Status epilepticus (SE) is a neurological emergency resulting from prolonged clinical or electroencephalographic seizure activity. Refractory SE refers to the persistence of seizure activity despite the initiation of first- and second- line anticonvulsant therapy. Sinister outcomes are often attributed to the etiology of SE. Despite randomized multicentre trials of established and promising therapeutic options, the management and prognostication in SE are fraught with challenges.

Status Epilepticus Page 4 Diagnosis The diagnosis of status epilepticus The clinical definition of status epilepticus is five minutes or more of convulsions or 2 or more convulsions in a 5-minute interval without return to preconvulsive neurological baseline. Status epilepticus is a neurologic emergency associated with signifi cant morbility and mortality. Status epilepticus is when seizure last 30 minutes or when a patient has two o more sequential crisis without a full recovery of con-sciousness between episodes. Ten percent in average of the patients with epilepsy could suffer status epilepti.

Neither the duration of SE nor time-delay to initiation o f therapy should discourage the aggressive approach to the management of SE. Neurointensive care of patients with SE c onsists of an algorithmic approach tailored to the etiology and systemic complications that arise as a consequence. This approach is also driven by the persistence of electrographic seizure activity, which is best followed with continu ous EEG monitoring. The extent of patient support has to be augmentative to the degree of encephalopathy/coma and impairment of vital functions. Potential interactions of anticonvulsant drugs with other co-medications need to be considered during the course of treatment.

This review discusses the existing literature on the epidemiological aspects, clinical approach, treatment and prognostication of SE. Changes in gene expression come to play later and are part ly annulled by the inhibition of protein synthesis. Maladaptive changes occur in protein expression which may contribute to the self-sustaining nature of the events There is depletion in hippocampus of the predominantly inhibitory peptides dynorphin, galanin, somatostatin, and neuropeptide Y, whereas the expression of the proconvulsant tachykinins, substance P and neurokinin B is increased. Seizure- induced neuronal death continues to occur even when motor manifestations are absent due to excitotoxic mechanisms which produce cell death.