Brain regions and epileptogenicity influence epileptic interictal spike production and propagation during NREM sleep in comparison with wakefulness

Epilepsia ◽  
2017 ◽  
Vol 59 (1) ◽  
pp. 235-243 ◽  
Author(s):  
Isabelle Lambert ◽  
Nicolas Roehri ◽  
Bernard Giusiano ◽  
Romain Carron ◽  
Fabrice Wendling ◽  
...  
2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Bowon Kim ◽  
Eunjin Hwang ◽  
Robert E. Strecker ◽  
Jee Hyun Choi ◽  
Youngsoo Kim

AbstractCompensatory elevation in NREM sleep EEG delta power has been typically observed following prolonged wakefulness and widely used as a sleep homeostasis indicator. However, recent evidence in human and rodent chronic sleep restriction (CSR) studies suggests that NREM delta power is not progressively increased despite of accumulated sleep loss over days. In addition, there has been little progress in understanding how sleep EEG in different brain regions responds to CSR. Using novel high-density EEG electrode arrays in the mouse model of CSR where mice underwent 18-h sleep deprivation per day for 5 consecutive days, we performed an extensive analysis of topographical NREM sleep EEG responses to the CSR condition, including period-amplitude analysis of individual slow waves. As previously reported in our analysis of REM sleep responses, we found different patterns of changes: (i) progressive decrease in NREM sleep duration and consolidation, (ii) persistent enhancement in NREM delta power especially in the frontal and parietal regions, and (iii) progressive increases in individual slow wave slope and frontal fast oscillation power. These results suggest that multiple sleep-wake regulatory systems exist in a brain region-specific manner, which can be modulated independently, especially in the CSR condition.


2016 ◽  
Vol 3 (10) ◽  
pp. 160201 ◽  
Author(s):  
Peter Achermann ◽  
Thomas Rusterholz ◽  
Roland Dürr ◽  
Thomas König ◽  
Leila Tarokh

Sleep is characterized by a loss of consciousness, which has been attributed to a breakdown of functional connectivity between brain regions. Global field synchronization (GFS) can estimate functional connectivity of brain processes. GFS is a frequency-dependent measure of global synchronicity of multi-channel EEG data. Our aim was to explore and extend the hypothesis of disconnection during sleep by comparing GFS spectra of different vigilance states. The analysis was performed on eight healthy adult male subjects. EEG was recorded during a baseline night, a recovery night after 40 h of sustained wakefulness and at 3 h intervals during the 40 h of wakefulness. Compared to non-rapid eye movement (NREM) sleep, REM sleep showed larger GFS values in all frequencies except in the spindle and theta bands, where NREM sleep showed a peak in GFS. Sleep deprivation did not affect GFS spectra in REM and NREM sleep. Waking GFS values were lower compared with REM and NREM sleep except for the alpha band. Waking alpha GFS decreased following sleep deprivation in the eyes closed condition only. Our surprising finding of higher synchrony during REM sleep challenges the view of REM sleep as a desynchronized brain state and may provide insight into the function of REM sleep.


Author(s):  
Fabrice Bartolomei

‘Irritative, epileptogenic, and ictal onset zones in depth EEG’ reviews the three classical brain regions that are to be defined by epileptologists during invasive EEG recordings. It first reviews the concept of the epileptogenic zone (EZ) and the different historical definitions and then the patterns of ictal onset observed from depth EEG recordings. It then discusses the concept of irritative zone, which is related to the interictal spike distribution, and its relationship with the EZ. Finally, the concept of ‘epileptogenic networks’ is developed, offering a modern framework for the functional anatomy of focal epilepsies.


2000 ◽  
Vol 84 (4) ◽  
pp. 1888-1893 ◽  
Author(s):  
Reto Huber ◽  
Tom Deboer ◽  
Irene Tobler

