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.

Other significant findings are present.