Question:

What can happen over a long period of time if you don't get enough sleep?

Answer:

Research shows, if you do not get enough sleep on a nightly basis, it can affect your decision making skills, cause stress and you will be over all cranky. Also, sleep deprivation affects how well the body fights infections.

More Info:

Sleep apnea (or sleep apnoea in British English; ) is a type of sleep disorder characterized by pauses in breathing or instances of shallow or infrequent breathing during sleep. Each pause in breathing, called an apnea, can last from at least ten seconds to minutes, and may occur 5 to 30 times or more an hour. Similarly, each abnormally shallow breathing event is called a hypopnea. Sleep apnea is often diagnosed with an overnight sleep test called a polysomnogram, or "sleep study". There are three forms of sleep apnea: central (CSA), obstructive (OSA), and complex or mixed sleep apnea (i.e., a combination of central and obstructive) constituting 0.4%, 84% and 15% of cases respectively. In CSA, breathing is interrupted by a lack of respiratory effort; in OSA, breathing is interrupted by a physical block to airflow despite respiratory effort, and snoring is common. Regardless of type, an individual with sleep apnea is rarely aware of having difficulty breathing, even upon awakening. Sleep apnea is recognized as a problem by others witnessing the individual during episodes or is suspected because of its effects on the body (sequelae). Symptoms may be present for years (or even decades) without identification, during which time the sufferer may become conditioned to the daytime sleepiness and fatigue associated with significant levels of sleep disturbance. Sleep apnea affects not only adults but some children as well. As stated by El-Ad, "patients complain about excessive daytime sleepiness (EDS) and impaired alertness". In other words, common effects of sleep apnea include daytime fatigue, a slower reaction time, and vision problems. Moreover, patients are examined using “standard test batteries” in order to further identify parts of the brain that are affected by sleep apnea. Tests have shown that certain parts of the brain cause different effects. The “executive functioning” part of the brain affects the way the patient plans and initiates tasks. Second, the part of the brain that deals with attention causes difficulty in paying attention, working effectively and processing information when in a waking state. Thirdly, the part of the brain that uses memory and learning is also affected. Due to the disruption in daytime cognitive state, behavioral effects are also present. This includes moodiness, belligerence, as well as a decrease in attentiveness and drive. Another symptom of sleep apnea is waking up in sleep paralysis. In severe cases, the fear of sleep due to sleep paralysis can lead to insomnia. These effects become very hard to deal with, thus the development of depression may transpire. There is also increasing evidence that sleep apnea may also lead to liver function impairment, particularly fatty liver diseases (see steatosis). Finally, because there are many factors that could lead to some of the effects previously listed, some patients are not aware that they suffer from sleep apnea and are either misdiagnosed, or just ignore the symptoms altogether. The diagnosis of sleep apnea is based on the conjoint evaluation of clinical symptoms (e.g. excessive daytime sleepiness and fatigue) and of the results of a formal sleep study (polysomnography, or reduced channels home based test). The latter aims at establishing an "objective" diagnosis indicator linked to the quantity of apneic events per hour of sleep (Apnea Hypopnea Index(AHI), or Respiratory Disturbance Index (RDI)), associated to a formal threshold, above which a patient is considered as suffering from sleep apnea, and the severity of their sleep apnea can then be quantified. Mild OSA (Obstructive Sleep Apneas) ranges from 5 to 14.9 events per hour of sleep, moderate OSA falls in the range of 15–29.9 events per hour of sleep, and severe OSA would be a patient having over 30 events per hour of sleep. Nevertheless, due to the number and variability in the actual symptoms and nature of apneic events (e.g., hypopnea vs apnea, central vs obstructive), the variability of patients' physiologies, and the intrinsic imperfections of the experimental setups and methods, this field is opened to debate. Within this context, the definition of an apneic event depends on several factors (e.g. patient's age) and account for this variability through a multi-criteria decision rule described in several, sometimes conflicting, guidelines. One example of a commonly adopted definition of an apnea (for an adult) includes a minimum 10 second interval between breaths, with either a neurological arousal (a 3-second or greater shift in EEG frequency, measured at C3, C4, O1, or O2) or a blood oxygen desaturation of 3–4% or greater, or both arousal and desaturation. Oximetry, which may be performed overnight in a patient's home, is an easier alternative to formal sleep study (polysomnography). In one study, normal overnight oximetry was very sensitive and so if normal, sleep apnea was unlikely. In addition, home oximetry may be equally effective in guiding prescription for automatically self-adjusting continuous positive airway pressure. Obstructive sleep apnea (OSA) is the most common category of sleep-disordered breathing. The muscle tone of the body ordinarily relaxes during sleep, and at the level of the throat the human airway is composed of collapsible walls of soft tissue which can obstruct breathing during sleep. Mild occasional sleep apnea, such as many people experience during an upper respiratory infection, may not be important, but chronic severe obstructive sleep apnea requires treatment to prevent low blood oxygen (hypoxemia), sleep deprivation, and other complications. Individuals with low muscle tone and soft tissue around the airway (e.g., because of obesity) and structural features that give rise to a narrowed airway are at high risk for obstructive sleep apnea. The elderly are more likely to have OSA than young people. Men are more likely to suffer sleep apnea than women and children are, though it is not uncommon in the last two population groups. The risk of OSA rises with increasing body weight, active smoking and age. In addition, patients with diabetes or "borderline" diabetes have up to three times the risk of having OSA. Common symptoms include loud snoring, restless sleep, and sleepiness during the daytime. Diagnostic tests include home oximetry or polysomnography in a sleep clinic. Some treatments involve lifestyle changes, such as avoiding alcohol or muscle relaxants, losing weight, and quitting smoking. Many people benefit from sleeping at a 30-degree elevation of the upper body or higher, as if in a recliner. Doing so helps prevent the gravitational collapse of the airway. Lateral positions (sleeping on a side), as opposed to supine positions (sleeping on the back), are also recommended as a treatment for sleep apnea, largely because the gravitational component is smaller in the lateral position. Some people benefit from various kinds of oral appliances to keep the airway open during sleep. Continuous positive airway pressure (CPAP) is the most effective treatment for severe obstructive sleep apnea but oral appliances are considered a first line approach equal to CPAP for mild to moderate sleep apnea according to the AASM parameters of care. There are also surgical procedures to remove and tighten tissue and widen the airway. Snoring is a common finding in people with this syndrome. Snoring is the turbulent sound of air moving through the back of the mouth, nose, and throat. Although not everyone who snores is experiencing difficulty breathing, snoring in combination with other conditions such as overweight and obesity has been found to be highly predictive of OSA risk. The loudness of the snoring is not indicative of the severity of obstruction, however. If the upper airways are tremendously obstructed, there may not be enough air movement to make much sound. Even the loudest snoring does not mean that an individual has sleep apnea syndrome. The sign that is most suggestive of sleep apneas occurs when snoring stops. Other indicators include (but are not limited to): hypersomnolence, obesity BMI >30, large neck circumference (16 in (410 mm) in women, 17 in (430 mm) in men), enlarged tonsils and large tongue volume, micrognathia, morning headaches, irritability/mood-swings/depression, learning and/or memory difficulties, and sexual dysfunction. The term "sleep-disordered breathing" is commonly used in the U.S. to describe the full range of breathing problems during sleep in which not enough air reaches the lungs (hypopnea and apnea). Sleep-disordered breathing is associated with an increased risk of cardiovascular disease, stroke, high blood pressure, arrhythmias, diabetes, and sleep deprived driving accidents. When high blood pressure is caused by OSA, it is distinctive in that, unlike most cases of high blood pressure (so-called essential hypertension), the readings do not drop significantly when the individual is sleeping. Stroke is associated with obstructive sleep apnea. It has been revealed that people with OSA show tissue loss in brain regions that help store memory, thus linking OSA with memory loss. Using magnetic resonance imaging (MRI), the scientists discovered that sleep apnea patients' mammillary bodies were nearly 20 percent smaller, particularly on the left side. One of the key investigators hypothesized that repeated drops in oxygen lead to the brain injury. In pure central sleep apnea or Cheyne–Stokes respiration, the brain's respiratory control centers are imbalanced during sleep. Blood levels of carbon dioxide, and the neurological feedback mechanism that monitors them, do not react quickly enough to maintain an even respiratory rate, with the entire system cycling between apnea and hyperpnea, even during wakefulness. The sleeper stops breathing and then starts again. There is no effort made to breathe during the pause in breathing: there are no chest movements and no struggling. After the episode of apnea, breathing may be faster (hyperpnea) for a period of time, a compensatory mechanism to blow off retained waste gases and absorb more oxygen. While sleeping, a normal individual is "at rest" as far as cardiovascular workload is concerned. Breathing is regular in a healthy person during sleep, and oxygen levels and carbon dioxide levels in the bloodstream stay fairly constant. The respiratory drive is so strong that even conscious efforts to hold one's breath do not overcome it. Any sudden drop in oxygen or excess of carbon dioxide (even if tiny) strongly stimulates the brain's respiratory centers to breathe. In central sleep apnea, the basic neurological controls for breathing rate malfunction and fail to give the signal to inhale, causing the individual to miss one or more cycles of breathing. If the pause in breathing is long enough, the percentage of oxygen in the circulation will drop to a lower than normal level (hypoxaemia) and the concentration of carbon dioxide will build to a higher than normal level (hypercapnia). In turn, these conditions of hypoxia and hypercapnia will trigger additional effects on the body. Brain cells need constant oxygen to live, and if the level of blood oxygen goes low enough for long enough, the consequences of brain damage and even death will occur. Fortunately, central sleep apnea is more often a chronic condition that causes much milder effects than sudden death. The exact effects of the condition will depend on how severe the apnea is and on the individual characteristics of the person having the apnea. Several examples are discussed below, and more about the nature of the condition is presented in the section on Clinical Details. In any person, hypoxia and hypercapnia have certain common effects on the body. The heart rate will increase, unless there are such severe co-existing problems with the heart muscle itself or the autonomic nervous system that makes this compensatory increase impossible. The more translucent areas of the body will show a bluish or dusky cast from cyanosis, which is the change in hue that occurs owing to lack of oxygen in the blood ("turning blue"). Overdoses of drugs that are respiratory depressants (such as heroin, and other opiates) kill by damping the activity of the brain's respiratory control centers. In central sleep apnea, the effects of sleep alone can remove the brain's mandate for the body to breathe. Some people with sleep apnea have a combination of both types. When obstructive sleep apnea syndrome is severe and longstanding, episodes of central apnea sometimes develop. The exact mechanism of the loss of central respiratory drive during sleep in OSA is unknown but is most commonly related to acid–base and CO2 feedback malfunctions stemming from heart failure. There is a constellation of diseases and symptoms relating to body mass, cardiovascular, respiratory, and occasionally, neurological dysfunction that have a synergistic effect in sleep-disordered breathing. In some cases, a side effect from the lack of sleep is a mild case of Excessive Daytime Sleepiness (EDS) where the subject has had minimal sleep and this extreme fatigue over time takes its toll on the subject. The presence of central sleep apnea without an obstructive component is a common result of chronic opiate use (or abuse) owing to the characteristic respiratory depression caused by large doses of narcotics. Complex sleep apnea has recently been described by researchers as a novel presentation of sleep apnea.] [ Patients with complex sleep apnea exhibit OSA, but upon application of positive airway pressure the patient exhibits persistent central sleep apnea. This central apnea is most commonly noted while on CPAP therapy after the obstructive component has been