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[Mesial temporal sclerosis (I): histological data, physiopathological hypothesis and etiological factors].

Authors
  • Serrano-Castro, P
  • Sánchez-Alvarez, J C
  • García-Gómez, T
Type
Published Article
Journal
Revista de neurologia
Publication Date
Apr 01, 1997
Volume
25
Issue
140
Pages
584–589
Identifiers
PMID: 9172925
Source
Medline
License
Unknown

Abstract

Probably these organic changes are both the cause and effect of repeated convulsions. Participation in this self-perpetuating circuit may be due to recognised risk factors of ETM (head injury, CNS infections, febrile convulsions in early stages of development) which cause, first of all, death of neurones of the dentate gyrus cells followed by reduced inhibitory activity of the 'basket' cells and therefore sustained hyper-excitability of the pyramidal cells (especially in the CA3 regions), which are responsible for complex partial seizures and massive liberation of glutamic acid. Glutamic acid can cause death of neurones of the granulosa cells of the dentate gyrus, thus closing the circuit. This hypothesis explains the progressive nature of the ETM syndrome. When there is pathology of the cortical structure there is another access via to this circuit--by means of cortical discharges of the so-called perforant pathway which stimulates activity of the pyramidal cells and sets off the chain of events described above. This hypothesis explains the so-called 'dual pathology'.

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