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Abstracts / Sleep Medicine 14S (2013) e18–e92
Introduction: Attention Deficit Hyperactivity Disorder (ADHD) is a neurodevelopmental disorder characterized by a triad of symptoms involving hyperactivity, impulsivity and inattention. Several studies in children with ADHD showed a high prevalence of excessive daytime sleepiness. To our knowledge, no study has objectively assessed sleepiness in adults with ADHD. Moreover, it has been shown that adults with ADHD were at risk for driving accidents. The objectives of this study are to quantify objective sleepiness and its impact on driving performance in adult with ADHD. Materials and methods: 36 subjects with ADHD (age (mean SE) = 36.3 1.6) and 18 control subjects (age (mean SE) = 31.2 1.2) were included. Nocturnal polysomnography was performed to identify potential sleep disorder. The next day patients were submitted to a Maintenance Wakefulness Test (MWT) at 10H, 12H, 14H, 16H to examine their level of daytime sleepiness. After a training of 15 min, a driving test of 1 h was carried out at 17H on a simulator (Oktal) to evaluate driving performance. Results: ADHD subjects were divided into 2 groups according to their level of sleepiness at the MWT: the ’’sleepy’’ group consisted of twenty subjects (mean sleep latency (SL) = 23.9 1.3 min) and the ‘‘alert’’ group included sixteen subjects (LE = 37.3 1 min)(p = 0.001). We observed that more than half of the ADHD subjects exhibit a sleep disorder: 31% among the alert ADHD subjects and 65% among sleepy ADHD subjects. But 35% of the sleepy ADHD subjects did not presented a sleep disorder. About driving performance, there were significant differences between driving performance (observed by the number of lines crossing) between the control group and the alert ADHD group (p = 0.05) and the control group and the sleepy ADHD group (p = 0.02). Conclusion: This study supports the hypothesis that there is a sub group of ADHD patients that present pathological sleepiness. In our sample, half of the patients suffer of excessive daytime sleepiness. But it is appropriate to question the origin of the sleepiness found in the other patients and to wonder if they represent a particular phenotype. ADHD impacts on driving performances, but it is not possible today to clearly explain them: attention deficit and/or sleepiness? But it is important to focus on this question to provide therapeutic strategy modulated by the clinic. Acknowledgements: JP rénéric. http://dx.doi.org/10.1016/j.sleep.2013.11.147
Symptoms of insomnia among OSA patients before and after 2 years of PAP treatment E. Bjornsdottir 1, C. Janson 2, E. Arnardóttir 1, A. Pack 3, T. Gislason 1, B. Benediktsdottir 1 1 Faculty of Medicine, University of Iceland, Iceland 2 Uppsala University, Sweden 3 Center for Sleep and Circadian Neurobiology, Division of Sleep Medicine, Department of Medicine, United States
Introduction: To assess the changes of insomnia symptoms among patients with obstructive sleep apnea (OSA) from starting treatment with positive airway pressure (PAP) to a two-year follow-up. Materials and methods: All subjects underwent a medical examination, type 3 sleep study and answered questionnaires on health and sleep before and 2 years after starting PAP treatment. The change in prevalence of insomnia symptoms by subtype were assessed by questionnaire and compared between individuals who were using or not using PAP at follow-up. Results: Symptoms of middle insomnia were most common at baseline and improved significantly among subjects using PAP (from 59.4% to 30.7%, p < 0.001). Symptoms of initial insomnia tended to
persist, regardless of PAP treatment and symptoms of late insomnia were more likely to improve among subjects not using PAP. Subjects with symptoms of initial and late insomnia at baseline were less likely to adhere with PAP (odds ratio (OR) 0.56, p = 0.007, and OR 0.53, p < 0.001, respectively). Conclusion: PAP treatment significantly reduced symptoms of middle insomnia. Symptoms of initial and late insomnia, however, tended to persist regardless of PAP treatment and had a negative effect on treatment adherence. Targeted treatment for insomnia may be beneficial for patients with OSA comorbid with insomnia and has the potential to positively affect adherence to PAP. Acknowledgements: Support: NIH grant HL72067 for ‘‘A Family Linkage Study of Obstructive Sleep Apnoea’’ and HL94307 for ‘‘Endophenotypes of Sleep Apnea and Role of Obesity’’, the Eimskip Fund of the University of Iceland and the Landspitali University Hospital Research Fund. http://dx.doi.org/10.1016/j.sleep.2013.11.148
A randomized controlled trial of the effects of bright light and melatonin for delayed sleep phase disorder B. Bjorvatn 1, I. Saxvig 1, A. Wilhelmsen-Langeland 1, Ø. Vedaa 2, I. Nordhus 1, S. Pallesen 1 1 Haukeland University Hospital, Norwegian Competence Center for Sleep Disorders, Norway 2 University of Bergen, Department of Psychosocial Science, Norway
Introduction: Delayed sleep phase disorder (DSPD) is a circadian rhythm sleep disorder. Patients with DSPD have problems initiating sleep if they go to bed at a conventional time and they have serious problems waking at desired times. In the present study we investigated short- and long-term effects of timed bright light and exogenous melatonin treatment alongside gradually advanced rise times in adolescents/young adults with DSPD in a randomized controlled two- week trial with an open label 3-month follow-up study. Materials and methods: Forty patients (16–25 years) diagnosed with DSPD were recruited to participate. The participants were randomized to receive treatment for 2 weeks in one of four treatment conditions: dim light + placebo capsules, bright light + placebo capsules, dim light + melatonin capsules or bright light + melatonin capsules. In the follow-up study, participants were re-randomized to either receive treatment with the combination of bright light and melatonin or no treatment in an open label trial for three months. Light and capsules were administered alongside gradual advancement of rise times. The main end points were sleep and daytime function as assessed by sleep diaries, actigraphy, sleepiness/fatigue recordings, cognitive function and circadian phase (assessed by salivary dim light melatonin onset (DLMO)). Results: During the two-week intervention, the timing of sleep and DLMO were advanced in all treatment conditions with no interaction effects (two-way ANOVA); about one hour advance of bed time, 2 h advance of rise time and two hours advance of DLMO in all four groups. Sleep duration was reduced with one hour. Subjective sleepiness, fatigue and cognitive function also improved significantly after two weeks of treatment, again with no interaction effects. At threemonth follow-up, the no-treatment group had returned to baseline on all measures, whereas the treatment group had maintained an advanced sleep phase as well as improved scores on sleepiness, fatigue, and cognitive function. Sleep duration had increased. Conclusion: Gradual advancement of rise time produced a phase advance and an improved daytime function during the two-week intervention, irrespective of treatment condition. Termination of treatment caused relapse into delayed sleep times and poor daytime