Treatment of late lithium-pilocarpine-induced status epilepticus with diazepam

Modeling epileptogenesis and temporal lobe epilepsy in a non-human primate

“…In the pilocarpine and kainate models of epilepsy in rodents, a severe episode of SE is essential for the subsequent development of SRS (Goffin et al, 2007;Lemos and Cavalheiro, 1996). By managing the severity of the SE, injecting sub-therapeutic doses of diazepam after the SE onset, one can decrease mortality without decreasing the development of epilepsy (Cunha et al, 2009;Gao et al, 2007;Hellier et al, 1998;Mello et al, 1993;Treiman et al, 1998;Walton and Treiman, 1988). The immediate seizures following pilocarpine injection in marmosets were similar to those described in pilocarpine-treated rodents (Racine et al, 1972;Turski et al, 1983).…”

Neuroprotective Effects of Diazepam, Carbamazepine, Phenytoin and Ketamine after Pilocarpine‐induced Status Epilepticus

“…Our findings point to neuroprotective effects of diazepam that could be attributed to treatment, that is, daily injections rather than a single administration. Indeed, according to Fujikawa [24] cell death still occur up to 72 hrs after the end of status epilepticus, and in a recent work abnormal discharges were continuously observed as late as 72 hrs after pilocarpine‐induced status epilepticus [31]. Another point is the reactive astrocytosis which is a common finding in brains of animals submitted to virtually all insults [32,33].…”

Prevention or Modification of Epileptogenesis after Brain Insults: Experimental Approaches and Translational Research

“…First, if SE is not effectively terminated, periodic paroxysmal discharges may recur over several days, as reported by Gao et al (2007). Second, as with other epileptogenic brain insults, such as TBI or stroke (Beghi et al, 2010), insultassociated acute symptomatic seizures may occur in the first 1 to 2 days after SE, which should not be confounded with spontaneous seizures.…”

“…Another experimental protocol often used in antiepileptogenesis studies involves no cessation 686 of SE duration, and the test drug is administered at delayed time-points after the SE (Tables 2 and 3). However, Gao et al (2007) reported that periodic hippocampal paroxysmal discharges occur for up to 24 to 72 h after onset of lithium-pilocarpine induced SE, so that onset of drug treatment after 24 h, for example, may induce alterations in SE duration compared with untreated SE control subjects. Furthermore, the large interindividual variation in SE duration forms a bias for antiepileptogenesis studies, which is a further argument for terminating SE at the same time in all animals per group.…”