Continuous Spike-and-Wave Activity during Slow-Wave Sleep

2008 ◽  
pp. 243-250
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Wave Activity

EEG delta power and auditory arousal in rested and sleep-deprived rabbits

1997 ◽  
Vol 272 (2) ◽  
pp. R648-R655 ◽  
Author(s):  
M. R. Opp ◽  
L. A. Toth ◽  
E. A. Tolley
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Rabbit Model ◽  
Stimulus Presentation ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Auditory Stimuli ◽  
Delta Power ◽  
Postural Changes ◽  
Behavioral Responsiveness

Slow-wave activity in the electroencephalogram is thought to reflect the depth or intensity of sleep. This hypothesis is primarily derived from studies of rats or humans. However, some characteristics of sleep of rabbits differ from those of rats or humans. To determine whether slow-wave activity (power density in the delta frequency band of 0.5-5.0 Hz) correlates with arousability in rabbits, we presented auditory stimuli (72-90 dB) to control or sleep-deprived animals during slow-wave sleep. The resulting behavioral responses, defined by changes in eye state and body posture, and the latency to return to sleep were used as measures of arousability. Behavioral responsiveness to auditory stimuli increased with increasing stimulus intensity in both control and sleep-deprived animals. Overall, however, sleep-deprived animals exhibited fewer postural changes and eye openings than did control rabbits. Sleep-deprived rabbits also more rapidly returned to sleep after the stimulus presentation than did control animals. Latency to return to sleep was correlated with delta power before stimulus presentation, but behavioral responsiveness was not. These data suggest that, in this rabbit model, delta power may not be predictive of behavioral arousability but may reflect sleep propensity.

scholarly journals Scalp EEG interictal high frequency oscillations as an objective EEG biomarker of infantile spasms

2020 ◽  
Author(s):  
Hiroki Nariai ◽  
Shaun A. Hussain ◽  
Danilo Bernardo ◽  
Hirotaka Motoi ◽  
Masaki Sonoda ◽  
...  
Keyword(s):  
Slow Wave ◽  
High Frequency ◽  
Slow Wave Sleep ◽  
Wave Activity ◽  
Infantile Spasms ◽  
Slow Wave Activity ◽  
List Type ◽  
Normal Children ◽  
High Frequency Oscillations ◽  
Epileptic Spasms

ABSTRACTObjectiveTo investigate the diagnostic utility of high frequency oscillations (HFOs) via scalp electroencephalogram (EEG) in infantile spasms.MethodsWe retrospectively analyzed interictal slow-wave sleep EEGs sampled at 2,000 Hz recorded from 30 consecutive patients who were suspected of having infantile spasms. We measured the rate of HFOs (80-500 Hz) and the strength of the cross-frequency coupling between HFOs and slow-wave activity (SWA) at 3-4 Hz and 0.5-1 Hz as quantified with modulation indices (MIs).ResultsTwenty-three patients (77%) exhibited active spasms during the overnight EEG recording. Although the HFOs were detected in all children, increased HFO rate and MIs correlated with the presence of active spasms (p < 0.001 by HFO rate; p < 0.01 by MIs at 3-4 Hz; p = 0.02 by MIs at 0.5-1 Hz). The presence of active spasms was predicted by the logistic regression models incorporating HFO-related metrics (AUC: 0.80-0.98) better than that incorporating hypsarrhythmia (AUC: 0.61). The predictive performance of the best model remained favorable (87.5% accuracy) after a cross-validation procedure.ConclusionsIncreased rate of HFOs and coupling between HFOs and SWA are associated with active epileptic spasms.SignificanceScalp-recorded HFOs may serve as an objective EEG biomarker for active epileptic spasms.HighlightsObjective analyses of scalp high frequency oscillations and its coupling with slow-wave activity in infantile spasms were feasible.Increased rate of high frequency oscillations and its coupling with slow-wave activity correlated with active epileptic spasms.The scalp high frequency oscillations were also detected in neurologically normal children (although at the low rate).

