ライフサイエンスコーパス: hypersomnia

1 depressive episodes, including insomnia and hypersomnia.

2 large number of neurons activated during PS hypersomnia.

3 ficacy of lower-sodium oxybate in idiopathic hypersomnia.

4 ory approval for the treatment of idiopathic hypersomnia.

5 atypical patients experience hyperphagia and hypersomnia.

6 mportant diagnostic tool in the diagnosis of hypersomnias.

7 Common symptoms were hypersomnia (100%), cognitive changes (96%, including a

8 rly morning awakening (38.9% vs. 12.7%), and hypersomnia (35.0% vs. 10.7%).

9 aracterized by atypical symptoms, especially hypersomnia, afternoon or evening slump, reverse diurnal

10 s in MDD include the presence of insomnia or hypersomnia and aberrations in sleep macro- and microstr

11 erity and reversed neurovegetative symptoms (hypersomnia and either hyperphagia or weight gain).

12 episode, in addition to atypical features of hypersomnia and hyperphagia.

13 ing only the reversed vegetative symptoms of hypersomnia and hyperphagia.

14 y information on 42 subjects with idiopathic hypersomnia and obtained detailed follow-up evaluations

15 large number of neurons activated during PS hypersomnia and projecting to the VLPAG/dDpMe.

16 In patients with central hypersomnia and thus a high pretest probability for narc

17 ay also aid more accurate phenotyping of the hypersomnias and in particular clarify heterogeneity amo

18 ave insomnia, 25% have sleep apnea, 28% have hypersomnia, and 4% have narcolepsy.

19 ted experiencing significantly more fatigue, hypersomnia, and psychomotor retardation during the most

20 h other sleep disorders, patients with other hypersomnias, and patients with narcolepsy with normal h

21 Narcolepsy and idiopathic hypersomnia are chronic brain disorders with an onset at

22 The features of idiopathic hypersomnia are not well defined.

23 trically opposite symptoms [eg, insomnia and hypersomnia]) as measured with the Patient Health Questi

24 e, failures were associated with fatigue and hypersomnia, but less so with sadness, anhedonia, and ap

25 disorder with symptoms that include periodic hypersomnia, cognitive and behavioural disturbances.

26 acterized by relapsing-remitting episodes of hypersomnia, cognitive disturbances, and behavioral dist

27 During episodes, all patients had hypersomnia, cognitive impairment, and derealization; 66

28 e therapy are recommended for narcolepsy and hypersomnia; continuous positive airway pressure, weight

29 agonists for the treatment of NT1 and other hypersomnia disorders.

30 by an unusual cohort of symptoms, including hypersomnia, executive dysfunction, as well as early ons

31 penditure balance (hyperphagia, weight gain, hypersomnia, fatigue, and leaden paralysis) and may mode

32 , but was characterized by increased eating, hypersomnia, frequent, relatively short episodes, and a

33 depressive disorder include mood reactivity, hypersomnia, hyperphagia, leaden paralysis, and rejectio

34 ve mood plus at least 2 additional symptoms: hypersomnia, hyperphagia, leaden paralysis, or lifetime

35 The pathophysiology of idiopathic hypersomnia (IH) remains unclear.

36 colepsy types 1 and 2 (NT1, NT2), idiopathic hypersomnia (IH), and Kleine-Levin syndrome (KLS) - for

37 alences were 23.1% for insomnia and 6.7% for hypersomnia in 1994.

38 ministration for the treatment of idiopathic hypersomnia in adults.

39 16 years.SUMMARY: Awareness of the extent of hypersomnia in children will allow physicians to effecti

40 Idiopathic hypersomnia is a central hypersomnolence disorder mainly

41 Idiopathic hypersomnia is a rare syndrome in which clinical heterog

42 ticipants (aged 18-75 years) with idiopathic hypersomnia (meeting criteria from the International Cla

43 tions for children with narcolepsy and other hypersomnias of central origin in order to raise awarene

44 falling asleep, early morning awakening, and hypersomnia) on the 3-year occurrence of attempting suic

45 1.88 [95% CI, 1.63-2.18]; P = 2.38 x 10-17; hypersomnia OR, 1.18 [95% CI, 1.05-1.33]; P = 5.80 x 10-

46 2.25 [95% CI, 2.00-2.53]; P = 9.03 x 10-41; hypersomnia OR, 1.22 [95% CI, 1.10-1.35]; P = 1.15 x 10-

47 more sleep disturbances including insomnia, hypersomnia, or nightmares than nonsuicidal patients.

48 nolence disorders (narcolepsy and idiopathic hypersomnia), other medical or psychiatric conditions, o

49 ole in the modulation of biological specific hypersomnia pathways.

50 Hypersomnia, rapid eye movement sleep disorder and/or na

51 nically meaningful improvement in idiopathic hypersomnia symptoms, with an overall safety profile con

52 The clinical usefulness of CSF testing in hypersomnia that is symptomatic of a neurological disord

53 ces neurological and sleep disorders such as hypersomnia; therefore, genetics allows us to uncover co

54 in MDD cases endorsing appetite increase and hypersomnia when contrasted with both controls (appetite

55 sease characterized by recurrent episodes of hypersomnia with behavioral and cognitive disturbances.

56 without cataplexy (N-C), 21 with idiopathic hypersomnia with long sleep time (IHL), 20 with BIISS an

57 nly 29% of subjects had 'classic' idiopathic hypersomnia with non-imperative sleepiness, long unrefre