There is evidence of acute post seizure change with increased hippocampal volume plus readily apparent T2-w positive edema (implying the seizure event is in either the hyperacute or early acute phase of evolution), or only minimally obvious implying the edema is recent, but not hyperacute. The area of involvement includes a significant portion of the hippocampus (more than just a small segment of one or both hippocampi).

There is abnormal volume and T2-w signal increase is limited to the hilum of the hippocampus.

There is abnormal volume and T2-w signal increase is limited to CA2.

There is abnormal volume and T2-w signal increase is limited to CA1.

There is abnormal volume and T2-w signal increase is limited to the subiculum.

There is abnormal volume and T2-w signal increase is limited to the tail of the hippocampus.

There is abnormally increased volume without apparent edema (implying the seizure evolutions is recent but not hyperacute) within the head/body/tail of hippocampus on one side or both sides.

There is abnormal concurrent volume and signal within both hippocampi, and/or the entorhinal cortex, the parahippocampal gyrus, or other parts of the limbic system to suggest status epilepticus.

There is abnormal reduced size or actual cavity formation in either hippocampus, usually with gliosis and loss of myelin signal; these are features of chronic hippocampal injury in epilepsy (i.e mesial temporal sclerosis or MTS).

There is abnormal volume and asymmetry of the amygdala on either side (dysgenesis).

There is evidence of a persistent hippocampal fissure remnants (variation of normal).

There is effacement of the internal hippocampal white matter pathways (i.e. ERC to dentate/CA2 tract, including the cisternal segment or hilar segment, and or Schaffer's collateral tract).

There is effacement of the external hippocampal white matter pathways (i.e. alveus, fimbria, infrasubicular tract, or pararhinal tract)

There is increased size and evidence of edema (increased T2 signal) in only a focal segment of either hippocampus.

There is increased size and evidence of edema (increased T2 signal) in CA1.

There is increased size and evidence of edema (increased T2 signal) in CA2.

There is increased size and evidence of edema (increased T2 signal) in the hilum (containing the dentate granular layer, CA3, and CA4).

There is increased size and evidence of edema (increased T2 signal) in the subiculum.

There is increased size and evidence of edema (increased T2 signal) involving the entorhinal cortex , as well as the hippocampus.

There is presence of an underlying hippocampal gray matter tumor: FTL ganglioglioma, DNET, or low grade glioma.

There is presence of an intercurrent infiltrative mass (gliomatosis or CNS lymphoma) in the brain.

There is presence of an intercurrent vascular malformation.

There is presence of intercurrent blood products either new or chronic.

There is presence of an intercurrent acute or subacute arterial/transcapillary/venous stroke.

There is presence of intercurrent CNS infectious process (i.e encephalitis, pia arachnoid granulomatous disease, empyema, etc.).

There is evidence of prior trauma including mesial temporal injury.

Other significant findings are present.