A growing body of evidence is now supporting a relationship between inflammation and epilepsy. Indeed, activated microglia, reactive astrocytes, local expression of pro-inflammatory cytokines, blood–brain barrier leakage and peripheral immune cell infiltration have all been observed in human TLE as well as in animal models [ 39 ]. Accordingly, inflammatory mechanisms are thought to play a central role in the initiation and maintenance of seizures, including those starting in the acute phase during SE induction. Although marked gliosis and inflammation are main features of hippocampal sclerosis in TLE, glial cells have been poorly investigated as possible candidates in promoting epileptogenesis. Because the role of astrocytes in epileptogenesis has been reviewed recently [ 27, 40, 41 ], we focus here on microglia.
Benzodiazepines may influence neurosteroid metabolism by virtue of their actions on translocator protein (TSPO; "peripheral benzodiazepine receptor").  The pharmacological actions of benzodiazepines at the GABA A receptor are similar to those of neurosteroids . Factors which affect the ability of individual benzodiazepines to alter neurosteroid levels may depend upon whether the individual benzodiazepine drug interacts with TSPO. Some benzodiazepines may also inhibit neurosteroidogenic enzymes reducing neurosteroid synthesis.