Abstract
Hippocampal pathology (Ammon’s horn sclerosis (AHS)) is a well-recognized finding in the brains of temporal lobe epileptics (Meldrum and Corsellis, 1984). Classical AHS involves extensive loss of neurons from hippocampal area CA1 (h1, Sommer sector), a less extensive neuronal deficit in the CA3-CA4 area (h3-h5, endblade, endfolium), and relative sparing of neurons in the h2 area (‘resistant zone’; area CA2 and the adjacent portion of area CA3a which contains the mossy fiber endbulb) and in the fascia dentata. Most commonly, some neuronal loss in other brain regions, particularly the amygdala, thalamus and cerebral neocortex, accompanies the hippocampal lesion. Although the near-total loss of neurons from area CA1 is the most striking feature of AHS in many patients, there is reason to believe that the most vulnerable neurons are the CA3 hippocampal pyramidal cells and the morphologically diverse neurons of area CA4 (Margerison and Corsellis, 1966).
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© 1986 Plenum Press, New York
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Nadler, J.V., Okazaki, M.M., Gruenthal, M., Ault, B., Armstrong, D.R. (1986). Kainic Acid Seizures and Neuronal Cell Death: Insights from Studies of Selective Lesions and Drugs. In: Schwarcz, R., Ben-Ari, Y. (eds) Excitatory Amino Acids and Epilepsy. Advances in Experimental Medicine and Biology, vol 203. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-7971-3_51
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