scholarly journals EEG desynchronization during phasic REM sleep suppresses interictal epileptic activity in humans

Epilepsia ◽  
2016 ◽  
Vol 57 (6) ◽  
pp. 879-888 ◽  
Author(s):  
Birgit Frauscher ◽  
Nicolás Ellenrieder ◽  
François Dubeau ◽  
Jean Gotman
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Daniel Gomes de Almeida-Filho ◽  
Bruna Del Vechio Koike ◽  
Francesca Billwiller ◽  
Kelly Soares Farias ◽  
Igor Rafael Praxedes de Sales ◽  
...  

AbstractHippocampal (HPC) theta oscillation during post-training rapid eye movement (REM) sleep supports spatial learning. Theta also modulates neuronal and oscillatory activity in the retrosplenial cortex (RSC) during REM sleep. To investigate the relevance of theta-driven interaction between these two regions to memory consolidation, we computed the Granger causality within theta range on electrophysiological data recorded in freely behaving rats during REM sleep, both before and after contextual fear conditioning. We found a training-induced modulation of causality between HPC and RSC that was correlated with memory retrieval 24 h later. Retrieval was proportional to the change in the relative influence RSC exerted upon HPC theta oscillation. Importantly, causality peaked during theta acceleration, in synchrony with phasic REM sleep. Altogether, these results support a role for phasic REM sleep in hippocampo-cortical memory consolidation and suggest that causality modulation between RSC and HPC during REM sleep plays a functional role in that phenomenon.


SLEEP ◽  
2018 ◽  
Vol 42 (2) ◽  
Author(s):  
Jun-Sang Sunwoo ◽  
Kwang Su Cha ◽  
Jung-Ick Byun ◽  
Tae-Joon Kim ◽  
Jin-Sun Jun ◽  
...  

1979 ◽  
Vol 47 (6) ◽  
pp. 1304-1310 ◽  
Author(s):  
C. E. Sullivan ◽  
E. Murphy ◽  
L. F. Kozar ◽  
E. A. Phillipson

Ventilatory responses to CO2 and to lung inflation were compared in four dogs during tonic and phasic segments of rapid-eye-movement (REM) sleep. Phasic REM sleep (P-REM) was identified by the presence of bursts of rapid eye movements, visible muscle twitchings, and frequent phasic discharges in the nuchal electromyogram. These features were absent during tonic REM sleep (T-REM). During P-REM the response of minute volume of ventilation (VI) to progressive hypercapnia (0.58 +/- 0.19 (l/min)/Torr, mean +/- SE) was significantly less than in slow-wave sleep (SWS) (1.40 +/- 0.14; P less than 0.05). In contrast, during T-REM the response (1.48 +/- 0.19) was similar to that in SWS. Similarly, during P-REM the duration of apnea (5.9 +/- 1.5 s) elicited by sustained inflation of the lungs with 1.0 liter of air, was significantly shorter than in SWS (25.8 +/- 0.8); in contrast, during T-REM the duration of apnea (17.8 +/- 3.6) was similar to that in SWS. The results indicate that previously described decreases in VI responses to CO2 and apneic responses to lung inflation during P-REM, compared to SWS, are related to the phasic phenomena of REM sleep, rather than to the REM sleep state per se.


2009 ◽  
Vol 106 (4) ◽  
pp. 1050-1056 ◽  
Author(s):  
Priscila A. Cassaglia ◽  
Robert I. Griffiths ◽  
Adrian M. Walker

