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to replace data storage media and batteries every 2448 hours, and the potential for faulty
recording due to poor electrode contact.

Ictal EEG
Certain seizure types have specific ictal EEG patterns, such as 3 per second generalised spike-
wave discharge in a typical absence seizure, the evolving temporal theta rhythm (57 Hz) in
mesial temporal lobe epilepsy, high frequency discharge in tonic seizures, and irregular slow
spike and wave (<2.5 Hz) in an atypical absence attack. Ictal changes can however be
obscured by artefact from movement or muscle, and scalp EEG may be unchanged or
unhelpful in simple partial seizures, some frontal lobe epilepsies and epilepsia partialis
continua, mostly because the epileptogenic focus is small and anatomically circumscribed or
distant from recording electrodes on the scalp. In partial epilepsies, the most important ictal
EEG changes for seizure localisation occur within the first 30 seconds after the seizure onset.
Broadly speaking, localised and lateralised changes are more likely to be found in temporal
lobe epilepsy than in extratemporal seizures, and epileptiform or high frequency discharge
tends to be seen in neocortical epilepsy, particularly when the focus is relatively
superficial289. Frontal lobe epilepsy often shows generalised or widespread high frequency
activity/slow rhythms/attenuation, as a result of rapid propagation or secondary
generalisation.

The EEG and status epilepticus

EEG is essential for correct diagnosis and management of status epilepticus (SE) in
convulsive and non-convulsive forms. The different electro-clinical types of SE show
common EEG features, manifest as waxing and waning rhythmic or patterns or epileptiform
discharges30.

In convulsive status epilepticus, EEG is used diagnostically to confirm that the patient has
status and not pseudostatus, in which ictal EEG is normal, and to differentiate causes of
altered mental status – ongoing seizure activity, drug-induced coma, or other
encephalopathy31. In refractory convulsive status, EEG monitoring to control and guide
treatment is essential once general anaesthesia has been induced, as clinical manifestations
of continuing seizure activity may be subtle or absent. A typical endpoint for general
anaesthesia treatment is EEG burst suppression; cessation of seizure activity or ED may be
sufficient, but is less easy to define. EEG can contribute prognostic information: continuing
electrographic status is associated with worse outcome in convulsive status32, and some
studies have shown that periodic epileptiform discharges are associated with poorer outcome
independent of aetiology of status33.

Non-convulsive status epilepticus (NCSE) covers a range of conditions, which have variable
clinical features and aetiological bases: generalised absence status, de novo absence status,
simple partial status epilepticus, complex partial status, electrographic status with subtle
clinical manifestations, and electrical status epilepticus in sleep34. EEG patterns described in
NCSE include continuous spike-wave discharge, discrete localised electrographic seizures,
diffuse slow activity with or without spikes, and periodic/repetitive ED. Electrographic
diagnosis is relatively easy in generalised absence status, when the prolonged state of altered
consciousness is accompanied by generalised 3 Hz spike-wave discharge. EEG confirmation
is usually straightforward in persistent electrographic status after control of convulsive status,
and in children with ESES. More problematic are cases of simple partial status, in which the
EEG can be unchanged or non-specific; or in acute cerebral damage due to anoxia, infection
or trauma, when EEG abnormalities, particularly repetitive complexes, may be due to the
primary pathology35.