scholarly journals Cortical monitoring of cardiac activity during rapid eye movement sleep: the heartbeat evoked potential in phasic and tonic REM microstates

SLEEP ◽  
2021 ◽  
Author(s):  
Péter Simor ◽  
Tamás Bogdány ◽  
Róbert Bódizs ◽  
Pandelis Perakakis

Abstract Sleep is a fundamental physiological state that facilitates neural recovery during periods of attenuated sensory processing. On the other hand, mammalian sleep is also characterized by the interplay between periods of increased sleep depth and environmental alertness. Whereas the heterogeneity of microstates during non-rapid-eye-movement (NREM) sleep was extensively studied in the last decades, transient microstates during REM sleep received less attention. REM sleep features two distinct microstates: phasic and tonic. Previous studies indicate that sensory processing is largely diminished during phasic REM periods, whereas environmental alertness is partially reinstated when the brain switches into tonic REM sleep. Here, we investigated interoceptive processing as quantified by the heartbeat evoked potential (HEP) during REM microstates. We contrasted the HEPs of phasic and tonic REM periods using two separate databases that included the nighttime polysomnographic recordings of healthy young individuals (N = 20 and N = 19). We find a differential HEP modulation of a late HEP component (after 500 ms post-R-peak) between tonic and phasic REM. Moreover, the late tonic HEP component resembled the HEP found in resting wakefulness. Our results indicate that interoception with respect to cardiac signals is not uniform across REM microstates, and suggest that interoceptive processing is partially reinstated during tonic REM periods. The analyses of the HEP during REM sleep may shed new light on the organization and putative function of REM microstates.

2020 ◽  
Author(s):  
Péter Simor ◽  
Bogdány Tamás ◽  
Robert Bodizs ◽  
Pandelis Perakakis

Sleep is a fundamental physiological state that facilitates neural recovery during periods of attenuated sensory processing. On the other hand, mammalian sleep is also characterized by the interplay between periods of increased sleep depth and environmental alertness. Whereas the heterogeneity of microstates during non-rapid-eye-movement (NREM) sleep was extensively studied in the last decades, transient microstates during REM sleep received less attention. REM sleep features two distinct microstates: phasic and tonic. Previous studies indicate that sensory processing is largely diminished during phasic REM periods, whereas environmental alertness is partially reinstated when the brain switches into tonic REM sleep. Here, we investigated interoceptive processing as quantified by the heartbeat evoked potential (HEP) during REM microstates. We contrasted the HEPs of phasic and tonic REM periods using two separate databases that included the nighttime polysomnographic recordings of healthy young individuals (N = 20 and N = 19). We find a differential HEP modulation of a late HEP component (after 500 ms post-R-peak) between tonic and phasic REM. Moreover, the late tonic HEP component resembled the HEP found in resting wakefulness. Our results indicate that interoception with respect to cardiac signals is not uniform across REM microstates, and suggest that interoceptive processing is partially reinstated during tonic REM periods. The analyses of the HEP during REM sleep may shed new light on the organization and putative function of REM microstates.


Author(s):  
Douglas J. Gelb

Sleep consists of a highly patterned sequence of cyclic activity in various regions of the brain; it is not simply a state of temporary unconsciousness. Although the brain is less responsive than normal during sleep, it is not totally unresponsive. In fact, during sleep the brain responds more readily to meaningful stimuli. Rapid eye movement (REM) sleep can be characterized as a period when the brain is active and the body is paralyzed, whereas in nonrapid eye movement (NREM) sleep, the brain is less active but the body can move. Sleep disorders are grouped into three general categories, based on whether patients have trouble staying awake, trouble sleeping, or abnormal behaviors during sleep.


