title: Diffusion- and perfusion-weighted MRI. The DWI/PWI mismatch region in acute stroke.
abstract: OBJECTIVE
  Diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) are relatively new MR techniques increasingly used in acute stroke. During the first hours of stroke evolution, the regions with abnormal perfusion are typically larger than the DWI lesions, and this mismatch region has been suggested to be "tissue at risk." The aim of this study was to evaluate the PWI/DWI mismatch region in acute stroke patients and find parameters indicative of both infarct progression and functional impairment.
  
  
  METHODS
  Twenty patients with nonlacunar ischemic stroke were imaged with DWI, PWI, and conventional MRI within 24 hours of symptom onset and after 1 week; in addition, the European Stroke Scale (ESS) score was recorded. With PWI, the volumes of regions with "time-to-peak" (TTP) delays of >/=2, 4, 6, 8, and 10 seconds were measured; these volumes were compared with the acute DWI lesion volumes, final infarct size, and ESS score.
  
  
  RESULTS
  In 80% of patients the acute DWI lesion was surrounded by regions with abnormal TTP delays (PWI>DWI lesion). A TTP delay of >/=6 s in the mismatch region was found to be associated with lesion enlargement between the initial and follow-up MRI scans. Lesions increased in 9 of 12 patients (75%) in whom the area with TTP delay >/=6 s was larger than the DWI lesion, but they increased in only 1 of 8 (12.5%) of the remaining patients, in whom the area with a TTP delay >/=6 s was smaller than the DWI lesion. The volume of the regions with TTP delays of >/=4 s correlated better with ESS (r=-0.88, P<0.001) than other PWI (or DWI) volumes, which indicated that a TTP delay of approximately 4 s might be the threshold for functional impairment of brain tissue.
  
  
  CONCLUSIONS
  Only patients with severe perfusion deficits in the PWI/DWI mismatch (TTP delays of >/=6 s) are at high risk of lesion enlargement. Functionally, more moderate perfusion deficits (TTP delays >/=4 and <6 s) appear to also contribute to the acute clinical deficit.
authors.affiliation: Department of Neurology, Institute of Diagnostic Radiology, Heinrich-Heine University, Düsseldorf, Germany. tnh@s-word.stanford.edu
authors.forename: T
authors.initials: T
authors.lastname: Neumann-Haefelin
authors.forename: H J
authors.initials: HJ
authors.lastname: Wittsack
authors.forename: F
authors.initials: F
authors.lastname: Wenserski
authors.forename: M
authors.initials: M
authors.lastname: Siebler
authors.forename: R J
authors.initials: RJ
authors.lastname: Seitz
authors.forename: U
authors.initials: U
authors.lastname: Mödder
authors.forename: H J
authors.initials: HJ
authors.lastname: Freund
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D001921:Brain / Q000098:blood supply / Q000473:pathology*; D002536:Cerebral Arteries; D002544:Cerebral Infarction / Q000175:diagnosis* / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D004058:Diffusion; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008279:Magnetic Resonance Imaging / Q000379:methods*; D008297:Male; D008875:Middle Aged; D015588:Observer Variation; D010477:Perfusion; D012189:Retrospective Studies; D012720:Severity of Illness Index