title: Anoxic injury-associated cerebral hyperperfusion identified with arterial spin-labeled MR imaging.
abstract: OBJECTIVE
  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.
  
  
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Radiology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA. jeffmpollock@gmail.com
authors.forename: J M
authors.initials: JM
authors.lastname: Pollock
authors.forename: C T
authors.initials: CT
authors.lastname: Whitlow
authors.forename: A R
authors.initials: AR
authors.lastname: Deibler
authors.forename: H
authors.initials: H
authors.lastname: Tan
authors.forename: J H
authors.initials: JH
authors.lastname: Burdette
authors.forename: R A
authors.initials: RA
authors.lastname: Kraft
authors.forename: J A
authors.initials: JA
authors.lastname: Maldjian
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001783:Blood Flow Velocity / Q000502:physiology; D001921:Brain / Q000098:blood supply*; D002648:Child; D002675:Child, Preschool; D004292:Dominance, Cerebral / Q000502:physiology; D005260:Female; D006323:Heart Arrest / Q000150:complications / Q000503:physiopathology; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D006940:Hyperemia / Q000175:diagnosis* / Q000503:physiopathology; D002534:Hypoxia, Brain / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology; D007089:Image Enhancement / Q000379:methods*; D007091:Image Processing, Computer-Assisted / Q000379:methods*; D007223:Infant; D020244:Infarction, Middle Cerebral Artery / Q000175:diagnosis / Q000503:physiopathology; D018810:Magnetic Resonance Angiography / Q000379:methods*; D008297:Male; D008875:Middle Aged; D012039:Regional Blood Flow / Q000502:physiology; D012189:Retrospective Studies; D014655:Vascular Resistance / Q000502:physiology