title: Geography, structure, and evolution of diffusion and perfusion lesions in Diffusion and perfusion imaging Evaluation For Understanding Stroke Evolution (DEFUSE).
abstract: OBJECTIVE
  The classical representation of acute ischemic lesions on MRI is a central diffusion-weighted imaging (DWI) lesion embedded in a perfusion-weighted imaging (PWI) lesion. We investigated spatial relationships between final infarcts and early DWI/PWI lesions before and after intravenous thrombolysis in the Diffusion and perfusion imaging Evaluation For Understanding Stroke Evolution (DEFUSE) study.
  
  
  METHODS
  Baseline and follow-up DWI and PWI lesions and 30-day fluid-attenuated inversion recovery scans of 32 patients were coregistered. Lesion geography was defined by the proportion of the DWI lesion superimposed by a Tmax (time when the residue function reaches its maximum) >4 seconds PWI lesion; Type 1: >50% overlap and Type 2: < or = 50% overlap. Three-dimensional structure was dichotomized into a single lesion (one DWI and one PWI lesion) versus multiple lesions. Lesion reversal was defined by the percentage of the baseline DWI or PWI lesion not superimposed by the early follow-up DWI or PWI lesion. Final infarct prediction was estimated by the proportion of the final infarct superimposed on the union of the DWI and PWI lesions.
  
  
  RESULTS
  Single lesion structure with Type 1 geography was present in only 9 patients (28%) at baseline and 4 (12%) on early follow-up. In these patients, PWI and DWI lesions were more likely to correspond with the final infarcts. DWI reversal was greater among patients with Type 2 geography at baseline. Patients with multiple lesions and Type 2 geography at early follow-up were more likely to have early reperfusion.
  
  
  CONCLUSIONS
  Before thrombolytic therapy in the 3- to 6-hour time window, Type 2 geography is predominant and is associated with DWI reversal. After thrombolysis, both Type 2 geography and multiple lesion structure are associated with reperfusion.
authors.affiliation: Department of Neurology, Neurological Sciences and the Stanford Stroke Center, Stanford University Medical Center, Stanford, CA, USA. jmolivot@stanford.edu
authors.forename: Jean-Marc
authors.initials: JM
authors.lastname: Olivot
authors.forename: Michael
authors.initials: M
authors.lastname: Mlynash
authors.forename: Vincent N
authors.initials: VN
authors.lastname: Thijs
authors.forename: Archana
authors.initials: A
authors.lastname: Purushotham
authors.forename: Stephanie
authors.initials: S
authors.lastname: Kemp
authors.forename: Maarten G
authors.initials: MG
authors.lastname: Lansberg
authors.forename: Lawrence
authors.initials: L
authors.lastname: Wechsler
authors.forename: Garry E
authors.initials: GE
authors.lastname: Gold
authors.forename: Roland
authors.initials: R
authors.lastname: Bammer
authors.forename: Michael P
authors.initials: MP
authors.lastname: Marks
authors.forename: Gregory W
authors.initials: GW
authors.lastname: Albers
mesh_terms: D000368:Aged; D002536:Cerebral Arteries / Q000187:drug effects / Q000473:pathology* / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology; D038524:Diffusion Magnetic Resonance Imaging / Q000379:methods*; D018450:Disease Progression; D005260:Female; D005343:Fibrinolytic Agents / Q000494:pharmacology*; D006801:Humans; D008297:Male; D017063:Outcome Assessment, Health Care / Q000379:methods; D015427:Reperfusion Injury / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D020521:Stroke / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology*; D016896:Treatment Outcome
chemical_list: D005343:Fibrinolytic Agents
references.citation: Stroke. 2008 Aug;39(8):2257-63
references.pmid: 18566302
references.citation: Stroke. 2003 Nov;34(11):2729-35
references.pmid: 14576370
references.citation: Ann Neurol. 2000 Apr;47(4):462-9
references.pmid: 10762157
references.citation: Radiology. 2009 Jan;250(1):184-92
references.pmid: 19017923
references.citation: Stroke. 2009 May;40(5):1692-7
references.pmid: 19299632
references.citation: Lancet Neurol. 2008 Apr;7(4):299-309
references.pmid: 18296121
references.citation: Brain. 2006 Sep;129(Pt 9):2384-93
references.pmid: 16891322
references.citation: Stroke. 2008 Mar;39(3):870-7
references.pmid: 18258831
references.citation: Lancet Neurol. 2009 Mar;8(3):261-9
references.pmid: 19233036
references.citation: Neurology. 2006 Sep 12;67(5):824-9
references.pmid: 16966545
references.citation: Ann Neurol. 2006 Nov;60(5):508-17
references.pmid: 17066483
references.citation: Stroke. 2009 Feb;40(2):469-75
references.pmid: 19109547
references.citation: Lancet. 2007 Jan 27;369(9558):293-8
references.pmid: 17258669
references.citation: Neurology. 1999 Oct 22;53(7):1528-37
references.pmid: 10534263
references.citation: Neurology. 2009 Mar 31;72(13):1140-5
references.pmid: 19332690