Impact of sleep on epileptic manifestations

Liborio Parrino MD (Dr. Parrino of the University of Parma has no relevant financial relationships to disclose.)
Antonio Culebras MD, editor. (Dr. Culebras of SUNY Upstate Medical University has no relevant financial relationships to disclose.)
Originally released June 5, 2010; last updated May 6, 2017; expires May 6, 2020

Overview

The circadian, homeostatic, ultradian, and microstructural processes that regulate the sleep-wake cycle are endowed with modulatory properties on epileptic events. In particular, sleep is a powerful trigger of both ictal and interictal manifestations. Non-REM sleep and cyclic alternating pattern promote strong activating effects, although REM sleep tends to exert a more inhibitory action. These characteristics are highly expressed in nocturnal frontal lobe epilepsy.

Key points

 

• Sleep is a powerful enhancer of epileptic features.

 

• Synchronized non-REM sleep facilitates seizures, whereas desynchronized REM sleep dampens seizure occurrence.

 

• The presence of nocturnal seizures affects the regular profile of the sleep architecture.

 

• Marked sleep instability, as expressed by cyclic alternating pattern (CAP), is often observed in epileptic patients, even in the absence of nocturnal seizures.

 

• Sleep-related seizures mostly affect conventional sleep measures, whereas nocturnal interictal discharges basically have a destabilizing impact on CAP parameters.

Historical note and terminology

So far, sleep has been exploited by neurologists in clinical routine as a nontraumatic method to trigger EEG abnormalities in putative epileptic patients. Both non-REM (NREM) and REM sleep can disclose EEG discharges that remain silent in the wakefulness condition and, therefore, provide useful diagnostic information (Bazil and Walczak 1997). However, sleep is not a passive neurophysiological state, but reflects highly dynamic processes that reciprocally interfere with the underlying mechanisms of epileptogenesis. This explains why epileptic manifestations can affect sleep and, in turn, be modulated by sleep itself. This reciprocal influence opens new perspectives on the interaction between epilepsy and the multiple biological processes that regulate the sleep-wake cycle. Moreover, the intrinsic properties of vigilance control can explain why a number of epileptic disorders, particularly nocturnal frontal lobe epilepsy, are confined exclusively in sleep.

Occurrence of epileptic phenomena during sleep is strongly modulated by the 4 major regulatory processes (circadian, homeostatic, ultradian, and microstructural).

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