eliminated. This has long been seen in sleep laboratories and has historically been managed either by CPAP or BiLevel therapy. Adaptive servo-ventilation (ASV) modes of therapy have been introduced to attempt to manage this complex sleep apnea. Studies have demonstrated marginally superior performance of the adaptive servo ventilators in treating Cheyne–Stokes breathing; however, no longitudinal studies have yet been published, nor have any results been generated that suggest any differential outcomes versus standard CPAP therapy. At the AARC 2006 in Las Vegas, NV, researchers reported successful treatment of hundreds of patients on ASV therapy; however, these results have not been reported in peer-reviewed publications as of July 2007[update]. It is suggested that transient central apnea produced during CPAP titration (the so-called "complex sleep apnea") is "…transient and self-limited." The central apneas may in fact be secondary to sleep fragmentation during the titration process. As of July 2007[update], there has been no alternate convincing evidence produced that these central sleep apnea events associated with CPAP therapy for obstructive sleep apnea are of any significant pathophysiologic importance.][ It has been proposed to add dead space to positive airway pressure for treatment of complex sleep-disordered breathing. Treatment often starts with behavioral therapy. Many patients are told to avoid alcohol, sleeping pills, and other sedatives, which can relax throat muscles, contributing to the collapse of the airway at night. Possibly owing to changes in pulmonary oxygen stores, sleeping on one's side (as opposed to on one's back) has been found to be helpful for central sleep apnea with Cheyne–Stokes respiration. Medications like acetazolamide lower blood pH and encourage respiration. Low doses of oxygen are also used as a treatment for hypoxia but are discouraged due to side effects. General dentists can fabricate an oral appliance. The oral appliance, called a mandibular advancement splint, is a custom-made mouthpiece that shifts the lower jaw forward and opens the bite slightly, which opens up the airway. Oral appliance therapy (OAT) is usually successful in patients with mild to moderate obstructive sleep apnea. OAT is a relatively new treatment option for sleep apnea in the United States, but it is much more common in Canada and Europe. For moderate to severe sleep apnea, the most common treatment is the use of a continuous positive airway pressure (CPAP) or automatic positive airway pressure (APAP) device, which 'splints' the patient's airway open during sleep by means of a flow of pressurized air into the throat. The patient typically wears a plastic facial mask, which is connected by a flexible tube to a small bedside CPAP machine. The CPAP machine generates the required air pressure to keep the patient's airways open during sleep. Advanced models may warm or humidify the air and monitor the patient's breathing to ensure proper treatment. Although CPAP therapy is extremely effective in reducing apneas and less expensive than other treatments, some patients find it extremely uncomfortable. Many patients refuse to continue the therapy or fail to use their CPAP machines on a nightly basis, especially in the long term. One way to ensure CPAP therapy remains comfortable and effective for patients is to carefully consider the right CPAP face mask to be used. CPAP masks come in different shapes, sizes and materials to ensure effective treatment for obstructive sleep apnea. It is important to select the right mask to fit each patient. It is not clear that CPAP reduces hypertension or cardiovascular events in patients who do not have daytime sleepiness; however, the lack of benefit may be partly due to noncompliance with therapy. Several surgical procedures (sleep surgery) are used to treat sleep apnea, although they are normally a second line of treatment for those who reject CPAP treatment or are not helped by it. Surgical treatment for obstructive sleep apnea needs to be individualized in order to address all anatomical areas of obstruction. Often, correction of the nasal passages needs to be performed in addition to correction of the oropharynx passage. Septoplasty and turbinate surgery may improve the nasal airway. Tonsillectomy and uvulopalatopharyngoplasty (UPPP or UP3) are available to address pharyngeal obstruction. Base-of-tongue advancement by means of advancing the genial tubercle of the mandible may help with the lower pharynx. Many other treatments are available, including hyoid bone myotomy and suspension and various radiofrequency Other surgery options may attempt to shrink or stiffen excess tissue in the mouth or throat; procedures done at either a doctor's office or a hospital. Small shots or other treatments, sometimes in a series, are used for shrinkage, while the insertion of a small piece of stiff plastic is used in the case of surgery whose goal is to stiffen tissues. The Pillar Procedure is a minimally invasive treatment for snoring and obstructive sleep apnea. This procedure was FDA indicated in 2004. During this procedure, three to six or more Dacron (the material used in permanent sutures) strips are inserted into the soft palate, using a modified syringe and local anesthetic. While the procedure was initially approved for the insertion of three "pillars" into the soft palate, it was found that there was a significant dosage response to more pillars, with appropriate candidates. After this brief and virtually painless outpatient operation, which usually lasts no more than 30 minutes, the soft palate is more rigid and snoring and sleep apnea can be reduced. This procedure addresses one of the most common causes of snoring and sleep apnea — vibration or collapse of the soft palate (the soft part of the roof of the mouth). If there are other factors contributing to snoring or sleep apnea, such as the nasal airway or an enlarged tongue, it will likely need to be combined with other treatments to be more effective. The Stanford Center for Excellence in Sleep Disorders Medicine achieved a 95% cure rate of sleep apnea patients by surgery. Maxillomandibular advancement (MMA) is considered the most effective surgery for sleep apnea patients, because it increases the posterior airway space (PAS). The main benefit of the operation is that the oxygen saturation in the arterial blood increases. In a study published in 2008, 93.3.% of surgery patients achieved an adequate quality of life based on the Functional Outcomes of Sleep Questionnaire (FOSQ). Surgery led to a significant increase in general productivity, social outcome, activity level, vigilance, intimacy, and intercourse. Overall risks of MMA surgery are low: The Stanford University Sleep Disorders Center found 4 failures in a series of 177 patients, or about one out of 44 patients. However, health professionals are often unsure as to who should be referred for surgery and when to do so: some factors in referral may include failed use of CPAP or device use; anatomy which favors rather than impeding surgery; or significant craniofacial abnormalities which hinder device use. Maxillomandibular advancement surgery is often combined with Genioglossus Advancement, as both are skeletal surgeries for sleep apnea. Several inpatient and outpatient procedures use sedation. Many drugs and agents used during surgery to relieve pain and to depress consciousness remain in the body at low amounts for hours or even days afterwards. In an individual with either central, obstructive or mixed sleep apnea, these low doses may be enough to cause life-threatening irregularities in breathing or collapses in a patient’s airways. Use of analgesics and sedatives in these patients postoperatively should therefore be minimized or avoided. Surgery on the mouth and throat, as well as dental surgery and procedures, can result in postoperative swelling of the lining of the mouth and other areas that affect the airway. Even when the surgical procedure is designed to improve the airway, such as tonsillectomy and adenoidectomy or tongue reduction, swelling may negate some of the effects in the immediate postoperative period. Once the swelling resolves and the palate becomes tightened by postoperative scarring, however, the full benefit of the surgery may be noticed. A sleep apnea patient undergoing any medical treatment must make sure his or her doctor and anesthetist are informed about the sleep apnea. Alternative and emergency procedures may be necessary to maintain the airway of sleep apnea patients. If an individual suspects he or she may have sleep apnea, communication with their doctor about possible preprocedure screening may be in order. Other studies have also suggested that strengthening the muscles around the upper airway may combat sleep apnea. A 2001 study investigated changes after Tongue Muscle Training (ZMT®) in respiratory parameters during night-time sleep of patients with increased respiratory disease index. 40 sleep apnea patients, which up to this time had been treated with nCPAP, underwent electrostimulation of the suprahyoidal musculature for 5 weeks with a special EMS-device. The apnea, hypopnea and desaturation indexes were reduced in 26 of the 40 patients (65%) by an average of approximately one half. A 2005 study in the British Medical Journal found that learning and practicing the didgeridoo helped reduce snoring and sleep apnea as well as daytime sleepiness. This appears to work by strengthening muscles in the upper airway, thus reducing their tendency to collapse during sleep. A 2009 study published in the American Journal of Respiratory and Clinical Care Medicine found that patients who practiced a series of tongue and throat exercises for 30 minutes a day showed a marked decline in sleep apnea symptoms after three months. Patients experienced an average of 39% fewer apnea episodes after successfully completing the treatments. Cannabis derivatives have also been studied in the treatment of sleep apnea. A 2002 study found that orally administered THC was able to stabilize respiration in rats and bulldogs during all sleep stages, decreasing apnea indexes during NREM and REM sleep stages by 42% and 58% respectively. A 2013 proof of concept trial found that dronabinol (synthetic THC) was able to reduce apnea indexes by 32% on average in the 17 human subjects that were studied. Lead study author Dr. David Carley subsequently received a $5 million grant from the National Institutes of Health (NIH) to conduct a Phase II clinical trial.][ The Wisconsin Sleep Cohort Study estimated in 1993 that roughly one in every 15 Americans were affected by at least moderate sleep apnea. It also estimated that in middle-age as many as nine percent of women and 24 percent of men were affected, undiagnosed and untreated. The costs of untreated sleep apnea reach further than just health issues. It is estimated that in the U.S. the average untreated sleep apnea patient's annual health care costs $1,336 more than an individual without sleep apnea. This may cause $3.4 billion/year in additional medical costs. Whether medical cost savings occur with treatment of sleep apnea remains to be determined. A 2012 study has shown that hypoxia (an inadequate supply of oxygen) that characterizes sleep apnea promotes angiogenesis which increase vascular and tumor growth, which in turn results in a higher incidence of cancer mortality. The clinical picture of this condition has long been recognized as a character trait, without an understanding of the disease process. The term "Pickwickian syndrome" that is sometimes used for the syndrome was coined by the famous early 20th century physician, William Osler, who must have been a reader of Charles Dickens. The description of Joe, "the fat boy" in Dickens's novel The Pickwick Papers, is an accurate clinical picture of an adult with obstructive sleep apnea syndrome. The early reports of obstructive sleep apnea in the medical literature described individuals who were very severely affected, often presenting with severe hypoxemia, hypercapnia and congestive heart failure. The management of obstructive sleep apnea was revolutionized with the introduction of continuous positive airway pressure (CPAP), first described in 1981 by Colin Sullivan and associates in Sydney, Australia. The first models were bulky and noisy, but the design was rapidly improved and by the late 1980s CPAP was widely adopted. The availability of an effective treatment stimulated an aggressive search for affected individuals and led to the establishment of hundreds of specialized clinics dedicated to the diagnosis and treatment of sleep disorders. Though many types of sleep problems are recognized, the vast majority of patients attending these centers have sleep-disordered breathing. 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Rapid eye movement sleep (REM sleep) is a normal stage of sleep characterized by the rapid and random movement of the eyes. Rapid eye movement sleep is classified into two categories: tonic and phasic. It was identified and defined by Nathaniel Kleitman and his student Eugene Aserinsky in 1953. Criteria for REM sleep includes rapid eye movement, low muscle tone and a rapid, low-voltage EEG; these features are easily discernible in a polysomnogram, the sleep study typically done for patients with suspected sleep disorders. REM sleep in adult humans typically occupies 20–25% of total sleep, about 90–120 minutes of a night's sleep. REM sleep is considered the lightest stage of sleep, and normally occurs close to morning. During a normal night of sleep, humans usually experience about four or five periods of REM sleep; they are quite short at the beginning of the night and longer toward the end. Many animals and some people tend to wake, or experience a period of very light sleep, for a short time immediately after a bout of REM. The relative amount of REM sleep varies considerably with age. A newborn baby spends more than 80% of total sleep time in REM. During REM, the activity of the brain's neurons is quite similar to that during waking hours; for this reason, the REM-sleep stage may be called paradoxical sleep. REM sleep is physiologically different from the other phases of sleep, which are collectively referred to as non-REM sleep (NREM sleep). Subjects' vividly recalled dreams mostly occur during REM sleep. Physiologically, certain neurons in the brain stem, known as REM sleep-on cells, (located in the pontine tegmentum), are particularly active during REM sleep, and are probably responsible for its occurrence. The release of certain neurotransmitters, the monoamines (norepinephrine, serotonin and histamine), is completely shut down during REM. This causes][ REM atonia, an almost complete paralysis of the body, due to motor neuron inhibition. Lack of such REM atonia causes REM behavior disorder; sufferers act out the movements occurring in their dreams. Heart rate and breathing rate are irregular during REM sleep, again similar to the waking hours. Body temperature is not well regulated during REM. Erections of the penis (nocturnal penile tumescence or NPT) normally accompany REM sleep. 