2020 ◽  
pp. 1-12
Author(s):  
Sue Llewellyn

Dreaming happens during sleep. When we aren’t interacting with the world, our minds turn inwards. We dream. These dreams differ. Rapid eye movement (REM) dreams are visual, vivid, bizarre, emotional, and highly associative with embodied narratives, whereas non-rapid eye movement (NREM) dreams tend to be shorter and more thought-like. During REM dreams, the brain is as active, or even more active, than it is during wakefulness. In some dreams, during REM sleep, the dreamer is lucid—they become aware they are dreaming and can, sometimes control the dream content. These different types of dream happen at different times in the sleep cycle. Across the night, we experience NREM sleep (including light sleep and deep sleep) and REM sleep in a fixed sequence. The night isn’t a uniform period of rest. This introductory chapter explains these basic issues about sleep and dreams.


2012 ◽  
Vol 92 (3) ◽  
pp. 1087-1187 ◽  
Author(s):  
Ritchie E. Brown ◽  
Radhika Basheer ◽  
James T. McKenna ◽  
Robert E. Strecker ◽  
Robert W. McCarley

This review summarizes the brain mechanisms controlling sleep and wakefulness. Wakefulness promoting systems cause low-voltage, fast activity in the electroencephalogram (EEG). Multiple interacting neurotransmitter systems in the brain stem, hypothalamus, and basal forebrain converge onto common effector systems in the thalamus and cortex. Sleep results from the inhibition of wake-promoting systems by homeostatic sleep factors such as adenosine and nitric oxide and GABAergic neurons in the preoptic area of the hypothalamus, resulting in large-amplitude, slow EEG oscillations. Local, activity-dependent factors modulate the amplitude and frequency of cortical slow oscillations. Non-rapid-eye-movement (NREM) sleep results in conservation of brain energy and facilitates memory consolidation through the modulation of synaptic weights. Rapid-eye-movement (REM) sleep results from the interaction of brain stem cholinergic, aminergic, and GABAergic neurons which control the activity of glutamatergic reticular formation neurons leading to REM sleep phenomena such as muscle atonia, REMs, dreaming, and cortical activation. Strong activation of limbic regions during REM sleep suggests a role in regulation of emotion. Genetic studies suggest that brain mechanisms controlling waking and NREM sleep are strongly conserved throughout evolution, underscoring their enormous importance for brain function. Sleep disruption interferes with the normal restorative functions of NREM and REM sleep, resulting in disruptions of breathing and cardiovascular function, changes in emotional reactivity, and cognitive impairments in attention, memory, and decision making.


2015 ◽  
Author(s):  
Sudhansu Chokroverty

Recent research has generated an enormous fund of knowledge about the neurobiology of sleep and wakefulness. Sleeping and waking brain circuits can now be studied by sophisticated neuroimaging techniques that map different areas of the brain during different sleep states and stages. Although the exact biologic functions of sleep are not known, sleep is essential, and sleep deprivation leads to impaired attention and decreased performance. Sleep is also believed to have restorative, conservative, adaptive, thermoregulatory, and consolidative functions. This review discusses the physiology of sleep, including its two independent states, rapid eye movement (REM) and non–rapid eye movement (NREM) sleep, as well as functional neuroanatomy, physiologic changes during sleep, and circadian rhythms. The classification and diagnosis of sleep disorders are discussed generally. The diagnosis and treatment of the following disorders are described: obstructive sleep apnea syndrome, narcolepsy-cataplexy sydrome, idiopathic hypersomnia, restless legs syndrome (RLS) and periodic limb movements in sleep, circadian rhythm sleep disorders, insomnias, nocturnal frontal lobe epilepsy, and parasomnias. Sleep-related movement disorders and the relationship between sleep and psychiatric disorders are also discussed. Tables describe behavioral and physiologic characteristics of states of awareness, the international classification of sleep disorders, common sleep complaints, comorbid insomnia disorders, causes of excessive daytime somnolence, laboratory tests to assess sleep disorders, essential diagnostic criteria for RLS and Willis-Ekbom disease, and drug therapy for insomnia. Figures include polysomnographic recording showing wakefulness in an adult; stage 1, 2, and 3 NREM sleep in an adult; REM sleep in an adult; a patient with sleep apnea syndrome; a patient with Cheyne-Stokes breathing; a patient with RLS; and a patient with dream-enacting behavior; schematic sagittal section of the brainstem of the cat; schematic diagram of the McCarley-Hobson model of REM sleep mechanism; the Lu-Saper “flip-flop” model; the Luppi model to explain REM sleep mechanism; and a wrist actigraph from a man with bipolar disorder. This review contains 14 highly rendered figures, 8 tables, 115 references, and 5 MCQs.


