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Building up of absence epilepsy: a progressive process that takes place during brain maturation

on the October 26, 2017

The three steps composing epileptogenesis

Caroussel_17.10.31_Depaulis_epileptogenese_EN.jpg

Idiopathic Generalized Epilepsies represent one-third of all epilepsies. These epilepsies, most often diagnosed during childhood, are not associated with clear-cut inciting events or detectable structural brain abnormalities. Their early onset suggests that epileptogenic processes take place during brain development and maturation. The precise characterization of these processes is of crucial importance to better define an appropriate therapeutic window and specific treatments.

Absence epilepsy, which generally first occurs in children aged 5-7, is considered as a prototypic form of epilepsy that develops during brain maturation and provides a unique pathophysiological model to study idiopathic epileptogenesis in general and the processes that lead to the generation of spike-wave complex. Absence Epilepsy is an epileptic syndrome characterized by the recurrence of generalized non-convulsive seizures associated with a transient alteration of consciousness with a loss of responsiveness to environmental stimuli concomitant with a cessation of activity. While the ictogenesis process (i.e. epileptic discharge occurrence) has been extensively studied, little is known about the mechanisms leading to the occurrence of recurrent epileptic discharges (i.e. epileptogenesis).

The team “Synchronization and modulation of neural networks in epilepsy” investigated how epileptic discharges emerged and evolved during the postnatal period in a recognized model of absence epilepsy, the GAERS rat. They showed that cortical discharges start from the third post-natal week and follow a three steps maturation process during which their pattern, frequency and duration progressively evolve to reach a relative stability at adulthood. This epileptic discharge maturation is associated with an abnormal alteration of the intrinsic properties of deep layer pyramidal neurons of the somatosensory cortex, notably a progressive increase in the strength of the local synaptic activity associated with a growing propensity of somatosensory cortical neurons to generate synchronized oscillations.

To conclude, this study evidences the progressive nature of absence epileptogenesis with the acquisition over time of abnormal properties in cortical networks and neurons, leading to the seizure expression. Given the early onset of epileptic discharges in genetic epilepsies, drugs specifically targeting the changes occurring during cortical networks development should be able to prevent, reverse or interrupt the epileptogenic processes.


 

Three steps maturation process of absence seizures during brain development showed by EEG recordings and the corresponding time-frequency plots.


Reference: 
Guillaume Jarre,  Tristan Altwegg-Boussac,  Mark S. Williams,  Florian Studer, Mathilde Chipaux,  Olivier David,  Stéphane Charpier,  Antoine Depaulis,  Séverine Mahon, Isabelle Guillemain (2017). Building Up Absence Seizures in the Somatosensory Cortex: From Network to Cellular Epileptogenic Processes, Cerebral Cortex, Volume 27, Issue 9, Pages 4607–4623. 

 


Updated on October 31, 2017

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