Several recent results show that sleep and sleep regulation are not only global phenomena encompassing the entire brain, but have local features. It is well established that slow-wave activity [SWA; mean electroencephalographic (EEG) power density in the 0.75–4.0 Hz band] in non–rapid eye movement (NREM) sleep is a function of the prior history of sleep and wakefulness. SWA is thought to reflect the homeostatic component of the two-process model of sleep regulation. According to this model, originally formulated for the rat and later extended to human sleep, the timing and structure of sleep are determined by the interaction of a homeostatic Process S and a circadian process. Our aim was to investigate the dynamics of SWA in the EEG of two brain regions (frontal and occipital cortex) after sleep deprivation (SD) in two of the mice strains most often used in gene targeting. C57BL/6J ( n = 9) and 129/Ola ( n = 8) were recorded during a 24-h baseline day, 6-h SD, and 18-h recovery. Both derivations showed a significant increase in SWA in NREM sleep after SD in both strains. In the first hour of recovery, SWA was enhanced more in the frontal derivation than in the occipital derivation and showed a faster decline. This difference resulted in a lower value for the time constant for the decrease of SWA in the frontal derivation (frontal: 10.9 ± 2.1 and 6.8 ± 0.9 h in Ola and C57, respectively; occipital: 16.6 ± 2.1 and 14.1 ± 1.5 h; P < 0.02; for each of the strains; paired t-test). Neither time constant differed significantly between the strains. The subdivision of SWA into a slower and faster band (0.75–2.5 Hz and 2.75–4.0 Hz) further highlighted regional differences in the effect of SD. The lower frequency band had a higher initial value in the frontal derivation than in the occipital derivation in both strains. Moreover, in the higher frequency band a prominent reversal took place so that power in the frontal derivation fell below the occipital values in both strains. Thus our results indicate that there may be differences in the brain in the effects of SD on SWA in mice, suggesting regional differences in the dynamics of the homeostatic component of sleep regulation. The data support the hypothesis that sleep has local, use- or waking-dependent features that are reflected in the EEG, as has been shown for humans and the laboratory rat.


SLEEP ◽  
2020 ◽  
Vol 43 (11) ◽  
Author(s):  
Sandro Lecci ◽  
Jacinthe Cataldi ◽  
Monica Betta ◽  
Giulio Bernardi ◽  
Raphaël Heinzer ◽  
...  

Abstract Feeling awake although sleep recordings indicate clear-cut sleep sometimes occurs in good sleepers and to an extreme degree in patients with so-called paradoxical insomnia. It is unknown what underlies sleep misperception, as standard polysomnographic (PSG) parameters are often normal in these cases. Here we asked whether regional changes in brain activity could account for the mismatch between objective and subjective total sleep times (TST). To set cutoffs and define the norm, we first evaluated sleep perception in a population-based sample, consisting of 2,092 individuals who underwent a full PSG at home and estimated TST the next day. We then compared participants with a low mismatch (normoestimators, n = 1,147, ±0.5 SD of mean) with those who severely underestimated (n = 52, &lt;2.5th percentile) or overestimated TST (n = 53, &gt;97.5th percentile). Compared with normoestimators, underestimators displayed higher electroencephalographic (EEG) activation (beta/delta power ratio) in both rapid eye movement (REM) and non-rapid eye movement (NREM) sleep, while overestimators showed lower EEG activation (significant in REM sleep). To spatially map these changes, we performed a second experiment, in which 24 healthy subjects and 10 insomnia patients underwent high-density sleep EEG recordings. Similarly to underestimators, patients displayed increased EEG activation during NREM sleep, which we localized to central-posterior brain areas. Our results indicate that a relative shift from low- to high-frequency spectral power in central-posterior brain regions, not readily apparent in conventional PSG parameters, is associated with underestimation of sleep duration. This challenges the concept of sleep misperception, and suggests that instead of misperceiving sleep, insomnia patients may correctly perceive subtle shifts toward wake-like brain activity.


SLEEP ◽  
2019 ◽  
Vol 43 (5) ◽  
Author(s):  
Kevin M Swift ◽  
Karina Keus ◽  
Christy Gonzalez Echeverria ◽  
Yesenia Cabrera ◽  
Janelly Jimenez ◽  
...  

Abstract Sleep impacts diverse physiological and neural processes and is itself affected by the menstrual cycle; however, few studies have examined the effects of the estrous cycle on sleep in rodents. Studies of disease mechanisms in females therefore lack critical information regarding estrous cycle influences on relevant sleep characteristics. We recorded electroencephalographic (EEG) activity from multiple brain regions to assess sleep states as well as sleep traits such as spectral power and interregional spectral coherence in freely cycling females across the estrous cycle and compared with males. Our findings show that the high hormone phase of proestrus decreases the amount of nonrapid eye movement (NREM) sleep and rapid eye movement (REM) sleep and increases the amount of time spent awake compared with other estrous phases and to males. This spontaneous sleep deprivation of proestrus was followed by a sleep rebound in estrus which increased NREM and REM sleep. In proestrus, spectral power increased in the delta (0.5–4 Hz) and the gamma (30–60 Hz) ranges during NREM sleep, and increased in the theta range (5–9 Hz) during REM sleep during both proestrus and estrus. Slow-wave activity (SWA) and cortical sleep spindle density also increased in NREM sleep during proestrus. Finally, interregional NREM and REM spectral coherence increased during proestrus. This work demonstrates that the estrous cycle affects more facets of sleep than previously thought and reveals both sex differences in features of the sleep–wake cycle related to estrous phase that likely impact the myriad physiological processes influenced by sleep.


