Neurophysiology of sleep and wakefulness

Arousals from sleep
Although the mechanisms of sleep–wake control tend to promote either the state of sleep or the state of wakefulness, neither of these conditions is stable. The level of alertness fluctuates constantly, mainly due to factors affecting the adaptive drive. There may also be an ultradian tendency to enter REM sleep during the day, leading to, for instance, a predisposition to daydream during wakefulness. During sleep, arousal mechanisms are continually active and may lead the subject to awaken in response to any stimulus, especially in stages 1 and 2 NREM sleep and in the elderly [28]. Arousals are heterogeneous, and while many are endogenous, some are triggered, or at least facilitated, by external stimuli.

The tendency towards arousal is a normal feature of sleep and is usually reversible in that a deeper level of sleep is then re-entered. Arousals are more frequent in infants and adults than in young children, and are most common in the elderly, particularly arousals from NREM sleep. They are also more frequent at times when NREM sleep is lightening rather than becoming deeper.

In NREM sleep there is a regular periodicity when arousals are most likely to occur. This is known as the cyclic alternating pattern (CAP) [29]. Arousals occur at intervals of 10–60s, usually 20–40s. The neurological basis for this may be an instability in the thalamocortical synchronization, or the failure of this mechanism to filter or suppress impulses reaching the thalamus. The K-complexes and spindles that are seen in arousals are attempts to re-establish NREM sleep.

Although the CAP is not detectable in REM sleep some of the aspects of phasic activity characteristic of this state may be analogous to it.

Stimuli that may lead to arousals from sleep do so more frequently if they are combined, such as an increase in noise and simultaneous physical stimulation, and when they coincide with the moment of arousal within the CAP [30]. This probably applies to conditions as diverse as arousal disorders from stages 3 and 4 NREM sleep, such as sleep walking, arousals from obstructive sleep apnoeas, bruxism, and periodic limb movements. Interictal spikes and epileptic seizures both occur particularly at the time of CAP arousals. The failure to arouse appropriately probably contributes to nocturnal enuresis, and possibly to the sudden infant death syndrome (SIDS).

The arousals may be manifested only by autonomic responses such as an increase in heart rate or blood pressure, but other features of brainstem activity may be seen, such as an increase in respiratory rate or depth, and gross body or limb movements. Subcortical arousals due to activation of aminergic and other brainstem nuclei increase the activity in the ascending reticular activating system but do not cause any electroencephalogram changes. They may or may not lead to a cortical arousal. These can be detected by an abrupt increase in the frequency of the electroencephalogram, alpha waves, high-voltage delta bursts or the appearance of K-complexes and spindles in NREM sleep. In REM sleep cortical arousal may be detected by the reappearance of muscle tone. Arousals, by definition, are transient and are followed by restoration of sleep.


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