Enhancement of quiet sleep in rabbit neonates by muramyl dipeptide

1987 ◽  
Vol 253 (4) ◽  
pp. R646-R654 ◽  
Author(s):  
D. Davenne ◽  
J. M. Krueger
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Muramyl Dipeptide ◽  
Wave Activity ◽  
Synthetic Analogue ◽  
Active Sleep ◽  
Quiet Sleep ◽  
Delta Wave ◽  
Parallel Increase ◽  
Behavioral Criteria

Muramyl peptides that induce excess slow-wave sleep have been isolated from urine and brain. A synthetic analogue to those substances, muramyl dipeptide (MDP, N-acetylmuramyl-L-alanyl-D-isoglutamine), was found to induce prolonged increases in slow-wave sleep and to increase electroencephalographic (EEG) delta-wave activity. MDP is also pyrogenic, although this activity can be separated from its somnogenic activity. To further investigate the somnogenic actions of MDP, neonatal rabbits were used in the present study. Intraperitoneal injection of 100 micrograms/kg MDP induced differential somnogenic and pyrogenic effects; from postnatal days 7-9, MDP increased duration of quiet sleep (QS, the precursor of adult slow-wave sleep) and decreased active sleep (AS) as judged by behavioral criteria. These animals were not febrile during the period of enhanced QS, nor did MDP alter EEG delta-wave activity at this age. From postnatal days 10-15, MDP induced prolonged (6 h) increases in duration of QS; both behavioral and EEG criteria were used at this age to determine duration of QS and AS. Maximum MDP-induced effects occurred during the 2nd h, with a parallel increase in amplitudes of EEG delta-wave activity. At this age, MDP also elicited monophasic fevers and inhibition of AS, with maximum effects observed during hours 3-4 postinjection. After postnatal day 16, MDP-induced somnogenic and febrile responses were similar to those observed in adult rabbits. We conclude that the mechanisms responsible for behavioral sleep states are responsive to a sleep-promoting substance early in ontogenesis.

Continuous Spike-and-Wave Activity During Slow-Wave Sleep: Syndrome or EEG Pattern?

Epilepsia ◽  
1999 ◽  
Vol 40 (11) ◽  
pp. 1593-1601 ◽  
Author(s):  
Pierangelo Veggiotti ◽  
Francesca Beccaria ◽  
Renzo Guerrini ◽  
Giuseppe Capovilla ◽  
Giovanni Lanzi
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Wave Activity ◽  
Eeg Pattern

Ghrelin promotes slow-wave sleep in humans

2003 ◽  
Vol 284 (2) ◽  
pp. E407-E415 ◽  
Author(s):  
J. C. Weikel ◽  
A. Wichniak ◽  
M. Ising ◽  
H. Brunner ◽  
E. Friess ◽  
...  
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Wave Activity ◽  
Sleep Eeg ◽  
Endogenous Ligand ◽  
Plasma Gh ◽  
Electroencephalogram Eeg ◽  
Inverse Pattern ◽  
Ghs Receptor

Ghrelin, an endogenous ligand of the growth hormone (GH) secretagogue (GHS) receptor, stimulates GH release, appetite, and weight gain in humans and rodents. Synthetic GHSs modulate sleep electroencephalogram (EEG) and nocturnal hormone secretion. We studied the effect of 4 × 50 μg of ghrelin administered hourly as intravenous boluses between 2200 and 0100 on sleep EEG and the secretion of plasma GH, ACTH, cortisol, prolactin, and leptin in humans ( n = 7). After ghrelin administration, slow-wave sleep was increased during the total night and accumulated δ-wave activity was enhanced during the second half of the night. Rapid-eye-movement (REM) sleep was reduced during the second third of the night, whereas all other sleep EEG variables remained unchanged. Furthermore, GH and prolactin plasma levels were enhanced throughout the night, and cortisol levels increased during the first part of the night (2200–0300). The response of GH to ghrelin was most distinct after the first injection and lowest after the fourth injection. In contrast, cortisol showed an inverse pattern of response. Leptin levels did not differ between groups. Our data show a distinct action of exogenous ghrelin on sleep EEG and nocturnal hormone secretion. We suggest that ghrelin is an endogenous sleep-promoting factor. This role appears to be complementary to the already described effects of the peptide in the regulation of energy balance. Furthermore, ghrelin appears to be a common stimulus of the somatotropic and hypothalamo-pituitary-adrenocortical systems. It appears that ghrelin is a sleep-promoting factor in humans.

