Nervenheilkunde 2011; 30(09): 683-690
DOI: 10.1055/s-0038-1628412
Update Neurologie
Schattauer GmbH

Update Schlafmedizin 2010

Update sleep medicine 2010
G. Mayer
1   Neurologie, Schlafmedizin, Hephata Klinik, Schwalmstadt-Treysa
2   Klinik für Neurologie, Philipps-Universität Marburg
,
S. Javidi
1   Neurologie, Schlafmedizin, Hephata Klinik, Schwalmstadt-Treysa
› Institutsangaben
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Publikationsverlauf

Eingegangen am: 30. März 2011

Angenommen am: 04. April 2011

Publikationsdatum:
23. Januar 2018 (online)

Zusammenfassung

Schlafmedizinische Diagnostik kann gemäßder Leitlinie S3 der Deutschen Gesellschaft für Schlafforschung und Schlafmedizin „Nicht erholsamerSchlaf/Schlafstörungen” durchgeführtwerden. Die Auswertung der Polysomnografien (PSG) erfolgt seit 2007 nach neuenRichtlinien. Sie erfordern frontale und okzipitaleAbleitungen, um Grafoelemente, die dasSchlafstadium charakterisieren am Ort dermaximalen Ausprägung zu identifizieren. Tiefschlafwird auf ein Stadium N3 reduziert. DieIndikation für die ambulante Polygrafie zur Diagnostikschlafbezogener Atmungsstörungenwird mittels der Prätestwahrscheinlichkeit optimiert.Bei hoher Prätestwahrscheinlichkeit und geringer Apnoezahl in der Polygrafie sowiebei Verdacht auf eine alveoläre Hypoventilation,z. B. bei neuromuskulären Erkrankungen,ist immer eine PSG indiziert. SchlafbezogeneAtmungsstörungen und kurzer Schlafgehen mit hohem kardiovaskulärem-, metabolischem- und Mortalitätsrisiko einher. Ob die Insomnie ein Risikofaktor ist konnte nichteindeutig geklärt werden. Dafür finden sich zunehmend Belege für das zugrunde liegende Hyperarousal-Modell. Neue Therapien für die Insomnien bieten die Melatoninagonisten. In der Narkolepsie konnten mittels genomweiter Analysen mehrere Assoziationen gefunden werden, die eine Autoimmunhypothese stützen. Bei Narkolepsien ohne Kataplexie konnte inpostmortalen Untersuchungen eine quantitativgeringe Destruktion hypocretinerger Neuronefestgestellt werden. Das HLA-Allel DQB1*0602ist fast ausschließlich mit einem niedrigen Liquor Hypocretin assoziiert, sodass sich bei Vorliegendes Allels die diagnostische Liquorpunktionerübrigt. Die REM-Schlafverhaltensstörunghat sich als Prädiktor für neurodegenerativeErkrankungen etabliert. Ihre Diagnostikumfasst Fragebögen, Riechtests, transkraniellenUltraschall der Stammganglien, zerebralerBildgebung und Muskeltonusanalyse des REMSchlafes.

Summary

Diagnosis of sleep disorders can be performed according to the evidence based guideline“ nonrestorative sleep/sleep disorders” of the German Sleep Society. PSG scoring is performed according to a new system since 2007. Frontal and occipital derivations allow scoringof graphoelements that characterize sleep stages at their maximal representation. Deep sleep stages are reduced to one stage N3. Indication for ambulatory polygraphy for diagnosis of sleep related breathing disorders is optimized by introducing a “pretest probability”. PSG is indicated if it is high and polygraphy displays only little apneas, and when alveolar hypoventilation is probable. Sleep related breathing disorders and short sleep are associated with high cardiovascular, metabolic and mortality risk. If insomnia is a risk factor itself is unclear. However, many proofs for the hyperarousal model of insomnia have been discovered. New therapeutic options for insomnia are given by the introduction of melatonina gonists. Genome-wide analysis has found several associations with gene loci that support the autoimmune hypothesis of narcolepsy. Post mortem investigations displayed aminor loss of hypocretinergic cells in humans.The allele DQB1*0602 is almost always associated with a low CSF hypocretin, and.therefore does not require a diagnostic lumbarpuncture. REM sleep behaviour disorderhas become an established predictor for neurodegenerative diseases. The diagnostic procedures comprise specific questionnaires, olfactory tests, transcranial ultrasound of basal ganglia, cerebral imaging and muscle tone analysis of REM sleep.

