There is evidence of extraaxial post traumatic injury (similar search pattern as head CT).

There is evidence of intraaxial post traumatic injury (similar search pattern as head CT).

There is evidence of brain injury of mixed ages highly concerning for NAT.

There are extraaxial, blood products.

There is evidence of brain contusion(s).

There is evidence of mass effect producing brain herniation(s).

There are multiple sites of punctate edema or microhemorrhage within the white matter and/or along the gray-white subcortical junction/ within the corpus callosum, Centro nuclear structures, or brainstem consistent with brain shear acceleration-deceleration injury.

There is vasogenic edema (and likely microhemorrhage) along egress pathways or cortical veins or the deep thalamostriate veins indicating venous tether injuries.

There is evidence of abnormal fluid accumulation along the margin of any major artery suggesting para arterial hematoma without intimal dissection-(Denver type 1 arterial injury).

There is evidence of abnormal fluid signal along the margin of any major artery with evidence of intimal flap or pseudoaneurysm confirming traumatic arterial dissection.

There is cytogenic edema in a recognizable arterial perfusion zone consistent with stroke superimposed on the traumatic injuries.

There is abnormal MR flair signal within the lumen of any major cortical vein or dural sinus suggesting venous egress thrombosis.

There is evidence of ventriculomegaly with subependymal edema indicating hydrocephalus (likely caused by SAH (which may not be evident) or sequestered ventricles.

There is SWI evidence of abnormal susceptiblity artifact associated with extraaxial/ intraaxial/ intraventricular or subependymal/ subpial blood products.

There is SWI evidence of parenchymal linear susceptiblity artifact following a cortical vein consistent with venous tether injury and resultant brain laceration.

There is SWI evidence of a few, multiple, or even diffuse parenchymal punctate susceptiblity artifacts, especially in the subpial spaces, gray-white matter junction, major forceps corpus callosum, basal ganglia, thalamus, mesencephalon and central brain stem consistent with DAI.

There is SWI evidence of thrombus within the lumen (exhibiting blooming artifact) of any major cortical vein or dural sinus.

There is altered SWI appearance of the venocapillary pool and the deep venous system, either increased from dysautoregulation-related hyperemia or reduced from vasospasm.

There is evidence of positive MR-diffusion but negative ADC (edema shine-through effect) associated with intraaxial parenchymal injury not evident on CT or other MR sequences.

There is evidence of positive MR-diffusion and ADC (actual positive restriction) in areas of post traumatic or hypoxic cytogenic edema or intercurrent arterial occlusion.

The distrubution of the positive sites on the DWI are consistent with a single trauma vector versus vectors of different directions (shaking) in NAI patients.

There is positive diffusion and positive ADC associated with intraaxial parenchymal injury and local ischemic effects not evident on CT or other MR sequences. This is especially evident in infants (< 1 year old) with NAI.

There is evidence of concurrent abnormalities not likely related to recent brain injury.

There is evidence of major arterial post traumatic dissection.

There is evidence of pial or meningeal arterial entrapment in a fracture.

There is evidence of major arterial post traumatic injury producing a pseudoaneurysm.

There is evidence of major arterial post traumatic injury producing a high or low flow AV fistula.

There is evidence of deformity (external compression) or thrombosis of a dural sinus.

There is evidence of concurrent abnormalities not likely related to recent brain injury.