With aging, sleep becomes more unstable, with reduced sleep efficiency (the amount of sleep time for the total time in bed), and by increased microarousals. N3 (slow-wave) sleep accounts for about 20% of the total sleep time in this age group. Healthy young adults spend nearly 7.5 h sleeping and 80% of this time is spent in NREM sleep, while 20% represents REM sleep. Sleep cycles are characterized by an evolution from Non-Rapid Eye Movement (NREM) sleep N1, N2, and N3, with progressive sleep depth manifested by increasing amounts of slow-wave activity, followed by REM sleep, which is characterized by faster and desynchronized activity similar to wakefulness. In the first third of the night, slow-wave sleep (N3) preferentially occurs, rather than REM sleep, but as the night progresses, the contribution of REM sleep increases. Human sleep in adults occurs in cycles that last an average of 90–100 min each, although sleep cycles in infants and children are usually shorter at approximately 60 min. Such patients may merit consideration of anti-seizure medication even following a first seizure given their higher risk for recurrence. When a first seizure arises from sleep, there is a higher risk for recurrence within the first 2 years of follow-up, conferring a similar increased risk as if the patient had previous symptomatic brain pathology on imaging or an epileptiform abnormality on EEG. Predictors of break-through seizures during the day include withdrawal of therapy, polytherapy, and high seizure burden. The risk of seizures while awake is present even in “pure sleep epilepsies” and is 13% within 6 years and 30.9% within 10 years. Such seizures are nearly 80% focal onset. Seizures arising either exclusively from sleep, or at least 90% from sleep occur in between 7.5 and 45% of patients with epilepsy. Pure sleep epilepsies may represent 3–45% of epilepsies, depending on how such epilepsies are defined. A case report of a patient with generalized convulsive epilepsy but no other neurological conditions revealed decreased REM and N3 sleep for 4 nights following status epilepticus. When seizures occurred at night, the subsequent decrease in REM sleep was more pronounced than sleep subsequent to preceding daytime seizures, and there were also increases in stage 1 sleep and decreases in sleep efficiency following nighttime seizures. after daytime complex partial or secondarily generalized seizures, there was a significant decrease in REM sleep the following night, without significant changes in sleep efficiency or in other sleep stages. When patients with temporal lobe epilepsy were compared under baseline conditions (seizure free) vs. The specific effects of temporal lobe seizures on sleep structure were examined in patients undergoing video-EEG monitoring. Simply recording sleep during an EEG will increase the likelihood of detecting epileptiform activity, and recording of overnight sleep improves the yield of interictal epileptiform discharges compared with routine daytime EEGs. Further research is necessary to understand the complex relationships between sleep and epileptic disorders and their treatments. Sleep has an important key association with sudden unexpected death in epilepsy (SUDEP). Co-morbid sleep disorders also have the potential to worsen seizure control. Epileptiform discharges and antiepileptic medications may in turn detrimentally impact sleep. Diagnostic interictal epileptiform discharges on the electroencephalogram are also most likely to be activated during deep NREM sleep stage N3. Several forms of epilepsy predominantly or exclusively manifest during sleep and seizures tend to arise especially from light NREM sleep. This article reviews the manifold and complex relationships between sleep and epilepsy and discusses treatment of the sleep-related epilepsies. The normal changes in waking and sleeping states result in neurophysiological conditions that either increase or decrease the tendency of seizures and interictal discharges to occur. A healthy brain requires balancing of waking and sleeping states.
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