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I read with pleasure the short report of Van Paesschenet al.1 This finding perhaps may raise some interest again in corpora amylacea as well as in the pathology of temporal lobe epilepsy. As I studied corpora amylacea for about 25 years I call the attention of the authors to the first—but important—finding of Ramsey who published in her article in 19652 a case of a 35 year old man who had intractable temporal lobe epilepsy. Surgical intervention was performed with temporal lobe resection including 3 cm of hippocampus. The pathologist’s report stated that the tissue seemed histologically normal except for a few areas of pyknosis and shrinkage of neurons and a decrease in the number of neurons in the hippocampus. The presence of corpora amylacea without gliosis was noted and was especially prominent in the hippocampus. The diagnosis was “mild presenile cortical atrophy of the temporal lobe with corpora amylacea in the hippocampus.”
I studied the occurrence of corpora amylacea in 1407 cases of various diseases with special reference to the so called predilection sites of corpora amylacea, and I sometimes found large numbers of corpora amylacea in the hippocampal area and other regions with and without special pathology, even in young people. The conditions which favour the development of corpora amylacea vary greatly (aging, chronic vascular—hypoxic—diseases, ALS, multiple sclerosis, dementias, etc) as well as various pathogenetic mechanisms promoting formation, which included chronic hypoxia, neuronal degeneration, external hydrocephalus—as a consequence of local cortical atrophy—diabetes mellitus, and other processes which induce stress states expressed by strong HSP 60 positivity in our investigations (see3-7for appropriate references). So the corpora amylacea formation really is an epiphenomenon in different diseases, as Van Paesschen et al state.
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