Background and Purpose-A mismatch between diffusion-and perfusion-weighted MRI is thought to define tissue at risk of infarction. This concept is based on the assumption that diffusion slowing of and decreases in the apparent diffusion coefficient (ADC) serve as indicator of tissue proceeding to infarction. We tested this hypothesis. Methods-MRI (diffusion weighted, perfusion weighted, MRA, T2 weighted) was performed in 15 patients with acute stroke within 2.9Ϯ0.8 hours (meanϮSD) of onset and on days 1 and 7. After intraindividual realignment of the ADC maps, the development of ADC range volumes and ADC values was determined. Results-An increase (354%, group A1) in the total ADC-based lesion volume below a threshold of Ͻ80% occurred in 4 patients on day 1, persisting on day 7 with a pronounced increase of ADC range volumes with low ADC values. An increase in total ADC-based lesion volume (201%, group A2) followed by a secondary drop to day 7 was found in 7 patients. A significant reduction in total ADC-based lesion volume (14%, group B) was found in 4 patients. ADC-based lesion volume increase was associated with persistent vessel occlusion in group A, whereas recanalization in group B resulted in ADC volume decrease. ADC normalization was observed independently from the degree of the initial ADC decrease on days 1 and 7 in group B. Conclusions-In

P21 Diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) are MR techniques increasingly used in acute stroke. The aim of this study was to evaluate the DWI/PWI mismatch volumes in acute stroke patients before and after intravenous thrombolytic therapy. METHODS: Seven patients with ischemic stroke were treated with intravenous recombinant tissue plasminogen activator (rtPA) and imaged with DWI, PWI, MRA, and conventional MRI within 3 hours of symptom onset and on day 1 and 7. Clinical scores (National Institutes of Health Stroke Scale [NIHSS] and Barthel Index) were assessed on each time point. The perfusion deficit was defined using a threshold function measuring the volumes of regions with “time-to-peak” (TTP) delays of 2–4s, 4–6s, 6–8s and above 8 s; these volumes were compared with the DWI lesion volumes, infarct progression and final infarct size. RESULTS: In all patients (n=7) the DWI lesion (< 3 hrs) was significantly smaller (45%) as compared to the PWI lesion volume. The mismatch area decreased from day 0 (113 ml) to day 7 (3 ml) in all patients except for two. Mean NIHSS in these two patients improved by 5 and 2 points, while the other patients improved by a mean of 12 points from day 0 to day 7. The DWI lesion volume - measured by manually outlining the lesion - increased from a mean of 78 ml (day 0) to 136 ml (day 7) measured on T2-weighted imaging. Contributing 31% to the PWI lesion on day 0, TTP delay interval of 2–4 s was found to increase to 47% by day 7 while the region with severely delayed perfusion (> 8 s) underwent a decrease of 13%. Overall the perfusion deficit on day 7 showed a reduction by 27%. The infarct volume measured by manually outlining the DWI-lesion on day 0 increased from a mean of 78 ml to 136 ml on day 7 measured on T2-weighted imaging. CONCLUSIONS: 1.) Intravenous thrombolytic therapy in selected patients with a severe PWI/DWI mismatch is associated with lesion enlargement taking in account that not all of the “tissue at risk” will be safed by thrombolytic therapy. 2.) Temporal development of the PWI/DWI mismatch serves as a parameter of the therapeutic efficacy of thrombolysis.

P31 Animal experiments indicated that the severity of the apparent diffusion coefficient (ADC) decrease might serve as indicator of tissue viability. We followed the temporal and spatial development of ADC values after acute human stroke to test this hypothesis. Methods We enrolled 10 consecutive patients with acute ischemic stroke during the last 4 hours. Multimodal MRI (DWI, PWI, MRA, T2w) was performed within 4 h after symptom onset and at days 1 and 7. NIH-stroke-scale was assessed. The mean ADC value for the not affected hemisphere served as reference for the relative ADC-reduction of <50%, 50–60%, 60–70% and 70–80%. Volume of these regions was determined for each imaging timepoint using a threshold function. In a second approach we transferred the previously obtained ADC-theshold areas of day 0 to day 1 and 7 for detection of ADC-changes to determine ADC-changes in reference to the initial ADC. Results In 4 patients with clear neurological improvement at day 1 we found a mean reduction of the ADC- lesion“-volume to 56%. The ADC-threshold-volume of 70–80% increased by 38.9% and areas below 70% decreased by between 56.7% (<50% ADC) and 23.5% (60–70%). Some areas with severe ADC decreases showed partial pseudo-normalization (lesion in T2w / normal ADC values, n=3) and normalization (normal T2w / normal ADC values, n=1) at day 1 and 7. Patients without change or a minor clinical improvement showed a mean increase of the ADC-lesion size at day 1 by 83.6 %. In these patients volume with ADC<50% increased by 275.7% while 70–80%-threshold-volume decreased to 52.2%. ADC values within the initial ADC-threshold-volumes differed significantly at day 1 (n=7), reflecting a different dynamics dependent on the initial ADC. Conclusion Ischemic tissue with severe ADC decreases may recover completely. However, areas with severe ADC decreases usually transform towards a less severe decrease in patients with good neurological recovery. In patients without clinical improvement the area of severe diffusion impairment spreads to adjacent areas.