2020 ◽  
Author(s):  
Tomomi Tsunematsu ◽  
Shuzo Sakata ◽  
Tomomi Sanagi ◽  
Kenji F. Tanaka ◽  
Ko Matsui

AbstractNeural activity is diverse, and varies depending on brain regions and sleep/wakefulness states. However, whether astrocyte activity differs between sleep/wakefulness states, and whether there are differences in astrocyte activity among brain regions remain poorly understood. In this study, we recorded astrocyte intracellular calcium (Ca2+) concentrations of mice during sleep/wakefulness states in the cortex, hippocampus, hypothalamus, cerebellum, and pons using fiber photometry. For this purpose, male transgenic mice in which their astrocytes specifically express the genetically encoded ratiometric Ca2+ sensor YCnano50 were used. We demonstrated that Ca2+ levels in astrocytes significantly decrease during Rapid Eye Movement (REM) sleep and increase after the onset of wakefulness. In contrast, differences in Ca2+ levels during non-Rapid Eye Movement (NREM) sleep were observed among different brain regions, and no significant decrease was observed in the hypothalamus and pons. Further analyses focusing on the transition between sleep/wakefulness states and correlation analysis with episode duration of REM showed that Ca2+ dynamics differed among brain regions, suggesting the existence of several clusters. To quantify region-specific Ca2+ dynamics, principal component analysis was performed to uncover three clusters; i.e., the first comprised the cortex and hippocampus, the second comprised the cerebellum, and the third comprised the hypothalamus and pons. Our study demonstrated that astrocyte Ca2+ levels change substantially according to sleep/wakefulness states. These changes were generally consistent, unlike neural activity. However, we also clarified that Ca2+ dynamics varies depending on the brain region, implying that astrocytes may play various physiological roles in sleep.Significance statementSleep is an instinctive behavior of many organisms. In the previous five decades, the mechanism of the neural circuits controlling sleep/wakefulness states and the neural activities associated with sleep/wakefulness states in various brain regions have been elucidated. However, whether astrocytes, which are a type of glial cell, change their activity during different sleep/wakefulness states is poorly understood. Here, we demonstrated that dynamic changes in intracellular Ca2+ concentrations occur in the cortex, hippocampus, hypothalamus, cerebellum, and pons of genetically modified mice during natural sleep. Further analyses demonstrated that Ca2+ dynamics slightly differ among different brain regions, implying that the physiological roles of astrocytes in sleep/wakefulness might vary depending on the brain region.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A127-A127
Author(s):  
K K Lui ◽  
B A Mander ◽  
S Radom-Aizik ◽  
M G Chappel-Farley ◽  
A Dave ◽  
...  

Abstract Introduction The prefrontal cortex, an area known for executive functioning (including inhibition and self-monitoring) develops during childhood and adolescents, with a pattern of posterior to anterior brain development. Slow-wave activity (SWA) in NREM sleep, tracks brain development with high SWA power migrating from occipital to frontal region as brain maturation occurs. This pilot study aimed to examine whether slow wave topography is correlated with executive function in youth. Methods Seventeen healthy children and adolescents (ages 11-17; 10 females) underwent overnight polysomnography (PSG) with high-density electroencephalography (hdEEG). Behavior Rating Inventory of Executive Function (BRIEF) was administered to assess executive function. SWA (SWA1: 0.5-1 Hz; SWA2: 1-4.5 Hz) and spindle (slow sigma: 11-13 Hz; fast sigma: 13-16 Hz) activity was analyzed with spectral analysis using Welch’s method. BRIEF subscales of inhibition and monitor were correlated with SWA and sigma power across all derivations, with Holm-Bonferroni correction (126 channels). Significant derivations were then controlled for sex and self-reported Tanner stage using multiple regression Results BRIEF-Inhibition scale (i.e., ability to repress impulsivity) and SWA1 in anterior frontal derivations were negatively correlated (R2=0.58, p=0.047 corrected). BRIEF-Monitor scale (i.e., self-perception of one’s own behavior and interpersonal awareness) was negatively correlated with fast sigma in anterior frontal derivations (R2=0.65, p=0.013 corrected). These associations were significant after controlling for sex and Tanner stage. Conclusion These results support the hypothesis that NREM sleep oscillations are associated with executive function and reflect changes in neuroplasticity related to “back-to-front” brain maturation. Future longitudinal studies should combine multi-modal neuroimaging of brain structure and local sleep with comprehensive assessments of executive function to evaluate the possible link between local sleep and development of higher-order cognition in frontal brain regions in youth. Support NCATS grant #UL1TR001414 & PERC Systems Biology Fund


