P rognosis of functional outcome after ischemic stroke is influenced by a variety of factors already assessable in the acute phase and within the first days after symptom onset. In clinical trials, stroke outcome is most commonly rated by the modified Rankin Scale (mRS) 1 because of the validity and rapid application of this rating scale and its ability to discriminate clinically relevant levels of disability and recovery.2-4 Brain imaging in the early phase after stroke onset provides valuable information related to individual functional recovery. 5,6 In particular, structural MRI identifies injured brain regions and allows for assessment of extent and location, both known to influence and predict functional outcome measured by the mRS.3 However, infarct volume from early MRI correlates only moderately with the mRS at later time points, 7,8 indicating that additional factors, such as lesion location, influence functional outcome. It is therefore of major interest to elucidate the relationship between early lesion patterns and functional impairment in the later course of stroke.Clinical impact of lesion locations can be inferred from voxel-based lesion symptom mapping (VLSM). This statistical method examines effects of brain lesions on behavioral scores on a voxel-by-voxel base. Therefore, a statistical test is conducted for each voxel to detect differences in a behavioral score based on the presence or absence of injury.9 VLSM produces statistical results that map structural lesions to a behavioral scale. In patients with chronic stroke, it has been Background and Purpose-In the early days after ischemic stroke, information on structural brain damage from MRI supports prognosis of functional outcome. It is rated widely by the modified Rankin Scale that correlates only moderately with lesion volume. We therefore aimed to elucidate the influence of lesion location from early MRI (days 2-3) on functional outcome after 1 month using voxel-based lesion symptom mapping. Methods-We analyzed clinical and MRI data of patients from a prospective European multicenter stroke imaging study (I-KNOW). Lesions were delineated on fluid-attenuated inversion recovery images on days 2 to 3 after stroke onset. We generated statistic maps of lesion contribution related to clinical outcome (modified Rankin Scale) after 1 month using voxel-based lesion symptom mapping. Results-Lesion maps of 101 patients with middle cerebral artery infarctions were included for analysis (right-sided stroke, 47%). Mean age was 67 years, median admission National Institutes of Health Stroke Scale was 11. Mean infarct volumes were comparable between both sides (left, 37.5 mL; right, 43.7 mL). Voxel-based lesion symptom mapping revealed areas with high influence on higher modified Rankin Scale in regions involving the corona radiata, internal capsule, and insula. In addition, asymmetrically distributed impact patterns were found involving the right inferior temporal gyrus and left superior temporal gyrus. Conclusions-In this group of patients with strok...

Background and Purpose-Early neurological deterioration (END) is a relatively common unfavorable course after anterior circulation ischemic stroke that can lead to worse clinical outcome. None of the END predictors identified so far is sufficiently reliable to be used in clinical practice and the mechanisms underlying END are not fully understood. We review the evidence from the literature for a role of hemodynamic and perfusion abnormalities, more specifically infarction of the oligemia, in END. Summary of Review-After an overview of the neuroimaging, including perfusion imaging, predictors of END, we review the putative mechanisms of END with a special focus on hemodynamic factors. The evidence relating perfusion abnormalities to END is addressed and potential hemodynamic mechanisms are suggested. Conclusions-Hemodynamic factors and perfusion abnormalities are likely to play a critical role in END. Infarction of the oligemic tissue surrounding the penumbra could be the putative culprit leading to END as a result of perfusion, but also physiological and biochemical abnormalities. Further studies addressing the role of the oligemia in END and developing measures to protect its progression to infarction are now needed. (Stroke. 2009;40:e443-e450.)