NCT03998020: Somnobank

Constitution of a Clinical, Neurophysiological and Biological Cohort for Chronic Sleep Disorders Responsible of Hypersomnolence

Recruiting now NA Last updated 2 January 2024

What this trial tests

NA trial testing scale of severity in Somnolence Disorder, Excessive in 5,000 participants. Currently enrolling.

Timeline

16 June 2020

Primary endpoint
16 June 2030

16 June 2033

Quick facts

Lead sponsor	University Hospital, Montpellier
Phase	NA
Status	Recruiting now
Study type	INTERVENTIONAL
Allocation	na
Design	single group
Masking	none
Primary purpose	basic science
Enrollment	5,000
Start date	16 June 2020
Primary completion	16 June 2030
Estimated completion	16 June 2033
Sites	1 location across France

Drugs / interventions tested

• scale of severity
• blood sample — full drug profile →

Conditions studied

• Somnolence Disorder, Excessive — all drugs for Somnolence Disorder, Excessive →

Sponsor

University Hospital, Montpellier

Who can join

6 and older, any sex, with Somnolence Disorder, Excessive. Patients with the condition only — healthy volunteers not accepted.

Sponsor's own description

Chronic sleep disorders result from multiple pathophysiological mechanisms and are often associated with severe hypersomnolence, responsible for major disability. Hypersomnolence may be secondary to sleep disturbances at night by sleep fragmentation, both overall in restless leg syndrome (RLS) or specific to slow or paradoxical sleep in parasomnias (sleepwalking, sleep behavior disorder). paradoxical). Attention-Deficit / Hyperactivity Disorder (ADHD) is another cause of secondary hypersomnolence, unsolved pathophysiology, leading to a major disturbance of alertness. More rarely, hypersomnolence may be primary (central hypersomnia), representing then the most severe form existing in humans. The best-known central hypersomnia is narcolepsy type 1 (NT1), affecting 0.02% of the population. It is thanks to the existence of well-characterized clinical, biological and neuropathological patients that its pathophysiology is better understood. It is due to a selective loss of hypothalamic neurons secreting orexin / hypocretin, in connection with a probable autoimmune process, in genetically predisposed subjects. Narcolepsy type 2 (NT2), idiopathic hypersomnia (HI) and Kleine-Levin syndrome (SKL), are rarer forms of central hypersomnia, the pathophysiology of which is still unknown, due to the small number of patients studied.

Publications & conference data

1 peer-reviewed publication reference this trial (live from Europe PMC):

1. Systematic Assessment of Dysexecutive Syndrome, Hypersomnolence and Dysautonomia in Kleine-Levin Syndrome.
   Barateau L, Diab J, Thobois O, Chenini S, et al · · 2025 · PMID 40576450 · DOI 10.1111/ene.70259