Hippocampal sclerosis (HS) is the most frequent aetiology for medically refractory epilepsy [1]. It was first described by Bouchet and Cazauvielh in 1825 on pathological examination of a patient who had died following seizures [2]. In 1880, Sommer studied pathological samples from over 90 patients with chronic epilepsy, and reported gliosis and pyramidal cell loss in the hippocampus, predominantly in the CA1 region, originally known as Sommer’s sector. He proposed that these abnormalities were the cause of the epilepsy. In 1889, Jackson associated focal lesions in the hippocampus with the clinical symptoms of temporal lobe seizures. In addition to the loss of pyramidal cells, the loss of hilar interneurons was recognized as an important feature [3] and is dominant in the type of pathology that came to be described as end-folium sclerosis [4]. Loss of both inhibitory gamma-aminobutyric acid (GABA) neurons and excitatory mossy cells in the hilus reduces their control of the dentate granule cells, and such loss of neurons in the hilus (sometimes included as part of CA4) is one of the most consistent findings in TLE [5,6]. The International League Against Epilepsy has proposed a classification of the distinct patterns of HS to correlate the type of pathological changes to post-surgical outcome [7]. In the 1950s with the development of electroencephalography, HS was linked to electrophysiologic temporal lobe seizures.