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. The function of REM sleep is not well understood; several theories have been proposed. According to one theory, certain memories are consolidated during REM sleep. Numerous studies have suggested that REM sleep is important for consolidation of procedural memory and spatial memory. (Slow-wave sleep, part of non-REM sleep, appears to be important for declarative memory.) A recent study shows that artificial enhancement of the non-REM sleep improves the next-day recall of memorized pairs of words. Tucker et al. demonstrated that a daytime nap containing solely non-REM sleep enhances declarative memory but not procedural memory. Monoamine oxidase (MAO) inhibitors and tricyclic antidepressants can suppress REM sleep and these drugs show no evidence of impairing memory. Some studies show MAO inhibitors improve memory. Moreover, one case study of an individual who had little or no REM sleep due to a shrapnel injury to the brainstem did not find the individual's memory to be impaired. (For a more detailed critique on the link between sleep and memory, see Ref.) Intimately related to views on REM function in memory consolidation, Mitchison and Crick have proposed that by virtue of its inherent spontaneous activity, the function of REM sleep "is to remove certain undesirable modes of interaction in networks of cells in the cerebral cortex", which process they characterize as "unlearning". As a result, those memories which are relevant (whose underlying neuronal substrate is strong enough to withstand such spontaneous, chaotic activation), are further strengthened, whilst weaker, transient, "noise" memory traces disintegrate. According to another theory, known as the Ontogenetic Hypothesis of REM sleep, this sleep stage (also known as active sleep in neonates) is particularly important to the developing brain, possibly because it provides the neural stimulation that newborns need to form mature neural connections and for proper nervous system development. Studies investigating the effects of active sleep deprivation have shown that deprivation early in life can result in behavioral problems, permanent sleep disruption, decreased brain mass, and result in an abnormal amount of neuronal cell death. Further supporting this theory is the fact that the amount of REM sleep in humans decreases with age, as well as data from other species (see below). One important theoretical consequence of the Ontogenetic Hypothesis is that REM sleep may have no essentially vital function in the mature brain, i.e., once the development of CNS has completed. However, because processes of neuronal plasticity do not cease altogether in the brain, REM sleep may continue to be implicated in neurogenesis in adults as a source of sustained spontaneous stimulation. According to Tsoukalas (2012) REM sleep is an evolutionary transformation of a well-known defensive mechanism, the tonic immobility reflex. This reflex, also known as animal hypnosis or death feigning, functions as the last line of defense against an attacking predator and consists of the total immobilization of the animal: the animal appears dead (cf. “playing possum”). The neurophysiology and phenomenology of this reaction shows striking similarities to REM sleep, a fact which betrays a deep evolutionary kinship. For example, both reactions exhibit brainstem control, paralysis, sympathetic activation, and thermoregulatory changes. This theory integrates many earlier findings into a unified, and evolutionary well informed, framework. According to "scanning hypothesis," the directional properties of REM sleep are related to a shift of gaze in dream imagery. Against this hypothesis is that such eye movements occur in those born blind and in fetuses in spite of lack of vision. Also, binocular REMs are non-conjugated (i.e., the two eyes do not point in the same direction at a time) and so lack a fixation point. In support of this theory, research finds that in goal-oriented dreams, eye gaze is directed towards the action described by the dreamer. Yet another theory suggests that monoamine shutdown is required so that the monoamine receptors in the brain can recover to regain full sensitivity. Indeed, if REM sleep is repeatedly interrupted, the person will compensate for it with longer REM sleep, "rebound sleep", at the next opportunity. It has been suggested that acute REM sleep deprivation can improve certain types of depression when depression appears to be related to an imbalance of certain neurotransmitters. Although sleep deprivation in general annoys most of the population, it has repeatedly been shown to alleviate depression, albeit temporarily. More than half the individuals who experience this relief report it to be rendered ineffective after sleeping the following night. Thus, researchers have devised methods such as altering the sleep schedule for a span of days following a REM deprivation period and combining sleep-schedule alterations with pharmacotherapy to prolong this effect. Though most antidepressants selectively inhibit REM sleep due to their action on monoamines, this effect decreases after long-term use. It is interesting to note that REM sleep deprivation stimulates hippocampal neurogenesis much the same as antidepressants. Some researchers argue that the perpetuation of a complex brain process such as REM sleep indicates that it serves an important function for the survival of mammalian and avian species. It fulfills important physiological needs vital for survival to the extent that prolonged REM sleep deprivation leads to death in experimental animals.][ In both humans and experimental animals, REM sleep loss leads to several behavioral and physiological abnormalities.][ Loss of REM sleep has been noticed during various natural and experimental infections. Survivability of the experimental animals decreases when REM sleep is totally attenuated during infection; this leads to the possibility that the quality and quantity of REM sleep is generally essential for normal body physiology. The sentinel hypothesis of REM sleep was put forward by Frederick Snyder in 1966. It is based upon the observation that REM sleep in several mammals (the rat, the hedgehog, the rabbit, and the rhesus monkey) is followed by a brief awakening. This does not occur for either cats or humans, although humans are more likely to wake from REM sleep than from NREM sleep. Snyder hypothesized that REM sleep activates an animal periodically, to scan the environment for possible predators. This hypothesis does not explain the muscle paralysis of REM sleep; however, a logical analysis might suggest that the muscle paralysis exists to prevent the animal from fully waking up unnecessarily, and allowing it to return easily to deeper sleep. Other theories are that they lubricate the cornea, warm the brain, stimulate and stabilize the neural circuits that have not been activated during waking, create internal stimulation to aid development of the CNS, or lack any purpose, being random creations of brain activation. REM deprivation causes a significant increase in the number of attempts to go into REM stage while asleep. On recovery nights, an individual will most likely to move to stage 3 and REM sleep more quickly and experience a REM rebound, which refers to a great increase in the time spent in REM stage over normal levels. These findings are consistent with the idea that REM sleep is crucial and perhaps the most important stage of sleep. After the deprivation is complete, mild psychological disturbances, such as anxiety, irritability, hallucinations, and difficulty concentrating, may develop and appetite may increase. There are also positive consequences of REM deprivation. Some symptoms of depression are found to be suppressed by REM deprivation; Interest in sex and general pleasure seeking activity, aggression, and eating behavior may increase. Animal studies of REM deprivation are markedly different than human studies. There is evidence that REM sleep deprivation in animals has more serious consequences than in humans. This may be because the length of time animals have been REM deprived for is much longer than humans. Evidence suggests that REM deprivation in rats impairs learning of new material, but does not effect existing memory. In one study, rats did not learn to avoid a painful stimulus after REM deprivation as well as they could before the deprivation. No learning impairments have been found in humans undergoing one night of REM deprivation. REM deprivation in rats produces an increase in attempts to enter REM, and after deprivation, REM rebound. In rats, as well as cats, REM sleep deprivation increased brain excitability (e.g. electrical amplification of sensory signals), and which lowered the threshold for waking seizures threshold. This increase in brain excitability seems to be similar in humans. One study also found a decrease in hindbrain sensory excitability. The hindbrain was less receptive overall to information in the afferent pathway, because of the increase in the amplification of those pathways that it is receptive to. Ultimately, REM deprivation in rats is fatal. One of the main symptoms during this time was hypothermia, despite observable effects to increase heat production (e.g., by eating). This has led to the hypothesis that the function of REM is to prevent heat loss. This is interesting because one of the state characteristics of REM is loss of thermoregulation. Sleep aids the process by which creativity forms associative elements into new combinations that are useful or meet some requirement. This occurs in REM sleep rather than in NREM sleep. Rather than being due to memory processes, this has been attributed to changes during REM sleep in cholinergic and noradrenergic neuromodulation. During REM sleep, high levels of acetylcholine in the hippocampus suppress feedback from hippocampus to the neocortex, and lower levels of acetylcholine and norepinephrine in the neocortex encourage the spread of associational activity within neocortical areas without control from the hippocampus. This is in contrast to waking consciousness, where higher levels of norepinephrine and acetylcholine inhibit recurrent connections in the neocortex. REM sleep through this process adds creativity by allowing "neocortical structures to reorganise associative hierarchies, in which information from the hippocampus would be reinterpreted in relation to previous semantic representations or nodes." REM sleep occurs in all land mammals as well as in birds. The phenomenon of REM sleep and its association with dreaming was discovered by Eugene Aserinsky and Nathaniel Kleitman with assistance from William C. Dement, a medical student at the time, in 1952 during their tenures at the University of Chicago. Kleitman and Aserinsky's seminal article was published September 10, 1953. [Add reference: Carson III, Culley C., Kirby, Roger S., Goldstein, Irwin, editors, "Textbook of Erectile Dysfunction" Oxford, U.K.; Isis Medical Media, Ltd., 1999; Moreland, R.B. & Nehra, A.; Pathosphysiology of erectile dysfunction; a molecular basis, role of NPT in maintaining potency: pp. 105–15.] M: PSO/PSI mepr dsrd (o, p, m, p, a, d, s), sysi/epon, spvo proc (eval/thrp), drug (N5A/5B/5C/6A/6B/6D) M: CNS anat (n/s/m/p/4/e/b/d/c/a/f/l/g)/phys/devp noco (m/d/e/h/v/s)/cong/tumr, sysi/epon, injr proc, drug (N1A/2AB/C/3/4/7A/B/C/D)
