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Background <p>Epilepsy is subject, among other things, to the rhythm of day and night and to the cycle of the various stages of sleep. The manifestation and severity of epilepsy is influenced by the sleep quality and continuity of the patient.</p> Objective <p>This article gives an overview of the interaction between sleep and epilepsy and the resulting potential benefits for the diagnostics and treatment.</p> Method <p>This a review article.</p> Results and discussion <p>Different types of epileptic and nonepileptic seizures follow a&#xa0;specific circadian or wake/sleep rhythm, which can be used for the differential diagnosis. Sleep deprivation leads to increased epilepsy activity, not least due to increased but unstable sleep the following day. In non-rapid eye movement (NREM) sleep, epilepsy-typical patterns (ETP) become more frequent and have a larger spatial distribution and therefore there is an increased likelihood of seizures and seizure generalization. In contrast, REM sleep is seizure-protective due to electroencephalograph (EEG) desynchronization and amplitude reduction as well as due to REM-specific functional disconnection, especially of the frontal lobe, and REM sleep is even more protective than the waking state. If it is nevertheless possible to record ETP or seizures in REM sleep, valuable localization information about the seizure onset zone can often be derived from these data due to the low tendency of ETP propagation in REM. Seizures during sleep and awake but even the occurrence of interictal ETP during sleep worsen sleep continuity, structure and quality. This can be the cause of affective, cognitive and mnestic disorders in the daily life of the patient; however, sleep fragmentation and lack of sleep also have a proconvulsive potency and can thus lead to a&#xa0;further worsening of seizures, which in turn further impairs sleep quality. This vicious circle is further fueled by the existence of comorbid sleep disorders or sleep-disturbing side effects of anti-seizure treatment. If such connections are recognized and treated, with an orientation towards the individual chronobiological and somnological conditions, this can result in good prospects for transforming a&#xa0;previously treatment-refractory patient into a&#xa0;responder.</p>

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Epilepsy in the rhythm of the night and in the cycle of sleep. English version

  • 期刊论文

  • 发表日期：

    2025年6月17日

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  • Berthold Voges

摘要

Background

Epilepsy is subject, among other things, to the rhythm of day and night and to the cycle of the various stages of sleep. The manifestation and severity of epilepsy is influenced by the sleep quality and continuity of the patient.

Objective

This article gives an overview of the interaction between sleep and epilepsy and the resulting potential benefits for the diagnostics and treatment.

Method

This a review article.

Results and discussion

Different types of epileptic and nonepileptic seizures follow a specific circadian or wake/sleep rhythm, which can be used for the differential diagnosis. Sleep deprivation leads to increased epilepsy activity, not least due to increased but unstable sleep the following day. In non-rapid eye movement (NREM) sleep, epilepsy-typical patterns (ETP) become more frequent and have a larger spatial distribution and therefore there is an increased likelihood of seizures and seizure generalization. In contrast, REM sleep is seizure-protective due to electroencephalograph (EEG) desynchronization and amplitude reduction as well as due to REM-specific functional disconnection, especially of the frontal lobe, and REM sleep is even more protective than the waking state. If it is nevertheless possible to record ETP or seizures in REM sleep, valuable localization information about the seizure onset zone can often be derived from these data due to the low tendency of ETP propagation in REM. Seizures during sleep and awake but even the occurrence of interictal ETP during sleep worsen sleep continuity, structure and quality. This can be the cause of affective, cognitive and mnestic disorders in the daily life of the patient; however, sleep fragmentation and lack of sleep also have a proconvulsive potency and can thus lead to a further worsening of seizures, which in turn further impairs sleep quality. This vicious circle is further fueled by the existence of comorbid sleep disorders or sleep-disturbing side effects of anti-seizure treatment. If such connections are recognized and treated, with an orientation towards the individual chronobiological and somnological conditions, this can result in good prospects for transforming a previously treatment-refractory patient into a responder.