ライフサイエンスコーパス: restless legs syndrome

1 ms associated with brain iron acquisition in restless legs syndrome.

2 n brain iron acquisition in individuals with restless legs syndrome.

3 in the epithelial cells of choroid plexus in restless legs syndrome.

4 or were upregulated in the choroid plexus in restless legs syndrome.

5 sleep disorders center received diagnoses of restless legs syndrome.

6 istory are characteristic of childhood-onset restless legs syndrome.

7 the activity of this protein is decreased in restless legs syndrome; a finding similar to our earlier

8 ls were isolated from the motor cortex of 11 restless legs syndrome and 14 control brains obtained at

9 entified and replicated 13 new risk loci for restless legs syndrome and confirmed the previously iden

10 small effects have been identified for both restless legs syndrome and narcolepsy with cataplexy.

11 and studied the genetic correlations between restless legs syndrome and traits of interest.

12 on's disease, dystonia, Tourette's syndrome, restless legs syndrome, and akathisia, have traditionall

13 nized conditions (motor stereotypy disorder, restless legs syndrome, and infantile masturbation) as w

14 onia, chorea, tics, myoclonus, stereotypies, restless legs syndrome, and various other disorders with

15 particular circadian disorders, narcolepsy, restless-legs syndrome, and OSAS.

16 clinical characteristics of childhood-onset restless legs syndrome are described.

17 r, a significant percentage of patients with restless legs syndrome are responsive to intravenous iro

18 id eye movement sleep behavior disorder, and restless legs syndrome, as well as circadian disorders,

19 loss of iron regulatory protein activity in restless legs syndrome brain tissue further implicates t

20 derlying cause of the iron deficiency in the restless legs syndrome brain.

21 erlying the decreased iron concentrations in restless legs syndrome brains is unknown.

22 f relative brain iron deficiency reported in restless legs syndrome brains may underlie the problems

23 romelanin cells from the substantia nigra of restless legs syndrome brains.

24 ns in the iron management protein profile in restless legs syndrome compared with controls at the sit

25 on in the brain is lower in individuals with restless legs syndrome compared with neurologically norm

26 ng of the molecular mechanisms that underlie restless legs syndrome could lead to new treatment optio

27 This issue provides a clinical overview of restless legs syndrome, focusing on diagnosis, treatment

28 medical condition, obstructive sleep apnea, restless legs syndrome, idiopathic insomnia, and circadi

29 For restless legs syndrome, implicated variants are typicall

30 Restless legs syndrome is a curious neurological disorde

31 Restless legs syndrome is a neurological disorder charac

32 Restless legs syndrome is a prevalent chronic neurologic

33 ted odds ratio =1.26; 95% CI = 1.02-1.54) or restless legs syndrome (n = 108, adjusted odds ratio = 1

34 med as the strongest genetic risk factor for restless legs syndrome (odds ratio 1.92, 95% CI 1.85-1.9

35 xt of another primary sleep disorder such as restless legs syndrome, or secondary to another underlyi

36 ies suggested a positive association between restless legs syndrome (RLS) and coronary heart disease

37 Most research on the association between restless legs syndrome (RLS) and depression has involved

38 minergic medications relieve symptoms of the restless legs syndrome (RLS) but have the potential to c

39 Restless legs syndrome (RLS) is a CNS disorder involving

40 Restless legs syndrome (RLS) is a common neurologic cond

41 Restless legs syndrome (RLS) is a common neurological di

42 Although restless legs syndrome (RLS) is a disorder recognized in

43 revious cross-sectional study, we found that restless legs syndrome (RLS) was associated with erectil

44 Restless legs syndrome (RLS), also known as Willis-Ekbom

45 Restless Legs Syndrome (RLS), first chronicled by Willis

46 spinal cord is implicated in the etiology of Restless Legs Syndrome (RLS), which is more prevalent in

47 1 dopaminergic systems in the development of restless legs syndrome (RLS)-like movements during sleep

48 uding 46 drug-naive patients with idiopathic restless legs syndrome (RLS).

49 ief from dysaesthesias and motor symptoms in restless legs syndrome (RLS).

50 on deficiency (BID), a pathogenetic model of restless legs syndrome (RLS).

51 ales (p = 0.007), had a higher proportion of restless legs syndrome (RLS; p < 0.001), had a higher bo

52 A family history of restless legs syndrome was present in 23 of 32 (72%) sub

53 in and its receptor in the microvessels from restless legs syndrome was significantly decreased compa

54 controls and 14 individuals who had primary restless legs syndrome was subjected to histochemical st

55 (parkinsonism, dystonia, tremor, chorea, and restless legs syndrome) were included.