Sleep is a naturally recurring state characterized by reduced or absent consciousness, relatively suspended sensory activity, and inactivity of nearly all voluntary muscles. It is distinguished from wakefulness by a decreased ability to react to stimuli, and is more easily reversible than being in hibernation or a coma. Sleep is a heightened anabolic state, accentuating the growth and rejuvenation of the immune, nervous, skeletal and muscular systems. It is observed in mammals, birds, reptiles, amphibians, and fish. The purposes and mechanisms of sleep are only partially clear and the subject of substantial ongoing research. Sleep is sometimes thought to help conserve energy, though this theory is not fully adequate as it only decreases metabolism by about 5–10%. Additionally it is observed that mammals require sleep even during the hypometabolic state of hibernation, in which circumstance it is actually a net loss of energy as the animal returns from hypothermia to euthermia in order to sleep. In mammals and birds, sleep is divided into two broad types: rapid eye movement (REM) and non-rapid eye movement (NREM or non-REM) sleep. Each type has a distinct set of associated physiological and neurological features. The American Academy of Sleep Medicine (AASM) further divides NREM into three stages: N1, N2, and N3, the last of which is also called delta sleep or slow-wave sleep. Sleep proceeds in cycles of REM and NREM, usually four or five of them per night, the order normally being N1 → N2 → N3 → N2 → REM. There is a greater amount of deep sleep (stage N3) earlier in the night, while the proportion of REM sleep increases in the two cycles just before natural awakening. The stages of sleep were first described in 1937 by Alfred Lee Loomis and his coworkers, who separated the different electroencephalography (EEG) features of sleep into five levels (A to E), which represented the spectrum from wakefulness to deep sleep. In 1953, REM sleep was discovered as distinct, and thus William Dement and Nathaniel Kleitman reclassified sleep into four NREM stages and REM. The staging criteria were standardized in 1968 by Allan Rechtschaffen and Anthony Kales in the "R&K sleep scoring manual." In the R&K standard, NREM sleep was divided into four stages, with slow-wave sleep comprising stages 3 and 4. In stage 3, delta waves made up less than 50% of the total wave patterns, while they made up more than 50% in stage 4. Furthermore, REM sleep was sometimes referred to as stage 5. In 2004, the AASM commissioned the AASM Visual Scoring Task Force to review the R&K scoring system. The review resulted in several changes, the most significant being the combination of stages 3 and 4 into Stage N3. The revised scoring was published in 2007 as The AASM Manual for the Scoring of Sleep and Associated Events. Arousals and respiratory, cardiac, and movement events were also added. Sleep stages and other characteristics of sleep are commonly assessed by polysomnography in a specialized sleep laboratory. Measurements taken include EEG of brain waves, electrooculography (EOG) of eye movements, and electromyography (EMG) of skeletal muscle activity. In humans, the average length of the first sleep cycle is approximately 90 minutes and 100 to 120 minutes from the second to the fourth cycle, which is usually the last one. Each stage may have a distinct physiological function and this can result in sleep that exhibits loss of consciousness but does not fulfill its physiological functions (i.e., one may still feel tired after apparently sufficient sleep). Scientific studies on sleep have shown that sleep stage at awakening is an important factor in amplifying sleep inertia. Alarm clocks involving sleep stage monitoring appeared on the market in 2005. Using sensing technologies such as EEG electrodes or accelerometers, these alarm clocks are supposed to wake people only from light sleep. According to 2007 AASM standards, NREM consists of three stages. There is relatively little dreaming in NREM. Stage N1 refers to the transition of the brain from alpha waves having a frequency of 8–13 Hz (common in the awake state) to theta waves having a frequency of 4–7 Hz. This stage is sometimes referred to as somnolence or drowsy sleep. Sudden twitches and hypnic jerks, also known as positive myoclonus, may be associated with the onset of sleep during N1. Some people may also experience hypnagogic hallucinations during this stage. During N1, the subject loses some muscle tone and most conscious awareness of the external environment. Stage N2 is characterized by sleep spindles ranging from 11 to 16 Hz (most commonly 12–14 Hz) and K-complexes. During this stage, muscular activity as measured by EMG decreases, and conscious awareness of the external environment disappears. This stage occupies 45–55% of total sleep in adults. Stage N3 (deep or slow-wave sleep) is characterized by the presence of a minimum of 20% delta waves ranging from 0.5–2 Hz and having a peak-to-peak amplitude >75 μV. (EEG standards define delta waves to be from 0 to 4 Hz, but sleep standards in both the original R&K, as well as the new 2007 AASM guidelines have a range of 0.5–2 Hz.) This is the stage in which parasomnias such as night terrors, nocturnal enuresis, sleepwalking, and somniloquy occur. Many illustrations and descriptions still show a stage N3 with 20–50% delta waves and a stage N4 with greater than 50% delta waves; these have been combined as stage N3. Rapid eye movement sleep, or REM sleep (also known as paradoxical sleep), accounts for 20–25% of total sleep time in most human adults. The criteria for REM sleep include rapid eye movements as well as a rapid low-voltage EEG. During REM sleep, EEG patterns returns to higher frequency saw-tooth waves. Most memorable dreaming occurs in this stage. At least in mammals, a descending muscular atonia is seen. Such paralysis may be necessary to protect organisms from self-damage through physically acting out scenes from the often-vivid dreams that occur during this stage.][ Sleep timing is controlled by the circadian clock, sleep-wake homeostasis, and in humans, within certain bounds, willed behavior. The circadian clock—an inner timekeeping, temperature-fluctuating, enzyme-controlling device—works in tandem with adenosine, a neurotransmitter that inhibits many of the bodily processes associated with wakefulness. Adenosine is created over the course of the day; high levels of adenosine lead to sleepiness. In diurnal animals, sleepiness occurs as the circadian element causes the release of the hormone melatonin and a gradual decrease in core body temperature. The timing is affected by one's chronotype. It is the circadian rhythm that determines the ideal timing of a correctly structured and restorative sleep episode. Homeostatic sleep propensity (the need for sleep as a function of the amount of time elapsed since the last adequate sleep episode) must be balanced against the circadian element for satisfactory sleep. Along with corresponding messages from the circadian clock, this tells the body it needs to sleep. Sleep offset (awakening) is primarily determined by circadian rhythm. A person who regularly awakens at an early hour will generally not be able to sleep much later than his or her normal waking time, even if moderately sleep-deprived][. Sleep duration is affected by the gene DEC2. Some people have a mutation of this gene; they sleep two hours less than normal. Neurology professor Ying-Hui Fu and her colleagues bred mice that carried the DEC2 mutation and slept less than normal mice. The optimal amount of sleep is not a meaningful concept unless the timing of that sleep is seen in relation to an individual's circadian rhythms. A person's major sleep episode is relatively inefficient and inadequate when it occurs at the "wrong" time of day; one should be asleep at least six hours before the lowest body temperature. The timing is correct when the following two circadian markers occur after the middle of the sleep episode and before awakening: maximum concentration of the hormone melatonin, and minimum core body temperature. Human sleep needs can vary by age and among individuals, and sleep is considered to be adequate when there is no daytime sleepiness or dysfunction. Moreover, self-reported sleep duration is only moderately correlated with actual sleep time as measured by actigraphy, and those affected with sleep state misperception may typically report having slept only four hours despite having slept a full eight hours. A University of California, San Diego psychiatry study of more than one million adults found that people who live the longest self-report sleeping for six to seven hours each night. Another study of sleep duration and mortality risk in women showed similar results. Other studies show that "sleeping more than 7 to 8 hours per day has been consistently associated with increased mortality," though this study suggests the cause is probably other factors such as depression and socioeconomic status, which would correlate statistically. It has been suggested that the correlation between lower sleep hours and reduced morbidity only occurs with those who wake naturally, rather than those who use an alarm. Researchers at the University of Warwick and University College London have found that lack of sleep can more than double the risk of death from cardiovascular disease, but that too much sleep can also be associated with a doubling of the risk of death, though not primarily from cardiovascular disease. Professor Francesco Cappuccio said, "Short sleep has been shown to be a risk factor for weight gain, hypertension, and Type 2 diabetes, sometimes leading to mortality; but in contrast to the short sleep-mortality association, it appears that no potential mechanisms by which long sleep could be associated with increased mortality have yet been investigated. Some candidate causes for this include depression, low socioeconomic status, and cancer-related fatigue... In terms of prevention, our findings indicate that consistently sleeping around seven hours per night is optimal for health, and a sustained reduction may predispose to ill health." Furthermore, sleep difficulties are closely associated with psychiatric disorders such as depression, alcoholism, and bipolar disorder. Up to 90% of adults with depression are found to have sleep difficulties. Dysregulation found on EEG includes disturbances in sleep continuity, decreased delta sleep and altered REM patterns with regard to latency, distribution across the night and density of eye movements. Children need more sleep per day in order to develop and function properly: up to 18 hours for newborn babies, with a declining rate as a child ages. A newborn baby spends almost 9 hours a day in REM sleep. By the age of five or so, only slightly over two hours is spent in REM. Studies say that school age children need about 10 to 11 hours of sleep. The siesta habit has recently been associated with a 37% reduction in coronary mortality, possibly due to reduced cardiovascular stress mediated by daytime sleep. Nevertheless, epidemiological studies on the relations between cardiovascular health and siestas have led to conflicting conclusions, possibly because of poor control of moderator variables, such as physical activity. It is possible that people who take siestas have different physical activity habits, e.g., waking earlier and scheduling more activity during the morning. Such differences in physical activity may mediate different 24-hour profiles in cardiovascular function. Even if such effects of physical activity can be discounted for explaining the relationship between siestas and cardiovascular health, it is still unknown whether it is the daytime nap itself, a supine posture, or the expectancy of a nap that is the most important factor. It was recently suggested that a short nap can reduce stress and blood pressure (BP), with the main changes in BP occurring between the time of lights off and the onset of stage 1. Dr. Zaregarizi and his team have concluded that the acute time of falling asleep was when beneficial cardiovascular changes take place. This study has indicated that a large decline in BP occurs during the daytime sleep-onset period only when sleep is expected. However, when subjects rest in a supine position, the same reduction in BP is not observed. This BP reduction may be associated with the lower coronary mortality rates seen in Mediterranean and Latin American populations in which siestas are common. Dr. Zaregarizi assessed cardiovascular function (BP, heart rate, and measurements of blood vessel dilation) while nine healthy volunteers, 34 years of age on average, spent an hour standing quietly, reclining at rest but not sleeping, or reclining to nap. All participants were restricted to 4 hours of sleep on the night prior to each of the sleep laboratory tests. During the three phases of daytime sleep, he noted significant reductions in BP and heart rate. By contrast, they did not observe changes in cardiovascular function while the participants were standing or reclining at rest. These findings also show that the greatest decline in BP occurs between lights-off and onset of daytime sleep itself. During this sleep period, which lasted 9.7 minutes on average, BP decreased, while blood vessel dilation increased by more than 9 percent. “There is little change in blood pressure once a subject is actually asleep," Dr. Zaregarizi noted, and he found minor changes in blood vessel dilation during sleep. Kaul et al. found that sleep duration in long-term experienced meditators was lower than in non-meditators and general population norms, with no apparent decrements in vigilance. Sleep debt is the effect of not getting enough sleep; a large debt causes mental, emotional and physical fatigue. Sleep debt results in diminished abilities to perform high-level cognitive functions. Neurophysiological and functional imaging studies have demonstrated that frontal regions of the brain are particularly responsive to homeostatic sleep pressure. Scientists do not agree on how much sleep debt it is possible to accumulate; whether it is accumulated against an individual's average sleep or some other benchmark; nor on whether the prevalence of sleep debt among adults has changed appreciably in the industrialized world in recent decades. It is likely that children are sleeping less than previously in Western societies. It is theorized that a considerable amount of sleep-related behavior, such as when and how long a person needs to sleep, is regulated by genetics. Researchers have discovered some evidence that seems to support this assumption. ABCC9 is one gene found which influences the duration of human sleep. The multiple hypotheses proposed to explain the function of sleep reflect the incomplete understanding of the subject. (When asked, after 50 years of research, what he knew about the reason people sleep, William Dement, founder of Stanford University's Sleep Research Center, answered, "As far as I know, the only reason we need to sleep that is really, really solid is because we get sleepy.") It is likely that sleep evolved to fulfill some primeval function and took on multiple functions over time][ (analogous to the larynx, which controls the passage of food and air, but descended over time to develop speech capabilities). If sleep were not essential, one would expect to find: Outside of a few basal