"is awake, brain waves show a regular rhythm. When a person first falls asleep, the brain waves become slower and less regular, which is called non-rapid eye movement (NREM) sleep. After about an hour and a half of NREM sleep, the brain waves begin to show a more active pattern again, called REM sleep (rapid eye movement sleep), when most remembered dreaming occurs. Associated with the EEG-observed waves during REM sleep, muscle atonia is present called REM atonia. In narcolepsy, the order and length of NREM and REM sleep periods are disturbed, with REM sleep occurring at sleep onset instead"
"Narcolepsy Narcolepsy is a long-term neurological disorder that involves a decreased ability to regulate sleep-wake cycles. Symptoms include periods of excessive daytime sleepiness that usually last from seconds to minutes and may occur at any time. About 70% of those affected also experience episodes of sudden loss of muscle strength, known as cataplexy. These experiences can be brought on by strong emotions. Less commonly, there may be inability to move or vivid hallucinations while falling asleep or waking up. People with narcolepsy tend to sleep about the same number of hours per day as people without, but the quality of"
"behavior modification are utilized to train patients to only go to bed when tired, associating the bed itself with a sleepy state. Narcolepsy is a condition characterized by abnormal transitions between REM and non-REM cycles during sleep and the awake cycle. Cataplexy, on the other hand, is an involuntary loss of muscle tone during wakefulness. The mechanism of narcolepsy is unknown, though recent findings suggest that orexin neurons in the lateral and posterior hypothalamus may play a critical role in reinforcing wakefulness. Narcolepsy is often treated with psychostimulants or tricyclic antidepressants in order to suppress REM sleep patterns. Sleep apnea"
"asleep for a few seconds. Along with vivid dreaming, people with narcolepsy are known to have audio or visual hallucinations prior to falling asleep. Narcoleptics can gain excess weight; children can gain 20 to 40 lb (9 to 18 kg) when they first develop narcolepsy; in adults the body-mass index is about 15% above average. The exact cause of narcolepsy is unknown, and it may be caused by several distinct factors. Part of the mechanism involves the loss of orexin-releasing neurons within the lateral hypothalamus. In up to 10% of cases there is a family history of the disorder. There"
"""over-sleeping"". In fact, narcoleptics live their entire lives in a constant state of extreme sleep deprivation. Daytime naps may occur with little warning and may be physically irresistible. These naps can occur several times a day. They are typically refreshing, but only for a few hours or less. Vivid dreams may be experienced on a regular basis, even during very brief naps. Drowsiness may persist for prolonged periods or remain constant. In addition, night-time sleep may be fragmented, with frequent awakenings. A second prominent symptom of narcolepsy is abnormal REM sleep. Narcoleptics are unique in that they enter into the"
"narcolepsy are present, but if the sleep attacks are isolated and cataplexy is mild or absent, diagnosis is more difficult. It is also possible for cataplexy to occur in isolation. Three tests that are commonly used in diagnosing narcolepsy are the polysomnogram, the multiple sleep latency test (MSLT), and administration of the Epworth Sleepiness Scale. These tests are usually performed by a sleep specialist. The polysomnogram involves continuous recording of sleep brain waves and a number of nerve and muscle functions during night time sleep. When tested, people with narcolepsy fall asleep rapidly, enter REM sleep early, and may often"
"order of appearance of cataplexy, sleep paralysis, and hypnagogic hallucinations in individuals. Only about 20 to 25 percent of people with narcolepsy experience all four symptoms. The excessive daytime sleepiness generally persists throughout life, but sleep paralysis and hypnagogic hallucinations may not. A rare subset of narcoleptics also experience a heightened sense of taste and smell known as the supertaster phenomenon. Many people with narcolepsy also suffer from insomnia for extended periods of time. The excessive daytime sleepiness and cataplexy often become severe enough to cause serious problems in a person's social, personal, and professional life. Normally, when an individual"
