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AJNR - American Journal of Neuroradiology

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

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American Journal of Neuroradiology 29:1302-1307, August 2008
© 2008 American Society of Neuroradiology

BRAIN

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

J.M. Pollock^a, C.T. Whitlow^a, A.R. Deibler^a, H. Tan^b, J.H. Burdette^a, R.A. Kraft^b and J.A. Maldjian^a

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

Please address correspondence to Jeffrey M. Pollock, Wake Forest University School of Medicine, Department of Radiology, Medical Center Blvd, Winston-Salem, NC 27157; e-mail: jeffmpollock{at}gmail.com

BACKGROUND AND PURPOSE: Anoxic brain injury is a devastating result of prolonged hypoxia. The goal of this study was to use arterial spin-labeling (ASL) to characterize the perfusion patterns encountered after anoxic injury to the brain.

MATERIALS AND METHODS: Sixteen patients with a history of anoxic or hypoxic-ischemic injury ranging in age from 1.5 to 78.0 years (mean, 50.3 years) were analyzed with conventional MR imaging and pulsed ASL 1.0–13.0 days (mean, 4.6 days) after anoxic insult. The cerebral perfusion in each case was quantified by using pulsed ASL as part of the standard stroke protocol. Correlation was made among perfusion imaging, conventional imaging, clinical history, laboratory values, and outcome.

RESULTS: Fifteen of the 16 patients showed marked global hyperperfusion, and 1 patient showed unilateral marked hyperperfusion. Mean gray matter (GM) cerebral blood flow (CBF) in these patients was 142.6 mL/100 g of tissue per minute (ranging from 79.9 to 204.4 mL/100 g of tissue per minute). Global GM CBF was significantly higher in anoxic injury subjects, compared with age-matched control groups with and without infarction (F_2,39 = 63.11; P < .001). Three patients had global hyperperfusion sparing areas of acute infarction. Conventional imaging showed characteristic restricted diffusion in the basal ganglia (n = 10) and cortex (n = 13). Most patients examined died (n = 12), with only 4 patients surviving at the 4-month follow-up.

CONCLUSION: Pulsed ASL can dramatically demonstrate and quantify the severity of the cerebral hyperperfusion after a global anoxic injury. The global hyperperfusion probably results from loss of autoregulation of cerebral vascular resistance.