title: Relationship between magnetic resonance arterial patency and perfusion-diffusion mismatch in acute ischemic stroke and its potential clinical use.
abstract: BACKGROUND
  In patients with acute ischemic stroke the magnetic resonance (MR) perfusion-diffusion mismatch pattern (perfusion lesion at least 20% larger than the lesion on diffusion-weighted imaging) may indicate ischemically threatened but viable tissue. To our knowledge, the relationship of this MR pattern to serial changes in MR angiography (MRA) has not been reported.
  
  
  OBJECTIVE
  To investigate the relationship between MRA changes and patterns of diffusion-weighted imaging and perfusion abnormalities and to determine if the information obtained could be used in clinical management.
  
  
  METHODS
  The MR studies of 35 patients who had undergone sequential multimodality MR imaging studies within the first 4 days of stroke were reviewed. All lesions were in the internal carotid artery territory distribution. Magnetic resonance angiographies were read by 2 observers blinded to the clinical data.
  
  
  RESULTS
  During the first 24 hours a perfusion-diffusion mismatch was present in 22 (92%) of the 24 patients with an MRA arterial occlusive lesion. (At this time 5 [46%] of the 11 patients with a normal MRA [P =.006] also had a mismatch.) Two to 4 days after stroke, of these 22 patients resolution of the mismatch occurred in 8 (87%) of 9 patients with recanalization on MRA compared with 5 (39%) of 13 patients without arterial recanalization (P =.03). Resolution of mismatch occurred in 3 (60%) of 5 patients with a normal MRA and a mismatch at the first time point.
  
  
  CONCLUSIONS
  Concordance between MRA and the MR perfusion-diffusion mismatch pattern provides supportive evidence for an arterial vascular basis for this MR signature in acute stroke. Discordance between MRA lesions and mismatch may result from arterial branch occlusions undetected by MRA or from an alternate mechanism for the mismatch. The MR imaging patterns identified extend our understanding of the pathophysiology of stroke and may contribute to the improvement of stroke management in the future.
authors.affiliation: Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
authors.forename: I A
authors.initials: IA
authors.lastname: Staroselskaya
authors.forename: C
authors.initials: C
authors.lastname: Chaves
authors.forename: B
authors.initials: B
authors.lastname: Silver
authors.forename: I
authors.initials: I
authors.lastname: Linfante
authors.forename: R R
authors.initials: RR
authors.lastname: Edelman
authors.forename: L
authors.initials: L
authors.lastname: Caplan
authors.forename: S
authors.initials: S
authors.lastname: Warach
authors.forename: A E
authors.initials: AE
authors.lastname: Baird
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001921:Brain / Q000098:blood supply* / Q000000981:diagnostic imaging* / Q000503:physiopathology; D002545:Brain Ischemia / Q000150:complications* / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology; D002343:Carotid Artery, Internal / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology; D002533:Cerebral Angiography / Q000379:methods*; D002560:Cerebrovascular Circulation; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D018810:Magnetic Resonance Angiography; D008297:Male; D008875:Middle Aged; D020521:Stroke / Q000000981:diagnostic imaging* / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D013997:Time Factors; D014654:Vascular Patency