Sympathetic nerve activity (SNA) in neurons projecting to skeletal muscle blood vessels increases during rapid-eye-movement (REM) sleep, substantially exceeding SNA of non-REM (NREM) sleep and quiet wakefulness (QW). Similar SNA increases to cerebral blood vessels may regulate the cerebral circulation in REM sleep, but this is unknown. We hypothesized that cerebral SNA increases during phasic REM sleep, constricting cerebral vessels as a protective mechanism against cerebral hyperperfusion during the large arterial pressure surges that characterize this sleep state. We tested this hypothesis using a newly developed model to continuously record SNA in the superior cervical ganglion (SCG) before, during, and after arterial pressure surges occurring during REM in spontaneously sleeping lambs. Arterial pressure (AP), intracranial pressure (ICP), cerebral blood flow (CBF), cerebral vascular resistance [CVR = (AP − ICP)/CBF], and SNA from the SCG were recorded in lambs ( n = 5) undergoing spontaneous sleep-wake cycles. In REM sleep, CBF was greatest (REM > QW = NREM, P < 0.05) and CVR was least (REM < QW = NREM, P < 0.05). SNA in the SCG did not change from QW to NREM sleep but increased during tonic REM sleep, with a further increase during phasic REM sleep (phasic REM > tonic REM > QW = NREM, P < 0.05). Coherent averaging revealed that SNA increases preceded AP surges in phasic REM sleep by 12 s ( P < 0.05). We report the first recordings of cerebral SNA during natural sleep-wake cycles. SNA increases markedly during tonic REM sleep, and further in phasic REM sleep. As SNA increases precede AP surges, they may serve to protect the brain against potentially damaging intravascular pressure changes or hyperperfusion in REM sleep.


2010 ◽  
Vol 104 (4) ◽  
pp. 2194-2202 ◽  
Author(s):  
Philip H. de Guzman ◽  
Farhang Nazer ◽  
Clayton T. Dickson

Non-REM (slow-wave) sleep has been shown to facilitate temporal lobe epileptiform events, whereas REM sleep seems more restrictive. This state-dependent modulation may be the result of the enhancement of excitatory synaptic transmission and/or the degree of network synchronization expressed within the hippocampus of the temporal lobe. The slow oscillation (SO), a ∼1 Hz oscillatory pattern expressed during non-REM sleep and urethane anesthesia, has been recently shown to facilitate the generation, maintenance, and propagation of stimulus-evoked epileptiform activity in the hippocampus. To further address the state-dependent modulation of epileptic activity during the SO, we studied the properties of short-duration interictal-like activity generated by focal application of penicillin in the hippocampus of urethane-anesthetized rats. Epileptiform spikes were larger but only slightly more prevalent during the SO as opposed to the theta (REM-like) state. More notably, however, epileptic spikes had a significant tendency to occur just following the peak negativity of ongoing SO cycles. Because of the known phase-dependent changes in 1) synaptic excitability (just following the positive peak of the SO) and 2) network synchronization (during the negative peak of the SO), these results suggest that it is the synchrony and not the changes in synaptic excitability that lead to the facilitation of epileptiform activity during sleep-like slow wave states.


2017 ◽  
Vol 40 ◽  
pp. e319-e320
Author(s):  
J.-S. Sunwoo ◽  
K.S. Cha ◽  
T.-J. Kim ◽  
J.-I. Byun ◽  
K.-Y. Jung

2017 ◽  
Vol 37 ◽  
pp. 74-76
Author(s):  
Sudhansu Chokroverty ◽  
Sushanth Bhat ◽  
Mitchell Rubinstein
Keyword(s):  

Author(s):  
Lino Nobili ◽  
Paola Proserpio ◽  
Steve Gibbs ◽  
Giuseppe Plazzi

This chapter on sleep and epilepsy examines the activating and deactivating properties of NREM and REM sleep states on interictal epileptic activity and seizures. It reviews specific epileptic syndromes in which seizures manifest a tendency to present exclusively or predominantly during sleep or upon wakening. Particular attention is paid to the description of the different forms of nocturnal frontal lobe epilepsy: autosomal dominant and lesional. There is also a discussion of the negative bidirectional relationship between epilepsy and sleep disorders (sleep apneas and parasomnias) and the effect of pharmacological and nonpharmacological treatments. Finally, a brief review of the relationship between sleep and sudden unexpected death in epilepsy is given.


2014 ◽  
Vol 125 ◽  
pp. S327
Author(s):  
J. Toppila ◽  
T. Naesi ◽  
J. Virtanen ◽  
T. Salmi ◽  
R. Ilmoniemi
Keyword(s):  

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