• Hypoxic ischemic injury (HII): Global hypoxic ischemic injury,
global anoxic injury, cerebral hypoperfusion injury
○ Etiologies: Cardiac arrest, cerebrovascular disease,
• Injury patterns highly variable depending on brain maturity,
severity, and length of insult
○ Mild to moderate: Watershed zone infarcts
○ Severe: Gray matter structures (basal ganglia, thalami,
cortex, cerebellum, hippocampi)
• MR best to assess overall extent of injury within hours after
○ DWI: 1st modality to be positive (within hours)
○ DWI: Restriction in deep nuclei ± cortex
○ T2/FLAIR: ↑ signal in cerebellum, basal ganglia, cortex
○ Acute changes not reliably identified with T2
• MRS: More sensitive and indicative of severity of injury in
○ ↑ lactate, ↑ glutamine-glutamate
• Ischemic territorial infarction
• Acute hypertensive encephalopathy, posterior reversible
encephalopathy syndrome (PRES)
• Common underlying process regardless of cause
○ ↓ cerebral blood flow and ↓ blood oxygenation
○ Switch from oxidative phosphorylation to anaerobic
○ Glutamate-related cytotoxic processes
(Left) Axial DTI trace image in
injury (HII). (Right) Axial T2 MR
visual and sensorimotor cortex
status post cardiac arrest. T2
subacute period (> 24 hours to
2 weeks) with increased signal
and swelling of the injured GM
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