animals that have no brain or a very simple one, no animals have been found to date that satisfy any of these criteria. While some varieties of shark, such as great whites and hammerheads, must remain in motion at all times to move oxygenated water over their gills, it is possible they still sleep one cerebral hemisphere at a time as marine mammals do. However it remains to be shown definitively whether any fish is capable of unihemispheric sleep. Some of the many proposed functions of sleep are as follows: Wound healing has been shown to be affected by sleep. A study conducted by Gumustekin et al. in 2004 shows sleep deprivation hindering the healing of burns on rats. It has been shown that sleep deprivation affects the immune system. In a study by Zager et al. in 2007, rats were deprived of sleep for 24 hours. When compared with a control group, the sleep-deprived rats' blood tests indicated a 20% decrease in white blood cell count, a significant change in the immune system. It is now possible to state that "sleep loss impairs immune function and immune challenge alters sleep," and it has been suggested that mammalian species which invest in longer sleep times are investing in the immune system, as species with the longer sleep times have higher white blood cell counts. Sleep has also been theorized to effectively combat the accumulation of free radicals in the brain, by increasing the efficiency of endogeneous antioxidant mechanisms. The effect of sleep duration on somatic growth is not completely known. One study by Jenni et al. in 2007 recorded growth, height, and weight, as correlated to parent-reported time in bed in 305 children over a period of nine years (age 1–10). It was found that "the variation of sleep duration among children does not seem to have an effect on growth." It has been shown that sleep—more specifically, slow-wave sleep (SWS)—does affect growth hormone levels in adult men. During eight hours' sleep, Van Cauter, Leproult, and Plat found that the men with a high percentage of SWS (average 24%) also had high growth hormone secretion, while subjects with a low percentage of SWS (average 9%) had low growth hormone secretion. There are multiple arguments supporting the restorative function of sleep. The metabolic phase during sleep is anabolic; anabolic hormones such as growth hormones (as mentioned above) are secreted preferentially during sleep. The duration of sleep among species is, in general, inversely related to animal size][ and directly related to basal metabolic rate. Rats, which have a high basal metabolic rate, sleep for up to 14 hours a day, whereas elephants and giraffes, which have lower BMRs, sleep only 3–4 hours per day. Energy conservation could as well have been accomplished by resting quiescent without shutting off the organism from the environment, potentially a dangerous situation. A sedentary nonsleeping animal is more likely to survive predators, while still preserving energy. Sleep, therefore, seems to serve another purpose, or other purposes, than simply conserving energy; for example, hibernating animals waking up from hibernation go into rebound sleep because of lack of sleep during the hibernation period. They are definitely well-rested and are conserving energy during hibernation, but need sleep for something else. Rats kept awake indefinitely develop skin lesions, hyperphagia, loss of body mass, hypothermia, and, eventually, fatal sepsis. According to the ontogenetic hypothesis of REM sleep, the activity occurring during neonatal REM sleep (or active sleep) seems to be particularly important to the developing organism (Marks et al., 1995). Studies investigating the effects of deprivation of active sleep have shown that deprivation early in life can result in behavioral problems, permanent sleep disruption, decreased brain mass (Mirmiran et al., 1983), and an abnormal amount of neuronal cell death. REM sleep appears to be important for development of the brain. REM sleep occupies the majority of time of sleep of infants, who spend most of their time sleeping. Among different species, the more immature the baby is born, the more time it spends in REM sleep. Proponents also suggest that REM-induced muscle inhibition in the presence of brain activation exists to allow for brain development by activating the synapses, yet without any motor consequences that may get the infant in trouble. Additionally, REM deprivation results in developmental abnormalities later in life. However, this does not explain why older adults still need REM sleep. Aquatic mammal infants do not have REM sleep in infancy; REM sleep in those animals increases as they age. Scientists have shown numerous ways in which sleep is related to memory. In a study conducted by Turner, Drummond, Salamat, and Brown (2007), working memory was shown to be affected by sleep deprivation. Working memory is important because it keeps information active for further processing and supports higher-level cognitive functions such as decision making, reasoning, and episodic memory. The study allowed 18 women and 22 men to sleep only 26 minutes per night over a four-day period. Subjects were given initial cognitive tests while well-rested, and then were tested again twice a day during the four days of sleep deprivation. On the final test, the average working memory span of the sleep-deprived group had dropped by 38% in comparison to the control group. The relation between working memory and sleep can also be explored by testing how working memory works during sleep. Daltrozzo, Claude, Tillmann, Bastuji, Perrin, using Event-Related Potentials to the perception of sentences during sleep showed that working memory for linguistic information is partially preserved during sleep with a smaller capacity compared to wake. Memory seems to be affected differently by certain stages of sleep such as REM and slow-wave sleep (SWS). In one study, multiple groups of human subjects were used: wake control groups and sleep test groups. Sleep and wake groups were taught a task and were then tested on it, both on early and late nights, with the order of nights balanced across participants. When the subjects' brains were scanned during sleep, hypnograms revealed that SWS was the dominant sleep stage during the early night, representing around 23% on average for sleep stage activity. The early-night test group performed 16% better on the declarative memory test than the control group. During late-night sleep, REM became the most active sleep stage at about 24%, and the late-night test group performed 25% better on the procedural memory test than the control group. This indicates that procedural memory benefits from late, REM-rich sleep, whereas declarative memory benefits from early, slow wave-rich sleep. A study conducted by Datta indirectly supports these results. The subjects chosen were 22 male rats. A box was constructed wherein a single rat could move freely from one end to the other. The bottom of the box was made of a steel grate. A light would shine in the box accompanied by a sound. After a five-second delay, an electrical shock would be applied. Once the shock commenced, the rat could move to the other end of the box, ending the shock immediately. The rat could also use the five-second delay to move to the other end of the box and avoid the shock entirely. The length of the shock never exceeded five seconds. This was repeated 30 times for half the rats. The other half, the control group, was placed in the same trial, but the rats were shocked regardless of their reaction. After each of the training sessions, the rat would be placed in a recording cage for six hours of polygraphic recordings. This process was repeated for three consecutive days. This study found that during the posttrial sleep recording session, rats spent 25.47% more time in REM sleep after learning trials than after control trials. These trials support the results of the Born et al. study, indicating an obvious correlation between REM sleep and procedural knowledge. An observation of the Datta study is that the learning group spent 180% more time in SWS than did the control group during the post-trial sleep-recording session. This phenomenon is supported by a study performed by Kudrimoti, Barnes, and McNaughton. This study shows that after spatial exploration activity, patterns of hippocampal place cells are reactivated during SWS following the experiment. In a study by Kudrimoti et al., seven rats were run through a linear track using rewards on either end. The rats would then be placed in the track for 30 minutes to allow them to adjust (PRE), then they ran the track with reward-based training for 30 minutes (RUN), and then they were allowed to rest for 30 minutes. During each of these three periods, EEG data were collected for information on the rats' sleep stages. Kudrimoti et al. computed the mean firing rates of hippocampal place cells during prebehavior SWS (PRE) and three ten-minute intervals in postbehavior SWS (POST) by averaging across 22 track-running sessions from seven rats. The results showed that ten minutes after the trial RUN session, there was a 12% increase in the mean firing rate of hippocampal place cells from the PRE level; however, after 20 minutes, the mean firing rate returned rapidly toward the PRE level. The elevated firing of hippocampal place cells during SWS after spatial exploration could explain why there were elevated levels of slow-wave sleep in Datta's study, as it also dealt with a form of spatial exploration. A study has also been done involving direct current stimulation to the prefrontal cortex to increase the amount of slow oscillations during SWSfe. The direct current stimulation greatly enhanced word-pair retention the following day, giving evidence that SWS plays a large role in the consolidation of episodic memories. The different studies all suggest that there is a correlation between sleep and the complex functions of memory. Harvard sleep researchers Saper and Stickgold point out that an essential part of memory and learning consists of nerve cell dendrites' sending of information to the cell body to be organized into new neuronal connections. This process demands that no external information is presented to these dendrites, and it is suggested that this may be why it is during sleep that memories and knowledge are solidified and organized. The "Preservation and Protection" theory holds that sleep serves an adaptive function. It protects the animal during that portion of the 24-hour day in which being awake, and hence roaming around, would place the individual at greatest risk. Organisms do not require 24 hours to feed themselves and meet other necessities. From this perspective of adaptation, organisms are safer by staying out of harm's way, where potentially they could be prey to other, stronger organisms. They sleep at times that maximize their safety, given their physical capacities and their habitats. This theory fails to explain why the brain disengages from the external environment during normal sleep. However, the brain consumes a large proportion of the body's calories at any one time and preservation of energy could only occur by limiting its sensory inputs. Another argument against the theory is that sleep is not simply a passive consequence of removing the animal from the environment, but is a "drive"; animals alter their behaviors in order to obtain sleep. Therefore, circadian regulation is more than sufficient to explain periods of activity and quiescence that are adaptive to an organism, but the more peculiar specializations of sleep probably serve different and unknown functions. Moreover, the preservation theory needs to explain why carnivores like lions, which are on top of the food chain and thus have little to fear, sleep the most. It has been suggested that they need to minimize energy expenditure when not hunting. Preservation also does not explain why aquatic mammals sleep while moving. Quiescence during these vulnerable hours would do the same and would be more advantageous, because the animal would still be able to respond to environmental challenges like predators, etc. Sleep rebound that occurs after a sleepless night will be maladaptive, but obviously must occur for a reason. A zebra falling asleep the day after it spent the sleeping time running from a lion is more, not less, vulnerable to predation. Dreaming is the perceived experience of sensory images and sounds during sleep, in a sequence which the dreamer usually perceives more as an apparent participant than as an observer. Dreaming is stimulated by the pons and mostly occurs during the REM phase of sleep. Dreams can also be suppressed or encouraged; taking anti-depressants, acetaminophen, ibuprofen, or alcohol is thought to potentially suppress dreams, whereas melatonin may have the ability to encourage them. People have proposed many hypotheses about the functions of dreaming. Sigmund Freud postulated that dreams are the symbolic expression of frustrated desires that have been relegated to the unconscious mind, and he used dream interpretation in the form of psychoanalysis to uncover these desires. See Freud: The Interpretation of Dreams. While penile erections are commonly believed to indicate dreams with sexual content, they are not more frequent during sexual dreams than they are during nonsexual dreams. The parasympathetic nervous system experiences increased activity during REM sleep which may cause erection of the penis or clitoris. In males, 80% to 95% of erection accompanies REM sleep while only about 12% of men's dreams contain sexual content. Freud's work concerns the psychological role of dreams, which does not exclude any physiological role they may have. Recent research claims that sleep has the overall role of consolidation and organization of synaptic connections formed during learning and experience. As such, Freud's work is not ruled out. Nevertheless, Freud's research has been expanded on, especially with regard to