ReviewStatus epilepticus, blood-brain barrier disruption, inflammation, and epileptogenesis

- Experimentally induced status epilepticus results in persistent regional BBB disruption and inflammation.
- Subtle BBB leakage can be detected many weeks after SE using MRI using a step-down infusion protocol.
- Regional leakage of the serum protein albumin increases neuronal excitability.
- Treatment that targets the TGFβ pathway can be a promising strategy to prevent epilepsy in models of BBB disruption.
- The mTOR inhibitor rapamycin might affect epileptogenesis via targeting angiogenesis and inflammation.

Over the last 15 years, attention has been focused on dysfunction of the cerebral vasculature and inflammation as important players in epileptogenic processes, with a specific emphasis on failure of the blood-brain barrier (BBB; Fig. 1) (Seiffert et al., 2004; Marchi et al., 2007; Oby and Janigro, 2006; van Vliet et al., 2014; Vezzani et al., 2011) [3-7]. Here, we discuss how the BBB is disrupted as a consequence of SE and how this BBB breakdown may be involved in epileptogenesis.This article is part of a Special Issue entitled “Status Epilepticus”.