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A subset of acquired epilepsies is called post-traumatic epilepsy (PTE), which develops in the months or years following a TBI.[2] TBI may be caused by blows to the head, blasts, penetrating head injuries, accidental falls, sports-related injuries, or motor vehicle accidents. It is currently not possible to predict who will develop PTE after a TBI.[3] Dr. Annamaria Vezzani, head of the Laboratory of Epilepsy and Therapeutic Strategies, Department of Acute Brain Injury at the Mario Negri Institute for Pharmacological Research in Milan, has been an important part of CURE Epilepsy’s efforts to understand acquired epilepsies for decades as an early (2002) and repeat (2015) grantee, and more recently, as part of the PTE Initiative. Dr. Vezzani’s work centers on the role of inflammation in epilepsy. Her work looks at neuroinflammation (i.e., the inflammatory response that is sustained by cells in the brain after insult or injury) and has shown that neuroinflammation can play an important role in the generation of seizures.[4] Through a study funded by CURE Epilepsy, Dr. Vezzani first studied a specific signaling pathway in the brain called interleukin-1 (IL-1) type 1 receptor/Toll-like receptor (IL-1R/TLR4). Her experiments in experimental animals showed that IL-1beta and an inflammatory molecule known as High Mobility Group Box 1 (HMGB1) are released from specific brain cells known as “glia” during seizures.[5] The levels of HMGB1 increased in the brain and the blood before animals developed epilepsy, and this increase in HMGB1 levels was maintained during the development of epilepsy.[6,7] These results gave her precise biological mechanisms that could be targeted to stop seizures.
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