There is evidence of abnormal increase in size and/or reduced T1-w signal (i.e. edema) of either hippocampus.

There is evidence of recent or chronic intracranial parenchymal hemorrhage.

There is T1-w signal abnormality (either reduced or increased) suggesting an underlying intraaxial or extraaxial CNS abnormality.

There is global background signal intensity 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.

There is focal/regional loss of sulci with compression of cisterns, & ventricles (not in a recognizable arterial zone), but is indicative of local or regional mass effect.

There may be extravasation of contrast from recent earlier CTA; not to be confused with recent subarachnoid hemorrhage.

There is abnormal brain calciification consistent with prior TORCH infection, as a cause of a seizure event.

There is apparent parenchymal dysgenesis (i.e. Sturge-Weber, NF, tuberous sclerosis, etc) or brain formation abnormality, as a cause of a seizure event.

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

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.

There is hyperemic pial circulation without contrast leak consistent with dysautoregulation post seizure.

There is reduced or absent post contrast signal intensity within brain parenchyma to suggest oligemic stroke (arterial, venous, or transcapillary).

There is thrombus in either dural sinus(es) and or cortical veins (CVT), as a cause for edema and seizure.

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 pial AVM, or dural AV fistula plus dural sinus stenosis/thrombosis.

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

There is abnormal intraaxial parenchymal enhancement to suggest an infiltrative neoplastic tumor or encephalitis.

There is evidence of tumoral regional hypervascularity with or without neoplastic type of AV shunting.

There is abnormal extraaxial enhancement to suggest an aggressive meningeal process (infectious or neoplastic).

Other significant findings are present.