Since the formal characterization of sleep stages, there have been reports that seizures may preferentially occur in certain phases of sleep. Through ascending cholinergic connections from the brainstem, rapid eye movement (REM) sleep is physiologically characterized by low voltage fast activity on the electroencephalogram, REMs, and muscle atonia. Multiple independent studies confirm that, in REM sleep, there is a strikingly low proportion of seizures (~1% or less). We review a total of 42 distinct conventional and intracranial studies in the literature which comprised a net of 1458 patients. Indexed to duration, we found that REM sleep was the most protective stage of sleep against focal seizures, generalized seizures, focal interictal discharges, and two particular epilepsy syndromes. REM sleep had an additional protective effect compared to wakefulness with an average 7.83 times fewer focal seizures, 3.25 times fewer generalized seizures, and 1.11 times fewer focal interictal discharges. In further studies REM sleep has also demonstrated utility in localizing epileptogenic foci with potential translation into postsurgical seizure freedom. Based on emerging connectivity data in sleep, we hypothesize that the influence of REM sleep on seizures is due to a desynchronized EEG pattern which reflects important connectivity differences unique to this sleep stage. 1. Introduction A bidirectional relationship between epilepsy and sleep has been observed since the time of Hippocrates [1]. It was not until the first formal characterization of sleep stages that this relationship became successively attuned to each specific sleep stage. It became apparent that seizures may preferentially occur during certain phases of sleep with the least likelihood of occurrence in rapid eye movement (REM) sleep. The purpose of this review is to focus on the impact of REM sleep on seizures. We discuss REM sleep physiology, a review of the available literature regarding seizures during REM sleep, and a consideration of the potential mechanisms which may underlie this intriguing but often overlooked phenomenon. 2. REM Sleep Physiology Based on a wealth of animal and human data accumulated since the discovery of REM sleep in 1953 [2], an exciting and coherent model of REM sleep physiology has emerged. In the pontomesencephalic junction of the brainstem, there are two populations of cholinergic neurons in the laterodorsal tegmentum (LDT) and pedunculopontine tegmentum (PPT) [3]. Within these populations, there is a subset of cells that are most active in REM sleep, as well as
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