[The neuropathology of temporal lobe epilepsy: primary and secondary changes in the cortical circuits and epileptogenicity].
BACKGROUND
Temporal lobe epilepsy is associated to many disorders localized to the neocortex, the hippocampal formation or both (dual pathology). The most common pathologies are mesial sclerosis, tumours, malformations and scars. However, these alterations are not intrinsically epileptogenic, as they are also seen in patients who do not develop epilepsy. Thus, the cortical tissue in the damaged brain undergoes changes that may become a primary epileptogenic region. This region, in turn, may induce the formation of secondary epileptogenic regions situated at some distance from the primary focus.


METHODS
In this paper we consider the possibility that in both the primary and secondary epileptogenic regions there are similar changes in the neuronal circuits which induce epileptic activity. In the case of the primary epileptogenic regions, these changes occur non specifically following an initial lesion or precipitating factor (e.g. a tumour) which induces gliosis and neuronal loss around the lesion. These changes give rise to a perilesional synaptic reorganization (elimination of connections with or without the formation of new synapses) which causes the onset and continuation of epileptic activity. However, the changes in the circuits in the secondary epileptogenic regions are the result of epileptic activity originated in the primary epileptogenic region which is propagated by specific anatomical connections. This anomalous activity causes changes in the target region (gliosis and neuronal loss) which leads to epileptogenic synaptic reorganization similar to that occurring in the primary perilesional areas.
DeFelipe Oroquieta
J
J
Unidad de Neuropatología, Instituto Cajal, CSIC, Madrid, 28002, España. defelipe@cajal.csic.es
Arellano
J I
JI
Alonso
L
L
Muñoz
A
A
D002540:Cerebral Cortex / Q000033:anatomy & histology / Q000473:pathology*; D004833:Epilepsy, Temporal Lobe / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D008959:Models, Neurological; D009474:Neurons / Q000166:cytology / Q000378:metabolism*