Hypoxic-ischemic brain injury is a diagnostic term that encompasses a complex constellation of pathophysiological and molecular injuries to the brain induced by hypoxia, ischemia, cytotoxicity, or combinations of these conditions.

Typical causes includes cardiac arrest, respiratory arrest, drowning, hanging, and other forms of incomplete suffocation or carbon monoxide and other poisonous gas exposures and/or severely diminished blood supply. 

The diffuse abnormality might be difficult to detect and history is key to suspecting the bilateral and symmetric pattern. 

Diffuse loss of grey/white differentiation with presence of pseudo-subarachnoid sign, diffuse edema and loss of sulci, and tonsillar herniation through foramen magnum in keeping with diffuse hypoxic ischemic injury.

Stroke Mimic - Not every hypoattenuation on CT is indicative of acute stroke. Given the preservation of cortical gray white in the insula, and in fact cortical expansion, this was a tumor with underlying vasogenic edema producing this appearance. 

Striatocapsular infarcts involve the striatum (ie the caudate nucleus and putamen), without involvement of the cortex secondary to either a complete or partial proximal MCA occlusion limiting flow to the lenticulostriate arteries.

Classically patients exhibit both cortical (e.g. aphasia, sensory neglect or extinction, apraxia) and subcortical (e.g. upper limb hemiparesis, dysarthria) neurological signs.

Tmax (red) and CBV (blue) demonstrate very increased time of transit of blood, and very low blood volume in the exact same areas. This is no perfusion mismatch here and all the brain tissue has been infarcted with no pneumbra present to save.

Susceptibility sequences SWI demonstrate diffuse hemorrhagic change within an area of previous Infarct. With corresponding diffusion DWI restriction in the right panel.