CME ARTICLE Sleep disruption, daytime somnolence and ‘sleep attacks’ in Parkinson’s disease: a clinical survey in PD patients and age-matched healthy volunteers J. J. Ferreira a , K. Desboeuf b , M. Galitzky c , C. Thalamas c , C. Brefel-Courbon b,c , N. Fabre c , J.-M. Senard b , J.-L. Montastruc b , C. Sampaio a and O. Rascol b,c a Neurological Clinical Research Unit, Lisbon School of Medicine, Lisbon, Portugal; b Department of Clinical Pharmacology, INSERM U455, Toulouse, France; and c Clinical Investigation Centre, University Hospital, Toulouse, France Keywords: Parkinson’s Disease, Sleep, Somnolence Received 7 April 2005 Accepted 10 May 2005 Recent case reports of ‘sleep attacks’ (SA) in patients with Parkinson’s disease (PD) generated concerns about drug-induced daytime somnolence in this population. However, there are nearly no comparative data on sleep and vigilance problems be- tween PD patients and normal controls. We performed a cross-sectional survey in PD patients and age-matched controls using a structured questionnaire on PD history, treatments, co-morbidity, activities of daily living, habits, exercise, sleep pattern, driving, pre-existing nocturnal problems, daytime somnolence, episodes of SA and the circumstances in which such episodes occurred. Daytime somnolence was also mea- sured with the Epworth Sleepiness Scale (ESS) and sleep quality with the Pittsburgh Sleep Quality Index (PSQI). 176 PD patients and 174 controls were included. The same proportion of PD patients (27%) and controls (32%) reported episodes of SA, but these were more frequent in PD patients and occurred more frequently during situations requiring attention (10.8% vs. 1.7%, p<10 )3 ). More PD patients had ab- normal daytime somnolence (ESS) and poor sleeping quality (PSQI). The most con- sistent factor associated with SA was the duration of levodopa therapy and the predictive value of an abnormal ESS score was rather poor (40.7%). Abnormal daytime somnolence and poor sleep quality at night are more frequent in PD patients than in normals. However, SA are reported in both groups, although less frequently in the normals during activities that requires attention. Introduction Although sleep disruption and daytime somnolence are common complaints in patients with Parkinson’s dis- ease (PD) [1,2], these symptoms have been largely neglected until the description of sudden sleep episodes designated as ‘sleep attacks’, causing car accidents in patients on the two newly marketed dopamine agonists (pramipexole and ropinirole) [3]. ‘Sleep attacks’ did not refer to any previously known sleep disorder [4] and were subsequently defined as ‘an event of overwhelming sleepiness that occurred without warning, or that oc- curred with a prodrome that was sufficiently short or overpowering to prevent the patient from taking appropriate protective measures’ [5]. Although there was no consensus regarding its acceptance as a ‘new’ drug-induced sleep disorder, this syndrome generated major safety concerns because of the related risk of falling asleep at the wheel [6,7]. Subsequent case reports reinforced a possible causal relationship with other dopamine agonists and levodopa itself [8–11]. Ques- tions on prevalence, pathophysiology, predictive fac- tors, protective measures and treatment strategies became pressing. However, data available were almost all anecdotal and did not allow further progress in our understanding of the problem. For PD, the closest sleep disorder previously studied on an epidemiological basis was ‘excessive daytime sleepiness’ and even for this symptom, information was scarce [12,13]. Furthermore, either old or recent studies had no control group, while ageing, for instance, is probably a major contributing and confounding factor [14]. For these reasons, we conducted a cross-sectional study to assess the prevalence and characteristics of ‘sleep attacks’, daytime somnolence, sleep problems in idiopathic PD patients compared with an age-matched non-parkinsonian population. We used logistic regres- sion analysis to identify risk factors such as types of an- tiparkinsonian medication and other clinical parameters. Correspondence: Joaquim J. Ferreira, Centro de Estudos Egas Moniz, Faculdade de Medicina de Lisboa, 1649-028 Lisboa, Portugal (tel.: +351 217930629; fax: +351 217957474; e-mail: joaquimjferreira@ net.sapo.pt). This is a Continuing Medical Education paper and can be found with corresponding questions on the Internet at: http://www. blackwellpublishing.com/products/journals/ene/mcqs. Certificates for correctly answering the questions will be issued by the EFNS. Ó 2006 EFNS 209 European Journal of Neurology 2006, 13: 209–214