"in managing symptoms of cataplexy, however, it has notable side-effects including sleep disruption. In the United States, it is estimated that this condition afflicts as many as 200,000 Americans, but fewer than 50,000 are diagnosed. It is as widespread as Parkinson's disease or multiple sclerosis and more prevalent than cystic fibrosis, but it is less well known. Narcolepsy is often mistaken for depression, epilepsy, or the side effects of medications. It can also be mistaken for poor sleeping habits, recreational drug use, or laziness. Narcolepsy can occur in both men and women at any age, although its symptoms are usually"
"the French ""narcolepsie"". The French term was first used in 1880 by Jean-Baptiste-Édouard Gélineau, who used the Greek νάρκη (""narkē""), meaning ""numbness"", and λῆψις (""lepsis"") meaning ""attack"". There are two main characteristics of narcolepsy: excessive daytime sleepiness and abnormal REM sleep. The first, excessive daytime sleepiness (EDS), occurs even after adequate night time sleep. A person with narcolepsy is likely to become drowsy or fall asleep, often at inappropriate times and places, or just be very tired throughout the day. Narcoleptics are not able to experience the amount of restorative deep sleep that healthy people experience – they are not"
"with impairments due to a greatly reduced number of hypothalamic orexin projection neurons and significantly fewer orexin neuropeptides in cerebrospinal fluid and neural tissue, compared to non-narcoleptic individuals. Those with narcolepsy generally experience the REM stage of sleep within five minutes of falling asleep, while people who do not have narcolepsy (unless they are significantly sleep deprived) do not experience REM until after a period of slow-wave sleep, which lasts for about the first hour or so of a sleep cycle. Measuring orexin levels in a person's cerebrospinal fluid sampled in a spinal tap may help in diagnosing narcolepsy, with"
"of) rapid eye movement (REM) sleep. As a consequence night time sleep does not include as much deep sleep, so the brain tries to ""catch up"" during the day, hence EDS. People with narcolepsy may visibly fall asleep at unpredicted moments (such motions as head bobbing are common). People with narcolepsy fall quickly into what appears to be very deep sleep, and they wake up suddenly and can be disoriented when they do (dizziness is a common occurrence). They have very vivid dreams, which they often remember in great detail. People with narcolepsy may dream even when they only fall"
"states of arousal. Hypocretin deficiency is further associated with decreased levels of histamine and epinephrine, which are chemicals important in promoting wakefulness, arousal and alertness. The diagnosis of narcolepsy and cataplexy is usually made by symptom presentation. Presenting with the tetrad of symptoms (Excessive daytime sleepiness, sleep onset paralysis, hypnagogic hallucinations, cataplexy symptoms) is strong evidence of the diagnosis of narcolepsy. A Multiple Sleep Latency Test (MSLT) is often conducted in order to quantify daytime sleepiness. Cataplexy is treated with medications. There are no behavioral treatments. People with narcolepsy will often try to avoid thoughts and situations that they know"
"jerkings of arms, which were characterized as muscle spasms. Finally, a patient with a homozygous c.810T>A showed signs of Gower's sign, hypotonia, and proximal muscle weakness. Narcolepsy is a neurological disabling sleep disorder, characterized by excessive daytime sleepiness, sleep fragmentation, symptoms of abnormal rapid-eye-movement (REM) sleep, cataplexy, hypnagogic hallucinations, and sleep paralysis. Cataplexy is a sudden loss of muscle tone triggered by emotions, which is the most valuable clinical feature used to diagnose narcolepsy. Human narcolepsy is primarily a sporadically occurring disorder but familial clustering has been observed. CHKB has been shown to have Protein-protein interactions with the following. CHKB"
"are made of the time taken to reach various stages of sleep (sleep onset latency). This test measures the degree of daytime sleepiness and also detects how soon REM sleep begins. Again, people with narcolepsy fall asleep rapidly and enter REM sleep early. Occasionally, a multiple sleep latency test can result in a false-negative for a narcoleptic. The system which regulates sleep, arousal, and transitions between these states in humans is composed of three interconnected subsystems: the orexin projections from the lateral hypothalamus, the reticular activating system, and the ventrolateral preoptic nucleus. In narcoleptic individuals, these systems are all associated"
