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1 leepiness Scale (ESS, which assesses daytime hypersomnolence).
2 sential for the proinflammatory response and hypersomnolence.
3 of superoxide in the oxidation injury and in hypersomnolence.
4 ysis was used to assess the risk factors for hypersomnolence.
5 stages, was also an independent predictor of hypersomnolence.
6 d slow wave sleep (SWS) were protective from hypersomnolence.
7 o significant association with the degree of hypersomnolence.
8 treatment for narcolepsy and other types of hypersomnolence.
9 option in patients with treatment-refractory hypersomnolence.
10 decreased sleep efficiency, without daytime hypersomnolence.
11 pitolisant to be effective in treating both hypersomnolence and cataplexy while generally being well
12 obstructive sleep apnea, results in lasting hypersomnolence and is associated with nitration and oxi
13 itical role for NADPH oxidase in the lasting hypersomnolence and oxidative and proinflammatory respon
15 to not only long-term hypoxia/reoxygenation hypersomnolence but also to carbonylation, lipid peroxid
16 cterize the prevalence of persistent daytime hypersomnolence, difficulties initiating and maintaining
18 pnoea syndrome, circadian disorders, central hypersomnolence disorders (narcolepsy and idiopathic hyp
19 ntiation with CSF from patients with central hypersomnolence disorders, with no significant differenc
21 olysomnographic parameters and the degree of hypersomnolence in 741 patients with SDB (apnea-hypopnea
28 ols (9 males and 6 females) with unspecified hypersomnolence (n = 7) and miscellaneous neurological c
29 tween genetics and some central disorders of hypersomnolence - narcolepsy types 1 and 2 (NT1, NT2), i
30 derate-severe sleep apnea, result in lasting hypersomnolence, oxidative injury, and proinflammatory r
32 g with breakfast and lunch, in patients with hypersomnolence syndromes (excluding narcolepsy with cat
37 p a mouse model of cranial radiation-induced hypersomnolence which recapitulates the human experience