 
  • Literatur

  • 1 Mayer G. et al. S3-Leitlinie nicht erholsamer Schlaf/ Schlafstörungen. Somnologie 2009; 13 (Suppl. 01) 1-160.
  • 2 Rechtschaffen A, Kales A. A manual of standardized terminology, techniques, and scoring system for sleep stages of human subjects. US Department of Health, Education, and Welfare Public Health Service – National Institutes of Health. 1968
  • 3 Iber C. et al. The AASM manual for the scoring of sleep and associated events: rules, terminology and technical specifications. Westchester. Illinois: American Academy of Sleep Medicine; 2007
  • 4 Redline S. et al. The scoring of respiratory events in sleep: reliability and validity. J Clin Sleep Med 2007; 03: 169-200.
  • 5 American Academy of Sleep Medicine. International classification of sleep disorders. 2nd ed.. Diagnostic and coding manual. Westchester. Illinois: American Academy of Sleep Medicine; 2005
  • 6 Haniffa M, Lasserson TJ, Smith I. Interventions to improve compliance with continuous positive airway pressure for obstructive sleep apnoea. Cochrane Database Syst Rev. 2004 18(4).
  • 7 Kryger MH, Dement WC, Roth T. Principles and practice of sleep medicine. London: Saunders WB; 2001
  • 8 Lyall RA. et al. A prospective study of quality of life in ALS patients treated with noninvasive ventilation. Neurology 2001; 57: 153-6.
  • 9 Storre JH. et al. Transcutaneous pCO2 monitoring during initiation of noninvasive ventilation. Chest 2007; 132: 1810-6.
  • 10 Fletcher EC. et al. Survival in COPD patients with a daytime PaO2 greater than 60 mm Hg with and without nocturnal oxyhemoglobin desaturation. Chest 1992; 101: 649-55.
  • 11 Budhiraja R, Budhiraja P, Quan SF. Sleep disordered breathing and cardiovascular disorders. Respir Care 2010; 55 (10) 1322-32.
  • 12 Gottlieb DJ. et al. Prospective study of obstructive sleep apnea and incident coronary heart disease and heart failure: the sleep heart health study. Circulation 2010; 122 (04) 352-60.
  • 13 Peppard PE. Is obstructive sleep apnea a risk factor for hypertension? Differences between the Wisconsin sleep cohort and the sleep heart health study. J Clin Sleep Med 2009; 05 (05) 404-5.
  • 14 Gangwisch JE. et al. Sleep duration as a risk factor for diabetes incidence in a large US sample. Sleep 2007; 30: 1667-73.
  • 15 Cappuccio FP. et al. Sleep duration and all-cause mortality: a systematic review and meta-analysis of prospective studies. Sleep 2010; 33 (05) 585-92.
  • 16 Gangwisch JE. et al. Sleep duration associated with mortality, but not middle-aged adults in a large US sample. Sleep 2008; 31: 1087-96.
  • 17 Gao B. et al. Sleep disruption aggravates focal cerebral ischemia in the rat. Sleep 2010; 33 (07) 879-87.
  • 18 Rupprecht S. et al. Central sleep apnea indicates autonomic dysfunction in asymptomatic carotid stenosis: a potential marker of cerebrovascular and cardiovascular risk. Sleep 2010; 33 (03) 327-33.
  • 19 Hallmayer J. et al. Narcolepsy is strongly associated with the T-cell receptor alpha locus. Nature Genetics 2009; 41: 708-11.
  • 20 Cvetkovic-Lopes V. et al. Elevated tribbles homolog 2-specific antibody levels in narcolepsy patients. J Clin Invest 2010; 120: 713-9.
  • 21 Thannickal TC, Nienhuis R, Siegel JM. Localized loss of hypocretin cells in narcolepsy without cataplexy. Sleep 2009; 32 (08) 993-8.
  • 22 Knudsen S. et al. Validation of the ICSD-2 criteria for csf-hypocretin-1 measurements in the diagnosis of narcolepsy in the Danish population. Sleep 2010; 33 (02) 169-76.
  • 23 Sakurai E. et al. Decreased csf histamine in narcolepsy with and without low csf hypocretin-1 in comparison to healthy controls. Sleep 2009; 32 (02) 175-80.
