scholarly journals High-voltage, diffuse delta rhythms coincide with wakeful consciousness and complexity in Angelman syndrome

2020 ◽  
Vol 2020 (1) ◽  
Author(s):  
Joel Frohlich ◽  
Lynne M Bird ◽  
John Dell’Italia ◽  
Micah A Johnson ◽  
Joerg F Hipp ◽  
...  

Abstract Abundant evidence from slow wave sleep, anesthesia, coma, and epileptic seizures links high-voltage, slow electroencephalogram (EEG) activity to loss of consciousness. This well-established correlation is challenged by the observation that children with Angelman syndrome (AS), while fully awake and displaying volitional behavior, display a hypersynchronous delta (1–4 Hz) frequency EEG phenotype typical of unconsciousness. Because the trough of the delta oscillation is associated with down-states in which cortical neurons are silenced, the presence of volitional behavior and wakefulness in AS amidst diffuse delta rhythms presents a paradox. Moreover, high-voltage, slow EEG activity is generally assumed to lack complexity, yet many theories view functional brain complexity as necessary for consciousness. Here, we use abnormal cortical dynamics in AS to assess whether EEG complexity may scale with the relative level of consciousness despite a background of hypersynchronous delta activity. As characterized by multiscale metrics, EEGs from 35 children with AS feature significantly greater complexity during wakefulness compared with sleep, even when comparing the most pathological segments of wakeful EEG to the segments of sleep EEG least likely to contain conscious mentation and when factoring out delta power differences across states. These findings (i) warn against reverse inferring an absence of consciousness solely on the basis of high-amplitude EEG delta oscillations, (ii) corroborate rare observations of preserved consciousness under hypersynchronization in other conditions, (iii) identify biomarkers of consciousness that have been validated under conditions of abnormal cortical dynamics, and (iv) lend credence to theories linking consciousness with complexity.

Brain ◽  
2021 ◽  
Author(s):  
Joel Frohlich ◽  
Daniel Toker ◽  
Martin M Monti

Abstract A common observation in EEG research is that consciousness vanishes with the appearance of delta (1 – 4 Hz) waves, particularly when those waves are high amplitude. High amplitude delta oscillations are very frequently observed in states of diminished consciousness, including slow wave sleep, anaesthesia, generalised epileptic seizures, and disorders of consciousness such as coma and vegetative state. This strong correlation between loss of consciousness and high amplitude delta oscillations is thought to stem from the widespread cortical deactivation that occurs during the “down states” or troughs of these slow oscillations. Recently, however, many studies have reported the presence of prominent delta activity during conscious states, which casts doubt on the hypothesis that high amplitude delta oscillations are an indicator of unconsciousness. These studies include work in Angelman syndrome, epilepsy, behavioural responsiveness during propofol anaesthesia, postoperative delirium, and states of dissociation from the environment such as dreaming and powerful psychedelic states. The foregoing studies complement an older, yet largely unacknowledged, body of literature that has documented awake, conscious patients with high amplitude delta oscillations in clinical reports from Rett syndrome, Lennox-Gastaut syndrome, schizophrenia, mitochondrial diseases, hepatic encephalopathy, and nonconvulsive status epilepticus. At the same time, a largely parallel body of recent work has reported convincing evidence that the complexity or entropy of EEG and magnetoencephalogram or MEG signals strongly relates to an individual’s level of consciousness. Having reviewed this literature, we discuss plausible mechanisms that would resolve the seeming contradiction between high amplitude delta oscillations and consciousness. We also consider implications concerning theories of consciousness, such as integrated information theory and the entropic brain hypothesis. Finally, we conclude that false inferences of unconscious states can be best avoided by examining measures of electrophysiological complexity in addition to spectral power.


2021 ◽  
Vol 16 (1-2) ◽  
pp. 63-68
Author(s):  
S. L. Kulikova ◽  
I. V. Kozyreva ◽  
S. A. Likhachev ◽  
M. Yu. Bobylova

The article presents a description of a clinical case of a child 3 years 8 months old with Rett syndrome caused by the mutation of p.Val485fs in the MECP2 gene. According to electroencephalography data at the age of 1 year and 6 months, diffuse continued epileptiform activity in the form of high-amplitude (up to 300 μV) acute – slow wave complexes (continuous spike-waves during slow-wave sleep, CSWS) with an index of 90–100 % was revealed. At the control examination at the age of 2 years and 10 months diffuse epileptiform activity was replaced by multifocal activity with an index of up to 70–80 % at certain epochs, in general, not exceeding 50–60 %. During the entire observation period there were no epileptic seizures. It remains unknown whether the presence of CSWS at such an early age is a predictor of a more severe course of Rett syndrome – in our observation the girl did not acquire walking skills and a delay in psychic and speech development was evident already before the 12 month of life. more research is needed on the frequency of the CSWS phenomenon and its role in the development of clinical features in Rett syndrome.


