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It has been clear for many years that some patients with epilepsy have seizures mainly during
sleep2,3. Particularly frontal lobe seizures often occur from both daytime and night-time sleep.
However, if temporal lobe seizures occur during sleep, the seizures are more likely to
secondarily generalise4. There may also be diurnal variation of certain types of epileptic
syndromes such as juvenile myoclonic epilepsy or epilepsy with generalised tonic-clonic
seizures on awakening5. Both benign (such as benign focal epilepsy with centrotemporal
spikes [BECTS]) and severe epilepsy syndromes (such as Landau-Kleffner and Lennox-
Gastaut syndrome with electrical status epilepticus during sleep [ESES]) show a predilection
for sleep.

Thalamocortical rhythms are activated during NREM sleep giving rise to sleep spindles.
Similar circuits are involved in the generation of spike-wave discharges in primary
generalised epilepsy, providing a possible explanation for the promotion of spike-wave
discharges seen during NREM sleep6.

Inter-ictal epileptiform discharges (IED) are facilitated following sleep deprivation, even in
the absence of sleep during the EEG recordings7. The reasons for this remain unclear but it
has been suggested that the increase in spike-wave activity seen after sleep deprivation may
be due to more frequent fluctuations in vigilance levels both during wakefulness and sleep8.
Using transcranial magnetic stimulation (TMS), increased cortical excitability has been
shown in epilepsy patients after sleep deprivation. This has not been the case for control
subjects or at least not to the same extent. Interestingly, changes have been seen bilaterally
in patients with generalised epilepsies but only ipsilateral to seizure onset zone in patients
with focal epilepsies9,10. Changes may reflect reduced intracortical inhibition, as the most
likely mechanism for an increase in excitability at the stimulation intervals used is reduced
GABA activity

The propensity for IED as well as seizures also varies throughout the night and IED are more
commonly seen during NREM sleep than REM sleep11-13. Epileptic seizures can occur at any
stage of NREM sleep but are more frequent during changes between sleep stages and lighter
stages than deep sleep. Seizures rarely occur during REM sleep4.

Interaction between sleep disorders, antiepileptic drugs and epilepsy

Excessive daytime sleepiness (EDS) is common in patients with epilepsy and is often
attributed to antiepileptic medication. Tiredness is often a dose-related side effect of many
antiepileptic drugs (AEDs). AEDs may, however, also interfere with the normal sleep pattern.
AEDs have different effects on sleep (summarised in Table 1) and some also have different
long- and short-term effects. For example, carbamazepine initially reduces and fragments
REM sleep but this effect is reversed after a month of treatment. GABAergic drugs (such as
phenobarbitone and benzodiazepines) prolong NREM sleep and shorten REM sleep and
gabapentin and pregablin have been shown to increase slow-wave sleep (SWS) and have even
been suggested as a treatment option for primary insomnia14.

Seizures and frequent IED can also disrupt sleep architecture, causing more unstable sleep in
both partial and generalised epilepsies. Patients with epilepsy may have increased sleep
latency and number of awakenings during the night, as well as reduction or fragmentation of
REM sleep. Reduced amount of REM sleep has been seen after both daytime and nocturnal
temporal lobe seizures15. The effect was most pronounced when seizures occurred during
sleep but also significant when seizures occurred on the previous day. Disrupted sleep may
hence contribute to the prolonged recovery time that some patients report following seizures.
Polysomnography of patients with juvenile myoclonic epilepsy (JME) have also shown
reduced sleep efficiency and increased sleep latency, unrelated to seizures as well16.