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Deep sleep pills9/25/2023 The major class of drugs indicated for the treatment of insomnia is the benzodiazepine receptor agonists (BzRAs). Given this hypothesis and the extensive data supportive of the hypothesis, drugs which enhance slow wave sleep should have important functional and clinical significance. One important caveat is that all of these studies involved acute, not chronic, manipulations of sleep. Numerous studies, that have deprived sleep, extended sleep, or added daytime naps, have shown that slow wave sleep and slow wave activity increase and decrease in the predicted directions (i.e., the index increases with increasing hours of wake and decreases with increasing hours of sleep), as one would hypothesize for a sleep homeostat. Quantitative EEG methods yield several indicies of slow wave activity that prove to be more sensitive than visual scoring of slow wave sleep. This hypothesis was established and supported with many studies using both visual scoring and various quantitative EEG methods such as spectral analysis. The observation that slow wave sleep diminishes progressively across NREM-REM cycles over the night led to the hypothesis that slow wave sleep/slow wave activity is precisely controlled, reflecting the operation of a sleep homeostat ( 3). During the third and fourth NREM-REM cycles there is minimal delta wave activity and REM periods are of 20–30 min duration. The duration of each episode of NREM stage 3 and 4 decreases each cycle and the duration of each REM episode increases with each cycle. Each cycle is about 90 minutes, but the sleep stages in those cycles change across the night. NREM and REM sleep continue to cycle in this manner for 4–5 cycles per eight hours. This first episode of NREM stages 3 and 4 lasts approximately 10–30 min, depending of age, and sleep lightens to stage 2 before the initiation of the first REM episode, which occurs 90–120 min after sleep onset. As stage 2 progresses a gradual appearance of high-voltage slow wave activity occurs, eventually reaching criteria for scoring stage 3 and 4 NREM sleep. Sleep is entered through NREM stage 1, which normally lasts 1–7 min before the sleep spindles and K-complexes of NREM stage 2 appear ( 1, 2). In contrast to this aroused EEG, the EMG shows a total atonia of voluntary muscles. The EOG of REM displays bursts of rapid eye movements, for which this stage is named. The EEG of REM sleep, in dramatic contrast, reverts to the low-voltage, mixed frequency pattern seen in stage 1 NREM sleep. NREM stages 3 and 4 are merely differentiated by the quantity of slow wave activity (SWA) on a given epoch (20–50% vs >50%) and often to maintain scoring reliability are not differentiated in visual sleep scoring. When arousal threshold is highest, the EEG of NREM stage 3 and 4 sleep has 0.5 – 2 Hz waves of 75 microvolts and greater, termed slow waves. Stage 2 NREM sleep is characterized by phasic events of sleep spindles (12–14 Hz) and K-complexes (negative sharp waves of 0.5 Hz and greater) and elevated arousal thresholds relative to stage 1 NREM sleep. Relaxed wakefulness with eyes closed exhibits an alpha (8–12 Hz) EEG pattern of 20–40 microvolts, which further slows to 3–7 Hz and decreases in amplitude during drowsy, stage 1 NREM, sleep. In terms of EEG activity, NREM sleep is characterized by EEG slowing and increased voltage relative to the low voltage (10–30 microvolts) and fast frequency (16–26 Hz) of activated wakefulness. Polysomnographic (PSG) studies, which refers to the simultaneous recording of multiple electrophysiological parameters during sleep, have demonstrated that sleep is a complex, highly organized biological state composed of two distinct brain states, rapid eye movement (REM) and non rapid eye movement (NREM) sleep ( 1, 2).
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