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Neurology 2002;58:1019-1024
© 2002 American Academy of Neurology

Parkinson’s disease and sleepiness

An integral part of PD

I. Arnulf, MD, E. Konofal, MD, M. Merino–Andreu, MD, J. L. Houeto, MD, V. Mesnage, MD, M. L. Welter, MD, L. Lacomblez, MD, J. L. Golmard, MD PhD, J. P. Derenne, MD and Y. Agid, MD PhD

From Fédération des Pathologies du Sommeil (Drs. Arnulf, Konofal, Merino–Andreu, and Derenne), Centre d’Investigation Clinique, Fédération de Neurologie and Inserm U289 (Drs. Houeto, Mesnage, Welter, and Agid), Service de Neuropharmacologie (Dr. Lacomblez), and Service d’Informatique Médicale (Dr. Golmard), Hôpital Pitié–Salpêtrière, Assistance Publique-Hôpitaux de Paris, France.

Address correspondence and reprint requests to Dr. Isabelle Arnulf, Pavillon Rambuteau, Hôpital Pitié–Salpêtrière, 47-83 Boulevard de l’Hôpital, 75651 Paris Cedex 13, France; e-mail: isabelle.arnulf{at}psl.ap-hop-paris.fr

Objective: To investigate the potential causes of excessive daytime sleepiness in patients with PD—poor sleep quality, abnormal sleep–wakefulness control, and treatment with dopaminergic agents.

Methods: The authors performed night-time polysomnography and daytime multiple sleep latency tests in 54 consecutive levodopa-treated patients with PD referred for sleepiness, 27 of whom were also receiving dopaminergic agonists.

Results: Sleep latency was 6.3 ± 0.6 minutes (normal >8 minutes), and the Epworth Sleepiness score was 14.3 ± 4.1 (normal <10). A narcolepsy-like phenotype (>=2 sleep-onset REM periods) was found in 39% of the patients, who were sleepier (4.6 ± 0.9 minutes) than the other 61% of patients (7.4 ± 0.7 minutes). Periodic leg movement syndromes were rare (15%, range 16 to 43/h), but obstructive sleep apnea–hypopnea syndromes were frequent (20% of patients had an apnea–hypopnea index >15/h; range 15.1 to 50.0). Severity of sleepiness was weakly correlated with Epworth Sleepiness score (r = -0.34) and daily dose of levodopa (r = 0.30) but not with dopamine-agonist treatment, age, disease duration, parkinsonian motor disability, total sleep time, periodic leg movement, apnea–hypopnea, or arousal indices.

Conclusions: In patients with PD preselected for sleepiness, severity of sleepiness was not dependent on nocturnal sleep abnormalities, motor and cognitive impairment, or antiparkinsonian treatment. The results suggest that sleepiness—sudden onset of sleep—does not result from pharmacotherapy but is related to the pathology of PD.




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