Low cerebrospinal fluid hypocretin levels during sudden infant death syndrome (SIDS) risk period

• Published in: Sleep medicine Vol. 33; pp. 57 - 60
• Main Authors: Lancien, Marion, Inocente, Clara Odilia, Dauvilliers, Yves, Kugener, Beatrice, Scholz, Sabine, Raverot, Veronique, Lin, Jian-Sheng, Guyon, Aurore, Gustin, Marie-Paule, Franco, Patricia
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01-05-2017; Elsevier
• Subjects: Adolescent; Child; Child, Preschool; Female; Humans; Hypocretin/orexin; Incidence; Infant; Infant, Newborn; Life Sciences; Male; Maturation; Neurology; Orexins - analysis; SIDS; Sleep; Sleep - physiology; Sleep Medicine; Spinal Puncture - methods; Sudden Infant Death - cerebrospinal fluid; Sudden Infant Death - epidemiology; Sudden Infant Death - etiology; Wakefulness - physiology; Infant; hypocretin/orexin; SIDS; Sleep; Maturation; Hypocretin/orexin; Orexins; Spinal Puncture; Humans; Preschool; Male; Incidence; Newborn; Wakefulness; Adolescent; Sudden Infant Death; Female; Child
• ISSN: 1389-9457; 1878-5506
• DOI: 10.1016/j.sleep.2016.12.027

Abstract Objectives The temporal association between sudden infant death syndrome (SIDS) and sleep suggests that the arousability from sleep provides a protective mechanism for survival. Recently, the hypocretin system, which promotes wakefulness, has been implicated in SIDS, since it has been reported that SIDS victims have fewer hypocretin neurons than infants who have died from other causes. To understand the role of hypocretin in SIDS, it is essential to better understand how this system matures. The present study compared cerebrospinal fluid (CSF) hypocretin in children aged 2-6 months, which is the age of peak incidence for SIDS, to both younger and older children. Method Hypocretin levels were measured in CSF samples from 101 children who underwent a clinically relevant lumbar puncture. Children were separated into five age groups: 0-2 months, 2-6 months, 1-5 years, 5-10 years, and 10-18 years. Results Hypocretin levels were not significantly different between 1-5 years, 5-10 years, and 10-18 years. Between the 0-2 month, 2-6 month, and 1-18 year groups, a significant difference in CSF hypocretin levels existed ( p =0.0012). Simple comparisons showed that CSF hypocretin levels in the 2-6 month age group were significantly lower than hypocretin levels in both the 0-2 month and 1-18 year group ( p <0.001 and p =0.008, respectively), but not significantly between 0-2 month and 1-18 year children. Conclusions The CSF hypocretin levels were lower at the age of peak incidence for SIDS. This could underlie an increased vulnerability to SIDS at this specific age.