makalah hiperinsomnia

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18. Nishino S, Kanbayashi T. Symptomatic narcolepsy, cataplexy and hypersomnia, and theirimplications in the hypothalamic hypocretin/orexin system. Sleep Med Rev. Aug 2005;9(4):269-310.[Medline].
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19. Yamanaka A, Tsujino N, Funahashi H, Honda K, Guan JL, Wang QP, et al. Orexins activatehistaminergic neurons via the orexin 2 receptor. Biochem Biophys Res Commun. 2002;290:1237-45.[Medline].[Full Text].

20. Ohayon MM, Dauvilliers Y, Reynolds CF 3rd. Operational Definitions and Algorithms forExcessive Sleepiness in the General Population: Implications for DSM-5 Nosology.Arch GenPsychiatry. Jan 2012;69(1):71-9.[Medline].

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28. [Best Evidence] [Guideline] Morgenthaler TI, Kapur VK, Brown T, Swick TJ, Alessi C, Aurora RN,et al. Practice parameters for the treatment of narcolepsy and other hypersomnias of central

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Background

The International Classification of Sleep Disorders (ICSD) describes primary hypersomnia as anidiopathic disorder of presumed central nervous system (CNS) cause that is associated with excessivesleepiness (ie, prolonged episodes of nonrapid eye movement [NREM] sleep). (See Etiology andPresentation.)[1]

The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR)defines primary (idiopathic) hypersomnia as excessive daytime sleepiness withoutnarcolepsyor theassociated features of othersleep disorders.[2]

In 1966, William Dement proposed that patients with excessive daytime sleepiness, but without cataplexy,sleep paralysis, or sleep-onset rapid eye movement (REM), should not be considered narcoleptic.[3] In1972, Roth et al described a type of hypersomnia with sleep drunkenness that consists of difficultycoming to complete wakefulness, confusion, disorientation, poor motor coordination, and slowness,accompanied by deep and prolonged sleep.[4] The abrupt sleep attacks seen in classic narcolepsy are notpresent in this disorder.

In comparison with narcolepsy, which is characterized by well-defined clinical, polysomnographic, andimmunogenetic features, primary hypersomnia is not well characterized.[5, 6] Moreover, while the DSM-IV-TRand the ICSD each define 2 types of idiopathic/primary hypersomnia based on the sleep time duration

(ie, with or without long sleep), the presentation is often heterogeneous. (See Presentation, DDX, andWorkup.)[7]

Please note that while the ICSD prefers the diagnostic label of idiopathic hypersomnia, the DSM prefersthe diagnostic label ofprimary hypersomnia. As the terms are interchangeable, this article will refer tothem alternately.

Classification

Primary hypersomnia can be classified as monosymptomatic or polysymptomatic. Isolated excessivedaytime sleepiness that is not due to abnormal nocturnal awakenings characterizes themonosymptomatic form. The polysymptomatic form consists of abnormally long nocturnal sleep and signsof sleep drunkenness upon awakening.[8]

In the literature, 3 possible subgroups of idiopathic CNS hypersomnia have been suggested.

Subgroup I

These patients have a positive family history, and associated clinical symptoms suggest dysfunction ofthe autonomic nervous system. These symptoms include headache, syncope, orthostatic hypotension,and peripheral vasoconstriction (cold hands and feet).

Subgroup II

This group includes patients who had a viral infection associated with neurologic symptoms, such asGuillain-Barr syndrome, infectious mononucleosis, or atypical viral pneumonia. Even after theirinfectious disease resolves, these patients continue to require significantly more nocturnal sleep andcontinue to feel very tired.

Although initially these patients are fatigued, they subsequently have difficulty differentiating fatigue fromsleepiness. To fight tiredness, these patients nap and eventually present with complaints of excessivedaytime sleepiness. Analysis of cerebral spinal fluid demonstrates moderate lymphocytosis (30-50cells/L with mild to moderate elevation in protein).

Subgroup III

These patients do not have a positive family or viral infection history, and the cause of the disorder truly isidiopathic.
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Recurrent primary hypersomnia

Kleine-Levin syndrome (KLS) is a rare disorder that starts during adolescence and has a male genderpreference. The patients have recurrent episodes of hypersomnia, which are often associated withcompulsive overeating and hypersexuality.[9] The periods of hypersomnia occur for days to weeks at atime and recur several times a year. In between the symptomatic periods, the patients have normal sleeprequirements and do not have excessive daytime sleepiness. Some patients may develop symptoms of

irritability, impulsive behavior, depersonalization, hallucinations, depression, and confusion. The etiologyof this disorder is not known.[10, 11]

The disorder mainly affects males (68%). The median age of onset is 15 years (range, 4-82y; 81% duringthe second decade), and the syndrome may last up to 8 years. The episodes recur every 3-4 months andmay last up to 10 days, but they may last longer in women.(See Epidemiology.)