"getting enough sleep. Cataplexy may be mistaken for seizures. While there is no cure, a number of lifestyle changes and medications may help. Lifestyle changes include taking regular short naps and sleep hygiene. Medications used include modafinil, sodium oxybate and methylphenidate. While initially effective, tolerance to the benefits may develop over time. Tricyclic antidepressants and selective serotonin reuptake inhibitors (SSRIs) may improve cataplexy. About 0.2 to 600 per 100,000 people are affected. The condition often begins in childhood. Men and women are affected equally. Untreated narcolepsy increases the risk of motor vehicle collisions and falls. The term ""narcolepsy"" is from"
"treat diseases of the CNS for example Alzheimer's disease (AD), attention deficit hyperactivity syndrome (ADHD), schizophrenia (SCH), pain, and narcolepsy. Narcolepsy is a sleeping disorder which is characterised by chronic sleepiness. Cataplexy, hypnagogic hallucinations and sleep paralysis can also be present in narcolepsy. HR antagonism leads to histamine release into the cerebrospinal fluid which promotes wakefulness. Therefore, HR antagonists have been studied in the hope of treating narcolepsy. Pitolisant has been approved for treatment of narcolepsy and other HR antagonists are in clinical trials. Alzheimer’s disease is a progressive neurodegenerative disease of the brain. Histamine plays a well documented role"
"sleep tends to be worse. The exact cause of narcolepsy is unknown, with potentially several causes. In up to 10% of cases, there is a family history of the disorder. Often, those affected have low levels of the neuropeptide ""orexin"", which may be due to an autoimmune disorder. Trauma, infections, toxins or psychological stress may also play a role. Diagnosis is typically based on the symptoms and sleep studies, after ruling out other potential causes. Excessive daytime sleepiness can also be caused by other sleep disorders such as sleep apnea, major depressive disorder, anemia, heart failure, drinking alcohol and not"
"hypocretin, is a neuropeptide that acts within the brain to regulate appetite and wakefulness as well as a number of other cognitive and physiological processes. While there are billions of cells in the human brain, only 10,000–20,000 neurons secrete orexin peptides; all of these neurons project out of the lateral hypothalamus. Loss of these orexin-producing neurons causes narcolepsy and most individuals with narcolepsy have a reduced number of these neurons in their brains. The neural control of normal sleep states and the relationship to narcolepsy are only partially understood. In humans, narcoleptic sleep is characterized by a tendency to go"
"wakefulness in the day (and sleep at night), and cataplexy, which is the loss of muscle tone in response to strong, usually positive, emotions. Dogs that lack a functional receptor for orexin have narcolepsy, while animals and people lacking the orexin neuropeptide itself also have narcolepsy. Central administration of orexin-A strongly promotes wakefulness, increases body temperature and locomotion, and elicits a strong increase in energy expenditure. Sleep deprivation also increases orexin-A transmission. The orexin system may thus be more important in the regulation of energy expenditure than food intake. In fact, orexin-deficient narcoleptic patients have increased obesity rather than decreased"
"narcolepsy is central nervous system stimulants such as methylphenidate, amphetamine, dextroamphetamine, modafinil, and armodafinil. In late 2007 an alert for severe adverse skin reactions to modafinil was issued by the FDA. Another drug that is used is atomoxetine, a non-stimulant and a norepinephrine reuptake inhibitor (NRI), which has no addiction liability or recreational effects. In many cases, planned regular short naps can reduce the need for pharmacological treatment of the EDS, but only improve symptoms for a short duration. A 120-minute nap provided benefit for 3 hours in patient alertness whereas a 15-minute nap provided no benefit. Daytime naps are"