2010 ◽  
Vol 298 (5) ◽  
pp. R1428-R1434 ◽  
Author(s):  
Xiaorui Tang ◽  
Barry R. Dworkin

The sensitivity of the baroreflex determines its stability and effectiveness in controlling blood pressure (BP). Sleep and arousal are reported to affect baroreflex sensitivity, but the findings are not consistent across studies. After statistically correcting the effect of sleep on the baselines in chronically neuromuscular-blocked (NMB) rats, we found that sleep affects BP and heart period (HP) baroreflex gain similarly. This finding is consistent with baroreflex modulation of HP and BP before divergence of the sympathetic and parasympathetic pathways. Therefore, we hypothesized that the gain modulation occurs in the dorsal medial nucleus of the solitary tract (dmNTS). The present study used long-term dmNTS recordings in NMB rats and single-pulse aortic depressor nerve stimulation. Under these conditions, the magnitude of A-fiber evoked responses (ERs), recorded from second- or higher-order dmNTS baroreflex neurons, was reliably augmented during high-amplitude low-frequency EEG activity (slow-wave sleep) and reduced during low-amplitude high-frequency EEG activity (arousal; ΔER = 11%, t = 9.49, P < 0.001, degrees of freedom = 1,016). This result has methodological implications for techniques that use changes in HP to estimate baroreflex BP gain and general implications for understanding the relationship between sleep and cardiovascular control.


1998 ◽  
Vol 275 (4) ◽  
pp. R1127-R1137 ◽  
Author(s):  
Paul Franken ◽  
Alain Malafosse ◽  
Mehdi Tafti

The genetic variation in spontaneous rhythmic electroencephalographic (EEG) activity was assessed by the quantitative analysis of the EEG in six inbred mice strains. Mean spectral EEG profiles (0–25 Hz) over 24 h were obtained for paradoxical sleep (PS), slow-wave sleep (SWS), and wakefulness. A highly significant genotype-specific variation was found for theta peak frequency during both PS and SWS, which strongly suggests the presence of a gene with a major effect. The strain distribution of theta peak frequency during exploratory behavior differed from that during sleep. In SWS, the relative contributions of delta (1–4 Hz) and sigma (11–15) power to the EEG varied with genotype and power in both frequency bands was negatively correlated. In addition, the EEG dynamics at state transitions were analyzed with a 4-s resolution. The onset of PS, but not that of wakefulness, was preceded by a pronounced peak in high-frequency (>11 Hz) power. These findings are discussed in terms of the neurophysiological mechanisms underlying rhythm generation and their control and modulation by the brain stem reticular-activating system.


1988 ◽  
Vol 8 (2) ◽  
pp. 215-226 ◽  
Author(s):  
Boris A. Vern ◽  
William H. Schuette ◽  
Boris Leheta ◽  
Vern C. Juel ◽  
Miodrag Radulovacki

To study the changes in cortical oxidative metabolism and blood volume during behavioral state transitions, we employed reflectance spectrophotometry of the cortical cytochrome c oxidase (cyt aa3) redox state and blood volume in unanesthetized cats implanted with bilateral cortical windows and EEG electrodes. Continuous oscillations in the redox state and blood volume (∼9/min) were observed during waking and sleep. These primarily metabolic oscillations of relatively high amplitude were usually synchronous in homotopic cortical areas, and persisted during barbiturate-induced electrocortical silence. Their mean amplitude and frequency did not vary across different behavioral/EEG states, although the mean levels of cyt aa3 oxidation and blood volume during rapid eye movement (REM) sleep significantly exceeded those during waking and slow-wave sleep. These data suggest the existence of a spontaneously oscillating metabolic phenomenon in cortex that is not directly related to neuroelectric activity. A superimposed increase in cortical oxidative metabolism and blood volume occurs during REM sleep. Experimental data concerning cerebral metabolism and blood flow that are obtained by clinical methods that employ relatively long sample acquisition times should therefore be interpreted with caution.


2021 ◽  
Vol 12 ◽  
Author(s):  
Guofang Shen ◽  
Wei-Xing Shi

Cortical neurons oscillate between Up and Down states during slow wave sleep and general anesthesia. Recent studies show that Up/Down oscillations also occur during quiet wakefulness. Arousal eliminates Down states and transforms Up/Down oscillations to a persistent Up state. Further evidence suggests that Up/Down oscillations are crucial to memory consolidation, whereas their transition to a persistent Up state is essential for arousal and attention. We have shown that D-amphetamine promotes cortical Up state, and the effect depends on activation of central α1A adrenergic receptors. Here, we report that dopamine also plays a role in D-amphetamine’s effect. Thus, using local-field-potential recording in the prefrontal cortex in chloral hydrate-anesthetized rats, we showed that the Up-state promoting effect of D-amphetamine was attenuated by antagonists at either D1 or D2-like dopamine receptors. The effect was also partially mimicked by co-activation of D1 and D2-like receptors. These results are consistent with the fact that D-amphetamine increases the release of both norepinephrine and dopamine. They are also in agreement with studies showing that dopamine promotes wakefulness and mediates D-amphetamine-induced emergence from general anesthesia. The effect of D-amphetamine was not mimicked, however, by activation of either D1 or D2-like receptors alone, indicating an interdependence between D1 and D2-like receptors. The dopamine/norepinephrine precursor L-DOPA also failed to promote the Up state. While more studies are needed to understand the difference between L-DOPA and D-amphetamine, our finding may provide an explanation for why L-DOPA lacks significant psychostimulant properties and is ineffective in treating attention-deficit/hyperactivity disorder.


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