Sleep and Epilepsy

Occurrence of Seizures across the Sleep-wake Cycle

Nearly two-thirds of seizures occurred between 8:00 PM and
8:00 AM, and insufficient sleep seemed to activate seizures.
Peaks in seizures occur in response to falling asleep and awakening.
Several epilepsy syndromes are characterized by seizures occurring
predominately or exclusively from sleep or upon awakening as
Sleep epilepsies

Benign focal epilepsy of childhood with centro-temporal spikes

Frontal lobe epilepsy

   Supplementary sensorimotor area

   Autosomal dominant nocturnal frontal lobe epilepsies

Lennox Gastaut syndrome (tonic seizures)

Epilepsy with continuous spike wave in sleep (CSWS)

Awakening epilepsies

Juvenile myoclonic epilepsy

Absence epilepsy

Epilepsy with grand mal seizures on awakening

Sudden withdrawal of medication and polytherapy were risk factors

for wake seizures.
Seizures in patients with frontal lobe epilepsies typically arise from
sleep, almost exclusively during NREM sleep.
Sleep appears to activate frontal seizures more often than temporal
seizures.
 Secondary generalization of partial seizures tends to occur more
often during sleep compared with wakefulness, and frontal lobe
seizures tend not to secondarily generalize during sleep.
Circadian influences appear to affect seizure timing in the partial
epilepsies, varying by the type and location of the epileptic generator.
Effects of Sleep on Interictal Epileptiform Discharges
Sleep activated additional epileptic foci in some patients who had
only one focus during wakefulness. Patients with psychomotor
seizures often had normal EEGs awake, but 95% had interictal
epileptiform discharges during sleep. Interest in this area spanning
decades has produced countless publications on the effects of sleep on the
EEG in epilepsy.
Partial Epilepsies
NREM sleep activates interictal epileptiform discharges in partial
epilepsies.
Interictal spikes increase at sleep onset, peaking in NREM 3, and
then falling in REM sleep to levels lower than wakefulness.
Idiopathic Generalized Epilepsies
Sleep is a less important activator in most idiopathic generalized
epilepsies because interictal epileptiform discharges are usually
present in the wake EEG. Spikes increase with sleep onset
progressively through NREM 3, diminish sharply in REM sleep, and
increase again in the morning after awakening. The EEG is most
abnormal after awakening or nighttime arousals in patients with
awakening epilepsy. In contrast, in the sleep epilepsies, the EEG
tends to be normal during wakefulness and shows a marked increase
in interictal epileptiform discharges during sleep.
Effects of Sleep Deprivation on Epilepsy
Total sleep deprivation is defined as at least 24 hours of sleep loss;
shorter periods of sleep loss are considered partial sleep deprivation
(PSD).
on Seizures
Modest amounts of sleep loss can precipitate seizures
on Interictal Epileptiform Discharges in EEG
Seizures were more likely to be activated by sleep or sleep deprivation in
patients with idiopathic generalized epilepsy than partial epilepsy.
Total sleep deprivation activates interictal epileptiform discharges of
patients with definite or suspected seizures. Whether PSD is a
comparable activator remains to be proven.
Effects of Antiepileptic Drugs on Sleep
Antiepileptic drugs have variable effects on nocturnal sleep and
wakefulness (CBZ)
Effects of Vagal Nerve Stimulation on Sleep and Wakefulness
Similarly, vagal nerve stimulation (VNS) has a variety of effects on
sleep and wakefulness.
Sleep Organization in Epilepsy
Sleep organization appears to be more disrupted in temporal lobe
epilepsy than frontal lobe epilepsies.
Sleep Disorders Symptoms in Epilepsy
Excessive daytime sleepiness is the most common sleep/wake
complaint among people with epilepsy, typically attributed to the
effects of antiepileptic drugs (AEDs) and seizures.
Primary Sleep Disorders in Epilepsy
Obstructive sleep apnea (OSA) may be more common in patients
with epilepsy than suspected. In older patients with epilepsy, the
presence of sleep apnea is associated with worsening seizure control
or late-onset seizures due to the adverse effect of central nervous
system depressants, such as barbiturates and benzodiazepines, and
possibly phenytoin on upper airway tone, weight gain associated with
some AEDs, reduced physical activity of people with epilepsy, and
comorbid endocrinopathies such as hypothyroidism and polycystic
ovarian syndrome.
Sleep-disordered breathing, and sleep disorders in general, increase
excitability in the epileptic brain.
Differentiating Nocturnal Seizures from Parasomnias and Other
Paroxysmal Events
Frontal lobe seizures are often misdiagnosed as sleep terrors,
sleepwalking, or nightmares.
Most previously undiagnosed epilepsy in sleeping children is in
fact nocturnal frontal lobe epilepsy.
In contrast to parasomnias, nocturnal frontal lobe seizures
typically:
(1) Have an abrupt, explosive, onset awakening the patient from
NREM 2 sleep;
(2) Are accompanied by sustained asymmetric dystonic, tonic
posturing, and hypermotor behaviors including thrashing, pedaling
and kicking;
(3) Tend to be stereotyped in appearance for the individual patient;
(4) Are brief, typically lasting 20 to 30 seconds
(5) are associated with preserved awareness
(6) Have no postictal confusion or amnesia
(7) Have no scalp-recorded
Special planning is required when performing PSG
The detection of epileptiform activity in the sleep laboratory is
greater with expanded EEG montages and video analysis.