scholarly journals An essential role for MEF2C in the cortical response to loss of sleep

2020 ◽  
Author(s):  
Theresa E. Bjorness ◽  
Ashwinikumar Kulkarni ◽  
Volodymer Rybalchenko ◽  
Ayako Suzuki ◽  
Catherine Bridges ◽  
...  
Keyword(s):  
Gene Expression ◽  
Slow Wave ◽  
Transcriptional Activity ◽  
Slow Wave Sleep ◽  
Sleep Loss ◽  
Wave Activity ◽  
Altered Gene Expression ◽  
Mepsc Frequency ◽  
Differential Gene ◽  
Altered Gene

AbstractNeuronal activity and gene expression in response to the loss of sleep can provide a window into the enigma of sleep function. Sleep loss is associated with brain differential gene expression, an increase in pyramidal cell mEPSC frequency and amplitude, and a characteristic rebound and resolution of slow wave sleep-slow wave activity (SWS-SWA). However, the molecular mechanism(s) mediating the sleep loss response are not well understood. We show that sleep-loss regulates MEF2C phosphorylation, a key mechanism regulating MEF2C transcriptional activity, and that MEF2C function in postnatal excitatory forebrain neurons is required for the biological events in response to sleep loss. These include altered gene expression, the increase and recovery of synaptic strength, and the rebound and resolution of SWS-SWA, which implicate MEF2C as an essential regulator of sleep function.One Sentence SummaryMEF2C is critical to the response to sleep loss.

scholarly journals Epilepsy with continuous spike-waves during slow wave sleep: a clinical and electroencephalographic study

1995 ◽  
Vol 53 (2) ◽  
pp. 252-257 ◽  
Author(s):  
Délrio F. Silva ◽  
Márcia Marques Lima ◽  
Luzinete V.A.t. Gonzalez ◽  
Odyna J. Lr. Lopez ◽  
Renato Anghinah ◽  
...  
Keyword(s):  
Mental Retardation ◽  
Slow Wave ◽  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Wave Activity ◽  
Motor Deficit ◽  
Epileptic Children ◽  
Electroencephalographic Study ◽  
Nearly Continuous ◽  
Eeg Pattern

We report four children with epilepsy with "continuous spike-waves during slow wave sleep" (CSWSS). The main clinical features were partial motor seizures, mental retardation and motor deficit. The EEG findings were characterized by nearly continuous (>85%) diffuse slow spike and wave activity in two patients, and localized to one hemisphere in two other cases during non-REM sleep. The treatment was effective in improving the clinical seizures, but not the EEG pattern. We believe that this epileptic syndrome has been overlooked and routine sleep EEG studies on epileptic children may disclose more cases of CSWSS.

scholarly journals An essential role for MEF2C in the cortical response to loss of sleep in mice

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Theresa E Bjorness ◽  
Ashwinikumar Kulkarni ◽  
Volodymyr Rybalchenko ◽  
Ayako Suzuki ◽  
Catherine Bridges ◽  
...  
Keyword(s):  
Gene Expression ◽  
Slow Wave ◽  
Transcriptional Activity ◽  
Slow Wave Sleep ◽  
Sleep Loss ◽  
Wave Activity ◽  
Altered Gene Expression ◽  
Mepsc Frequency ◽  
Differential Gene ◽  
Altered Gene

Neuronal activity and gene expression in response to the loss of sleep can provide a window into the enigma of sleep function. Sleep loss is associated with brain differential gene expression, an increase in pyramidal cell mEPSC frequency and amplitude, and a characteristic rebound and resolution of slow wave sleep-slow wave activity (SWS-SWA). However, the molecular mechanism(s) mediating the sleep-loss response are not well understood. We show that sleep-loss regulates MEF2C phosphorylation, a key mechanism regulating MEF2C transcriptional activity, and that MEF2C function in postnatal excitatory forebrain neurons is required for the biological events in response to sleep loss in C57BL/6J mice. These include altered gene expression, the increase and recovery of synaptic strength, and the rebound and resolution of SWS-SWA, which implicate MEF2C as an essential regulator of sleep function.

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