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. 1989 Dec 29;505(2):271-82.
doi: 10.1016/0006-8993(89)91453-4.

Mechanisms of seizure suppression during rapid-eye-movement (REM) sleep in cats

M N Shouse  1 , J M Siegel, M F Wu, R Szymusiak, A R Morrison
Affiliations

Mechanisms of seizure suppression during rapid-eye-movement (REM) sleep in cats

M N Shouse et al. Brain Res. .

Abstract

REM sleep is the most antiepileptic state in the sleep-wake cycle for human generalized epilepsy, yet the neural mechanism is unknown. This study verified the antiepileptic properties of REM sleep in feline generalized epilepsy and also isolated the responsible factors. Conclusions are based on 20 cats evaluated for generalized EEG and motor seizure susceptibility before and after dissociation of specific REM sleep components. Bilateral electrolytic lesions of the medial-lateral pontine tegmentum created a syndrome of REM sleep without atonia. Systemic atropine created a syndrome of REM sleep without thalamocortical EEG desynchronization. Identical results were obtained in two seizure models, systemic penicillin epilepsy and electroconvulsive shock. (1) Normal REM sleep retarded the spread of EEG seizure discharges and had even more potent anticonvulsant effects. (2) Selective loss of 'sleep paralysis' (skeletal muscle atonia) during REM abolished REM sleep protection against myoclonus and convulsions without affecting generalized EEG paroxysms. (3) Conversely, selective loss of thalamocortical EEG desychronization abolished REM sleep protection against generalized EEG seizures without affecting clinical motor accompaniment. These results suggest that the descending brainstem pathways which mediate lower motor neuron inhibition also protect against generalized motor seizures during REM sleep. Protection against spread of EEG paroxysms is governed by a separate mechanism, presumably the ascending brainstem pathways mediating intense thalamocortical EEG desynchronization during REM sleep.

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Figures

Fig. 1.
Fig. 1.
Polygraphic characteristics of rapid-eye-movement (REM) sleep before and after REM sleep syndromes. The top tracing depicts normal REM sleep, defined by thalamocortical EEG desynchronization, rapid eye movements in the EOG, PGO spikes in the lateral geniculate nucleus (LGN) and atonia, reflected by silence in the neck EMG. The middle tracing shows a post-atropine REM sleep example, which had all REM sleep components except thalamoeortical EEG desynchronization. The bottom tracing shows a post-lesion record, which had all REM sleep components except atonia.
Fig. 2.
Fig. 2.
Reconstructions comparing size and location of typical lesions which induced REM sleep without atonia and those which did not affect atonia in REM sleep. Extent of lesions are shown from APO through P4 in 3 cats. Coordinates correspond to Berman's atlas. Reconstructions are shown to illustrate lesions in the medial-lateral pontine tegmentum that created REM sleep without atonia in two cats (left and middle). Lesions in control cats, who did not display REM sleep without atonia, are typified by the reconstruction on the right. Control lesions were smaller and situated more dorsolaterally in the pontine tegmentum than lesions which affected REM sleep atonia (see text).
Fig. 3. A:
Fig. 3. A:
systemic penicillin epilepsy during slow-wave-sleep (SWS) and REM sleep before and after dissociation of REM sleep components. Spike-wave paroxysms are visible in the EEG tracing, and myoclonic seizures were associated with discharges in the EMG tracing in this cat.
Fig. 3. B:
Fig. 3. B:
electroconvulsive shock (ECS) trials conducted during REM sleep without thalamocortical EEG desynchronization (top) and during REM sleep without atonia (bottom). Stimulus artifact is visible in the middle of each tracing.
Fig. 4.
Fig. 4.
Susceptibility to generalized EEG vs motor seizures in a control condition (clear bars) and after treatments to dissociate REM sleep polygraphic components (dark bars). Each bar reflects the mean and S.D. from multiple measure of seizure activity during alert waking, SWS or REM sleep per cat. For example, penicillin seizure activity is indexed by the mean number of spike- wave complexes (left) or myoclonic seizures (right) per 20-s epoch of each state. ECS thresholds represent at least three thresholds to generalized afterdischarge (AD; left) or convulsions (GTCs right) per state in each cat. A: EEG and motor seizure susceptibility before atropine (clear bars) and after atropine (dark bars) in penicillin (top) and ECS (bottom) epilepsy models. B: EEG and motor seizure susceptibility after pontine lesions which did not affect atonia in REM sleep (clear bars) and lesions which eliminated atonia during REM sleep (dark bars). Data are provided for penicillin (top) and ECS (bottom) epilepsy models. ECS data: note that threshold is inversely related to susceptibility; the ECS ordinate is inverted to so that high bars reflect increased seizure susceptibility in both epilepsy models.
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