2015 ◽  
Author(s):  
Sudhansu Chokroverty

Recent research has generated an enormous fund of knowledge about the neurobiology of sleep and wakefulness. Sleeping and waking brain circuits can now be studied by sophisticated neuroimaging techniques that map different areas of the brain during different sleep states and stages. Although the exact biologic functions of sleep are not known, sleep is essential, and sleep deprivation leads to impaired attention and decreased performance. Sleep is also believed to have restorative, conservative, adaptive, thermoregulatory, and consolidative functions. This review discusses the physiology of sleep, including its two independent states, rapid eye movement (REM) and non–rapid eye movement (NREM) sleep, as well as functional neuroanatomy, physiologic changes during sleep, and circadian rhythms. The classification and diagnosis of sleep disorders are discussed generally. The diagnosis and treatment of the following disorders are described: obstructive sleep apnea syndrome, narcolepsy-cataplexy sydrome, idiopathic hypersomnia, restless legs syndrome (RLS) and periodic limb movements in sleep, circadian rhythm sleep disorders, insomnias, nocturnal frontal lobe epilepsy, and parasomnias. Sleep-related movement disorders and the relationship between sleep and psychiatric disorders are also discussed. Tables describe behavioral and physiologic characteristics of states of awareness, the international classification of sleep disorders, common sleep complaints, comorbid insomnia disorders, causes of excessive daytime somnolence, laboratory tests to assess sleep disorders, essential diagnostic criteria for RLS and Willis-Ekbom disease, and drug therapy for insomnia. Figures include polysomnographic recording showing wakefulness in an adult; stage 1, 2, and 3 NREM sleep in an adult; REM sleep in an adult; a patient with sleep apnea syndrome; a patient with Cheyne-Stokes breathing; a patient with RLS; and a patient with dream-enacting behavior; schematic sagittal section of the brainstem of the cat; schematic diagram of the McCarley-Hobson model of REM sleep mechanism; the Lu-Saper “flip-flop” model; the Luppi model to explain REM sleep mechanism; and a wrist actigraph from a man with bipolar disorder. This review contains 14 highly rendered figures, 8 tables, 115 references, and 5 MCQs.


SLEEP ◽  
2021 ◽  
Author(s):  
Andreas Brink-Kjær ◽  
Matteo Cesari ◽  
Friederike Sixel-Döring ◽  
Brit Mollenhauer ◽  
Claudia Trenkwalder ◽  
...  

Abstract Study objectives Patients diagnosed with isolated rapid eye movement (REM) sleep behavior disorder (iRBD) and Parkinson’s disease (PD) have altered sleep stability reflecting neurodegeneration in brainstem structures. We hypothesize that neurodegeneration alters the expression of cortical arousals in sleep. Methods We analyzed polysomnography data recorded from 88 healthy controls (HC), 22 iRBD patients, 82 de novo PD patients without RBD and 32 with RBD (PD+RBD). These patients were also investigated at a 2-year follow-up. Arousals were analyzed using a previously validated automatic system, which used a central EEG lead, electrooculography, and chin electromyography. Multiple linear regression models were fitted to compare group differences at baseline and change to follow-up for arousal index (ArI), shifts in electroencephalographic signals associated with arousals, and arousal chin muscle tone. The regression models were adjusted for known covariates affecting the nature of arousal. Results In comparison to HC, patients with iRBD and PD+RBD showed increased ArI during REM sleep and their arousals showed a significantly lower shift in α-band power at arousals and a higher muscle tone during arousals. In comparison to HC, the PD patients were characterized by a decreased ArI in NREM sleep at baseline. ArI during NREM sleep decreased further at the 2-year follow-up, although not significantly Conclusions Patients with PD and iRBD present with abnormal arousal characteristics as scored by an automated method. These abnormalities are likely to be caused by neurodegeneration of the reticular activation system due to alpha-synuclein aggregation.


