There is evidence of subperiosteal hemorrhage along either the inner or outer calvarial surface.

There is evidence of epidural hemorrhage (acute-meningeal artery bleed vs delayed-diploic venous bleed).

There is evidence of intradural hemorrhage (usually Peds patients).

There is evidence of subdural hemorrhage.

There is evidence of hemorrhage into CSF spaces including subarachnoid, intraventricular, or subpial spaces.

There is evidence epidural/sub periosteal/parenchymal blood outside dural sinuses, especially for injury adjacent to the superior sagittal or transverse sinuses.

There is evidence of epidural blood adjacent to fx near meningeal arteries.

Mixed-age CNS injuries in the absence of clear history in a child is very suspicious for NAI.

There is evidence of intraaxial direct impact injuries: brain contusion or superficial gliding contusions (over orbital roof or petrous bone).

There is evidence of intraaxial/extraaxial direct impact injuries (coup event) and opposite side (contre coup event), which can include intraventricular hemorrhage.

There is evidence of brain laceration from missile type penetrating injuries.

There is evidence of intraaxial (non-direct impact acceleration-deceleration) brain shear injuries or diffuse axonal injuries (i.e. DAI) causing microhemorrhages at the gray-white junction or along the major forceps of the corpus callosum.

There is evidence of microhemorrhage from arterial microvascular shear effect (from acceleration-deceleration vector) in corpus callosum.

There is evidence of microhemorrhage from arterial microvascular shear effect (from acceleration-deceleration vector) in the BG/thalamus, or brainstem.

There is evidence of venous tether avulsion injuries, possibly with brain laceration (linear parenchymal hemorrhage).

There is evidence of any focal intracranial post traumatic mass (or hydrocephalus) producing brain herniation.

There is evidence of regional brain swelling from dysautoregulation and expanded intravascular pool, but without apparent brain edema.

There is evidence of intercurrent PCA or circummesencephalic artery stroke(s) from tentorial herniation.

There is evidence of intercurrent ACA stroke from subfalcine shift.

There is evidence of intercurrent ICA stroke from traumatic injury or from uncal brain herniation compressing across the interclinoidal ligament. Can also be caused by choking compressing ICA in neck in NAI.

There is evidence of an extraaxial hemorrhage adjacent to, and displacing or occluding a dural sinus.

There is evidence of focal posterior temporal intra or extraaxial mass effect (usually associated with temporal bone fracture) compressing or occluding the V of Labbe’ and/or transverse sinus.

There is evidence of global (diffuse) cytogenic edema likely related to concurrent apneic episode with cytotoxic brain edema.

There is evidence of major proximal or pial 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 abnormal capillary leak in areas of lost blood brain barrier, abnormal venocapillary pool density, or actual abnormal contrast enhancement if a focal lesion.

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