ライフサイエンスコーパス: migraine headache

1 actions contribute to the pathophysiology of migraine headache.

2 as a novel therapeutic for the treatment of migraine headache.

3 eading depolarization with migraine aura and migraine headache.

4 s a complex and unresolved relationship with migraine headache.

5 iceptive responses in two distinct models of migraine headache.

6 calcium levels were associated with risk of migraine headache.

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

8 vestibular migraine largely mirror those for migraine headache.

9 ESK mutation increases the susceptibility of migraine headache.

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

11 se resembling the development of the delayed migraine headache.

12 on the mechanism by which light exacerbates migraine headache.

13 on the mechanism by which light intensifies migraine headache.

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

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

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

17 sensitization, leading to the generation of migraine headache.

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

19 t regulates pain signaling and generation of migraine headache.

20 D) receptor agonists commonly prescribed for migraine headache.

21 eningeal and brainstem events that cause the migraine headache.

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

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

24 rrent sinusitis, cough, and both tension and migraine headaches.

25 ological pathways linking phytochemicals and migraine headaches.

26 operties of a diet in the pathophysiology of migraine headaches.

27 eadaches are common in both migraine and non-migraine headaches.

28 ry acid load (DAL) in the pathophysiology of migraine headaches.

29 osition to CAD was inversely associated with migraine headaches.

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

31 treatment of choice for moderate and severe migraine headaches.

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

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

34 8-65 years) from 62 sites in the USA who had migraine headaches 8-14 days per month.

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

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

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

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

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

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

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

42 %) had current CRS symptoms, 1,765 (23%) had migraine headache, and 1,930 (25%) had higher levels of

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

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

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

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

47 Male sex, migraine headache, and prior sinus surgery were associat

48 l therapeutics for patent ductus arteriosus, migraine headache, and sepsis; however, the lack of sele

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

50 al unsolved issue is whether visual aura and migraine headache are parallel or sequential processes.

51 Migraine headaches are often precipitated by stress and

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

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

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

55 on of meningeal afferents play a key role in migraine headache, but the underlying mechanisms remain

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

57 e common practice of attempting to alleviate migraine headaches by targeting the greater and lesser o

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

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

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

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

62 zumab group had on average 4.1 fewer monthly migraine headache days compared with baseline (13.4), wh

63 an change from baseline in number of monthly migraine headache days during the 3-month treatment peri

64 ents with >=50%, >=75% and 100% reduction in migraine headache days from baseline at months 1, 2 and

65 .11 (galcanezumab) vs -0.53+/-0.11 (placebo) migraine headache days indicated onset at week 1.

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

67 per month; chronic migraine, at least eight migraine headache days per month and at least 15 headach

68 igh frequency episodic migraine, eight to 14 migraine headache days per month and fewer than 15 heada

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

70 dache Disorders 3rd edition criteria for 2-8 migraine headache days per month were recruited and rand

71 episodic migraine, four to fewer than eight migraine headache days per month; high frequency episodi

72 The number of migraine headache days per week, and onset of efficacy m

73 ients had significantly greater reduction in migraine headache days versus placebo across months 1-3.

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

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

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

77 neural substrate underlying the worsening of migraine headache during physical activity.

78 sociated with an increased risk of new-onset migraine, headache, epilepsy, sleep disorder, or mental

79 come was a composite neurological outcome of migraine, headache, epilepsy, sleep disorder, or mental

80 ew the importance of the cranial meninges to migraine headaches, explore the properties of trigeminal

81 ine the pathophysiology of migraine aura and migraine headache, exploring evidence from clinical obse

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

83 he cranial meninges as a key site underlying migraine headache genesis through complex interplay betw

84 ular and neuroimmune interactions, underlies migraine headache genesis.

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

86 cluding duration, frequency, and severity of migraine headaches, Headache Impact Test-6 (HIT-6), and

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

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

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

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

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

92 l data challenge the notion that aura causes migraine headache in patients.

93 Systemic infusion of PACAP-38 induces migraine headache in people with migraine and mild heada

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

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

96 etween dietary phytochemical index (DPI) and migraine headaches in Iranian patients, analyzing both c

97 greater or less than 50% improvement of the migraine headache index (MHI) after surgery.

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

99 = 0.191, P = 0.03) between serum calcium and migraine headache, indicating that these traits have a g

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

101 Migraine headache is a pain condition characterized by s

102 Migraine headache is common in children and adolescents,

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

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

105 Migraine headache is hypothesized to involve the activat

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

107 Migraine headache is proposed to be mediated by nitric o

108 Migraine headache is triggered by and associated with a

109 Migraine headache is uniquely exacerbated by light.

110 ilepsy, major depressive disorder (MDD), and migraine headaches (MH) that can significantly affect pa

111 ; 3 studies) and among patients with chronic migraine headaches (n = 1508, -2.30 headaches per month;

112 ly that one theory will explain all types of migraine headache or the mechanisms of action of drugs t

113 sociation was observed between the score and migraine headaches (OR: 0.94; 95% CI: 0.93 to 0.96).

114 urbing symptom, the characteristic throbbing migraine headache pain, is widely agreed to be caused by

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

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

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

118 re followed up at 3, 6, and 12 months, and a migraine headache questionnaire was administered at each

119 The underlying causes of migraine headache remained enigmatic for most of the 20t

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

121 How these interactions might generate migraine headaches remains incompletely understood and a

122 on of inflammation in the context of CSD and migraine headaches remains poorly understood.

123 Migraine headache results from activation of meningeal n

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

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

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

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

128 ent believed to underlie aura, might trigger migraine headaches through inflammatory signalling that

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

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

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

132 Using mouse models of migraine headache, we show that peroxynitrite-modulating

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

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

135 nerve oedema, splenomegaly, anhidrosis, and migraine headache), while the ALPK1[V1092A] mutation acc

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

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

138 enopausal and had a long-standing history of migraine headaches without hormonal or drug therapy.