical strokes, with no difference in gray matter. General linear modeling confirmed significantly greater postcontrast enhancement in cerebrospinal fluid in lacunar patients than in cortical controls (t=3.37, P<0.0008).
  
  
  CONCLUSIONS
  These preliminary data suggest that the blood-brain barrier may be dysfunctional throughout subcortical white matter (white matter drains via interstitial spaces to cerebrospinal fluid) in patients with lacunar stroke. Further studies are required to confirm these findings and determine whether abnormal blood-brain barrier might predate development of lacunar disease. Blood-brain barrier dysfunction may be an important mechanism for brain damage in cerebral microvascular disease.
authors.forename: Joanna M
authors.initials: JM
authors.lastname: Wardlaw
authors.forename: Andrew
authors.initials: A
authors.lastname: Farrall
authors.forename: Paul A
authors.initials: PA
authors.lastname: Armitage
authors.forename: Trevor
authors.initials: T
authors.lastname: Carpenter
authors.forename: Francesca
authors.initials: F
authors.lastname: Chappell
authors.forename: Fergus
authors.initials: F
authors.lastname: Doubal
authors.forename: Debashish
authors.initials: D
authors.lastname: Chowdhury
authors.forename: Vera
authors.initials: V
authors.lastname: Cvoro
authors.forename: Martin S
authors.initials: MS
authors.lastname: Dennis
mesh_terms: D000368:Aged; D001812:Blood-Brain Barrier / Q000378:metabolism / Q000473:pathology*; D020520:Brain Infarction / Q000145:classification / Q000378:metabolism / Q000473:pathology*; D002545:Brain Ischemia / Q000145:classification / Q000378:metabolism / Q000473:pathology*; D002555:Cerebrospinal Fluid / Q000378:metabolism; D003287:Contrast Media; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology; D019786:Gadolinium DTPA; D006801:Humans; D008279:Magnetic Resonance Imaging; D009413:Nerve Fibers, Myelinated / Q000473:pathology; D020521:Stroke / Q000145:classification / Q000378:metabolism / Q000473:pathology*
chemical_list: D003287:Contrast Media; D019786:Gadolinium DTPA