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patients on medication for HIV, and in these patients intravenous loading with 24 g of
magnesium sulphate over 20 minutes may help with seizure control and prevention of
arrhythmias.

Seizure and EEG monitoring. In prolonged status epilepticus, or in comatose ventilated
patients, motor activity can be barely visible. In this situation, continuous EEG monitoring
using a full EEG or a cerebral function monitor is necessary, and at the very least intermittent
daily EEGs should be recorded. The latter must be calibrated individually to register both
burst-suppression and seizure activity. Burst-suppression provides an arbitrary physiological
target for the titration of barbiturate or anaesthetic therapy. Drug dosing is commonly set at
a level that will produce burst-suppression with interburst intervals of between 2 and 30
seconds.

Intracranial pressure monitoring and cerebral oedema. Continuous intracranial pressure
monitoring is sometimes needed, especially in children in the presence of persisting, severe,
or progressive elevated intracranial pressure. The need for active therapy is usually
determined by the underlying cause rather than the status epilepticus. Intermittent positive
pressure ventilation, high-dose corticosteroid therapy (4 mg dexamethasone every six hours),
or mannitol infusion may be used (the latter is usually reserved for temporary respite for
patients in danger of tentorial coning). Neurosurgical decompression is occasionally required.

Long-term anticonvulsant therapy. Long-term, maintenance, anticonvulsant therapy must be
given in tandem with emergency treatment. The choice of drug depends on previous therapy,
the type of epilepsy, and the clinical setting. If phenytoin or phenobarbitone has been used in
emergency treatment, maintenance doses can be continued orally (through a nasogastric tube)
guided by serum level monitoring. Other maintenance AEDs can be started also, giving oral
loading doses. Care needs to be taken with nasogastric feeds, which can interfere with the
absorption of some AEDs (especially phenytoin).

Treatment of tonic-clonic status epilepticus

Tonic-clonic status epilepticus is treated as an emergency in order to avoid both systemic
complications and also cerebral damage. Cerebral damage is partly caused by physiological
compromise and the consequent hypoxia/ischaemia, but it also results from excitotoxicity
consequent upon continuous seizure activity. In the initial stages of a tonic-clonic seizure,
there are compensatory mechanisms that result in increased cerebral perfusion. By 6090
minutes these compensatory mechanisms fail; there is hypotension and, importantly, loss of
cerebral autoregulation. This results in cerebral hypoperfusion and cerebral damage. In
addition, at this stage, the continuous seizure activity results in intraneuronal calcium
accumulation and neuronal death. Thus, treatment regimens should be staged. These stages
are: the premonitory (pre-hospital) stage, the early status epilepticus stage from 030
minutes, the stage of established status epilepticus from 3060/90 minutes and then the
refractory (late) stage during which substantial neuronal damage can occur.

Stages in emergency drug treatment

The suggested regimen for a typical new case presenting to a casualty department as an
emergency is given in Table 2. These are guidelines, and obviously in some circumstances
intensive care management and general anaesthesia may be required earlier.

Premonitory stage
In patients with established epilepsy, tonic-clonic status epilepticus seldom develops without
warning. Usually, a prodromal phase (the premonitory stage), during which seizures become
increasingly frequent or severe, precedes status epilepticus. Urgent drug treatment will