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5 - Excessive somnolence disorders

from SECTION 2 - SLEEP DISORDERS

Published online by Cambridge University Press:  08 August 2009

By
Geert Mayer
Edited by
Harold R. Smith ,
Cynthia L. Comella  and
Birgit Högl
Geert Mayer
Affiliation:
Schwalmstadt-Treysa, Germany
Harold R. Smith
Affiliation:
University of California, Irvine
Cynthia L. Comella
Affiliation:
Rush University Medical Center, Chicago
Birgit Högl
Affiliation:
Inssbruck Medical University
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Summary

Introduction

Excessive somnolence is characterized by the inability to stay awake during the desired wake period resulting in falling asleep in monotonous situations or developing unintended naps. Excessive somnolence can be a consequence of lifestyle, environmental and circadian influences, medical disorders, drugs or substances. When persisting for several weeks it is considered to be pathological, whereas it is a normal condition when occurring for a few days only, such as after sleep deprivation.

Excessive daytime sleepiness (EDS) is the term used for pathological states, defined as falling asleep in inappropriate situations and which cannot be controlled voluntarily. Between 4% and 9% of the general population are affected by EDS. The consequences on quality of life, performance, and concentration are dependent on the severity of EDS. The high socioeconomic costs of EDS have fostered efforts for early diagnosis and treatment. The underlying cause of EDS is determined by an assessment of multiple factors involved in the sleep/wake system. These may include environmental factors, lifestyle, genetics, inflammation, trauma, or tumor.

Sleep disturbances with EDS as the primary symptom have been classified by the International Classification of Sleep Disorders 2nd edition (ICSD-2) as “hypersomnias of central origin.” EDS may also be a prominent but not primary feature in other sleep disorders that are classified according to their main features, e.g., sleep-disordered breathing or sleep-related movement disorders. Since the discovery of REM sleep, enormous scientific progress has taken place in the understanding of sleep/wake disorders, giving rise to modern treatment options.

Keywords

excessive somnolence disordersgenetic disordershepatic encephalopathyidiopathic hypersomniarecurrent hypersomniapsychiatric disordersnarcolepsy
Type
Chapter
Information
Sleep Medicine , pp. 78 - 96
Publisher: Cambridge University Press
Print publication year: 2008

