Progressive sleep “destructuring” in Parkinson’s disease. A polysomnographic study in 46 patients. Sleep Med 6:313-318

Department of Neuroscience, Centre Hospitalier de Luxembourg, 4, rue Barblé, L-1210 Luxembourg, Luxembourg.
Sleep Medicine (Impact Factor: 3.15). 08/2005; 6(4):313-8. DOI: 10.1016/j.sleep.2005.03.011
Source: PubMed

ABSTRACT Sleep abnormalities in Parkinson's disease (PD) are frequent, but it is unknown whether or not there is progressive loss of physiological sleep architecture or what the causes could be.
Retrospective review of medical records and polysomnographic data from 46 non-demented PD patients.
Sleep latency was correlated with disease duration (F1,44=4.87, P=0.03). Total sleep time (F1,44=8.54, P=0.005), deep sleep time (F1,44=4.06, P=0.05), REM sleep time (F1,44=9.15, P=0.004) and sleep efficiency (SE) (F1,44=10.20, P=0.003) were inversely correlated with disease duration. The same sleep parameters were independent from the degree of motor impairment, dosage of the dopaminergic medications, and age. Subjective sleep complaints could only partially predict abnormalities in polysomnographic (PSG) studies.
In PD nocturnal sleep 'destructuring' is linked to disease duration and evolves independently from other major disease parameters.

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    Sleep Medicine Reviews 02/2015; DOI:10.1016/j.smrv.2015.02.005 · 8.51 Impact Factor
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    • "1Sturrock and Rao (1985), 2Zhang et al. (2005), 3Naidoo et al. (2011), 4van der Zee et al. (1991), 5Carskadon et al. (1982), 6Foley et al. (2007), 7Magri et al. (1997), 8Touitou (1995), 9Whitehead et al. (2008), 10Huang et al. (2002), 11Davidson et al. (2008), 12Turek et al. (1995), 13Dykierek et al. (1998), 14Feinberg et al. (1967), 15Myers and Badia (1995), 16Brun and Englund (1981), 17Teipel et al. (2005), 18Vitiello et al. (1991), 19Satlin et al. (1995), 20Wu et al. (2007), 21Montplaisir et al. (1995), 22Tseng et al. (2010), 23Bonanni et al. (2005), 24Wu and Swaab (2007), 25Kang et al. (2009), 26Braak et al. (2004), 27Thannickal et al. (2007), 28Factor et al. (1990), 29Schenck et al. (1996), 30Postuma and Montplaisir (2009), 31Hartmann et al. (1997), 32Emser et al. (1988), 33Mouret (1975), 34Diederich et al. (2005), 35Willis and Turner (2007), 36Vonsattel et al. (1985), 37Kremer et al. (1991), 38Arnulf et al. (2008), 39Morton et al. (2005), 40Fish et al. (1991), 41Wiegand et al. (1991), 42Aziz et al. (2010), 43Maywood et al. (2010), 44Pallier et al. (2007), 45Sandyk (2006), 46Kimura et al. (1999), 47Atalaia et al. (2007), 48Lo Coco et al. (2011), 49Patacchioli et al. (2003), 50Barthlen and Lange (2000), 51Howard et al. (1989), 52David et al. (1997), 53Weishaupt et al. (2006). "
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    Frontiers in Neurology 10/2011; 2:66. DOI:10.3389/fneur.2011.00066
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