KLS may be precipitated by infections (38.2%), head trauma (9%), or alcohol consumption (5.4%).Characteristic symptoms include the following [11] :

Hypersomnia - 100%

Cognitive changes - 96%, including a specific feeling of derealization

Eating disturbances - 80%

Hypersexuality - 43%

Compulsions - 29%

Depressed mood - 48%Menstrual-related hypersomnia is diagnosed when excessive daytime sleepiness occurs on a periodicbasis over a few days preceding menstruation.[12] It is assumed that the symptoms follow hormonalchanges, but the etiology of the syndrome, as well as its prevalence and course, are virtually unknown.

The ICSD recurrent hypersomnia is classified separately to describe the recurrent form of primaryhypersomnia according to the DSM-IV-TR.

Etiology

Primary hypersomnia is an idiopathic disorder. Although head injury or viral infections can cause adisorder resembling primary hypersomnia, the true causes for most cases remain unknown. No genetic,environmental, or other predisposition has been identified.[6]

Excessive daytime sleepiness has been described in a subset of patients following viral illnesses such asGuillain-Barr syndrome, hepatitis, mononucleosis, and atypical viral pneumonia. Familial casesassociated with HLA-Cw2 and HLA-DR11 genotypes have also been reported.[13] However, the majority ofthe patients diagnosed with idiopathic hypersomnia have neither a positive family history nor a pastmedical history of viral illnesses.

In experimental animal studies, destruction of the nonadrenergic neurons of the rostral third of the locusceruleus complex has produced hypersomnia. While trauma has been associated with excessive daytimesleepiness in a case series, cerebrospinal fluid (CSF) analysis for specific neurotransmitter metabolitesdid not differentiate patients with posttraumatic excessive daytime sleepiness from patients withnarcolepsy or other patients with excessive daytime sleepiness.[14]Injury to the adrenergic neurons at thebundle of isthmus has led to hypersomnia associated with a proportional increase of both NREM and

REM sleep.[15]

Evidence suggests that a dopamine system dysfunction may occur in narcolepsy, while a similarmalfunction of the norepinephrine system may occur in idiopathic hypersomnia. Decreased CSFhistamine levels have been reported in primary hypersomnia, as well as in narcolepsy, but not in non-CNS hypersomnias, suggesting that histamine may be an indicator of a central (versus a peripheral)origin for hypersomnias.[16]

A major advance in the understanding of the pathology of narcolepsy, a disorder closely related toprimary hypersomnia, was made after the discovery of narcolepsy-associated genes in animals; ie, genes
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involved in the pathology of the hypocretin/orexin ligand and its receptor.[17, 18] Low CSF concentrations ofhypocretin-1 and hypocretin-2 in HLA DQB1*0602 were also found in primary hypersomnia, and ageneralized defect in hcrt-2 transmission may be present in this disorder. As hypocretin peptides excitethe histaminergic system by the hypocretin receptor 2,[19] hypocretin deficiency may result in excessivedaytime sleepiness via decreased histaminergic function.[16]

EpidemiologyOccurrence in the United States

While the rates of excessive daytime sleepiness complaints in the general population are between 0.5-5%of adults (in surveys without a specific consideration of causes/diagnoses), idiopathic hypersomnia isdiagnosed in about 5-10% of individuals who are self referred to a sleep clinic with a chief complaint ofdaytime sleepiness.[1]A precise estimation of idiopathic hypersomnia prevalence is complicated by a lackof clear biologic markers or unambiguous diagnostic criteria.

A study by Ohayon et al suggested that excessive sleepiness is more prevalent than previouslyestimated. The study found that with 27.8% of 15,929 individuals from 15 US states reported excessivesleepiness. Even when using restrictive criteria of frequency at least 3 times per week for at least 3months despite normal sleep duration, the prevalence was 4.7%.[20]

Sex- and age-related demographicsGender ratio for idiopathic hypersomnia is unknown. Kleine-Levin syndrome affects males approximately3 times more often than females.[1]

As with narcolepsy and Klein-Levin syndrome, onset of primary hypersomnia is most common duringadolescence and rare in people older than 30 years. The diagnosis of idiopathic hypersomnia iscomplicated by the fact that differentiating between excessive versus long sleep or normal versusabnormal wakefulness is often difficult in this population.

