The electroretinography to identify biomarkers of idiopathic hypersomnia and narcolepsy type 1

Author:

Rach Héloïse12,Kilic‐Huck Ulker12,Geoffroy Pierre A.134ORCID,Bourcier Tristan5,Braun Sophie12ORCID,Comtet Henri12,Ruppert Elisabeth12ORCID,Hugueny Laurence12,Hebert Marc67,Reynaud Eve12,Bourgin Patrice12

Affiliation:

1. Institute for Cellular and Integrative Neurosciences, CNRS UPR 3212 & Strasbourg University Strasbourg France

2. CIRCSom (International Research Center for ChronoSomnology) & Sleep Disorders Center Strasbourg University Hospital Strasbourg France

3. Département de psychiatrie et d'addictologie, AP‐HP, GHU Paris Nord, DMU Neurosciences Hopital Bichat‐Claude Bernard Paris France

4. Université de Paris, NeuroDiderot, Inserm, FHU I2‐D2 Paris France

5. Department of Ophthalmology & Gepromed, Education Department Strasbourg University Hospital Strasbourg France

6. Centre de Recherche CERVO Centre Intégré Universitaire de Santé et des Services Sociaux de la Capitale Nationale Québec Quebec Canada

7. Département d'Ophtalmologie et d'Oto‐Rhino‐Laryngologie‐Chirurgie Cervico‐Faciale, Faculté de Médecine Université Laval Québec Quebec Canada

Abstract

SummaryHypersomnia spectrum disorders are underdiagnosed and poorly treated due to their heterogeneity and absence of biomarkers. The electroretinography has been proposed as a proxy of central dysfunction and has proved to be valuable to differentiate certain psychiatric disorders. Hypersomnolence is a shared core feature in central hypersomnia and psychiatric disorders. We therefore aimed to identify biomarkers by studying the electroretinography profile in patients with narcolepsy type 1, idiopathic hypersomnia and in controls. Cone, rod and retinal ganglion cells electrical activity were recorded with flash‐electroretinography in non‐dilated eye of 31 patients with idiopathic hypersomnia (women 84%, 26.6 ± 5.9 years), 19 patients with narcolepsy type 1 (women 63%, 36.6 ± 12.7 years) and 43 controls (women 58%, 30.6 ± 9.3 years). Reduced cone a‐wave amplitude (p = 0.039) and prolonged cone (p = 0.022) and rod b‐wave (p = 0.009) latencies were observed in patients with narcolepsy type 1 as compared with controls, while prolonged photopic negative response‐wave latency (retinal ganglion cells activity) was observed in patients with idiopathic hypersomnia as compared with controls (p = 0.033). The rod and cone b‐wave latency clearly distinguished narcolepsy type 1 from idiopathic hypersomnia and controls (area under the curve > 0.70), and the photopic negative response‐wave latency distinguished idiopathic hypersomnia and narcolepsy type 1 from controls with an area under the curve > 0.68. This first original study shows electroretinography anomalies observed in patients with hypersomnia. Narcolepsy type 1 is associated with impaired cone and rod responses, whereas idiopathic hypersomnia is associated with impaired retinal ganglion cells response, suggesting different phototransduction alterations in both hypersomnias. Although these results need to be confirmed with a larger sample size, the electroretinography may be a promising tool for clinicians to differentiate hypersomnia subtypes.

Publisher

Wiley

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