[6] If researchers come to better understand epileptogenesis, the latent period may allow healthcare providers to interfere with the development of epilepsy or to reduce its severity.
[6] Changes that occur during epileptogenesis are poorly understood but are thought to include cell death, axonal sprouting, reorganization of neural networks, alterations in the release of neurotransmitters, and neurogenesis.
[5] Brain regions that are highly sensitive to insults and can cause epileptogenesis include temporal lobe structures such as the hippocampus, the amygdala, and the piriform cortex.
[3] Another proposed mechanism for epileptogenesis in TBI is that damage to white matter causes hyperexcitability by effectively undercutting the cerebral cortex.
[2] Excessive release of the neurotransmitter glutamate is widely recognized as an important part of epileptogenesis early after a brain injury, including in humans.
[6] Excessive glutamatergic activity is also a feature of neuronal circuits after epilepsy has developed, but glutamate does not appear to play an important role in epileptogenesis during the latent period.
[10][11] Furthermore, it was shown that albumin, the most frequent protein in the serum is the agent that leaks from the blood into the brain parenchyma under BBB disruption conditions and induces epileptogenesis by activation of the transforming growth factor beta receptor on astrocytes.
Losartan, a commonly used drug for the treatment of hypertension was shown to prevent epilepsy and facilitate BBB healing in animal models.
Testing the potential of antiepileptogenic agents (e.g. losartan) or BBB healing drugs necessitates biomarkers for patients selection and treatment-followup.