For example, it was shown that pilocarpine 9,12-Octadecadiynoic acid seizures cause cerebrovascular changes which are consistent with those seen on MRI of patients. These consist of homeostatic failure leading, in patients, to MRI hyperintensity and in animals to increased extravasation of intravascular or cerebral-to-serum indicators. In addition, pilocarpine induces seizures by an unexpected immunologic activation mediated by specific receptors and adhesion molecules. These same molecules are the target of corticosteroids, and depletion of these adhesion molecules appears to protect against pilocarpine or clinical seizures. While the link between steroidal efficacy and BBB needs to be fully demonstrated in patients, we believe that the results we present herein are adequate to warrant an in-depth investigation of the BBB-corticosteroid-epilepsy relationship. If BBB leakage is the main initiator of seizures, and if BBB repair is protective against neurological disease, which are the mechanisms involved? The experimental evidence provided herein, together with previous findings, point to an inflammatory-induced damage of the BBB. Corticosteroids have a profound effect on human and rodent BBB permeability. Moreover, corticosteroids have an impact on the number of circulating Ouabain octahydrate T-cells. Downstream signaling by IL1-b appears to be a common thread in pilocarpine-induced seizures. It therefore seems reasonable to assume that the immune system acts in concert to produce BBB leakage and seizures, while the counteraction of corticosteroids has the opposite effect. These results further suggest that seizures and inflammation belong to the same chapter of neuroimmunology, as also shown recently. An important correlate of our findings is the fact that animal data strongly suggest that anti-inflammatory treatments have a pronounced effect on survival, which in the pilocarpine model is usually achieved only by stopping SE with diazepam or barbiturates. This may bear significant relevance for the treatment of catastrophic epilepsies in pediatric or adult settings. It is important to note that a non-inflammatory mechanism for steroidal action exists, namely the modulation of GABA receptors.