Geography, structure, and evolution of diffusion and perfusion lesions in Diffusion and perfusion imaging Evaluation For Understanding Stroke Evolution (DEFUSE).
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.
Olivot
Jean-Marc
JM
Department of Neurology, Neurological Sciences and the Stanford Stroke Center, Stanford University Medical Center, Stanford, CA, USA. jmolivot@stanford.edu
Mlynash
Michael
M
Thijs
Vincent N
VN
Purushotham
Archana
A
Kemp
Stephanie
S
Lansberg
Maarten G
MG
Wechsler
Lawrence
L
Gold
Garry E
GE
Bammer
Roland
R
Marks
Michael P
MP
Albers
Gregory W
GW
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
D005343:Fibrinolytic Agents
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