Background-The efficiency of various strategies of neuroprotection is well
documented in animal experiments but is thus far disappointing in ischemic
stroke, for which only early reperfusion induced by thrombolysis has improv
ed clinical outcome. This discrepancy between expectation from experimental
research and clinical reality may be related to differences in the pathoge
netic factors contributing to infarction.
Summary of Comment-Positron emission tomography cerebral blood now studies
within 3 hours of onset were used to identify the various compartments of t
he infarct outlined on MRI 2 to 3 weeks after a hemispheric stroke in 10 pa
tients. Critical hypoperfusion below the viability threshold accounted for
the largest proportion (mean, 70%) of the final infarct, whereas penumbral
tissue (18%) and initially sufficiently perfused tissue (12%) were responsi
ble for considerably smaller portions of the final infarct.
Conclusions-These results indicate that early critical now disturbance lead
ing to rapid cell damage is the predominant cause of infarction, while seco
ndary and delayed pathobiochemical processes in borderline or initially suf
ficiently perfused regions contribute only little to the final infarct. The
refore, emerging therapeutic strategies should be targeted to the initially
critically perfused tissue subcompartments. Clinical drug trials might ben
efit from stratification of patients for target tissue compartments applyin
g functional imaging.