ライフサイエンスコーパス: migraine headache

1 NAP) at doses relevant to the human model of migraine headache.

2 vestibular migraine largely mirror those for migraine headache.

3 ESK mutation increases the susceptibility of migraine headache.

4 se genes that later in life are expressed as migraine headache.

5 se resembling the development of the delayed migraine headache.

6 on the mechanism by which light exacerbates migraine headache.

7 on the mechanism by which light intensifies migraine headache.

8 were specific for migraine compared with non-migraine headache.

9 veruse can lead to an increased frequency of migraine headache.

10 e the meninges--an event believed to set off migraine headache.

11 sensitization, leading to the generation of migraine headache.

12 ted peptide (CGRP) in the pathophysiology of migraine headache.

13 t regulates pain signaling and generation of migraine headache.

14 D) receptor agonists commonly prescribed for migraine headache.

15 eningeal and brainstem events that cause the migraine headache.

16 rain NO are proposed to initiate and mediate migraine headache.

17 calcium levels were associated with risk of migraine headache.

18 postulated to be responsible for the pain of migraine headache.

19 rol subjects and in 20 control patients with migraine headaches.

20 treatment of choice for moderate and severe migraine headaches.

21 ical, and clinical evidence link estrogen to migraine headaches.

22 based on the delayed development of typical migraine headache 4-6 h after infusing the NO donor nitr

23 8-65 years) from 62 sites in the USA who had migraine headaches 8-14 days per month.

24 primary efficacy end point was cessation of migraine headache 91 to 180 days after the procedure.

25 t somatic symptoms were stomach ulcer pains, migraine headaches, absence epilepsy (petit mal) episode

26 oposes a novel framework for conceptualizing migraine headache and its associated symptoms.

27 ciated with CMI among deployed veterans, and migraine headaches and gastritis were associated with CM

28 out one-half of the affected individuals had migraine headaches and several had episodes typical of b

29 ate the assumption of an association between migraine headaches and the presence of PFO by use of a l

30 We found no association between migraine headaches and the presence of PFO in this large

31 %) had current CRS symptoms, 1,765 (23%) had migraine headache, and 1,930 (25%) had higher levels of

32 n lesions, low-pitch hoarse voice, glaucoma, migraine headache, and arthritis were frequently observe

33 hat UNGD is associated with nasal and sinus, migraine headache, and fatigue symptoms in a general pop

34 natural gas development and nasal and sinus, migraine headache, and fatigue symptoms in Pennsylvania.

35 spondents with chronic rhinosinusitis (CRS), migraine headache, and fatigue symptoms.

36 aster rate occurs in women, in patients with migraine headaches, and in the presence of disc hemorrha

37 Migraine headaches are often precipitated by stress and

38 s at serotonin 1D (5-HT1D) receptors relieve migraine headache but are not clinically used as general

39 trongly implicated in the pathophysiology of migraine headache, but its role in migraine is still equ

40 g a potential explanation for selectivity to migraine headache, but not other pains, and a predominan

41 We found that exacerbation of migraine headache by light is prevalent among blind indi

42 diseases, including coronary artery disease, migraine headache, cervical artery dissection, fibromusc

43 nce was observed in the primary end point of migraine headache cessation between implant and sham gro

44 ribed for nonepileptic conditions, including migraine headache, chronic neuropathic pain, mood disord

45 up demonstrated a greater reduction in total migraine headache days (P=0.027).

46 ry endpoint was the mean change in number of migraine headache days per 28-day period assessed at 9-1

47 Patients aged 18-65 years with four to 14 migraine headache days per month were randomly assigned

48 ge from baseline to week 12 in the number of migraine headache days was -4.2 (SD 3.1; 62.5% decrease)

49 What do epilepsy, migraine headache, deafness, episodic ataxia, periodic p

50 vidence that hypercalcaemia is comorbid with migraine headache diagnoses, and that genetically elevat

51 th, arthritis, chronic musculoskeletal pain, migraines, headaches, fatigue, and family history of leu

52 traumatic brain injury, hepatic failure, and migraine headache has yet to be fully clarified.

53 ythms and pupil responses, and can intensify migraine headache in adults.

54 he premonitory phase without pain and during migraine headache in eight patients.

55 anced responses to an established trigger of migraine headache in humans.

56 finding of a neurophysiological correlate of migraine headache in meningeal nociceptors.

57 lycerin) to trigger premonitory symptoms and migraine headache in patients with episodic migraine wit

58 thase (NOS) inhibitor attenuates spontaneous migraine headaches in 67% of subjects.

59 bo to 99 outpatients with moderate or severe migraine headaches in a double blind, parallel group stu

60 it neurogenic dural inflammation, a model of migraine headache, indicating that these compounds may b

61 = 0.191, P = 0.03) between serum calcium and migraine headache, indicating that these traits have a g

62 and rACC/mPFC was associated with increased migraine headache intensity at the baseline.

63 Migraine headache is common in children and adolescents,

64 We propose that photoregulation of migraine headache is exerted by a non-image-forming reti

65 The perception of migraine headache is formed when nociceptive signals ori

66 Migraine headache is present in 12% of adults and has be

67 Migraine headache is proposed to be mediated by nitric o

68 Migraine headache is triggered by and associated with a

69 Migraine headache is uniquely exacerbated by light.

70 ; 3 studies) and among patients with chronic migraine headaches (n = 1508, -2.30 headaches per month;

71 ulinum toxin A was not associated with fewer migraine headaches per month vs valproate (standardized

72 were switched from TAC to CsA for recurrent migraine headaches, posttransplant diabetes, and chronic

73 rge on the nociceptive pathway that mediates migraine headache provide first set of scientific data o

74 The role of CSD in initiating a migraine headache remains to be determined, but it might

75 Medications clinically effective for migraine headache selectively elicit relief of ongoing c

76 esight we found that green light exacerbates migraine headache significantly less than white, blue, a

77 Clinical observations of migraine headache symptoms in patients with a patent for

78 ing hormonal contraceptives and bone health, migraine headaches, thrombosis risk, hypertension, weigh

79 lvarial sutures may be positioned to mediate migraine headache triggered by pathophysiology of extrac

80 meninges and participates in the genesis of migraine headaches, triggering mechanisms remain controv

81 s, including the onset of or exacerbation of migraine headaches, venous thromboembolism, and hyperten

82 rigeminovascular pathway thought to underlie migraine headache--we now report that CSD can activate c

83 The perception of migraine headache, which is mediated by nociceptive sign

84 addresses hypertension; atrial fibrillation; migraine headache with aura; and the epidemiology of typ

85 was no association of number or frequency of migraine headaches with progression of lesions.