Page 205 - ILAE_Lectures_2015

a. An EEG should be performed to support a diagnosis of epilepsy in patients in whom
the clinical history suggests that the event was likely to be epileptic

b. EEG cannot be used to exclude a diagnosis of epilepsy in a patient in whom the
clinical history suggests an event of non-epileptic origin

c. The EEG cannot and should not be used in isolation to make a diagnosis of epilepsy

(Adapted from NICE guidelines1)

Epileptiform phenomena

EEG features classified as epileptiform are spike discharges, spike or polyspike wave
complexes, and sharp waves. Some types of epileptiform phenomena are strongly correlated
with clinical epilepsy; others are weakly linked to active epilepsy, or have limited association
with seizure disorders. Three per second spike-wave discharge in childhood absence epilepsy
and the hypsarrhythmic pattern of West syndrome are examples of epileptiform phenomena
that are closely correlated with an epileptic disorder. The EEG of normal subjects can show
a range of spiky features, particularly during sleep. Physiological and pathological but non-
epileptogenic variants include wicket spikes, 14 and 6 Hz spikes, rhythmic mid-temporal
theta, and sub-clinical rhythmic epileptiform discharge in adults (SREDA). Mostly, these are
not associated with epilepsy, but non-epileptogenic variants are a potential source of
confusion and EEG misinterpretation.

Diagnostic yield

A number of factors influence whether patients with epilepsy will show inter-ictal
epileptiform discharge (ED) in a routine EEG. Children do so more often than older subjects,
and certain epilepsy syndromes or seizure types are more likely to show ED. The location of
an epileptogenic region is relevant: a majority of patients with temporal lobe epilepsy show
ED, whereas epileptic foci in mesial or basal cortical regions remote from scalp electrodes
are less likely to demonstrate spikes, unless additional recording electrodes are used. Patients
with frequent (one per month) seizures are more likely to have ED than those with rare (one
per year) attacks7. The timing of EEG recording may be important: investigation within 24
hours of a seizure revealed ED in 51%, compared with 34% who had later EEG8. Some
patients show discharges mainly during sleep, or there may be circadian variation as in the
idiopathic generalised epilepsies.

A routine EEG recording typically takes 2030 minutes, and should include standard
activation procedures of hyperventilation (up to three minutes) and photic stimulation, using
published protocols9, or specific triggers in rare types of reflex epilepsies (reading and
musicogenic epilepsy etc). It is good practice to warn patients of the small risk of seizure
induction and obtain consent to activation procedures. Breath counting is a reliable and
effective means to test transient cognitive impairment during generalised spike-wave
discharges induced by hyperventilation10. Most centres use the international 1020 system of
scalp electrode placement, but additional electrodes are often useful, especially those that
record from the anterior temporal lobe region (superficial sphenoidal electrodes). The yield
of routine EEG can be increased by repeat recordings (up to a total of four in adults), or by
use of sleep studies, achieved by recording natural sleep or through use of hypnotics to induce
sleep. The combination of wake and sleep records gives a yield of 80% in patients with
clinically confirmed epilepsy. Whether sleep deprivation is of additional value for induction
of ED is difficult to determine from reported studies, though there is some evidence that it
specifically activates ED in idiopathic generalised epilepsies11. An evaluation of different
EEG protocols in young people (<35 years) with possible epilepsy found that sleep-deprived
EEG (SD-EEG) provided significantly better yield of than routine EEG or drug-induced sleep