Table 2.

Structural and functional anatomic changes involved in the epilepsy syndromes covered in this review article.

Condition	Structural	Functional
Early life seizures	Neuronal injury in l. septal nuclei, amygdala, v. subiculum/CA1	CA1 unable to form spatial mapPrefrontal cortex short term potentiation alterations (LII/LIII-to-LV and LV-to-LV)
Temporal lobe epilepsy	Volume loss in thalamus, hippocampus, cerebellum Temporal and frontal cortical thinning (only frontal in some studies) With postictal psychosis: prefrontal and temporal thickening	Lateral amygdala stimulation causes experiential symptoms White matter abnormalities in a. and m. temporal, ips. cerebellum, p. callosum, con. frontoparietal Interictal hypometabolism in epileptic region Poorly segregated cognitive modules
Temporal lobe epilepsy with hippocampal sclerosis	Neuronal loss and gliosis centered around CA1 Granule cell dispersion and loss and sprouting of interneurons in dentate gyrus Mesiotemporal cortex sclerosis, neuronal loss, gliosis Increase in complexity of temporal and frontal cortical folding Cortical thinning in regions connected with hippocampus	Decrease connectivity between amygdalo-hippocampal complex and bil. v. prefrontal, temporal pole, con. p. cingulate; Increase connectivity with a. cingulate, d. m. prefrontal, bil. temporo-parietal junction Increased synchronization in ips. parahippocampus, midbrain, insula, callosum, bil. sensorimotor cortex, frontoparietal subcortical structures; Decreased synchronization in cerebellum, precuneus, p. cingulate, bil. i. l. parietal, m. PFC
Frontal lobe epilepsy	Frontal cortical volume loss in children for left FLE: (ips) s. frontal, paracentral, precuneus, cingulate, i. parietal, supramarginal, postcentral, s. temporal (con) s. and m. frontal, m. orbitofrontal, supramarginal, postcentral, s. temporal banks, parahippocampus; right FLE: (ips) precentral, postcentral, transverse temporal, parahippocampus, lingual, l. occipital (con) s. front, i. parietal, postcentral, s. temporal, p. cingulate, lingual	Frontal, temporal, parietal hypometabolism
Juvenile myoclonic epilepsy	Gray matter changes in s. m. frontal, p. cingulate and a. callosum Gray matter reduction in supplementary motor area and p. cingulate	White matter abnormalities in bil. a. and s. corona radiata, callosum genu and body, cingulum-temporal connections, p. parietal, and frontal Reduced connectivity between prefrontal and frontopolar regions; Increased connectivity between occipital cortex and supplementary motor area Hyperconnectivity in subnetwork involving primary motor cortex, precuneus, cerebellum lobules IV and V, basal ganglia, bil. parietal/postcentral, subcortical regions and right hippocampus
Childhood absence epilepsy		White matter abnormalities in bil. thalamus, a. callosum, upper brainstem, prefrontal, a. cingulate, parietal, p. cerebellum, bil. putamen, bil. p. internal capsule Altered whole-brain topology Impaired subcortical and orbitofrontal subnetworks Microstructural changes in callosum and bil. precuneus

Some changes span both categories, in which case we classified it according to its dominant feature. Abbreviations used are positional: a-anterior, p-posterior, v-ventral, d-dorsal, s-superior, i-inferior, l-lateral, m-medial, ips-ipsilateral, con-contralateral, bil-bilateral. Italicized text are animal studies.