SLEEP ◽  
2020 ◽  
Author(s):  
Jun-Sang Sunwoo ◽  
Kwang Su Cha ◽  
Jung-Ick Byun ◽  
Jin-Sun Jun ◽  
Tae-Joon Kim ◽  
...  

Abstract Study Objectives We investigated electroencephalographic (EEG) slow oscillations (SOs), sleep spindles (SSs), and their temporal coordination during nonrapid eye movement (NREM) sleep in patients with idiopathic rapid eye movement (REM) sleep behavior disorder (iRBD). Methods We analyzed 16 patients with video-polysomnography-confirmed iRBD (age, 65.4 ± 6.6 years; male, 87.5%) and 10 controls (age, 62.3 ± 7.5 years; male, 70%). SSs and SOs were automatically detected during stage N2 and N3. We analyzed their characteristics, including density, frequency, duration, and amplitude. We additionally identified SO-locked spindles and examined their phase distribution and phase locking with the corresponding SO. For inter-group comparisons, we used the independent samples t-test or Wilcoxon rank-sum test, as appropriate. Results The SOs of iRBD patients had significantly lower amplitude, longer duration (p = 0.005 for both), and shallower slope (p < 0.001) than those of controls. The SS power of iRBD patients was significantly lower than that of controls (p = 0.002), although spindle density did not differ significantly. Furthermore, SO-locked spindles of iRBD patients prematurely occurred during the down-to-up-state transition of SOs, whereas those of controls occurred at the up-state peak of SOs (p = 0.009). The phase of SO-locked spindles showed a positive correlation with delayed recall subscores (p = 0.005) but not with tonic or phasic electromyography activity during REM sleep. Conclusions In this study, we found abnormal EEG oscillations during NREM sleep in patients with iRBD. The impaired temporal coupling between SOs and SSs may reflect early neurodegenerative changes in iRBD.


SLEEP ◽  
2019 ◽  
Vol 43 (6) ◽  
Author(s):  
Sjoerd J van Hasselt ◽  
Maria Rusche ◽  
Alexei L Vyssotski ◽  
Simon Verhulst ◽  
Niels C Rattenborg ◽  
...  

Abstract Most of our knowledge about the regulation and function of sleep is based on studies in a restricted number of mammalian species, particularly nocturnal rodents. Hence, there is still much to learn from comparative studies in other species. Birds are interesting because they appear to share key aspects of sleep with mammals, including the presence of two different forms of sleep, i.e. non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. We examined sleep architecture and sleep homeostasis in the European starling, using miniature dataloggers for electroencephalogram (EEG) recordings. Under controlled laboratory conditions with a 12:12 h light–dark cycle, the birds displayed a pronounced daily rhythm in sleep and wakefulness with most sleep occurring during the dark phase. Sleep mainly consisted of NREM sleep. In fact, the amount of REM sleep added up to only 1~2% of total sleep time. Animals were subjected to 4 or 8 h sleep deprivation to assess sleep homeostatic responses. Sleep deprivation induced changes in subsequent NREM sleep EEG spectral qualities for several hours, with increased spectral power from 1.17 Hz up to at least 25 Hz. In contrast, power below 1.17 Hz was decreased after sleep deprivation. Sleep deprivation also resulted in a small compensatory increase in NREM sleep time the next day. Changes in EEG spectral power and sleep time were largely similar after 4 and 8 h sleep deprivation. REM sleep was not noticeably compensated after sleep deprivation. In conclusion, starlings display signs of NREM sleep homeostasis but the results do not support the notion of important REM sleep functions.


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