Hippocampus and Epilepsy Surgery

Abstract

Summary: Sclerosis of the cornu Ammonis, or Ammon's horn sclerosis (AHS), is an “often‐described, yet hitherto enigmatic phenomen,” as Spielmeyer described it in 1927. It has been detected in cases with ischemia, anoxia, or hypoglycemia and in more than half of the epileptic brains examined postmortem. Various theories about its pathogenesis have been propounded. Among them, the “Pathoklise” theory of the Vogts and the vascular theory of Spielmeyer et al. had prevailed until recently. In 1953, two articles were published to contribute to the pathogenesis of ictal automatism (a type of complex partial or temporal lobe seizure). One is the incisural sclerosis theory of Penfield et al., and the other is the AHS theory of Sano and Malamud. The former researchers described a diffuse sclerosis of the inferomesial temporal structures without, however, specifically relating it to AHS. They considered it to be the result of localized anoxia of that portion of the brain caused by incisural herniation occurring during parturition. Sano and Malamud maintained that AHS is a result of convulsions, a distinct scar adjacent to which epileptogenic foci may develop in the course of time to cause ictal automatism. The latter theory was corroborated by Sano, Falconer, and other investigators. Falconer expanded the theory to the assertion that not only ictal automatism but other types of intractable epilepsy may be due to “mesial temporal (Ammon's horn) sclerosis.” The most recent development in the pathogenesis of AHS is the excito‐toxicity theory, i.e., that AHS is caused by excessive excitation of neurons, probably by putative excitatory neurotransmitters, especially glutamate. For this theory, there is a significant body of evidence. Recent developments in glial physiology suggest that the existence of gliosis itself may actively exert a great influence on neurons so that neurons generate high‐frequency synchronous discharges as epileptogenic foci.