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makalah hiperinsomnia

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patofisiolgi, farmasi, hiperinsomnia
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  1. American Psychiatric Association. Primary hypersomnia. In: Diagnostic and Statistical Manual of Mental Disorders. Text Revision (DSM-IV-TR) . 4th Edition. Washington, DC: American Psychiatric Association; 2000:604-9. 2. American Academy of Sleep Medicine. The international classification of sleep disorders: diagnostic - coding manual  . 2 nd  ed. Westchester, IL: American Academy of Sleep Medicine; 2005. 3. Dement W, Rechtschaffen A, Gulevich G. The nature of the narcoleptic sleep attack. Neurology  . Jan 1966;16(1):18-33. [Medline].  4. Roth B, Nevsimalova S, Rechtschaffen A. Hypersomnia with sleep drunkenness .  Arch Gen Psychiatry  . May 1972;26(5):456-62. [Medline].    5. Roehrs T, Zorick F, Sicklesteel J. Excessive daytime sleepiness associated with insufficient sleep. Sleep . 1983;6(4):319-25. [Medline].    6. Billiard M. Diagnosis of narcolepsy and idiopathic hypersomnia. An update based on the International classification of sleep disorders, 2nd edition. Sleep Med Rev  . Oct 2007;11(5):377-88. [Medline].    7. Bassetti C, Pelayo R, Guilleminault C. Idiopathic Hypersomnia. In: Kryger MH, Roth T, Dement WC. Principles and Practices of Sleep Medicine . 4th Edition. Philadelphia, PA: Elsevier; 2005:791-800. 8. Roth T. Introduction: narcolepsy and excessive daytime sleepiness: from the bench to the bedside. J Clin Psychiatry  . 2007;68 Suppl 13:4. [Medline].    9. Guilleminault C. Disorders of excessive sleepiness.  Ann Clin Res . 1985;17(5):209-19. [Medline].    10. Roth B. Narcolepsy and hypersomnia: review and classification of 642 personally observed cases. Schweiz Arch Neurol Neurochir Psychiatr  . 1976;119(1):31-41. [Medline].    11. Arnulf I, Zeitzer JM, File J, et al. Kleine-Levin syndrome: a systematic review of 186 cases in the literature. Brain . Dec 2005;128(Pt 12):2763-76. [Medline].    12. Billiard M, Guilleminault C, Dement WC. A menstruation-linked periodic hypersomnia: Kleine-Levin syndrome or new clinical entity?. Neurology  . 1975;25:436-443. [Medline].    13. Montplaisir J, Poirier G. HLA in disorders of excessive sleepiness without cataplexy in Canada. In: Honda Y, Juti T. HLA in Narcolepsy  . Berlin, Germany: Springer-Verlag; 1988:186-190. 14. Guilleminault C, Faull KF, Miles L. Posttraumatic excessive daytime sleepiness: a review of 20 patients. Neurology  . Dec 1983;33(12):1584-9. [Medline].    15. Montplaisir J, de Champlain J, Young SN. Narcolepsy and idiopathic hypersomnia: biogenic amines and related compounds in CSF. Neurology  . Nov 1982;32(11):1299-302. [Medline].    16. Kanbayashi T, Kodama T, Kondo H, Satoh S, Inoue Y, Chiba S, et al. CSF histamine contents in narcolepsy, idiopathic hypersomnia and obstructive sleep apnea syndrome. Sleep . Feb 1 2009;32(2):181-7.[Medline].    17. Nishino S, Okuro M, Kotorii N, Anegawa E, Ishimaru Y, Matsumura M, et al. Hypocretin/orexin and narcolepsy: new basic and clinical insights.  Acta Physiol (Oxf) . Jun 25 2009;[Medline].    18. Nishino S, Kanbayashi T. Symptomatic narcolepsy, cataplexy and hypersomnia, and their implications in the hypothalamic hypocretin/orexin system. Sleep Med Rev  . Aug 2005;9(4):269-310. [Medline].   19. Yamanaka A, Tsujino N, Funahashi H, Honda K, Guan JL, Wang QP, et al. Orexins activate histaminergic 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 for Excessive Sleepiness in the General Population: Implications for DSM-5 Nosology.  Arch Gen Psychiatry  . Jan 2012;69(1):71-9. [Medline].    21. Guilleminault C, Faull KF. Sleepiness in nonnarcoleptic, non-sleep apneic EDS patients: the idiopathic CNS hypersomnolence. Sleep . 1982;5 Suppl 2:S175-81. [Medline].    22. Bassetti C, Gugger M, Bischof M. The narcoleptic borderland: a multimodal diagnostic approach including cerebrospinal fluid levels of hypocretin-1 (orexin A). Sleep Med  . Jan 2003;4(1):7-12. [Medline].  23. Ohayon MM. From wakefulness to excessive sleepiness: what we know and still need to know. Sleep Med Rev  . Apr 2008;12(2):129-41. [Medline].    24. Sangal RB; Mitler MM; Sangal JM. Subjective sleepiness ratings (Epworth sleepiness scale) do not reflect the same parameter of sleepiness as objective sleepiness (maintenance of wakefulness test) in patients with narcolepsy. Clin Neurophysiol  . Dec 1999;(110)12:2131-5. [Medline].    25. Sangal RB, Sangal JM, Belisle C. Subjective and objective indices of sleepiness (ESS and MWT) are not equally useful in patients with sleep apnea. Clin Electroencephalogr  . Apr 1999;30(2):73-5. [Medline].    26. Rechtschaffen A, Roth B. Nocturnal sleep of hypersomniacs.  Act Nerv Super (Praha) . 1969;11(3):229-33.[Medline].    27. Anderson KN, Pilsworth S, Sharples LD, Smith IE, Shneerson JM. Idiopathic hypersomnia: a study of 77 cases. Sleep . Oct 1 2007;30(10):1274-81. [Medline].    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 srcin. Sleep . Dec 1 2007;30(12):1705-11. [Medline].    29. Ballon JS, Feifel D. A systematic review of modafinil: Potential clinical uses and mechanisms of action. J Clin Psychiatry  . Apr 2006;67(4):554-66. [Medline].    30. Valentino RM, Foldvary-Schaefer N. Modafinil in the treatment of excessive daytime sleepiness. Cleve Clin J Med  . Aug 2007;74(8):561-6, 568-71. [Medline].    