the organization and consolidation of recent memory. Certain processes in the cerebral cortex have been studied by John Allan Hobson and Robert McCarley. In their activation synthesis theory, for example, they propose that dreams are caused by the random firing of neurons in the cerebral cortex during the REM period. Neatly, this theory helps explain the irrationality of the mind during REM periods, as, according to this theory, the forebrain then creates a story in an attempt to reconcile and make sense of the nonsensical sensory information presented to it. Ergo, the odd nature of many dreams. According to Tsoukalas (2012) REM sleep is an evolutionary transformation of a well-known defensive mechanism, the tonic immobility reflex. This reflex, also known as animal hypnosis or death feigning, functions as the last line of defense against an attacking predator and consists of the total immobilization of the animal: the animal appears dead (cf. “playing possum”). The neurophysiology and phenomenology of this reaction shows striking similarities to REM sleep, a fact which betrays a deep evolutionary kinship. For example, both reactions exhibit brainstem control, paralysis, sympathetic activation, and thermoregulatory changes. This theory integrates many earlier findings into a unified, and evolutionary well informed, framework. Insomnia is a general term describing difficulty falling asleep and staying asleep. Insomnia can have many different causes, including psychological stress, a poor sleep environment, an inconsistent sleep schedule, or excessive mental or physical stimulation in the hours before bedtime. Insomnia is often treated through behavioral changes like keeping a regular sleep schedule, avoiding stimulating or stressful activities before bedtime, and cutting down on stimulants such as caffeine. Patients are often counseled to improve their sleep environment by installing heavy drapes to shut out all sunlight, and keeping computers, televisions and work materials out of the sleeping area. A 2010 review of published scientific research suggested that exercise generally improves sleep for most people, and helps sleep disorders such as insomnia. The optimum time to exercise may be 4 to 8 hours before bedtime, though exercise at any time of day is beneficial, with the exception of heavy exercise taken shortly before bedtime, which may disturb sleep. However there is insufficient evidence to draw detailed conclusions about the relationship between exercise and sleep. Sleeping medications such as Ambien and Lunesta are an increasingly popular treatment for insomnia, and have become a major source of revenue for drug companies. Although these nonbenzodiazepine medications are generally believed to be better and safer than earlier generations of sedatives, they have still generated some controversy and discussion regarding side-effects. White noise appears to be a promising treatment for insomnia. Obstructive sleep apnea is a condition in which major pauses in breathing occur during sleep, disrupting the normal progression of sleep and often causing other more severe health problems. Apneas occur when the muscles around the patient's airway relax during sleep, causing the airway to collapse and block the intake of oxygen. As oxygen levels in the blood drop, the patient then comes out of deep sleep in order to resume breathing. When several of these episodes occur per hour, sleep apnea rises to a level of seriousness that may require treatment. Diagnosing sleep apnea usually requires a professional sleep study performed in a sleep clinic, because the episodes of wakefulness caused by the disorder are extremely brief and patients usually do not remember experiencing them. Instead, many patients simply feel tired after getting several hours of sleep and have no idea why. Major risk factors for sleep apnea include chronic fatigue, old age, obesity and snoring. Sleep disorders include narcolepsy, periodic limb movement disorder (PLMD), restless leg syndrome (RLS), and the circadian rhythm sleep disorders. Fatal familial insomnia, or FFI, is an extremely rare genetic disease with no known treatment or cure, is characterized by increasing insomnia as one of its symptoms; ultimately sufferers of the disease stop sleeping entirely, before dying of the disease. Somnambulism, known as sleep walking, is also a common sleeping disorder, especially among children. In somnambulism the individual gets up from his/her sleep and wanders around while still sleeping. Older people may be more easily awakened by disturbances in the environment and may to some degree lose the ability to consolidate sleep. Research suggests that sleep patterns vary significantly across cultures. The most striking differences are between societies that have plentiful sources of artificial light and ones that do not. The primary difference appears to be that pre-light cultures have more broken-up sleep patterns. For example, people might go to sleep far sooner after the sun sets, but then wake up several times throughout the night, punctuating their sleep with periods of wakefulness, perhaps lasting several hours. The boundaries between sleeping and waking are blurred in these societies. Some observers believe that nighttime sleep in these societies is most often split into two main periods, the first characterized primarily by deep sleep and the second by REM sleep. Some societies display a fragmented sleep pattern in which people sleep at all times of the day and night for shorter periods. In many nomadic or hunter-gatherer societies, people will sleep on and off throughout the day or night depending on what is happening. Plentiful artificial light has been available in the industrialized West since at least the mid-19th century, and sleep patterns have changed significantly everywhere that lighting has been introduced. In general, people sleep in a more concentrated burst through the night, going to sleep much later, although this is not always true. Historian Roger Ekrich thinks that the traditional pattern of "segmented sleep" as it is called began to disappear among the urban upper class in Europe in the late 17th century and the change spread over the next 200 years; by the 1920s "the idea of a first and second sleep had receded entirely from our social consciousness." Ekrich attributes the change to increases in "street lighting, domestic lighting and a surge in coffee houses," which slowly made nighttime a legitimate time for activity, decreasing the time available for rest. In some societies, people generally sleep with at least one other person (sometimes many) or with animals. In other cultures, people rarely sleep with anyone but a most intimate relation, such as a spouse. In almost all societies, sleeping partners are strongly regulated by social standards. For example, people might only sleep with their immediate family, extended family, spouses, their children, children of a certain age, children of specific gender, peers of a certain gender, friends, peers of equal social rank, or with no one at all. Sleep may be an actively social time, depending on the sleep groupings, with no constraints on noise or activity. People sleep in a variety of locations. Some sleep directly on the ground; others on a skin or blanket; others sleep on platforms or beds. Some sleep with blankets, some with pillows, some with simple headrests, some with no head support. These choices are shaped by a variety of factors, such as climate, protection from predators, housing type, technology, personal preference, and the incidence of pests. Neurological sleep states can be difficult to detect in some animals. In these cases, sleep may be defined using behavioral characteristics such as minimal movement, postures typical for the species, and reduced responsiveness to external stimulation. Sleep is quickly reversible, as opposed to hibernation or coma, and sleep deprivation is followed by longer or deeper rebound sleep. Herbivores, who require a long waking period to gather and consume their diet, typically sleep less each day than similarly sized carnivores, who might well consume several days' supply of meat in a sitting. Horses and other herbivorous ungulates can sleep while standing, but must necessarily lie down for REM sleep (which causes muscular atony) for short periods. Giraffes, for example, only need to lie down for REM sleep for a few minutes at a time. Bats sleep while hanging upside down. Some aquatic mammals and some birds can sleep with one half of the brain while the other half is awake, so-called unihemispheric slow-wave sleep. Birds and mammals have cycles of non-REM and REM sleep (as described above for humans), though birds' cycles are much shorter and they do not lose muscle tone (go limp) to the extent that most mammals do. Many mammals sleep for a large proportion of each 24-hour period when they are very young. However, killer whales and some other dolphins do not sleep during the first month of life. Instead, young dolphins and whales frequently take rests by pressing their body next to their mother’s while she swims. As the mother swims she is keeping her offspring afloat to prevent them from drowning. This allows young dolphins and whales to rest, which will help keep their immune system healthy; in turn, protecting them from illnesses. During this period, mothers often sacrifice sleep for the protection of their young from predators. However, unlike other mammals, adult dolphins and whales are able to go without sleep for a month. Also unlike terrestrial mammals, dolphins, whales, and pinnipeds (seals) cannot go into a deep sleep. The consequences of falling into a deep sleep for marine mammalian species is suffocation and drowning, or becoming easy prey for predators. Thus, dolphins, whales, and seals engage in unihemispheric sleep, which allows one brain hemisphere to remain fully functional, while the other goes to sleep. The hemisphere that is asleep, alternates so that both hemispheres can be fully rested. Just like terrestrial mammals, pinnipeds that sleep on land fall into a deep sleep and both hemispheres of their brain shut down and are in full sleep mode. M: PSO/PSI mepr dsrd (o, p, m, p, a, d, s), sysi/epon, spvo proc (eval/thrp), drug (N5A/5B/5C/6A/6B/6D) M: CNS anat (n/s/m/p/4/e/b/d/c/a/f/l/g)/phys/devp noco (m/d/e/h/v/s)/cong/tumr, sysi/epon, injr proc, drug (N1A/2AB/C/3/4/7A/B/C/D)
Sleep deprivation is the condition of not having enough sleep; it can be either chronic or acute. A chronic sleep-restricted state can cause fatigue, daytime sleepiness, clumsiness and weight loss or weight gain. It adversely affects the brain and cognitive function. Few studies have compared the effects of acute total sleep deprivation and chronic partial sleep restriction. Complete absence of sleep over long periods is impossible for humans to achieve (unless they suffer from fatal familial insomnia); brief microsleeps cannot be avoided. Long-term total sleep deprivation has caused death in lab animals. Generally, sleep deprivation may result in: In 2005, a study of over 1400 participants showed that participants who habitually slept few hours were more likely to have associations with type 2 diabetes. However, because this study was merely correlational, the direction of cause and effect between little sleep and diabetes is uncertain. The authors point to an earlier study which showed that experimental rather than habitual restriction of sleep resulted in impaired glucose tolerance (IGT). Sleep deprivation can adversely affect the brain and cognitive function. A 2000 study, by the UCSD School of Medicine and the Veterans Affairs Healthcare System in San Diego, used functional magnetic resonance imaging (fMRI) technology to monitor activity in the brains of sleep-deprived subjects performing simple verbal learning tasks. The study showed that regions of the brain's prefrontal cortex, an area that supports mental faculties such as working memory and logical and practical ("means-ends") reasoning, displayed more activity in sleepier subjects. Researchers interpreted this result as indicating that the brain of the average sleep-deprived subject had to work harder than that of the average non-sleep-deprived subject to accomplish a given task, and from this indication they inferred the conclusion the brains of sleep-deprived subjects were attempting to compensate for adverse effects caused by sleep deprivation. The temporal lobe, which is a brain region involved in language processing, was activated during verbal learning in rested subjects but not in sleep-deprived subjects. The parietal lobe, not activated in rested subjects during the verbal exercise, was more active when the subjects were deprived of sleep. Although memory performance was less efficient with sleep deprivation, greater activity in the parietal region was associated with better short term memory. A 2001 study at the Chicago Medical Institute suggested that sleep deprivation may be linked to serious diseases, such as heart disease and mental illness including psychosis and bipolar disorder.][ The link between sleep deprivation and psychosis was further documented in 2007 through a study at Harvard Medical School and the University of California at Berkeley. The study revealed, using MRI scans, that sleep deprivation causes the brain to become incapable of putting an emotional event into the proper perspective and incapable of making a controlled, suitable response to the event. A study tested 17 right-handed civilian males, between the ages of 21 and 29 years (mean 24.7 ± 2.8 years), with no history of medical, neurological, psychiatric, or sleep disorder conditions. Their histories also included 7–8 hours of nightly sleep on a regular basis, no nicotine use, and low caffeine use (less than 100 mg/day). The negative effects of sleep deprivation on alertness and cognitive performance suggest decreases in brain activity and function, primarily in the thalamus, structure involved in alertness