rapid eye movement sleep rapid eye movement sleep rapid eye movement sleep (rem sleep or rems) is a unique phase of sleep in mammals and birds, characterized by random rapid movement of the eyes, accompanied by low muscle tone throughout the body, and the propensity of the sleeper to dream vividly. a sample hypnogram (electroencephalogram of sleep) showing sleep cycles characterized by increasing paradoxical (rem) sleep. eeg of a mouse that shows rem sleep being characterized by prominent theta-rhythm the rem phase is also known as paradoxical sleep (ps) and sometimes desynchronized sleep or dreamy sleep, because of physiological similarities to waking states including rapid, low-voltage desynchronized brain waves. electrical and chemical activity regulating this phase seems to originate in the brain stem, and is characterized most notably by an abundance of the neurotransmitter acetylcholine, combined with a nearly complete absence of monoamine neurotransmitters histamine, serotonin and norepinephrine. experiences of rem sleep are not transferred to permanent memory due to absence of norepinephrine. rem sleep is physiologically different from the other phases of sleep, which are collectively referred to as non-rem sleep (nrem sleep, nrems, synchronized sleep). the absence of visual and auditory stimulation (sensory deprivation) during rem sleep can cause hallucinations. rem and non-rem sleep alternate within one sleep cycle, which lasts about 90 minutes in adult humans. as sleep cycles continue, they shift towards a higher proportion of rem sleep. the transition to rem sleep brings marked physical changes, beginning with electrical bursts called "ponto-geniculo-occipital waves" (pgo waves) originating in the brain stem. rem sleep occurs 4 times in a 7 hour sleep. organisms in rem sleep suspend central homeostasis, allowing large fluctuations in respiration, thermoregulation and circulation which do not occur in any other modes of sleeping or waking. the body abruptly loses muscle tone, a state known as rem atonia. in 1953, professor nathaniel kleitman and his student eugene aserinsky defined rapid eye movement and linked it to dreams. rem sleep was further described by researchers, including william dement and michel jouvet. many experiments have involved awakening test subjects whenever they begin to enter the rem phase, thereby producing a state known as rem deprivation. subjects allowed to sleep normally again usually experience a modest rem rebound. techniques of neurosurgery, chemical injection, electroencephalography, positron emission tomography, and reports of dreamers upon waking, have all been used to study this phase of sleep. physiology electrical activity in the brain polysomnographic record of rem sleep. eeg highlighted by red box. eye movement highlighted by red line. rem sleep is called "paradoxical" because of its similarities to wakefulness. although the body is paralyzed, the brain acts as if it is somewhat awake, with cerebral neurons firing with the same overall intensity as in wakefulness. electroencephalography during rem deep sleep reveals fast, low amplitude, desynchronized neural oscillation (brainwaves) that resemble the pattern seen during wakefulness, which differ from the slow δ (delta) waves pattern of nrem deep sleep. an important element of this contrast is the 3–10 hz theta rhythm in the hippocampus and 40–60 hz gamma waves in the cortex; patterns of eeg activity similar to these rhythms are also observed during wakefulness. the cortical and thalamic neurons in the waking and rem sleeping brain are more depolarized (fire more readily) than in the nrem deep sleeping brain. human theta wave activity predominates during rem sleep in both the hippocampus and the cortex. during rem sleep, electrical connectivity among different parts of the brain manifests differently than during wakefulness. frontal and posterior areas are less coherent in most frequencies, a fact which has been cited in relation to the chaotic experience of dreaming. however, the posterior areas are more coherent with each other; as are the right and left hemispheres of the brain, especially during lucid dreams. brain energy use in rem sleep, as measured by oxygen and glucose metabolism, equals or exceeds energy use in waking. the rate in non-rem sleep is 11–40% lower. brain stem neural activity during rem sleep seems to originate in the brain stem, especially the pontine tegmentum and locus coeruleus. rem sleep is punctuated and immediately preceded by pgo (ponto-geniculo-occipital) waves, bursts of electrical activity originating in the brain stem. (pgo waves have long been measured directly in cats but not in humans because of constraints on experimentation; however, comparable effects have been observed in humans during "phasic" events which occur during rem sleep, and the existence of similar pgo waves is thus inferred.) these waves occur in clusters about every 6 seconds for 1–2 minutes during the transition from deep to paradoxical sleep. they exhibit their highest amplitude upon moving into the visual cortex and are a cause of the "rapid eye movements" in paradoxical sleep. other muscles may also contract under the influence of these waves. forebrain research in the 1990s using positron emission tomography (pet) confirmed the role of the brain stem and suggested that, within the forebrain, the limbic and paralimbic systems showed more activation than other areas. the areas activated during rem sleep are approximately inverse to those activated during non-rem sleep and display greater activity than in quiet waking. the "anterior paralimbic rem activation area" (apra) includes areas linked with emotion, memory, fear and sex, and may thus relate to the experience of dreaming during rems. more recent pet research has indicated that the distribution of brain activity during rem sleep varies in correspondence with the type of activity seen in the prior period of wakefulness. the superior frontal gyrus, medial frontal areas, intraparietal sulcus, and superior parietal cortex, areas involved in sophisticated mental activity, show equal activity in rem sleep as in wakefulness. the amygdala is also active during rem sleep and may participate in generating the pgo waves, and experimental suppression of the amygdala results in less rem sleep. the amygdala may also regulate cardiac function in lieu of the less active insular cortex. chemicals in the brain compared to slow-wave sleep, both waking and paradoxical sleep involve higher use of the neurotransmitter acetylcholine, which may cause the faster brainwaves. the monoamine neurotransmitters norepinephrine, serotonin and histamine are completely unavailable. injections of acetylcholinesterase inhibitor, which effectively increases available acetylcholine, have been found to induce paradoxical sleep in humans