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References

American Academy of Sleep Medicine. International Classification of Sleep Disorders: Diagnostic and Coding Manual, 2nd edn (ICSD-2). Westchester, IL: American Academy of Sleep Medicine, 2005.
Arnulf, I, Zeitzer, JM, File, J, et al. Kleine–Levin syndrome: a systematic review of 186 cases in the literature. Brain 2005; 128:2763–76.CrossRefGoogle ScholarPubMed
Bassetti, C, Aldrich, MS. Idiopathic hypersomnia. Brain 1997; 120:1423–35.CrossRefGoogle ScholarPubMed
Billiard, M. Idiopathic hypersomnia. Neurol Clin 1996; 14:573–82.CrossRefGoogle ScholarPubMed
Billiard M. Hypersomnias. In: Billiard, M, ed. Sleep: Physiology, Investigations and Medicine. New York, NY: Kluwer/Plenum, 2003: 333–6.CrossRefGoogle Scholar
Billiard, M, Bassetti, C, Dauvilliers, Y, et al. EFNS guidelines on management of narcolepsy. Eur J Neurol 2006; 13:1035–48.CrossRefGoogle ScholarPubMed
Bruck, D, Parkes, JD. A comparison of idiopathic hypersomnia and narcolepsy–cataplexy using self report measures and sleep diary. J Neurol Neurosurg Psychiatry 1996; 60:576–8.CrossRefGoogle ScholarPubMed
Dauvilliers, Y, Montplaisir, J, Molinari, N, et al. Age at onset of narcolepsy in two large populations of patients in France and Quebec. Neurology 2001; 57:2029–33.CrossRefGoogle ScholarPubMed
Dauvilliers, Y, Mayer, G, Lecendreux, M, et al. Kleine–Levin syndrome: an autoimmune hypothesis based on clinical and genetic analyses in thirty unrelated patients. Neurology 2002; 59:1739–45.CrossRefGoogle Scholar
Dauvilliers, Y, Baumann, CR, Carlander, B, et al. CSF hypocretin-1 levels in narcolepsy, Kleine–Levin syndrome, and other hypersomnias and neurological conditions. J Neurol Neurosurg Psychiatry 2003; 74:1667–73.CrossRefGoogle ScholarPubMed
Dodel, R, Peter, H, Walbert, T, et al. The socioeconomic impact of narcolepsy. Sleep 2004; 27:1123–8.CrossRefGoogle ScholarPubMed
Dolenc, L, Besset, A, Billiard, M. Hypersomnia in association with dysthymia in comparison with idiopathic hypersomnia and normal controls. Eur J Physiol 1996; 431 (suppl): R303–4.CrossRefGoogle ScholarPubMed
Faull, KF, Guilleminault, C, Berger, PA, et al. Cerebrospinal fluid monoamine metabolites in narcolepsy and hypersomnia. Ann Neurol 1983; 13:258–63.CrossRefGoogle ScholarPubMed
Gélineau, J. De la narcolepsie. Gaz des Hôp 1880; 53:626–8; 54:635–7.Google Scholar
Goldberg, MA. The treatment of Kleine–Levin syndrome with lithium. Can J Psychiatry 1983; 28:491–3.CrossRefGoogle ScholarPubMed
Guilleminault, C, Yuen, KM, Gulevich, MG, et al. Hypersomnia after head–neck trauma: a medico-legal dilemma. Neurology 2000; 54:653–9.Google Scholar
Happe S, Trenkwalder C. Parkinson's disease. In: Ebadi, M, Pfeiffer, R, eds. Sleep Disorders in Parkinson's Disease. Boca Raton, FL: CRC Press, 2005: S217–27.Google Scholar
Honda, Y, Juji, T, Matsuki, K, et al. HLA-DR2 and Dw2 in narcolepsy and in other disorders of excessive somnolence without cataplexy. Sleep 1986; 9:133–42.CrossRefGoogle ScholarPubMed
Hublin, C, Kaprio, J, Partinen, M, et al. Daytime sleepiness in an adult, Finnish population. J Intern Med 1996; 239:417–23.CrossRefGoogle Scholar
Kanbayashi, T, Inoue, Y, Chiba, S, et al. CSF hypocretin-1 (orexin-A) concentrations in narcolepsy with and without cataplexy and idiopathic hypersomnia. J Sleep Res 2002; 11:91–3.CrossRefGoogle ScholarPubMed
Kawashima, M, Tamiya, G, Oka, A, et al. Genomewide association analysis of human narcolepsy and a new resistance gene. Am J Hum Genet 2006; 79:252–63.CrossRefGoogle Scholar
Littner, M, Johnson, SF, McCal, WV, et al. Practice parameters for the treatment of narcolepsy: an update for 2000. Standards of Practice Committee. Sleep 2001; 24:451–66.Google Scholar
Mayer, G, Blanke, J. Moebius syndrome, narcolepsy and parasomnias: report on two patients. Somnologie 2004; 3:110–14.CrossRefGoogle Scholar
Mayer, G, Leonhardt, E, Krieg, J, Meier-Ewert, K. Endocrinological and polysomnographic findings in Kleine–Levin syndrome: no evidence for hypothalamic and circadian dysfunction. Sleep 1998; 21:278–84.CrossRefGoogle ScholarPubMed
Mayer, G, Kesper, K, Ploch, T, Peter, H, Peter, J. The implications of gender and age at onset of first symptoms in narcoleptic patients in Germany: results from retrospective evaluation of hospital records. Somnologie 2002; 6:13–18.CrossRefGoogle Scholar
Montplaisir, J, Champlain, J, Young, SN, et al. Narcolepsy and idiopathic hypersomnia: biogenic amines and related compounds in CSF. Neurology 1982; 32:1299–302.CrossRefGoogle Scholar
Montplaisir J, Poirier G. HLA in disorders of excessive daytime sleepiness without cataplexy in Canada. In: Honda, Y, Jui, T, eds. HLA in Narcolepsy. Berlin: Springer, 1988: 186.CrossRefGoogle Scholar
Nevsímalova, S, Blazejová, K, Illnerová, H, et al. A contribution to pathophysiology of idiopathic hypersomnia. Suppl Clin Neurophysiol 2000; 53:366–70.CrossRefGoogle ScholarPubMed
Ohayon, MM. Prevalence and correlates of nonrestorative sleep complaints. Arch Intern Med 2005; 165:35–41.CrossRefGoogle ScholarPubMed
Perlis, ML, Pigeon, WR, Riemann, D.State-of-the-science for the treatment of chronic insomnia. Sleep Med Rev in press.
Riemann, D, Fischer, J, Mayer, G, Peter, HJ. The guidelines for “non-restorative sleep”: relevance for the diagnosis and therapy of insomnia. Somnologie 2003; 7:66–76.CrossRefGoogle Scholar
Rogers, AE, Aldrich, MS, Berrios, AM, Rosenberg, R. Compliance with stimulant medications in patients with narcolepsy. Sleep 1997; 20:28–33.CrossRefGoogle ScholarPubMed
Roth, B. Die Narkolepsie und die Hypersomnie vom Standpunkt der Physiologie des Schlafs. Berlin: VEB Volk und Gesundheit, 1962.Google Scholar
Roth, B, Nevsímalova, S, Rechtschaffen, A. Hypersomnia with sleep drunkenness. Arch Gen Psychiatry 1972; 26:456–62.CrossRefGoogle ScholarPubMed
Roth, B, Nevsímalova, S, Sagova, V, et al. Neurological, psychological and polygraphic findings in sleep drunkenness. Arch Suisse Neurochirurgie Psychiatrie 1981; 129:209–22.Google ScholarPubMed
Rye, DB, Bliwise, DL, Dihenia, B, Gurecki, P. Daytime sleepiness in Parkinson's disease. J Sleep Res 2000; 9:63–9.CrossRefGoogle ScholarPubMed
Schöls, L, Haan, J, Riess, O, et al. Sleep disturbance in spinocerebellar ataxias: is the SCA3 mutation a cause of restless legs syndrome?Neurology 1998; 51:1603–7.CrossRefGoogle ScholarPubMed
Schweitzer PK. Drugs that disturb sleep and wakefulness. In: Kryger, MH, Roth, T, Dement, WC, eds. Principles and Practice of Sleep Medicine, 4th edn. Philadelphia, PA: Saunders, 2005: 499–518.Google Scholar
Sforza, E, Gaudreau, H, Petit, D, Montplaisir, J. Homeostatic sleep regulation in patients with idiopathic hypersomnia. Clin Neurophysiol 2000; 111:277–82.CrossRefGoogle ScholarPubMed
Standards of Practice Committee. Practice Parameters for the treatment of narcolepsy: An update for 2000. Sleep 2001; 24: 451–66.
Vanková, J, Nevsímalová, S, Sonka, K, Spacková, N, Svejdová-Blazejova, K. Increased REM density in narcolepsy–cataplexy and the polysymptomatic form of idiopathic hypersomnia. Sleep 2001; 24:707–11.CrossRefGoogle ScholarPubMed

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