Epilepsy and stroke

My team and I have made major conceptual advances in the understanding of epilepsy and, in particular, temporal lobe epilepsy, which in itself only constitutes a large part of the types of epilepsy that does not respond to treatments. We were the first to develop the animal model that mimics the best electro-graphic, clinical and histopathological signatures of this type of epilepsy. We have also shown that the administration of a molecule, kainic acid (a structural analogue of the isolated glutamic acid from the red seaweed Digenea simplex), generates seizures associated with lesions in brain regions sensitive to crises, followed by a reorganization of the neural network and the formation of new connections between neurons.

In other words, after injury, the brain forms new connections whose properties will contribute to the expression of the syndrome. The neurodegenerative process is a continuous process with a “reactive plasticity” that plays a central role in causing the syndrome. Thus, “the crisis leads to the crisis” through a cascade: crisis, injury, budding, formation of new synapses and genesis of new crises. These observations have been, for the most part, confirmed on humans and the concept of reactive plasticity is a focus of current studies. Especially since this reactive plasticity seems to operate in other neurological diseases, and particularly in the aftermath of episodes of stroke.

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