and other animals already in slow-wave sleep. carbachol, which mimics the effect of acetylcholine on neurons, has a similar influence. in waking humans, the same injections produce paradoxical sleep only if the monoamine neurotransmitters have already been depleted. two other neurotransmitters, orexin and gamma-aminobutyric acid (gaba), seem to promote wakefulness, diminish during deep sleep, and inhibit paradoxical sleep. unlike the abrupt transitions in electrical patterns, the chemical changes in the brain show continuous periodic oscillation. models of rem regulation according to the activation-synthesis hypothesis proposed by robert mccarley and allan hobson in 1975–1977, control over rem sleep involves pathways of "rem-on" and "rem-off" neurons in the brain stem. rem-on neurons are primarily cholinergic (i.e., involve acetylcholine); rem-off neurons activate serotonin and noradrenaline, which among other functions suppress the rem-on neurons. mccarley and hobson suggested that the rem-on neurons actually stimulate rem-off neurons, thereby serving as the mechanism for the cycling between rem and non-rem sleep. they used lotka–volterra equations to describe this cyclical inverse relationship. kayuza sakai and michel jouvet advanced a similar model in 1981. whereas acetylcholine manifests in the cortex equally during wakefulness and rem, it appears in higher concentrations in the brain stem during rem. the withdrawal of orexin and gaba may cause the absence of the other excitatory neurotransmitters; researchers in recent years increasingly include gaba regulation in their models. eye movements most of the eye movements in "rapid eye movement" sleep are in fact less rapid than those normally exhibited by waking humans. they are also shorter in duration and more likely to loop back to their starting point. about seven such loops take place over one minute of rem sleep. in slow-wave sleep, the eyes can drift apart; however, the eyes of the paradoxical sleeper move in tandem. these eye movements follow the ponto-geniculo-occipital waves originating in the brain stem. the eye movements themselves may relate to the sense of vision experienced in the dream, but a direct relationship remains to be clearly established. congenitally blind people, who do not typically have visual imagery in their dreams, still move their eyes in rem sleep. an alternative explanation suggests that the functional purpose of rem sleep is for procedural memory processing, and the rapid eye movement is only a side effect of the brain processing the eye-related procedural memory. circulation, respiration, and thermoregulation generally speaking, the body suspends homeostasis during paradoxical sleep. heart rate, cardiac pressure, cardiac output, arterial pressure, and breathing rate quickly become irregular when the body moves into rem sleep. in general, respiratory reflexes such as response to hypoxia diminish. overall, the brain exerts less control over breathing; electrical stimulation of respiration-linked brain areas does not influence the lungs, as it does during non-rem sleep and in waking. the fluctuations of heart rate and arterial pressure tend to coincide with pgo waves and rapid eye movements, twitches, or sudden changes in breathing. erections of the penis (nocturnal penile tumescence or npt) normally accompany rem sleep in rats and humans. if a male has erectile dysfunction (ed) while awake, but has npt episodes during rem, it would suggest that the ed is from a psychological rather than a physiological cause. in females, erection of the clitoris (nocturnal clitoral tumescence or nct) causes enlargement, with accompanying vaginal blood flow and transudation (i.e. lubrication). during a normal night of sleep, the penis and clitoris may be erect for a total time of from one hour to as long as three and a half hours during rem. body temperature is not well regulated during rem sleep, and thus organisms become more sensitive to temperatures outside their thermoneutral zone. cats and other small furry mammals will shiver and breathe faster to regulate temperature during nrems—but not during rems. with the loss of muscle tone, animals lose the ability to regulate temperature through body movement. (however, even cats with pontine lesions preventing muscle atonia during rem did not regulate their temperature by shivering.) neurons which typically activate in response to cold temperatures—triggers for neural thermoregulation—simply do not fire during rem sleep, as they do in nrem sleep and waking. consequently, hot or cold environmental temperatures can reduce the proportion of rem sleep, as well as amount of total sleep. in other words, if at the end of a phase of deep sleep, the organism's thermal indicators fall outside of a certain range, it will not enter paradoxical sleep lest deregulation allow temperature to drift further from the desirable value. this mechanism can be 'fooled' by artificially warming the brain. muscle rem atonia, an almost complete paralysis of the body, is accomplished through the inhibition of motor neurons. when the body shifts into rem sleep, motor neurons throughout the body undergo a process called hyperpolarization: their already-negative membrane potential decreases by another 2–10 millivolts, thereby raising the threshold which a stimulus must overcome to excite them. muscle inhibition may result from unavailability of monoamine neurotransmitters (restraining the abundance of acetylcholine in the brainstem) and perhaps from mechanisms used in waking muscle inhibition. the medulla oblongata, located between pons and spine, seems to have the capacity for organism-wide muscle inhibition. some localized twitching and reflexes can still occur. pupils contract. lack of rem atonia causes rem behavior disorder, those affected physically act out their dreams, or conversely "dream out their acts", under an alternative theory on the relationship between muscle impulses during rem and associated mental imagery (which would also apply to people without the condition, except that commands to their muscles are suppressed). this is different from conventional sleepwalking, which takes place during slow-wave sleep, not rem. narcolepsy, by contrast, seems to involve excessive and unwanted rem atonia: cataplexy and excessive daytime sleepiness while awake, hypnagogic hallucinations before entering slow-wave sleep, or sleep paralysis while waking. other psychiatric disorders including depression have been linked to disproportionate rem sleep. patients with suspected sleep disorders are typically evaluated by polysomnogram. lesions of the pons to prevent atonia have induced functional "rem behavior disorder" in animals. psychology dreaming rapid eye movement sleep (rem) has since its discovery been closely associated with dreaming. waking up sleepers during a