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Excessive daytime sleepiness in patients with Parkinson's disease: A polysomnography study

Authors

  • Isaac Shpirer MD,

    Corresponding author
    1. Sleep Laboratory, Assaf Harofeh Medical Center, Zerifin, Israel, affiliated to Sackler School of Medicine, Tel Aviv University, Israel
    • Pulmonary Institute, Assaf Harofeh Medical Center, Zerifin 70300, Israel
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  • Ala Miniovitz MD,

    1. Department of Neurology, Assaf Harofeh Medical Center, Zerifin, Israel affiliated to Sackler School of Medicine, Tel Aviv University, Israel
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  • Colin Klein MD,

    1. Department of Neurology, Assaf Harofeh Medical Center, Zerifin, Israel affiliated to Sackler School of Medicine, Tel Aviv University, Israel
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  • Richard Goldstein MD,

    1. Sleep Laboratory, Assaf Harofeh Medical Center, Zerifin, Israel, affiliated to Sackler School of Medicine, Tel Aviv University, Israel
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  • Tatiana Prokhorov MD,

    1. Department of Neurology, Assaf Harofeh Medical Center, Zerifin, Israel affiliated to Sackler School of Medicine, Tel Aviv University, Israel
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  • Jack Theitler MD,

    1. Department of Neurology, Assaf Harofeh Medical Center, Zerifin, Israel affiliated to Sackler School of Medicine, Tel Aviv University, Israel
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  • Lea Pollak MD,

    1. Department of Neurology, Assaf Harofeh Medical Center, Zerifin, Israel affiliated to Sackler School of Medicine, Tel Aviv University, Israel
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  • Jose Martin Rabey MD

    1. Department of Neurology, Assaf Harofeh Medical Center, Zerifin, Israel affiliated to Sackler School of Medicine, Tel Aviv University, Israel
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Abstract

To investigate excessive daytime sleepiness (EDS) in patients with Parkinson's disease (PD), the reasons for which have not yet been clarified, polysomnography (PSG) and the Multiple Sleep Latency Test (MSLT) were performed in 46 patients with PD, and, in addition, PSG was performed in 30 healthy controls. Assessment included Epworth Sleepiness Score (ESS), Mini-Mental State Examination (MMSE), and Hamilton Test (HT) for depression. Fifty percent of PD patients reported EDS (ESS, 10 ± 4.5 vs. 6.9 ± 3.7; P = 0.01). Compared with controls, PD patients as a group had lower sleep efficiency (65 ± 22 vs. 77 ± 14; P = 0.03), a longer Stage 2 (73 ± 12 vs. 67 ± 12; P = 0.03), and a shorter rapid eye movement stage (8 ± 8 vs. 17 ± 8; P < 0.001). Clinical data and sleep characteristics were similar in PD with/without EDS. Of interest, patients treated with clonazepam (CLNZ) had lower EDS than those without CLNZ (ESS, 7.9 ± 4.7 vs. 11.3 ± 4.0; P = 0.03). These patients suffered less periodic leg movement during sleep (2.1 ± 2.7 vs. 12.4 ± 28; P = 0.04), which might explain the finding. No correlation was found between ESS, MSLT, and all other clinical features analyzed. In PD patients, according to the data obtained, severity of EDS does not depend on any specific clinical factor and the etiology is probably multifactorial. Paradoxically, PD patients treated with CLNZ were less sleepy than patients not treated with CLNZ. © 2006 Movement Disorder Society

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