Abstract

This chapter discusses the pathological findings in mesial temporal sclerosis. Ammon's horn sclerosis describes a severe segmental neuronal loss and astrogliosis that predominantly involves the most vulnerable neuronal populations of Ammon's horn. A diagnosis of Ammon's horn sclerosis in a surgical specimen requires that the anatomic integrity of the hippocampal formation is sufficiently preserved to allow an unambiguous identification of its different segments. The presence of Ammon's horn sclerosis and focal lesions are not independent variables. Ammon's horn sclerosis is much more common in patients without as compared to those with focal lesions such as tumors, malformative or vascular lesions. It is found that Ammon's horn sclerosis is not only associated with a loss of ganglion cells but that some neuronal populations are actually increased in numbers as compared to the normal hippocampus. A widely accepted hypothesis with respect to seizure susceptability of the hippocampal formation in Ammon's horn sclerosis is that of aberrant axonal reorganization. It is observed that in Ammon's horn sclerosis there is a homogeneous increase in tenascin-C (TN-C) immunoreactivity without distinct TN-C boundaries. It is suggested that the loss of TN-C boundaries is most prominent in areas characterized by severe neuronal cell loss, reactive astrogliosis, and synaptic reorganization in the dentate gyrus molecular layer.

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