TY - JOUR
T1 - Boundary-Dependent Sleep–Wake Dysregulation in Idiopathic Hypersomnia
AU - Mombelli, Samantha
AU - Lacourse, Karine
AU - Blais, Hélène
AU - Deshaies-Rugama, Anne Sophie
AU - Thompson, Cynthia
AU - Desautels, Alex
AU - Montplaisir, Jacques
AU - Nigam, Milan
AU - Moderie, Christophe
AU - Khajehpiri, Boshra
AU - Duclos, Catherine
AU - Lina, Jean Marc
AU - Carrier, Julie
AU - Gosselin, Nadia
N1 - Publisher Copyright:
© 2026 The Author(s). Annals of Clinical and Translational Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.
PY - 2026
Y1 - 2026
N2 - Objective: Idiopathic hypersomnia (IH) presents with excessive daytime sleepiness (EDS) despite apparently preserved nocturnal sleep, challenging traditional models of hypersomnolence based on sleep loss or fragmentation. We aimed to test the hypothesis that EDS in IH reflects excessive stabilization of the sleep state, consistent with dysfunctional thalamocortical control rather than impaired sleep quantity or continuity. Methods: We analyzed overnight polysomnography from 62 IH and 81 age- and sex-matched healthy controls using sleep bout duration, sleep stage transition dynamics, and automated spindle detection. Principal component analyses derived composite indices of NREM and REM sleep stability. Group differences were assessed using ANCOVAs controlling for age and sex, and associations with EDS severity were examined. Results: Compared with controls, IH patients showed reduced transitions from N3 sleep toward lighter stages and wakefulness. Moreover, REM sleep was characterized by longer durations, fewer transitions to wakefulness, and more frequent transitions to lighter stages. In parallel, spindle amplitude was reduced in IH while spindle density was preserved, and smaller spindle amplitudes were associated with shorter latencies on the Multiple Sleep Latency Test. Interpretation: IH is characterized by excessive N3 stabilization and reduction in transitions toward wakefulness in both NREM and REM sleep. These findings suggest that altered sleep–wake dynamics, rather than impaired sleep continuity, may contribute to persistent daytime sleepiness in IH and support sleep stability as a potential target for future research and therapeutic strategies.
AB - Objective: Idiopathic hypersomnia (IH) presents with excessive daytime sleepiness (EDS) despite apparently preserved nocturnal sleep, challenging traditional models of hypersomnolence based on sleep loss or fragmentation. We aimed to test the hypothesis that EDS in IH reflects excessive stabilization of the sleep state, consistent with dysfunctional thalamocortical control rather than impaired sleep quantity or continuity. Methods: We analyzed overnight polysomnography from 62 IH and 81 age- and sex-matched healthy controls using sleep bout duration, sleep stage transition dynamics, and automated spindle detection. Principal component analyses derived composite indices of NREM and REM sleep stability. Group differences were assessed using ANCOVAs controlling for age and sex, and associations with EDS severity were examined. Results: Compared with controls, IH patients showed reduced transitions from N3 sleep toward lighter stages and wakefulness. Moreover, REM sleep was characterized by longer durations, fewer transitions to wakefulness, and more frequent transitions to lighter stages. In parallel, spindle amplitude was reduced in IH while spindle density was preserved, and smaller spindle amplitudes were associated with shorter latencies on the Multiple Sleep Latency Test. Interpretation: IH is characterized by excessive N3 stabilization and reduction in transitions toward wakefulness in both NREM and REM sleep. These findings suggest that altered sleep–wake dynamics, rather than impaired sleep continuity, may contribute to persistent daytime sleepiness in IH and support sleep stability as a potential target for future research and therapeutic strategies.
KW - non-restorative sleep
KW - sleep microstructure
KW - sleepiness
KW - sleep–wake balance
KW - thalamocortical network
UR - https://www.scopus.com/pages/publications/105049181729
U2 - 10.1002/acn3.70522
DO - 10.1002/acn3.70522
M3 - Journal Article
C2 - 42687137
AN - SCOPUS:105049181729
SN - 2328-9503
JO - Annals of Clinical and Translational Neurology
JF - Annals of Clinical and Translational Neurology
ER -