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Ze Zhang ◽  
Corinne Beier ◽  
Tenley Weil ◽  
Samer Hattar

AbstractLight regulates daily sleep rhythms by a neural circuit that connects intrinsically photosensitive retinal ganglion cells (ipRGCs) to the circadian pacemaker, the suprachiasmatic nucleus. Light, however, also acutely affects sleep in a circadian-independent manner. The neural circuits involving the acute effect of light on sleep remain unknown. Here we uncovered a neural circuit that drives this acute light response, independent of the suprachiasmatic nucleus, but still through ipRGCs. We show that ipRGCs substantially innervate the preoptic area (POA) to mediate the acute light effect on sleep in mice. Consistently, activation of either the POA projecting ipRGCs or the light-responsive POA neurons increased non-rapid eye movement (NREM) sleep without influencing REM sleep. In addition, inhibition of the light-responsive POA neurons blocked the acute light effects on NREM sleep. The predominant light-responsive POA neurons that receive ipRGC input belong to the corticotropin-releasing hormone subpopulation. Remarkably, the light-responsive POA neurons are inhibitory and project to well-known wakefulness-promoting brain regions, such as the tuberomammillary nucleus and the lateral hypothalamus. Therefore, activation of the ipRGC-POA circuit inhibits arousal brain regions to drive light-induced NREM sleep. Our findings reveal a functional retina-brain circuit that is both necessary and sufficient for the acute effect of light on sleep.


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A13-A14
Author(s):  
Natalia Machado ◽  
William Todd ◽  
Clifford Saper

Abstract Introduction Previous studies suggest that the median preoptic nucleus (MnPO) plays an important role in regulating the wake-sleep cycle and in particular homeostatic sleep drive. However, the precise cellular phenotypes, targets and central mechanisms by which the MnPO neurons regulate the wake-sleep cycle remain unknown. Both glutamatergic (Vglut2+) and GABAergic (Vgat+) MnPO neurons innervate brain regions implicated in sleep promotion and maintenance, suggesting that both cell types may participate on sleep control. Methods In this study, we used two genetically-targeted approaches associated with electroencephalographic (EEG) and electromyographic (EMG) recordings in Vgat-IRES-cre and Vglut2-IRES-cre mice to investigate the role of the MnPOVgat and MnPOVglut2 neurons in modulating wake-sleep behavior. Results First, using a chemogenetic approach, we found that activation of MnPOVgat neurons reduced the latency for the first NREM sleep episode, produced an increase in NREM sleep and reduced wakefulness. Then, to test the role of MnPOVgat and MnPOVglut2 neurons in regulating sleep homeostasis, we recorded EEG and EMG responses in mice that had the Vgat+ or Vglut2+ neurons deleted from the MnPO. After deletion of MnPOVgat neurons, mice showed a reduction of NREM sleep and an increase in wakefulness during the light phase. Deletion of MnPOVgat neurons also reduced sleep recovery after 4 hours of sleep deprivation (SD). On the other hand, deletion of the MnPOVglut2 neurons did not change the wake-sleep cycle during the 24h baseline condition, but prevented the sleep recovery immediately after SD. To understand the underlying mechanism in preventing sleep recovery in both MnPOVglut2- and MnPOVgat-deleted mice groups, we exposed these animals to a psychological stress protocol. In response to a psychological stressor, mice with deletion of glutamatergic, but not GABAergic MnPO neurons, had an exacerbation of the stress-induced insomnia. Conclusion Our results suggest that both neuron populations differentially participate in wake-sleep control, with MnPOVgat neurons being critically involved in sleep homeostasis, and MnPOVglut2 neurons promoting sleep during allostatic (stressful) challenges. Support (if any) NIH Grants NS085477, NS072337, HL095491 and Sleep Research Society Foundation (Award 026-JP-20).


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