Effect of Cerebral Glutamate on Epileptogenesis after Stroke

Xian Hu*

One of the most significant causes of adult acquired epilepsy is stroke. Although cortical involvement and hemorrhage have been linked to an increased risk of seizures, the mechanisms behind the onset of epilepsy following a stroke remain a mystery. An excitotoxic effect of abnormal glutamate release following a stroke is one hypothesised mechanism. As a result of direct measurement of glutamate from the epileptic brain and  analysis of receptors and transporters essential to glutamate homeostasis, numerous studies have implicated glutamate in the pathogenesis of seizures and epilepsy. Acute stroke is known to raise cerebral extracellular glutamate levels. There is little direct
evidence linking the rise in glutamate during stroke with the later development of epilepsy, despite the fact that experimental evidence suggests that the cellular injury caused by glutamate exposure may result in the development of an epileptic phenotype. The lack of non-invasive methods for measuring cerebral glutamate has hampered clinical research in this area. Nonetheless, with the rising accessibility of 7T X-ray innovation, attractive reverberation spectroscopy is ready to more readily determine glutamate from other synthetic species at this field strength and Glutamate Substance Trade immersion move (GluCEST) imaging has been applied to confine epileptic foci in non-lesional central epilepsy.