There is T2 evidence of hyperacute hemorrhage (nearly isointense T2 and isointense T1) evident only by local mass effect (parenchyma) or lack of phase loss from active blood flow for arteries, veins, or dural sinuses.

There is T2 evidence of acute hemorrhage (hypointense T2 while T1 is also isointense).

There is T2 evidence of early subacute hemorrhage (persistent hypointense T2 while T1 is hyperintense from met-Hgb).

There is T2 evidence of late subacute hemorrhage (after clot lysis T2 is now hyperintense T2 while T1 remains hyperintense from met-Hgb).

There is T2 evidence of chronic residua of prior hemorrhage (both T2 and T1 are hypointense from hemosiderin).

There is T2 evidence of an underlying AV malformation or AV fistula.

There is T2 evidence of an underlying intraaxial mass lesion(s).

There is T2 evidence of tissue edema in the affected venous egress zone and/or acute thrombus within intracranial veins or dural sinuses.

There is T2 evidence of acute edema in a recognizable arterial perfusion zone, or thrombus (no longer detect the normal loss of signal caused by patent blood flow) within the arterial lumen.

There is T2 evidence of ventricular enlargement with evidence of raised CSF pressure consistant with primary or secondary hydrocephalus.

Given mass effects from hemorrhage, underlying stroke or mass, and/or hydrocephalus, there is evidence of significant brain displacements and herniation.

Other significant imaging findings are present.