REM sleep is characterized by: Rapid and random movement of the eyes, dreaming often with vivid dreams, low muscle tone, and a rapid, low-voltage EEG. REM sleep in adult humans typically occupies 20–25 % of total sleep or about 90–120 min of a night’s sleep. In a normal night, REM sleep does not begin during the first hour of sleep and is of shortest duration early in sleep with longer duration toward morning.

The neurophysiology of sleep is complex and is considered here only in brief overview. Key brain anatomy for generating REM sleep is in the pontine tegmentum and adjacent portions of the midbrain. Destruction of these areas prevents REM sleep. These brain areas and the hypothalamus contain REM-on neurons that are maximally active during REM sleep and REM-off neurons which are minimally active during REM sleep. During REM sleep; REM-off neurons stop firing and thus fail to stimulate motor neurons, which in turn causes REM muscle atonia. As such, limb and face muscles do not move but the diaphragm functions normally. In addition to muscle atonia , the heart rate and respiratory rate become irregular similar to behavior during the waking hours. In addition, the body temperature is poorly regulated and falls toward environmental temperature. Erections of the penis occur called nocturnal penile tumescence.

NREM sleep is generated by neurons in the preoptic region of the hypothalamus and adjacent basal forebrain. Stimulation of these regions produce sleep onset and in contrast lesions in the same area produce insomnia.

Neurons in the posterior hypothalamus are important in maintaining the waking state. These neurons are tonically active during wakefulness, greatly reduce their discharging in NREM sleep, and are almost silent in REM sleep. Neurons that fire in a similar profile are also present in the locus coeruleus, raphe nuclei, and hypocretin containing neurons of the hypothalamus.

Our body maintains many daily rhythms involving physiological and behavioral processes that are controlled by a network of circadian clocks linking the brain and peripheral organs. Fundamental circadian rhythms have several components: Photoreceptors and visual pathways that transduce photic entraining information, pacemakers that generate a circadian signal, and output pathways that couple the pacemaker to effector systems.

The master clock in our body is located in the suprachiasmatic nuclei (SCN) of the hypothalamus. The SCN clock is autonomous and spontaneously cycles about every 24 h. However, it receives exogenous input to modify it to follow environmental time whose daylight changes by season as well as other factors such as mealtime, locomotor activity, and chronobiotic drugs. However, the most efficient synchronizer is the daily light–dark cycle. Specific wavelengths of blue light (roughly 460–480 nm) are detected by a newly discovered photopigment, melanopsin, which is present in a small percentage (1–2 %) of the retinal ganglion cells. The axons of the melanopsin-containing retinal ganglion cells project directly to the suprachiasmatic nuclei (SCN) via the retinohypothalamic tract in the optic nerve so the visual cortex is not involved.

Critical to afferent control of circadian rhythms of other tissues is the pineal gland. This gland is an unpaired neuroendocrine organ situated in the midline of the brain. Its primary function is to transduce light and dark information to the whole body physiology via release of the hormone melatonin. The light–dark cycle of the pineal gland is under the control of the SCN via a multisynaptic pathway that eventually terminates on pinealocytes. Amazingly, this pathway travels down to the thoracic sympathetic neurons in the intermediolateral cell column. The signal then exits the spinal cord and travels back up external sympathetic nerves to innervate the pineal gland. Release of norepinephrine via this pathway onto pinealocytes, which occurs during the night, stimulates the synthesis of melatonin. Melatonin is then rapidly discharged into the blood vascular system and possibly also into the cerebrospinal fluid of the third ventricle and acts on cells in many organs including SCN neurons that contain melatonin receptors MT1 and MT2. Thus, the pineal gland releases melatonin only at night and not in daylight.

Many parts of the brain and systemic organs also have circadian oscillators that are under the control of multisynaptic SCN axons and melatonin. Examples of circadian rhythms are body temperature, potassium excretion, and several pituitary hormones (prolactin, growth hormone, thyroxin, and adrenal corticosteroid secretion).

During wakefulness, neuronal activity from the brainstem ascending reticular activating system sends signals to the thalamus and onto the cerebral cortex. This input results in nonrhythmic cortical activity, stimulating behavioral arousal that is stimulus dependent, and producing a desynchronized EEG with tracings appearing almost random.

The onset of sleep is produced by GABA-ergic neurons located in the basal forebrain, anterior hypothalamus, and medulla that inhibit the ascending reticular activating system and suppress the thalamocortical activity. Hypocretin (or orexin) neurons located in the lateral hypothalamus are important in regulating sleep and wakefulness. Hypocretin neurons project widely to ascending reticular activating system neurons as well as other parts of the CNS. The normal hypocretin system inhibits REM sleep, promotes wakefulness, and stimulates feeding and motor activity.

In summary, normal sleep wake cycles are governed by SCN output and melatonin from the pineal gland producing the sleep circadian rhythm. However, the sleep circadian rhythm can be temporarily influenced by the duration of prior wakefulness. The longer a person is awake, the greater the tendency to sleep. Aging also affects sleep patterns. Babies and children have longer normal sleep times (8–10 h ) while older adults tend to sleep less (often 6 h a night) and normally have 3–6 transient nocturnal periods of wakefulness.