AJDRAJNR - American Journal of Neuroradiology

Published ahead of print on May 1, 2008
doi: 10.3174/ajnr.A1095

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Anoxic Injury-Associated Cerebral Hyperperfusion Identified with Arterial Spin-Labeled MR Imaging

J.M. Pollocka, C.T. Whitlowa, A.R. Deiblera, H. Tanb, J.H. Burdettea, R.A. Kraftb and J.A. Maldjiana

a Department of Radiology, Wake Forest University School of Medicine, Winston-Salem, NC
b Department of Biomedical Engineering, Wake Forest University, Winston-Salem, NC


Figure 1
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Fig 1. Segmentation map obtained by using the T1-weighted image shows CSF (blue), white matter (red), and GM (green). The green areas are used for the mean GM CBF measurements.


Figure 2
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Fig 2. Axial diffusion-weighted, apparent diffusion coefficient (ADC), and quantitative CBF map from patient 2 shows the typical sequelae from anoxic injury, including diffuse bilateral symmetric restricted diffusion in the cerebral cortex (arrow) and the basal ganglia and thalami (arrowhead). The ADC image reflects the subacute nature of the ischemic change, because the imaging was done 9 days after the anoxic event. CBF map shows global hyperperfusion and the second highest average GM blood flow recorded in this study (190.6 mL/100 g of tissue per minute).


Figure 3
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Fig 3. A, Diffusion, ADC, and quantitative CBF map generated from the PASL sequence obtained in patient 8 one day before the global anoxic event shows restricted diffusion and hypoperfusion in the left posterior watershed territory corresponding with areas of subacute infarction (arrowheads). B, Diffusion, ADC, and quantitative CBF map obtained 3 days after the episode of pulseless electrical activity in patient 8 shows interval worsening of the diffusion abnormality (arrowhead) with new marked global hyperperfusion. There is relative sparing of the previous subacute infarct in the left posterior MCA territory (arrow). Quantitative analysis performed by placing regions of interest over the entire section showed an average CBF increase from 31.4 to 188.6 mL/100 g of tissue per minute.


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Fig 4. Graph demonstrates rates of global GM CBF (in milliliters per 100 grams per minute), expressed as means ± SDs for 3 groups (infarction negative, infarction positive, and anoxic injury). Rates of global CBF in the anoxic injury group are 109% and 154% higher than rates of CBF in the infarction-negative and infarction-positive control groups, respectively. Data show a statistically significant difference between the anoxic injury and infarction-negative (*) groups and infarction-positive ({dagger}) groups. There was no statistically significant difference in global rates of CBF between the infarction-positive and infarction-negative groups.