31. Schwartz JR. Modafinil: new indications for wake promotion. Expert Opin Pharmacother  . Jan 2005;6(1):115-29. [Medline].    32. Poppe M, Friebel D, Reuner U, Todt H, Koch R, Heubner G. The Kleine-Levin syndrome - effects of treatment with lithium. Neuropediatrics . 2003;34:113-9. [Medline].   Background The International Classification of Sleep Disorders (ICSD) describes primary hypersomnia as an idiopathic disorder of presumed central nervous system (CNS) cause that is associated with excessive sleepiness (ie, prolonged episodes of non  – rapid eye movement [NREM] sleep). (See Etiology and Presentation.) [1]  The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision  ( DSM-IV-TR  ) defines primary (idiopathic) hypersomnia as excessive daytime sleepiness without narcolepsy or the associated features of other  sleep 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] In 1972, Roth et al described a type of hypersomnia with sleep drunkenness that consists of difficulty coming 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 not present in this disorder. In comparison with narcolepsy, which is characterized by well-defined clinical, polysomnographic, and immunogenetic features, primary hypersomnia is not well characterized. [5, 6] Moreover, while the DSM-IV-TR   and 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, and Workup.) [7]  Please note that while the ICSD prefers the diagnostic label of idiopathic hypersomnia , the DSM prefers the diagnostic label of  primary hypersomnia . As the terms are interchangeable, this article will refer to them alternately. Classification Primary hypersomnia can be classified as monosymptomatic or polysymptomatic. Isolated excessive daytime sleepiness that is not due to abnormal nocturnal awakenings characterizes the monosymptomatic form. The polysymptomatic form consists of abnormally long nocturnal sleep and signs of 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 of the 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 as Guillain-Barré syndrome, infectious mononucleosis, or atypical viral pneumonia. Even after their infectious disease resolves, these patients continue to require significantly more nocturnal sleep and continue to feel very tired.  Although initially these patients are fatigued, they subsequently have difficulty differentiating fatigue from sleepiness. To fight tiredness, these patients nap and eventually present with complaints of excessive daytime sleepiness. Analysis of cerebral spinal fluid demonstrates moderate lymphocytosis (30-50 cells/µL 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 is idiopathic.  Recurrent primary hypersomnia Kleine-Levin syndrome (KLS) is a rare disorder that starts during adolescence and has a male gender preference. The patients have recurrent episodes of hypersomnia, which are often associated with compulsive overeating and hypersexuality. [9] The periods of hypersomnia occur for days to weeks at a time and recur several times a year. In between the symptomatic periods, the patients have normal sleep requirements and do not have excessive daytime sleepiness. Some patients may develop symptoms of irritability, impulsive behavior, depersonalization, hallucinations, depression, and confusion. The etiology of 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% during the second decade), and the syndrome may last up to 8 years. The episodes recur every 3-4 months and may 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 periodic basis over a few days preceding menstruation. [12] It is assumed that the symptoms follow hormonal changes, 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 primary hypersomnia according to the DSM-IV-TR  . Etiology Primary hypersomnia is an idiopathic disorder. Although head injury or viral infections can cause a disorder 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 as Guillain-Barré syndrome, hepatitis, mononucleosis, and atypical viral pneumonia. Familial cases associated with HLA-Cw2 and HLA-DR11 genotypes have also been reported. [13] However, the majority of the patients diagnosed with idiopathic hypersomnia have neither a positive family history nor a past medical history of viral illnesses. In experimental animal studies, destruction of the nonadrenergic neurons of the rostral third of the locus ceruleus complex has produced hypersomnia. While trauma has been associated with excessive daytime sleepiness in a case series, cerebrospinal fluid (CSF) analysis for specific neurotransmitter metabolites did not differentiate patients with posttraumatic excessive daytime sleepiness from patients with narcolepsy or other patients with excessive daytime sleepiness. [14] Injury to the adrenergic neurons at the bundle 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 similar malfunction of the norepinephrine system may occur in idiopathic hypersomnia. Decreased CSF histamine 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) srcin for hypersomnias. [16]   A major advance in the understanding of the pathology of narcolepsy, a disorder closely related to primary hypersomnia, was made after the discovery of narcolepsy-associated genes in animals; ie, genes

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Jul 23, 2017
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