and attention, and in the prefrontal cortex, a region sub-serving alertness, attention, and higher-order cognitive processes. This study used a combination of positron emission tomography (PET) and Fluorine-2-deoxyglucose (FDG), a marker for regional cerebral metabolic rate for glucose (CMRglu) and neuronal synaptic activity. A time series design was used, with progressive sleep deprivation as the independent variable. Repeated measures of absolute regional CMRglu, cognitive performance, alertness, mood, and subjective experiences were collected after 0, 24, 48, and 72 h of sleep deprivation. Additional measures of alertness, cognitive performance, and mood were collected at fixed intervals throughout the sleep deprivation period. These measures were included to place the performance results associated with the PET scans in the context of the circadian rhythm of cognitive performance, as well as to impose a moderate-to-heavy near continuous workload on the subjects as might be anticipated in a real-world sustained operation. A noted 2002 University of California animal study indicated that non-rapid eye movement sleep (NREM) is necessary for turning off neurotransmitters and allowing their receptors to "rest" and regain sensitivity which allows monoamines (norepinephrine, serotonin and histamine) to be effective at naturally produced levels. This leads to improved regulation of mood and increased learning ability. The study also found that rapid eye movement sleep (REM) deprivation may alleviate clinical depression because it mimics selective serotonin reuptake inhibitors (SSRIs). This is because the natural decrease in monoamines during REM is not allowed to occur, which causes the concentration of neurotransmitters in the brain, that are depleted in clinically depressed persons, to increase. Sleep outside of the REM phase may allow enzymes to repair brain cell damage caused by free radicals. High metabolic activity while awake damages the enzymes themselves preventing efficient repair. This study observed the first evidence of brain damage in rats as a direct result of sleep deprivation. Animal studies suggest that sleep deprivation increases stress hormones, which may reduce new cell production in adult brains. A 1999 study found that sleep deprivation resulted in reduced cortisol secretion the next day, driven by increased subsequent slow-wave sleep. Sleep deprivation was found to enhance activity on the hypothalamic-pituitary-adrenal axis (which controls reactions to stress and regulates body functions such as digestion, the immune system, mood, sex, or energy usage) while suppressing growth hormones. The results supported previous studies, which observed adrenal insufficiency in idiopathic hypersomnia. A study conducted in 2005 showed that a group of rats which were deprived of REM sleep for five days experienced no significant changes in their ability to heal wounds, compared to a group of rats not deprived of "dream" sleep. The rats were allowed deep (NREM) sleep. However, another study conducted by Gumustekin et al. in 2004 showed sleep deprivation hindering the healing of burns on rats. Among the numerous physical consequences of sleep deprivation, deficits in attention and working memory are perhaps the most important; such lapses in mundane routines can lead to unfortunate results, from forgetting ingredients while cooking to missing a sentence while taking notes. Working memory is tested by such methods as choice-reaction time tasks. The attentional lapses also extend into more critical domains in which the consequences can be life-or-death; car crashes and industrial disasters can result from inattentiveness attributable to sleep deprivation. To empirically measure the magnitude of attention deficits, researchers typically employ the psychomotor vigilance task (PVT) which requires the subject to press a button in response to a light at pseudo-random intervals. Failure to press the button in response to the stimulus (light) is recorded as an error, attributable to the microsleeps that occur as a product of sleep deprivation. Crucially, individuals' subjective evaluations of their fatigue often do not predict actual performance on the PVT. While totally sleep-deprived individuals are usually aware of the degree of their impairment, lapses from chronic (lesser) sleep deprivation can build up over time so that they are equal in number and severity to the lapses occurring from total (acute) sleep deprivation. Chronically sleep-deprived people, however, continue to rate themselves considerably less impaired than totally sleep-deprived participants. Since people usually evaluate their capability on tasks like driving subjectively, their evaluations may lead them to the false conclusion that they can perform tasks that require constant attention when their abilities are in fact impaired. The dangers of sleep deprivation are apparent on the road; the American Academy of Sleep Medicine (AASM) reports that one in every five serious motor vehicle injuries is related to driver fatigue, with 80,000 drivers falling asleep behind the wheel every day and 250,000 accidents every year related to sleep, though the National Highway Traffic Safety Administration suggests the figure for traffic accidents may be closer to 100,000. The AASM recommends pulling off the road and taking a 15- or 20-minute nap to alleviate drowsiness. According to a 2000 study published in the British Medical Journal, researchers in Australia and New Zealand reported that sleep deprivation can have some of the same hazardous effects as being drunk. People who drove after being awake for 17–19 hours performed worse than those with a blood alcohol level of .05 percent, which is the legal limit for drunk driving in most western European countries and Australia. Another study suggested that performance begins to degrade after 16 hours awake, and 21 hours awake was equivalent to a blood alcohol content of .08 percent, which is the blood alcohol limit for drunk driving in Canada, the U.S., and the U.K. In addition, as a result of continuous muscular activity without proper rest time, effects such as cramping are much more frequent in sleep-deprived individuals. Extreme cases of sleep deprivation have been reported to be associated with hernias, muscle fascia tears, and other such problems commonly associated with physical overexertion. A 2006 study has shown that while total sleep deprivation for one night caused many errors, the errors were not significant until after the second night of total sleep deprivation. However, combining alcohol with acute sleep deprivation results in a trebled rate of driving off the road when using a simulator. The National Sleep Foundation identifies several warning signs that a driver is dangerously fatigued, including rolling down the window, turning up the radio, trouble keeping eyes open, head-nodding, drifting out of the lane, and daydreaming. At particular risk are lone drivers between midnight and 6 am. Sleep deprivation can negatively impact performance in professional fields as well, potentially jeopardizing lives. Due largely to the February 2009 crash of Colgan Air Flight 3407, which killed 50 people and was partially attributed to pilot fatigue, the FAA reviewed its procedures to ensure that pilots are sufficiently rested. A 2004 study also found medical residents with less than four hours of sleep a night made more than twice as many errors as residents who slept for more than seven hours a night, an especially alarming trend given that less than 11% of surveyed residents were sleeping more than seven hours a night. Twenty-four hours of continuous sleep deprivation results in the choice of less difficult math tasks without decreases in subjective reports of effort applied to the task. Naturally caused sleep loss affects the choice of everyday tasks such that low effort tasks are mostly commonly selected. Adolescents who experience less sleep show a decreased willingness to engage in sports activities that require effort through fine motor coordination and attention to detail. Great sleep deprivation mimics psychosis: distorted perceptions can lead to inappropriate emotional and behavioral responses. Astronauts have reported performance errors and decreased cognitive ability during periods of extended working hours and wakefulness as well as due to sleep loss caused by circadian rhythm disruption and environmental factors. Microsleeps occur when a person has a significant sleep deprivation. The brain automatically shuts down, falling into a sleep state for a period that can last from a fraction of a second up to half a minute. The person falls asleep no matter what activity he or she is engaged in. Microsleeps are similar to blackouts and a person experiencing them is not consciously aware that they are occurring. An even lighter type of sleep has been seen in rats that have been kept awake for long periods of time. In a process known as local sleep, specific localized regions went into periods of short (~80 ms) but frequent (~40/min) NREM-like state. Despite the on and off periods where neurons shut off, the rats appeared awake, although they performed worse at tests. In rats, prolonged, complete sleep deprivation increased both food intake and energy expenditure with a net effect of weight loss and ultimately death. This study hypothesizes that the moderate chronic sleep debt associated with habitual short sleep is associated with increased appetite and energy expenditure with the equation tipped towards food intake rather than expenditure in societies where high-calorie food is freely available. Several large studies using nationally representative samples suggest that the obesity problem in the United States might have as one of its causes a corresponding decrease in the average number of hours that people are sleeping. The findings suggest that this might be happening because sleep deprivation could be disrupting hormones that regulate glucose metabolism and appetite. The association between sleep deprivation and obesity appears to be strongest in young and middle-age adults. Other scientists hold that the physical discomfort of obesity and related problems, such as sleep apnea, reduce an individual's chances of getting a good night's sleep. Sleep loss is currently proposed to disturb endocrine regulation of energy homeostasis leading to weight gain and obesity. For instance, laboratory sleep deprivation studies in young men have demonstrated that one night of wakefulness (typically found e.g. in shift workers) exerts significant effects on the energy balance the next morning, including reduced energy expenditure, enhanced hedonic stimulus processing in the brain underlying the drive to consume food, and overeating that goes beyond satiety. Further studies have shown that a reduction of sleep duration to 4 hours for two consecutive nights has recently been shown to decrease circulating leptin levels and to increase ghrelin levels, as well as self-reported hunger. Similar endocrine alterations have been shown to occur even after a single night of sleep restriction. In a balanced order, nine healthy normal-weight men spent three nights in a sleep laboratory separated by at least 2 weeks: one night with a total sleep time of 7 h, one night with a total sleep time of 4.5 hours, and one night with total sleep deprivation (SD). On a standard symptom-rating scale, subjects rated markedly stronger feelings of hunger after total SD than after 7-hour sleep (3.9 ± 0.7 versus 1.7 ± 0.3; P = 0.020) or 4.5 h sleep (2.2 ± 0.5; P = 0.041). Plasma ghrelin levels were 22 ± 10% higher after total SD than after 7 h sleep (0.85 ± 0.06 versus 0.72 ± 0.04 ng mL(−1); P = 0.048) with intermediate levels of the hormone after 4.5 h sleep (0.77 ± 0.04 ng mL(−1)). Feelings of hunger as well as plasma ghrelin levels are already elevated after one night of SD, whereas morning serum leptin concentrations remain unaffected. Thus, the results provide further evidence for a disturbing influence of sleep loss on endocrine regulation of energy homeostasis, which in the long run may result in weight gain and obesity. A sleepless week down-regulated 444 genes, and up-regulated 267. Genes that were affected are related to circadian rhythms, metabolism, inflammation, immune response and stress. In science, sleep deprivation (of rodents, e.g.) is used in order to study the function(s) of sleep and the biological mechanisms underlying the effects of sleep deprivation. Some sleep deprivation techniques are as follows: Sleep deprivation can be used as a means of interrogation, which has resulted in court trials over whether or not the technique is a form of torture. Under one interrogation technique, a subject might be kept awake for several days and when finally allowed to fall asleep, suddenly awakened and questioned. Menachem Begin, the Prime Minister of Israel from 1977 to 1983, described his experience of sleep deprivation as a prisoner of the NKVD in Russia as follows: Sleep deprivation was one of the five techniques used by the British government in the 1970s. The European Court of Human Rights ruled that the five techniques "did not occasion suffering of the particular intensity and cruelty implied by the word torture ... [but] amounted to a practice of inhuman and degrading treatment", in breach of the European Convention on Human Rights. The United States Justice Department released four memos in August 2002 describing interrogation techniques used by the Central Intelligence Agency. They first described 10 techniques used in the interrogations of Abu Zubaydah, described as a terrorist logistics specialist, including sleep deprivation. Memos from May 2005 introduced four more techniques and confirmed that the combination of interrogation methods did not constitute torture under United States law. The question of extreme use of sleep deprivation as torture has advocates on both sides of the issue. In 2006, Australian Federal Attorney-General