Status epilepticus (SE), defined as a seizure or series of seizures without recovery between lasting more than 30 min, takes a variety of forms, as illustrated in the report by Knake and colleagues1 in this issue of J Neurol Neurosurg Psychiatry (see page 588). In their paper, the response to intravenous levetiracetam of 16 patients with a total of 18 episodes of status epilepticus is described. The patients were all adults; the majority of episodes of SE were complex partial and symptomatic in aetiology, a case mix that might well be seen in an acute medical admissions unit. The duration of SE is not given, a pity particularly for the patients with convulsive SE where outcome is related to duration of seizure activity. All patients received intravenous benzodiazepine, usually lorazepam, before levetiracetam. Intravenous levetiracetam was given as a bolus dose of 250–1500 mg and was associated with seizure cessation in 16/18 episodes; it was the second drug given in 10 episodes, the third in seven. Sedation was observed in two patients but no other side effects were noted. The study was retrospective, unblinded and observational, but the results suggest the use of intravenous levetiracetam in SE should be investigated further.

The incidence of SE is between 6.8 and 41/100 000/year in population based studies2; prognosis depends predominantly on the aetiology. Early effective treatment is the goal. Despite being a relatively common neurological emergency, few randomised controlled trials of treatment in SE have been undertaken. A recent Cochrane review identified 11 studies of convulsive and non-convulsive status epilepticus.3 It concluded that intravenous lorazepam was superior to diazepam or phenytoin for initial treatment of established SE. When lorazepam fails in convulsive SE, current guidance recommends intravenous phenytoin, phenobarbital or fosphenytoin, all of which can cause hypotension, cardiac arrhythmia and hypoventilation. Approximately one-third of patients with convulsive SE fail to respond to secondline treatment and require admission to intensive care with the attendant risks of artificial ventilation. New, less toxic therapies for SE are needed.

Levetiracetam is one of the newer antiepileptic drugs. It has a broad spectrum of action being effective against both focal onset and primary generalised seizures. Since 2000, when it was licensed in Europe, the use of oral levetiracetam has increased swiftly; it has no significant interactions with other drugs, has a rapid titration schedule and is usually well tolerated. Significant side effects include behavioural change and unpredictable seizure exacerbation. The intravenous preparation became available in the UK in 2006; case reports of its use in convulsive and non-convulsive status epilepticus followed within months.

An alternative to intravenous levetiracetam or other standard therapies for SE is a drug that will be familiar to all neurologists—sodium valproate. Intravenous valproate has been compared with intravenous phenytoin in the treatment of SE in a randomised trial4; the numbers were small but suggested valproate 30 mg/kg over 15 min was at least as effective as phenytoin. The time has come for another trial of treatment for SE. This will not be easy; issues around consent and funding need to be resolved and setting up a large multicentre study will be difficult. But it is a challenge we should not shirk if we want to try to improve treatment of a common and life threatening neurological condition.