Prognosis

After a typical onset between the ages 15-30 years, untreated primary hypersomnia presents a chronic,but stable, course. Idiopathic hypersomnia is a lifelong disorder with no tendency to remit spontaneously.Consequences of this disease are mostly social and professional in nature.

Daytime sleepiness can lead to depression. Of note, in children, daytime sleepiness can present ashyperactivity.[1]

Patient Education

While treating patients with primary hypersomnia, the patient's close family should be involved in theoverall education and decision-making process.

Because these disorders may lead to marriage breakdown, extensive counseling for the patient'spartners, educating them about the symptomatology and treatment options, must be part of acomprehensive management plan.

Patients with primary hypersomnia often need significant support because they are at risk of being

misunderstood as being incompetent or slothful. Therefore, education of relatives, friends, and colleagueshelps the patient to function much better with this incurable disease.

For patient education information, see theSleep Disorders Center,as well asDisorders That DisruptSleep (Parasomnias)andNarcolepsy.

Medline Plus/National Institutes of Health (NIH) provides concise and to-the-point summaries of thediagnosis and recommendations for patients and families dealing withprimary hypersomniaandKleine-Levine syndrome.
http://www.emedicinehealth.com/sleep-disorders/center.htmhttp://www.emedicinehealth.com/sleep-disorders/center.htmhttp://www.emedicinehealth.com/sleep-disorders/center.htmhttp://www.emedicinehealth.com/Articles/42677-1.asphttp://www.emedicinehealth.com/Articles/42677-1.asphttp://www.emedicinehealth.com/Articles/42677-1.asphttp://www.emedicinehealth.com/Articles/42677-1.asphttp://www.emedicinehealth.com/Articles/42505-1.asphttp://www.emedicinehealth.com/Articles/42505-1.asphttp://www.emedicinehealth.com/Articles/42505-1.asphttp://www.nlm.nih.gov/medlineplus/ency/article/000803.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000803.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000803.htmhttp://www.ninds.nih.gov/disorders/kleine_levin/kleine_levin.htmhttp://www.ninds.nih.gov/disorders/kleine_levin/kleine_levin.htmhttp://www.ninds.nih.gov/disorders/kleine_levin/kleine_levin.htmhttp://www.ninds.nih.gov/disorders/kleine_levin/kleine_levin.htmhttp://www.ninds.nih.gov/disorders/kleine_levin/kleine_levin.htmhttp://www.ninds.nih.gov/disorders/kleine_levin/kleine_levin.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000803.htmhttp://www.emedicinehealth.com/Articles/42505-1.asphttp://www.emedicinehealth.com/Articles/42677-1.asphttp://www.emedicinehealth.com/Articles/42677-1.asphttp://www.emedicinehealth.com/sleep-disorders/center.htm


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Some people appear to have a genetic predisposition to hypersomnia; in others, there is no known

cause.

Typically, hypersomnia is first recognized in adolescence or young adulthood.

Hypersomnia Treatment

Treatment is symptomatic in nature.

Changes in behavior (for example avoiding night work and social activities that delay bed time) and diet

may offer some relief. Patients should avoid alcohol and caffeine.

Medications

Stimulants such as the following may be prescribed:

amphetamine,

methylphenidate(Concerta, Metadate CD, Metadate ER, Methylin, Methylin ER, Ritalin, Ritalin LA,

Ritalin-SR), and

modafinil(Provigil).

Other drugs used to treat hypersomnia include:

clonidine(Catapres),

levodopa(Larodopa),

bromocriptine(Parlodel),

antidepressants,and

monoamine oxidase inhibitors.

Outlook

The prognosis for persons with hypersomnia depends on the cause of the disorder. While the disorder

itself is not life threatening, it can have serious consequences, such as automobile accidents caused by

falling asleep while driving. The attacks usually continue indefinitely.

Research on Hypersomnia

The NINDS supports and conducts research on sleep disorders such as hypersomnia. The goal of this

research is to increase scientific understanding of the condition, find improved methods of diagnosing and

treating it, and discover ways to prevent it.

Hypersomnia Topic Guide
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Hypersomnia:Hypersomnia is a condition characterized by episodes of prolonged nighttime sleep or

excessive daytime sleepiness. Symptoms include anxiety, increased irritation, decreased energy, slow

thinking, slow speech, loss of appetite, and more. Causes of hypersomnia include other sleep disorders,

physical problems such as tumor or head trauma, medications, medical conditions such as multiple

sclerosis, depression, epilepsy, obesity, and encephalitis, and genetic predisposition. Treatment for

hypersomnia is generally with medication and changes in behavior.
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