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Results Five children with DM (33%) had profound nocturnal hypoglycemia, which was associated with increased sleep efficiency, increased slow wave sleep, and increased Δ power in spectral analysis of the electroencephalogram. Hypoglycemic episodes were not associated with sympathetic activation.
The SM patients had increased awakenings and the NSM patients had increased slow wave sleep and less fast arousals.
Statistical analyses, performed using Comprehensive Meta-Analysis software, revealed that chronic TBI is characterized by relatively increased slow wave sleep (SWS).
Polysomnographic analysis of TASK-3 mutants reveals increases in nocturnal active wake and suppressed REM sleep time while increased slow wave sleep typifies the inactive phase, findings that have implications for the cognitive impact of reduced TASK-3 activity.
Hughes et al. [7] noticed that both EEG and QEEG reveal marked abnormalities in alcoholic subjects, which might result in increased slow activity or the converse, while Waite et al. [8] using QEEG techniques confirmed that slow waves dominated the brain of alcoholics.
TRN stimulation increased slow wave power during natural NREM sleep.
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Females demonstrated a trend toward increased slow-wave sleep (SWS) which continued throughout most of their lives.
Therefore, the intensity of the E 1 emission increased slower than that of the E 0 emission.
In contrast to narcolepsy patients, idiopathic hypersomnia patients were likely to have increased slow-wave sleep [23].
In the experiment, ΔΦ increased slower and then even began to decay again while the light was still on.
SXB increased slow-wave sleep (SWS) and reduced sleep fragmentation in patients with narcolepsy [ 27, 28].
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