There is evidence of acute parenchymal cytogenic edema or post ischemic leukomalacia matching any arterial afferent perfusion zone, any watershed zone, nor any efferent venous egress zone.

There is evidence of hyperintense, acute, intraluminal arterial thrombosis in a major stem, trunk, division or pial artery perfusion zone.

There is evidence of hyperintense, acute, intraluminal arterial thrombosis in a recognizable perforator, choroidal, or deep subcortical penetrating artery/arteries.

There is evidence of hypo or hyperintensity within the deep medullary veins, or the deep venous system to suggest congestion, stasis, thrombosis, or increased (high flow) medullary venous hyperemia

There is hyperintensity within the cortical ribbon consistent with sequestered infarction (laminar necrosis)

There is hyperintensity within the centronuclear structures consistent with chronic low grade ischemic changes

There is enlargment of the Virchow-Robin spaces surrounding either the perforating arteries or the penetrating arteries.

There is luminal abnormal isointensity (lack of flow void) or hyperintensity within one or more dural sinuses (delta sign) indicative of acute thrombus on the noncontrast T1.

There is evidence of hyper or isointensity  within one or more cortical or central veins on noncontrast T1.

There is evidence of dilatation of the intraorbital veins, and optic hydrops (dilated CSF space around the optic nerves) on pre or post contrast T1 MR.

There is evidence of abnormal ventriculomegaly consistent with early hydrocephalus, pseudotumor, or PRES.

There is reduced or absent post contrast signal intensity within brain parenchyma (cortical ribbon and/or subcortcial white matter) consistent with low or absent transcapillary perfusion.

There is hyperemic pial circulation without contrast leak consistent with collateral pial drainage.

There is hyperemic perforator arterial circulation and deep medullary venous egress consistent with moyamoya vasculopathy.

There is hyperemic pial circulation with contrast leak consistent with dysautoregulation.

There is evidence of dural sinus filling defect (empty delta sign) indicating thrombosis within one or more dural sinuses on the post contrast T1.

There is evidence of pial venous collateral veins (typically appear serpiginous, enlarged size, draining the reversed directiong, with the size changed from being larger next to the dural sinus to being larger at there inception site on the post constrast T1 MR).

There is prominence of any of the pial/dural anastomotic sites (i.e. vertex venous lacunae, tenorial confluences, or cavernous sinus/retropharyngeal venous plexus) on the post contrast T1-w sequence.

There is evidence of mural enhancement or actual luminal filling defect within a cortical or central vein indicating acute thrombus on post contrast T1.

There is evidence of mural enhancement or intraluminal filling defect indicating thrombosis in an ophthalmic vein on post contrast T1.

There is evidence of dural sinus filling defect indicating thrombosis within the cavernous sinus and either its' afferent input or efferent egress veins on the post contrast T1.

There is contrast enhancement (contrast leak) which follows the parenchymal Virchow-Robin spaces surrounding the small metarterioles consistent with angiitis. This may create a patterns suggesting small nodule when viewed in axial plane.

There is evidence of unexpected regional cortical vein enlargement (arterialization of othersise NL veins), consistent with the combination of a dural AV fistula plus dural sinus stenosis/thrombosis on post contrast T1.

There is evidence of skull base destruction (infection/tumor) leading to cavernous or dural sinus thrombosis.

There is evidence of hemorrhagic conversion.

No other findings abnormalities are noted.