  • 24 Fronczek R, Verschuuren J, Lammers GJ. Response to intravenous immunoglobulins and placebo in a patient with narcolepsy cataplexy. J Neurol 2007; 254: 1607-8.
  • 25 Pincherle A. et al. Immunoabsorption fort he treatment of narcolepsy with cataplexy. Neurol Sci 2008; 29: 499-500.
  • 26 Riemann D. et al. Chronic insomnia and MRImeasured hippocampal volumes: a pilot study. Sleep 2007; 30 (08) 955-8.
  • 27 Nissen C. et al. Impaired sleep-related memory consolidation in primary insomnia. Sleep 2006; 29: 1068-73.
  • 28 Smith MT, Perlis ML. NREM sleep cerebral blood flow before and after behavior therapy for chronic insomnia: preliminary single photon emission computed tomography (SPECT) data. Sleep Med 2005; 06: 93-4.
  • 29 Vertes RP, Siegel J. Time for the sleep community to take a critical look at the purported role of sleep in memory processing. Sleep 2005; 28: 1228-9.
  • 30 Winkelman JW. et al. Reduced brain GABA in primary insomnia: preliminary data from 4T proton magnetic resonance spectroscopy (1H-MRS). Sleep 2008; 31: 1499-506.
  • 31 Riemann D, Perlis ML. The treatments of chronic insomnia: a review of benzodiazepine receptor agonists and psychological and behavioural therapies. Sleep Med Rev 2009; 13: 205-14.
  • 32 Lewy AJ, Ahmed S, Jackson JM. Melatonin shifts human circadian rhythms according to a phase-response curve. Chronobiol Int 1992; 09: 380-92.
  • 33 Wade AG. et al. Efficacy of prolonged release melatonin in insomnia patients aged 55–80 years: Quality of sleep and next day alertness outcomes. Curr Med Res Opinion 2007; 23 (04) 2597-605.
  • 34 Mayer G. et al. Efficacy and safety of 6-month nightly ramelteon administration in adults with chronic, primary insomnia. Sleep 2009; 32 (03) 351-60.
  • 35 Iranzo A. et al. Rapid-eye-movement sleep behaviour disorder as an early marker for a neurodegenerative disorder: a descriptive study. Lancet Neurology 2006; 05: 572-7.
  • 36 Schenck CH, Bundlie SR, Mahowald MW. REM sleep behaviour disorder (RBD) delayed emergence of parkinsonism and/or dementia in 65% of older men initially diagnosed with idiopathic RBD, and an analysis of the maximum & minimum tonic and/ or phasic electromyographic abnormalities found during REM sleep. Sleep. 2003; 26 A 316.
  • 37 Arnulf I. et al. REM sleep behavior disorder and REM sleep without atonia in patients with progressive supranuclear palsy. Sleep 2005; 28 (03) 349-54.
  • 38 Iranzo A, Santamaria J, Tolosa E. The clinical and pathophysiological relevance of REM sleep behavior disorder in neurodegenerative diseases. Sleep Med Rev 2009; 13 (06) 385-401.
  • 39 Mayer G. et al. Quantification of tonic and phasic muscle activity in REM sleep behavior disorder. J Clin Neurophysiol 2008; 25 (01) 48-55.
  • 40 Stiasny-Kolster K. et al. The REM sleep behavior disorder screening questionnaire (RBDSQ) – a new diagnostic instrument. Movement Disorders 2007; 22 (16) 2386-93.
  • 41 Stiasny-Kolster K. et al. Olfactory dysfunction in patients with narcolepsy with and without REM sleep behavior disorder. Brain. 2007; 130 (Pt 2): 442-9.
  • 42 Unger MM. et al. Assessment of idiopathic rapideye-movement sleep behaviour disorder by transcranial sonography, olfactory function test, and FPCIT-SPECT. Mov Disord 2008; 23 (04) 596-9.
  • 43 Miyamoto T. et al. Reduced cardiac 123I-MIBG scintigraphy in idiopathic REM sleep behavior disorder. Neurology 2006; 67: 2236-8.
  • 44 Ferini-Strambi L. et al. Neuropsychological assessment in idiopathic REM sleep behavior disorder (RBD): does the idiopathic form of RBD really exist?. Neurology 2004; 62 (01) 41-5.
  • 45 Lu J, Sherman D, Devor M, Saper CB. A putative flip-flop switch for control of REM sleep. Nature 2006; 441: 589.
  • 46 Thannickal TC, Lai YY, Siegel M. Hypocretin cell loss in Parkinson’s disease. Brain 2007; 130: 1586-95.