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Academia Mexicana de Neurología, A.C.

2007, Number 2

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Rev Mex Neuroci 2007; 8 (2)

Epilepsy. Developmental brain anomalies and Ammon’s horn salerosis associated to epileptogenesis. Which is its relevance?

Escobar A

Language: Spanish
References: 48
Page: 163-169
PDF size: 102.91 Kb.


ABSTRACT

The introduction of neuroimaging techniques in the diagnosis of epilepsy: Computerized axial tomography (CAT), Single photon emission tomography (SPECT), Magnetic resonance (IMR), Functional magnetic resonance (fMR), and Positron emission tomography (PET), constituted a stride in the in vivo detection of developmental brain anomalies that are significant to epileptogenesis. This valuable neuropathological data also led to a classification change of the so-called idiopathic epilepsies to symptomatic epilepsies associated to a known anatomical brain anomaly. A good number of developmental brain anomalies, termed dysgenesis, are readily identified by macroscopic examination, to name a few, corpus callosum agenesis, megalencephaly, lisencephaly, macrogiria and microgiria, focal cortical dysplasia, however, other anomalies require of microscopical exam, thus named microdysgenesis, for instance: columnar and or laminar disarrangement, subpial or in the white matter ectopic pyramidal neurons, inverted neurons, reduced neuronal number, mainly referring to interneurons.
The most common associated lesion to epileptogenesis is that of Ammon’s horn sclerosis, also named hippocampal or mesial temporal lobe sclerosis. This lesion, known since 1825, constitutes in itself the most frequent neuropathological finding in temporal lobe epilepsy. It is characterized by loss of pyramidal neurons in the CA1 sector of the hippocampus, usually unilateral, but occasionally affecting also sectors CA3 and CA4, and less frequently extending to the dentate gyrus. There is associated reactive astrocytic gliosis. These lesions are manifested clinically as partial complex seizures. Other associated lesion is the disruption of the blood.brain barrier, an event occurring at every seizure in acute or chronic epilepsy, the ensuing hematic protein leaking into the nervous parenchyma leads to progression of seizures and formation of epileptic focus.


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