There is evidence of acute or subacute parenchymal (intraaxial) hemorrhage.

There is evidence of concurrent intraaxial hematoma and subarachnoid hemorrhage (r/o aneurysm/sentinel bleed).

There is evidence of a pial, or choroidal, or deep parenchymal AVM (consisting of afferent arterial input, AVM nidus, and efferent egress veins).

There is evidence of an AVM with a component of higher flow AV fistula within the nidus.

There is evidence of parenchymal angiomatous transformation (AVM variant).

There is evidence of intra ventricular bleeding possibly from choroidal AVM.

There is evidence of a recently thrombosed AVM (perilesional edema).

There is evidence of a primary, intradual, AVF (consisting of afferent or efferent vessels but no nidus).

There is evidence of parenchymal hemosiderin deposition from chronic microhemorrhage caused by vascular steal effects produced by either a high flow AVF or AVM.

There is evidence of encephalomalacia or leukomalacia related to chronic vascular steal effects or injury related to hemorrhage.

There is evidence of rerouting of the venous efferents related to direct AV-shunt, venous-pressure-increase effects.

There is evidence of rerouting of the venous efferents from concurrent venous or dural thrombosis.

There is evidence of marked venous efferent dilatation or venous aneurysm related to the high flow across the AV shunt.

There is evidence of focal enlargement of dural sinuses possibly with enlarged orbital veins (often with proptosis) to suggest dural AV fistula or extradural AV fistula of carotid origin.

There is evidence of unexplained pial veins suggesting dural AV fistula.

There is evidence of hemorrhage associated with cortical vein or dural sinus thrombosis.

There is evidence of bleeding near falx (possibly post traumatic in origin - search for brain contusion).

There are the features of enlarge lenticulostriate arteries in the basal ganglia as evidence of Moya-Moya vasculopathy.

There is evidence of multicentric bleeding sites for coagulopathy as cause for bleeding.

There is evidence of focal cytogenic edema for intercurrent hemorrhagic stroke.

There is evidence of hemorrhagic met or other tumor as basis for intracranial hemorrhage.

There is evidence of intercurrent hydrocephalus or herniation syndromes.

There is evidence of a cavernous angioma or multiple consistent with familial cavernous angiomatous syndrome.

There is evidence of non-shunting, cavernous malformation(s).

There is evidence of a DVA.

There is evidence of concurrent DVA + cavernous malformation.

There is evidence of pontine telangiectasia.

Other abnormalities.