She started with an overview of how inflammatory events occur in the general tissues. Then, she introduced information on studies that found increased inflammatory substances during experimental animal models of epilepsy, as well as in brain tissues surgically ressected from Epileptic patients. She highlighted the question: Is inflammation the cause or a consequence of epilepsy? To address this, she mentioned studies that looked into IL-1beta, its receptors and antagonists, and showed that these were promising targets for future anti-epileptic therapy. She also added that blood-brain-barrier (BBB) disruption induced by inflammatory mediators in peripheral blood can help leukocytes to squeeze into vulnerable brain tissues and augment or perhaps initiate epileptogenic changes. Thus both local brain damage as well peripheral inflammatory processes can work in tandem to bring about clinical epilepsy. Also control of BBB disruption could be another important therapeutic target.
There were also some thought provoking discussions on the limitations of interpreting from the results of targeted gene-knock out studies.