"of excessive daytime sleepiness. A study has reported that transplantation of orexin neurons into the pontine reticular formation in rats is feasible, indicating the development of alternative therapeutic strategies in addition to pharmacological interventions to treat narcolepsy. Orexin Orexin (), also known as hypocretin, is a neuropeptide that regulates arousal, wakefulness, and appetite. The most common form of narcolepsy, in which the sufferer experiences brief losses of muscle tone (cataplexy), is caused by a lack of orexin in the brain due to destruction of the cells that produce it. There are only 10,000–20,000 orexin-producing neurons in the human brain, located"
"substantially to the disabling features of the disorder. Cognitive, educational, occupational, and psychosocial problems associated with the excessive daytime sleepiness of narcolepsy have been documented. For these to occur in the crucial teen years when education, development of self-image, and development of occupational choice are taking place is especially devastating. While cognitive impairment does occur, it may only be a reflection of the excessive daytime somnolence. The prevalence of narcolepsy is about 1 per 2,000 persons. It is a reason for patient visits to sleep disorder centers, and with its onset in adolescence, it is also a major cause of"
"wakefulness including the dopamine, norepinephrine, histamine and acetylcholine systems and appear to play an important role in stabilizing wakefulness and sleep. The discovery that an orexin receptor mutation causes the sleep disorder canine narcolepsy in Doberman Pinschers subsequently indicated a major role for this system in sleep regulation. Genetic knockout mice lacking the gene for orexin were also reported to exhibit narcolepsy. Transitioning frequently and rapidly between sleep and wakefulness, these mice display many of the symptoms of narcolepsy. Researchers are using this animal model of narcolepsy to study the disease. Narcolepsy results in excessive daytime sleepiness, inability to consolidate"
"associated with primary hypersomnia in general in mouse studies. “Mice with systemic carnitine deficiency exhibit a higher frequency of fragmented wakefulness and rapid eye movement (REM) sleep, and reduced locomotor activity.” Administration of acetyl-L-carnitine was shown to improve these symptoms in mice. A subsequent human trial found that narcolepsy patients given L-carnitine spent less total time in daytime sleep than patients who were given a placebo. Narcolepsy Narcolepsy is a long-term neurological disorder that involves a decreased ability to regulate sleep-wake cycles. Symptoms include periods of excessive daytime sleepiness that usually last from seconds to minutes and may occur at"
"first noticed in teenagers or young adults. There is strong evidence that narcolepsy may run in families; around 10 percent of people diagnosed with narcolepsy with cataplexy have a close relative with this neurological disorder. While narcolepsy symptoms are often confused with depression, there is a link between the two disorders. Research studies have mixed results on co-occurrence of depression in narcolepsy patients - the numbers quoted by different studies are anywhere between 6% and 50%. Narcolepsy has its typical onset in adolescence and young adulthood. There is an average 15-year delay between onset and correct diagnosis which may contribute"
"REM phase of sleep in the beginnings of sleep, even when sleeping during the day. The classic symptoms of the disorder, often referred to as the ""tetrad of narcolepsy,"" are cataplexy, sleep paralysis, hypnagogic hallucinations, and excessive daytime sleepiness. Other symptoms may include automatic behaviors and night-time wakefulness. These symptoms may not occur in all patients. In most cases, the first symptom of narcolepsy to appear is excessive and overwhelming daytime sleepiness. The other symptoms may begin alone or in combination months or years after the onset of the daytime naps. There are wide variations in the development, severity, and"
