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Julie Rolling1– 4*, Juliette Rabot1– 3,5,6*, Carmen M Schroder1– 6 1Department of Child and Adolescent Psychiatry, Strasbourg University Hospitals, Strasbourg, France; 2CNRS UPR3212- Research Team “Light, Circadian Rhythms, Sleep Homeostasis and Neuropsychiatry”, Institute of Cellular and Integrative Neurosciences, Strasbourg, France; 3Excellence Centre for Autism and Neurodevelopmental Disorders STRAS&ND, Strasbourg, France; 4Sleep Disorders Centre & International Research Centre for ChronoSomnology (Circsom), University Hospitals Strasbourg, Strasbourg, France; 5Expert Centre for High-Functioning Autism, Fondation FondaMental, Strasbourg, France; 6Autism Resources Centre 67 for Children and Adolescents, Strasbourg, France*These authors contributed equally to this workCorrespondence: Carmen M Schroder, Email schroderc@unistra.frAbstract: Sleep is a vital physiological function that is impaired in ranges from 10% in the typically developing pediatric population to over 80% in populations of children with neurodevelopmental disorders and/or psychiatric comorbidities. Pediatric insomnia disorder is an increasing public health concern given its negative impact on synaptic plasticity involved in learning and memory consolidation but also on mood regulation, hormonal development and growth, and its significant impact on quality of life of the child, the adolescent and the family. While first-line treatment of pediatric insomnia should include parental education on sleep as well as sleep hygiene measures and behavioural treatment approaches, pharmacological interventions may be necessary if these strategies fail. Melatonin treatment has been increasingly used off-label in pediatric insomnia, given its benign safety profile. This article aims to identify the possible role of melatonin treatment for pediatric insomnia, considering its physiological role in sleep regulation and the differential effects of immediate release (IR) versu

Léa Dormegny,1,2 Reana Velizarova,1 Carmen M Schroder,1,3 Ulker Kilic-Huck,1,3 Henri Comtet,1,3 Hélène Dollfus,4 Patrice Bourgin,1,3 Elisabeth Ruppert1,3 1Centre des Troubles du Sommeil - CIRCSom, Hôpital Civil, University of Strasbourg, Strasbourg, 67091, France; 2Department of Ophthalmology, Hôpital Civil, University of Strasbourg, Strasbourg, 67091, France; 3Institute for Cellular and Integrative Neurosciences, CNRS - UPR 3212, Strasbourg, 67000, France; 4Centre des Affections Rares en Génétique Ophtalmologique (CARGO), University of Strasbourg, Strasbourg, 67091, FranceCorrespondence: Elisabeth RuppertCentre des Troubles du Sommeil - CIRCSom - Hôpital Civil, 1, place de l’Hôpital, BP 426, Cedex, Strasbourg, 67091, FranceTel +33 3 88 11 64 30Fax +33 3 88 11 51 53Email elisabeth.ruppert@chru-strasbourg.frObjective/Background: Bardet–Biedl syndrome (BBS) is a rare but well-recognized ciliopathy with high genetic and phenotypic heterogeneity. Cardinal features include obesity, diabetes and high blood pressure (HBP), which are often associated with sleep-disordered breathing. Also, the high prevalence of blindness due to retinal dystrophy could affect circadian sleep–wake rhythms. We characterized in this cohort of adult BBS patients sleep-disordered breathing, sleep quality, daytime sleepiness and chronotype.Patients and Methods: Thirty-two patients with genetically confirmed BBS were included in this observational single center study. Overnight respiratory polygraphy was performed for sleep apnea syndrome (SAS) in 30 patients. Quality of sleep, daytime sleepiness, fatigue and chronotype were assessed in 25 patients using Pittsburgh sleep quality index (PSQI), 14-day sleep diary (SD), Epworth sleepiness scale (ESS), Pichot fatigue scale (PFS) and Horne and Ostberg morningness-eveningness questionnaire (MEQ).Results: Patients’ mean age was 32± 11 years and mean BMI 32.6± 7.7 kg/m2. Eleven (35%) patients had HBP and 7 (22%) diabetes. Moderate to sev