Philip Ruddock argued that sleep deprivation does not constitute torture. Nicole Bieske, a spokeswoman for Amnesty International Australia, has stated the opinion of her organization thusly: "At the very least, sleep deprivation is cruel, inhumane and degrading. If used for prolonged periods of time it is torture." Recent studies show sleep restriction has some potential in the treatment of depression. As many as 60% of patients, when sleep-deprived, show immediate recovery, although most relapse the following night. The effect has been shown to be linked to increases in the brain-derived neurotrophic factor (BDNF). It has been shown that chronotype is related to the effect of sleep deprivation on mood in normal people. Those with morningness preference become more depressed following sleep deprivation while those with eveningness preference show an improvement in mood. The incidence of relapse can be decreased by combining sleep deprivation with medication. Many tricyclic antidepressants suppress REM sleep, providing additional evidence for a link between mood and sleep. Similarly, tranylcypromine has been shown to completely suppress REM sleep at adequate doses. Sleep deprivation can sometimes be self-imposed due to a lack of desire to sleep and/or the habitual use of stimulant drugs (i.e. Cocaine, Amphetamines, etc.) Recent studies have also suggested that sleep deprivation produces similar effects in the brain to that of an SSRI in persons with depression, thus ensuing a clinical, self-imposed remedy. However, most individuals suffering from clinical depression are not aware that lack of sleep is having a direct positive effect on mood. Sleep deprivation is also self-imposed to achieve personal fame in the context of record-breaking stunts. People also use voluntary sleep deprivation to help them convert from monophasic sleep to polyphasic sleep. Sleep apnea (Obstructive sleep apnea, OSA) is a collapse of the upper airway during sleep, which reduces airflow to the lungs. It has many serious health outcomes if untreated, but can very often be effectively treated with positive air pressure therapy. Nasal problems such as a deviated septum will shut down the airway and increase swelling in the mucus lining and nasal turbinates. Corrective surgery (septoplasty) will maximise the airflow and correct the feedback loop to the brain which keeps awakening the sufferer so as not to asphyxiate. Central sleep apnea is repeated stops in breathing during sleep when the brain temporarily stops sending signals to the muscles that control breathing. The specific causal relationships between sleep loss and effects on psychiatric disorders have been most extensively studied in patients with mood disorders. Shifts into mania in bipolar patients are often preceded by periods of insomnia, and sleep deprivation has been shown to induce a manic state in susceptible individuals. Sleep deprivation may represent a final common pathway in the genesis of mania, and sleep loss is both a precipitating and reinforcing factor for the manic state. A National Sleep Foundation survey found that college/university-aged students get an average of 6.7 hours of sleep each night.][ Sleep deprivation is common in first year college students as they adjust to the stress and social activities of college life. A study performed by the Department of Psychology at the National Chung Cheng University in Taiwan concluded that freshmen received the shortest amount of sleep during the week. In 1997 the University of Minnesota did research that compared students who went to school at 7:15 am and those who went to school at 8:40 am. They found that students who went to school at 8:40 got higher grades and more sleep on weekday nights. One in four U.S. high school students admits to falling asleep in class at least once a week. It is known that during human adolescence, circadian rhythms and therefore sleep patterns typically undergo marked changes. Electroencephalogram (EEG) studies indicate a 50% reduction of deep (stage 4) sleep and a 75% reduction in the peak amplitude of delta waves during NREM sleep in adolescence. School schedules are often incompatible with a corresponding delay in sleep offset, leading to a less than optimal amount of sleep for the majority of adolescents. Several strategies are common in attempting to increase alertness and counteract the effects of sleep deprivation. Caffeine is often used over short periods to boost wakefulness when acute sleep deprivation is experienced; however, caffeine is less effective if taken routinely. Other strategies recommended by the American Academy of Sleep Medicine include prophylactic sleep before deprivation, naps, other stimulants, and combinations thereof. However, the only sure and safe way to combat sleep deprivation is to increase nightly sleep time. Recovery of cognitive function is accomplished more rapidly after acute total sleep deprivation than after chronic partial sleep restriction. Chronic deprivation is the more common in everyday life. Just one night of recovery sleep can reverse adverse effects of total sleep deprivation. Recovery sleep is more efficient than normal sleep with shorter sleep latency and increased amounts of deep and REM sleep. Randy Gardner holds the scientifically documented record for the longest period of time a human being has intentionally gone without sleep not using stimulants of any kind. Gardner stayed awake for 264 hours (11 days), breaking the previous record of 260 hours held by Tom Rounds of Honolulu. LCDR John J. Ross of the U.S. Navy Medical Neuropsychiatric Research Unit later published an account of this event, which became well-known among sleep-deprivation researchers. The Guinness World Records record stands at 449 hours (18 days, 17 hours), held by Maureen Weston, of Peterborough, Cambridgeshire in April 1977, in a rocking-chair marathon. Claims of not having slept in years have been made at times, for certain individuals, but either without scientific verification, or contradicted in independent verification: M: PSO/PSI mepr dsrd (o, p, m, p, a, d, s), sysi/epon, spvo proc (eval/thrp), drug (N5A/5B/5C/6A/6B/6D) M: CNS anat (n/s/m/p/4/e/b/d/c/a/f/l/g)/phys/devp noco (m/d/e/h/v/s)/cong/tumr, sysi/epon, injr proc, drug (N1A/2AB/C/3/4/7A/B/C/D)
Sleep inertia is a physiological state characterised by a decline in motor dexterity and a subjective feeling of grogginess immediately following an abrupt awakening. The impaired alertness may interfere with the ability to perform mental or physical tasks. Sleep inertia can also refer to the tendency of a person wanting to return to sleep. NASA studies have shown that a variety of factors influence the severity and duration of sleep inertia. These include: Sleep inertia can be more severe and last longer when a nap follows a prolonged period of wakefulness or an accumulated sleep debt. Sleep inertia can often be reversed by activity and noise as well as caffeine. Reaction time performance is directly related to sleep stage at awakening; persons awakened during the deepest sleep have the slowest reaction times. One theory is that sleep inertia is caused by the build-up of adenosine in the brain during NREM sleep. Adenosine then binds to receptors, and feelings of tiredness result. M: PSO/PSI mepr dsrd (o, p, m, p, a, d, s), sysi/epon, spvo proc (eval/thrp), drug (N5A/5B/5C/6A/6B/6D) M: CNS anat (n/s/m/p/4/e/b/d/c/a/f/l/g)/phys/devp noco (m/d/e/h/v/s)/cong/tumr, sysi/epon, injr proc, drug (N1A/2AB/C/3/4/7A/B/C/D)
Circadian rhythm sleep disorders are a family of sleep disorders affecting, among other things, the timing of sleep. People with circadian rhythm sleep disorders are unable to sleep and wake at the times required for normal work, school, and social needs. They are generally able to get enough sleep if allowed to sleep and wake at the times dictated by their body clocks. Unless they also have another sleep disorder, their sleep is of normal quality. Humans, like most animals and plants, have biological rhythms, known as circadian rhythms, which are controlled by a biological clock and work on a daily time scale. These affect body temperature, alertness, appetite, hormone secretion etc. as well as sleep timing. Due to the circadian clock, sleepiness does not continuously increase as time passes. A person's desire and ability to fall asleep is influenced by both the length of time since the person woke from an adequate sleep, and by internal circadian rhythms. Thus, the body is ready for sleep and for wakefulness at different times of the day. Sleep researcher Yaron Dagan states that "[t]hese disorders can lead to harmful psychological and functional difficulties and are often misdiagnosed and incorrectly treated due to the fact that doctors are unaware of their existence." Two of these disorders are extrinsic (from Latin extrinsecus, from without, on the outside) or circumstantial: Four of them are intrinsic (from Latin intrinsecus, on the inside, inwardly), "built-in": Among people with healthy circadian clocks, there is a continuum of chronotypes from "larks", "morning people", who prefer to sleep and wake early, to "owls", "evening people" or "night people", who prefer to sleep and wake at late times. Whether they are larks or owls, people with normal circadian systems: Researchers have placed volunteers in caves or special apartments for several weeks without clocks or other time cues. Without time cues, the volunteers tended to go to bed an hour later and to get up about an hour later each day. These experiments appeared to demonstrate that the "free-running" circadian rhythm in humans was about 25 hours long. However, these volunteers were allowed to control artificial lighting and the light in the evening caused a phase delay. More recent research shows that adults of all ages free-run at an average of 24 hours and 11 minutes. To maintain a 24-hour day/night cycle, the biological clock needs regular environmental time cues or Zeitgebers, e.g., sunrise, sunset, and daily routine. Time cues keep the normal human circadian clock aligned with the rest of the world. Non-24-hour sleep-wake syndrome and other persistent circadian rhythm sleep disorders are believed to be caused by an inadequate ability to reset the sleep/wake cycle in response to environmental time cues. These individuals' circadian clocks might have an unusually long cycle, and/or might not be sensitive enough to time cues. People with DSPS (Delayed sleep phase disorder), more common than Non-24, do entrain to nature's 24 hours, but are unable to sleep and awaken at socially preferred times, sleeping instead, for example, from 4 a.m. to noon. According to doctors Cataletto and Hertz at WebMD, "Altered or disrupted sensitivity to zeitgebers is probably the most common cause of circadian rhythm disorder." Circadian rhythm abnormalities are also extremely common in ADHD, especially in the form of delayed sleep (sleep initiation insomnia). It has been genetically linked by findings of polymorphism in genes in common between those apparently involved in ADHD and those involved in the circadian rhythm and a high proportion of DSPD among those with ADHD, however no specific or further cause-effect relationship has been proven. As of October 1, 2005, the diagnostic codes for circadian rhythm sleep disorders were changed from the 307-group to the 327-group in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR). The DSM updated to agree with the International Classification of Diseases (ICD-9). The new codes reflect the moving of these disorders from the Mental Disorders section to the Neurological section in the ICD. Possible treatments for circadian rhythm sleep disorders include: M: PSO/PSI mepr dsrd (o, p, m, p, a, d, s), sysi/epon, spvo proc (eval/thrp), drug (N5A/5B/5C/6A/6B/6D) M: CNS anat (n/s/m/p/4/e/b/d/c/a/f/l/g)/phys/devp noco (m/d/e/h/v/s)/cong/tumr, sysi/epon, injr proc, drug (N1A/2AB/C/3/4/7A/B/C/D) M: CNS anat (n/s/m/p/4/e/b/d/c/a/f/l/g)/phys/devp noco (m/d/e/h/v/s)/cong/tumr, sysi/epon, injr proc, drug (N1A/2AB/C/3/4/7A/B/C/D)
Sleep hygiene is the controlling of "all behavioural and environmental factors that precede sleep and may interfere with sleep." It is the practice of following guidelines in an attempt to ensure more restful, effective sleep which can promote daytime alertness and help treat or avoid certain kinds of sleep disorders. Trouble sleeping and daytime sleepiness can be indications of poor sleep hygiene or sleep habits. The International Classification of Sleep Disorders-Revised (ICSD-R) states on page 74: "The importance of assessing the contribution of inadequate sleep hygiene in maintaining a preexisting sleep disturbance cannot be overemphasized." In the ICSD-R, the diagnosis inadequate sleep hygiene is classified as an extrinsic sleep disorder, code 307.41-1. Doctors and clinicians who advise sleep hygiene strategies for patients and families have lists of suggestions which may include advice about timing of sleep and food intake in relationship to it, exercise, sleeping environment, etc. Which items are suggested for which patients are selected by the clinician, depending on knowledge of the individual situation; the counselling is presented as a form of patient education. Re-education involves a combination of advice about homeostatic, adaptive and circadian aspects of sleep control, how to avoid sleep deprivation, and how to respond to unwanted awakenings from sleep if these occur. As the second edition of the ICSD (ICSD2, 2005) points out, the "sleep disruptive effects of poor sleep hygiene are often obvious to others, but the patients show little insight into this fact." Recommendations to improve sleep quality include: Also, some medications cause drowsiness, and in such cases it may be beneficial to use a non-sedating alternative.
Sleep deprivation Effects of sleep deprivation on cognitive performance Rapid eye movement sleep Sleep Biology Neurophysiology
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