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. In this article, we will explore the relationship between seizures and sleep, including the effect of therapies for seizures upon sleep. Some anti-seizure medications also influence sleep structure independently of their effects on seizures. Seizure-related effects on sleep include interruption of sleep by ictal events and interictal epileptiform discharges. It has also become clear that there is a strong association between the sleep state and risk of SUDEP. Sleep stages have an impact on the activation and manifestations of seizures, including both the type of seizures and the likelihood of seizures occurring. Sleep disruption of any kind, including sleep disorders, can worsen epileptic seizures and contribute to the burden of epilepsy. Appropriately, the first description of sleep apnea came from the eminent French epileptologist Henri Gastaut in 1965. A number of interactions between the two have become apparent, and these are bidirectional. The systematic study of sleep and epilepsy is a relatively young discipline. 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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