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The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.

Surgical Treatment of Drug-Resistant Epilepsy Due to Mesial Temporal Sclerosis: Etiology and Significance

Falconer, Murray A.·1968·Archives of Neurology

Abstract

THERE is now general agreement 1-3 that in about 50% of institutionalized epileptic patients who die of natural causes, an autopsy will disclose a lesion. This was first demonstrated macroscopically in 1825, in 9 out of 18 cases, by Bouchet and Cazauvieilh, 1 who called it Ammon's horn (synonyms—sclerosis of the cornu Ammonis and hippocampal sclerosis). Its histopathology was subsequently described in 1880 by Sommer. 4 This lesion has also been called incisural sclerosis 5 and pararhinal sclerosis. 6,7 Both these terms, however, have now acquired rather misleading connotations, one of difficult birth and the other of olfactory perception. We therefore prefer the simpler term mesial temporal sclerosis (MTS) because the sclerotic process usually involves other structures, such as the amygdala and uncus, as well as the hippocampus, and because the term which has since been adopted by others is purely descriptive without etiological or functional implications 8 (Figure).

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Metadata

Authors
Falconer, M. A.
Venue
Archives of Neurology
Published
1968-10-01
Volume
19
Issue
4
Pages
353
ISSN
0003-9942 (ISSN-L)
OpenAlex
W2074878857
Cited by
273
References
16
FWCI
11.19
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Surgical Treatment of Drug-Resistant Epilepsy Due to Mesial Temporal Sclerosis: Etiology and Significance. https://app.cochat.ai/papers/10.1001/archneur.1968.00480040019001
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Falconer, M. A. (1968). Surgical Treatment of Drug-Resistant Epilepsy Due to Mesial Temporal Sclerosis: Etiology and Significance. Archives of Neurology. https://doi.org/10.1001/archneur.1968.00480040019001

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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