There is evidence of recent intracranial (subarachnoid/cisternal/intraventricular) hemorrhage.

There is evidence of recent intracranial parenchymal (intra axial) hemorrhage.

There is evidence of focal CT hyperdensity to suggest recent intracranial hemorrhagic conversion of an acute stroke.

There is evidence of “isodense focal mass” effect, which could be related to very recent hemorrhagic conversion or sequestered infarction.

There may be extravasation of contrast from recent earlier CTA.  

There is global background CT density asymmetry between the cerebrum vs cerebellum (only evident when using narrow/high contrast window widths), which if present, is consistent with global hypoxic-ischemic (HIE) event where the cerebrum is uniformly hypodense and the cerebellum is actually normal or near normal.

Generalized loss of sulci with compression of cisterns, & ventricles (not in a recognizable arterial zone) is indicative of other processes that causing asymmetric, nonfocal, brain swelling, as pseudotumor cerebri, drowning, respiratory arrest, etc.

There is evidence of dural sinus thrombosis ("delta or empty delta sign").

There is evidence of acute cortical or deep central vein CVT ("cord sign")..

There is evidence of aggressive otomastoid or paranasal sinus infectious disease, which could lead to cortical vein phlebothrombosis or dural sinus thrombosis.

There is hyperdensity within a recognizable cortical or deep central vein indicating hyperacute thrombus (CVT).

There is hyperdensity within a recognizable carotid or vertebral artery component (primary stem, secondary stem, division, trunk, or pial artery) in either the upper cervical, intracranial/extradural, or intracranial regions.

There is focal effacement of GW (gray matter-white matter) junction from early cytogenic edema.

There is evidence that the stroke-zone occupies more than 1/3 of the proximal stem artery or major venous expected perfusion zone.

There is hyperdense CT change in brain parenchyma to confirm an area of dense ischemic core (and likely sequestered infarction).

There is well delineated CT hypodense change (usually cytogenic edema) within a recognizable vascular territory indicating the stroke evolution time from ictus to imaging is at least 8 hours.

There is focal effacement of sulci confirming the presence of either cytogenic edema or expanded venocapillary bed from physiologic hyperemia in the collateral zone surrounding the (arterial or vneous) stroke-zone.

There is focal effacement of parts of the ventricles confirming presence of local post ischemic cytogenic edema.

There is protein leak into sulci (effacing the margins of the sulci) consistent with increasing blood brain barrier leak.

There is  sulcal dilatation and/or ventriculomegaly outside the range of normal consistent with brain atrophy out of proportion for the patients' age. The atrophy may be global, regional or focal in location and mild, moderate, or advanced in degree.

There are one or more lacunar defects or areas of encephalomalacia or evidence of subcortical leukomalacia consisent with post ischemic injury, or multiple other etiologies as trauma, post encephalitis, post HIE, toxic encepalopathy, etc.

No other abnormalities are noted.