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risk of relapse, such as photosensitive epilepsy, juvenile myoclonic epilepsy or symptomatic
seizure disorders.

Cognitive deterioration. Confusional states or acute/sub-acute cognitive decline in epilepsy
might be the result of a marked increase in ED; frequent subtle/clinically unrecognised
seizures; a metabolic or toxic encephalopathy; or non-convulsive status. EEG plays an
important role in differentiating these causes. However, electrographic confirmation of acute
encephalopathy or non-convulsive status in severe symptomatic epilepsies can be very
challenging, because these disorders often show substantial overlap of inter-ictal and ictal
EEG patterns.

Chronic cognitive decline in epilepsy may be due to a progressive neurological condition
underlying the seizure disorder, or an independent neurodegenerative process. EEG
demonstration of deterioration in background cortical activity can help to identify an organic
brain syndrome, but is unlikely to discriminate as to cause. Epileptic encephalopathy is an
emerging concept, notably in childhood seizure syndromes. The encephalopathy and
progressive disturbance in cerebral function is viewed as being directly related to
electrographic epileptiform abnormalities, but the required EEG features for a diagnosis of
epileptic encephalopathy have not yet been widely agreed or defined.

Long-term EEG monitoring

Long-term monitoring (LTM) in epilepsy is available in all age groups from neonates to the
elderly246, and applicable in hospital and community settings. There is now substantial
evidence that LTM has a crucial role in the assessment of seizure disorders, as indicated by
a recent ILAE Commission report27.

The clinical applications of EEG monitoring are:
 Differential diagnosis of paroxysmal neurological attacks
 Differentiation between nocturnal epilepsy and parasomnias
 Diagnosis of psychogenic non-epileptic seizures
 Characterisation of seizure type and the electro-clinical correlates of epileptic
seizures
 Quantification of ED or seizure frequency
 Evaluation of candidates for epilepsy surgery
 Identification of sleep-related epileptiform discharge/electrical status in children
 Electro-clinical characterisation of neonatal seizures
 Monitoring of status epilepticus (convulsive, non-convulsive, electrographic).

LTM methods comprise ambulatory and video-EEG telemetry. Ambulatory EEG is more
suited to clinical problems which do not require concurrent synchronised video to document
clinical features (though it can be combined with hand-held camcorder), or for monitoring in
an outpatient setting or specific environment. In-patient video EEG telemetry is expensive
and labour intensive, and often a limited resource. Specialised telemetry units have the
advantage of ward-based staff, experienced in identification of subtle clinical events and able
to care for patients during seizures. Methods to increase the likelihood of paroxysmal events
include reduction in dose of anti-epileptic medication or sleep deprivation. Provocation
techniques, such as saline injections, are not recommended as they can result in false
positives, and there are ethical issues if the patient is deliberately misled.

Optimal duration of LTM study depends on the clinical problem, and frequency of attacks.
Patients are unlikely to benefit from monitoring if paroxysmal events occur less than once
per week. Duration of outpatient LTM is to some extent limited by technical issues – the need