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Sleep: Widespread white matter changes in post-H1N1 narcolepsy type 1 patients and 1st degree relatives

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  • Sleep: Widespread white matter changes in post-H1N1 narcolepsy type 1 patients and 1st degree relatives

    Widespread white matter changes in post-H1N1 narcolepsy type 1 patients and 1st degree relatives

    Hilde T Juvodden Dag Aln?s Martina J Lund Ingrid Agartz Ole A Andreassen Espen Dietrichs Per M Thorsby Lars T Westlye Stine Knudsen

    Sleep, zsy145, https://doi.org/10.1093/sleep/zsy145

    Published:
    17 July 2018

    Article history




    Abstract

    Study Objectives
    To assess white matter involvement in H1N1-vaccinated hypocretin deficient narcolepsy type 1 (NT1) patients compared with 1st degree relatives (a potential risk group), and healthy controls.
    Methods
    We compared four diffusion tensor imaging-based microstructural indices (fractional anisotropy (FA), mean (MD), radial (RD), and axial diffusivity (AD)) in 57 NT1 patients (39 females, mean age 21.8 years, 51/57 H1N1-vaccinated, 57/57 HLA-DQB1*06:02-positive, 54/54 hypocretin-deficient), 54 1st degree relatives (29 females, mean age 19.1 years, 37/54 H1N1-vaccinated, 32/54 HLA-DQB1*06:02-positive), and 55 healthy controls (38 females, mean age 22.3 years). We tested for differences between these groups, for parametric effects (controls > 1st degree relatives > patients) and associations in patients (CSF hypocretin-1 and disease duration) and 1st degree relatives (HLA-DQB1*06:02 and H1N1-vaccination). We employed tract-based spatial statistics and used permutation testing and threshold-free cluster enhancement for inference.
    Results
    NT1 patients had a widespread, bilateral pattern of significantly lower FA compared with 1st degree relatives and healthy controls. Additionally, NT1 patients also exhibited significantly higher RD and lower AD in several focal white matter clusters. The parametric model showed that 1st degree relatives had intermediate values. Full sample of NT1 patients showed no significant associations with disease duration or CSF hypocretin-1.
    Conclusions
    Our study suggests widespread abnormal white matter involvement far beyond the already known focal hypothalamic pathology in NT1, possibly reflecting the combined effects of the loss of the widely projecting hypothalamic hypocretin neurons, and/or secondary effects of wake/sleep dysregulation. These findings demonstrate the importance of white matter pathology in NT1.


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