"unrefreshing naps). It is believed that this subgroup might have dysfunction in multiple arousal systems, including orexin and GABA (see idiopathic hypersomnia causes). People with narcolepsy can be substantially helped, but not cured. Treatment is tailored to the individual, based on symptoms and therapeutic response. The time required to achieve optimal control of symptoms is highly variable and may take several months or longer. Medication adjustments are frequently necessary, and complete control of symptoms is seldom possible. While oral medications are the mainstay of formal narcolepsy treatment, lifestyle changes are also important. The main treatment of excessive daytime sleepiness in"
"of mechanisms of action are needed before new classes of therapeutic agents can be developed. Narcolepsy is an underdiagnosed condition in the general population. This is partly because its severity varies, so it can be mistaken for other illnesses very easily. Some people with narcolepsy do not suffer from loss of muscle control. In 2015, it was reported that the British Department of Health was paying for sodium oxybate medication at a cost of £12,000 a year for 80 people who are taking legal action over problems linked to the use of the Pandemrix swine flu vaccine. Sodium oxybate is"
"not a replacement for night time sleep. Ongoing communication between the health care provider, patient, and the patient's family members is important for optimal management of narcolepsy. Another FDA-approved treatment option for narcolepsy is sodium oxybate, also known as sodium gamma-hydroxybutyrate (GHB). It can be used for cataplexy associated with narcolepsy and excessive daytime sleepiness associated with narcolepsy. Narcolepsy has sometimes been treated with selective serotonin reuptake inhibitors and tricyclic antidepressants, such as clomipramine, imipramine, or protriptyline, as well as other drugs that suppress REM sleep. Venlafaxine, an antidepressant which blocks the reuptake of serotonin and norepinephrine, has shown usefulness"
"Orexin Orexin (), also known as hypocretin, is a neuropeptide that regulates arousal, wakefulness, and appetite. The most common form of narcolepsy, in which the sufferer experiences brief losses of muscle tone (cataplexy), is caused by a lack of orexin in the brain due to destruction of the cells that produce it. There are only 10,000–20,000 orexin-producing neurons in the human brain, located predominantly in the perifornical area and lateral hypothalamus. They project widely throughout the central nervous system, regulating wakefulness, feeding, and other behaviours. There are two types of orexin peptide and two types of orexin receptor. Orexin was"
"on hypocretin gene therapy and hypocretin cell transplantation for narcolepsy-cataplexy. Cataplexy Cataplexy is a sudden and transient episode of muscle weakness accompanied by full conscious awareness, typically triggered by emotions such as laughing, crying, or terror. Cataplexy affects approximately 70% of people who have narcolepsy, and is caused by an autoimmune destruction of neurons that produce the neuropeptide hypocretin (also called orexin), which regulates arousal and wakefulness. Cataplexy without narcolepsy is rare and the cause is unknown. The term cataplexy originates from the Greek κατά (""kata"", meaning ""down""), and πλῆξις (""plēxis"", meaning ""stroke""). Cataplexy manifests itself as muscular weakness which"
"their muscles are suppressed). This is different from conventional sleepwalking, which takes place during slow-wave sleep, not REM. Narcolepsy by contrast seems to involve excessive and unwanted REM atonia—i.e., cataplexy and excessive daytime sleepiness while awake, hypnagogic hallucinations before entering slow-wave sleep, or sleep paralysis while waking. Other psychiatric disorders including depression have been linked to disproportionate REM sleep. Patients with suspected sleep disorders are typically evaluated by polysomnogram. Lesions of the pons to prevent atonia have induced functional “REM behavior disorder” in animals. Rapid eye movement sleep (REM) has since its discovery been closely associated with dreaming. Waking up"
"of after a period of NREM sleep. Also, some aspects of REM sleep that normally occur only during sleep, like lack of muscular control, sleep paralysis, and vivid dreams, occur at other times in people with narcolepsy. For example, the lack of muscular control can occur during wakefulness in a cataplexy episode; it is said that there is an intrusion of REM atonia during wakefulness. Sleep paralysis and vivid dreams can occur while falling asleep or waking up. Simply put, the brain does not pass through the normal stages of dozing and deep sleep but goes directly into (and out"