ライフサイエンスコーパス: migraine attack

1 dividual changes in gene expression during a migraine attack.

2 ing were treated during a moderate to severe migraine attack.

3 rtant role during the premonitory phase of a migraine attack.

4 tching placebo for the treatment of a single migraine attack.

5 re and ocular biometric parameters and acute migraine attack.

6 imescale compatible with the duration of the migraine attack.

7 te to explain the sensory alterations of the migraine attack.

8 eminal nociceptive pathways, and lead to the migraine attack.

9 ved study treatment for a moderate or severe migraine attack.

10 n nociception and associated symptoms of the migraine attack.

11 areas when examined during a fully developed migraine attack.

12 nsient hemiplegia during the aura phase of a migraine attack.

13 the conceptual model for the progression of migraine attacks.

14 e wide range of possible triggers for future migraine attacks.

15 re results in a lower incidence of new-onset migraine attacks.

16 involved in the initiation and modulation of migraine attacks.

17 l hypoperfusion and neuroinflammation during migraine attacks.

18 release of proinflammatory substances during migraine attacks.

19 central sensitization mechanisms involved in migraine attacks.

20 not support using rizatriptan for vestibular migraine attacks.

21 lity of life or reduction of the duration of migraine attacks.

22 ed to periodontitis, OnabotA seems to reduce migraine attacks.

23 cological agents that both trigger and treat migraine attacks.

24 of oxytocin, which has been shown to prevent migraine attacks.

25 tor have shown efficacy in the prevention of migraine attacks.

26 lonal antibodies can reduce and even prevent migraine attacks.

27 did not significantly vary during the acute migraine attacks.

28 ine during acute glyceryl trinitrate-induced migraine attacks.

29 certain brainstem areas are activated during migraine attacks.

30 auditory, and olfactory stimuli can trigger migraine attacks.

31 f the premonitory phase in spontaneous human migraine attacks.

32 tification spectra, experienced during their migraine attacks.

33 operidol is very effective in aborting acute migraine attacks.

34 ved in animal also develops in humans during migraine attacks.

35 Treating migraine attacks 1 hour (early) or 4 hours (late) after

36 e between the migraine patients during acute migraine attacks (15.07 mmHg), painless period (14.10 mm

37 9 days; p = 0.02), mean reduction of monthly migraine attacks (-2.0 vs. -1.4; p = 0.01), and number o

38 at are activated at the earliest stages of a migraine attack, a greater appreciation of the potential

39 patient (5%; 95% CI, 0%-24%) who developed a migraine attack after placebo (P < .001).

40 patient per group) presented with new-onset migraine attacks after 3 months.

41 New-onset migraine attacks after ASD closure improved or resolved

42 s been suggested that clopidogrel may reduce migraine attacks after ASD closure.

43 en patients (71%; 95% CI, 48%-89%) developed migraine attacks after VIP compared with 1 patient (5%;

44 administering eptinezumab treatment during a migraine attack and comparison with alternative treatmen

45 ccurrence of appetite loss in patients under migraine attack and investigated the neuronal substrate

46 The prodrome is the earliest phase of a migraine attack and is characterised by non-aura symptom

47 37 patients did not treat a migraine attack and were excluded from outcome analyses.

48 e responder rate defined as 50% reduction in migraine attacks and adverse events.

49 parameters in migraine patients during acute migraine attacks and compare them with painless period a

50 neffective at 1 hour for treating vestibular migraine attacks and had limited benefit on symptoms at

51 il size of 40 migraine patients during acute migraine attacks and painless period and 40 age- and sex

52 We suggest that the hemiplegic migraine attacks and the cerebellar degeneration are lin

53 isual stimuli, and sounds, commonly triggers migraine attacks, and hypersensitivities to sensory stim

54 oducibility in research quantifying episodic migraine attacks, and identifying attack onset, a sound

55 migraine attacks), mean reduction in monthly migraine attacks, and percentage of patients who experie

56 number of monthly migraine days and monthly migraine attacks, and resulted in a greater number of su

57 Susceptibility to migraine attacks appears to be related to brain hyperexc

58 nosed with menstrual migraine, perimenstrual migraine attacks are associated with substantially great

59 Migraine attacks are associated with the development of

60 Migraine attacks are delimited, allowing investigation o

61 Because migraine attacks are hardly predictable and thereby the

62 re, during or after an episode; seizures and migraine attacks are mostly not temporally linked.

63 In many cases, migraine attacks are thought to begin centrally.

64 Consideration of a migraine attack as a brain state provides an expanded fr

65 We currently conceive of a migraine attack as originating in the brain.

66 graineurs during glyceryl trinitrate-induced migraine attacks as well as in matched control subjects.

67 The incidence and severity of new-onset migraine attacks, as evaluated by the Migraine Disabilit

68 etworks and the average monthly frequency of migraine attacks, as well as allodynia.

69 TNS treatment of a single moderate or severe migraine attack at home.

70 7%) and 4 patients (2.3%) continuing to have migraine attacks at 6 and 12 months, respectively (vs 3

71 no differences between groups in the rate of migraine attacks at 6 months (initial clopidogrel group:

72 Incidence and severity of migraine attacks at 6- and 12-month follow-up.

73 ive correlation between the time of the last migraine attack before the scan and activation of the pa

74 ties to sensory stimuli are prominent during migraine attacks, but can persist with less magnitude be

75 ration of a nitric oxide (NO) donor triggers migraine attacks, but the mechanisms by which this occur

76 ced presynaptic inhibition may contribute to migraine attacks by favouring a persistent state of hype

77 s severe channel dysfunction, and paroxysmal migraine attacks can be accompanied by seizures, coma, a

78 Moderate to severe acute migraine attacks can be treated with dihydroergotamine m

79 itory phase of glyceryl trinitrate-triggered migraine attacks can explain many of the premonitory sym

80 termining the susceptibility to developing a migraine attack, changes in cortical energy metabolism m

81 Migraine attacks consist of head pain and hypersensitivi

82 monotherapy, the percentage of patients with migraine attacks decreased over time, with 8 (4.7%) and

83 mly misclassifying MM was based on number of migraine attacks during 3 menstrual cycles (3 x 28 days)

84 6; 95% CI, 1.24-2.24), better improvement of migraine attacks during late pregnancy (OR, 5.10; 95% CI

85 rence in incidence of experimentally induced migraine attacks during the observational period (0-12 h

86 rm skin areas in the absence of, and during, migraine attacks enabled us to determine the occurrence

87 d for quantifying the number and duration of migraine attacks, enabling researchers to procure data o

88 expression during and outside a spontaneous migraine attack exist which are specific to migraine.

89 to 0.91]; P = .04) and a lower incidence of migraine attacks following ASD closure (9.5% for the clo

90 network of perpetual feedback that drives a migraine attack for many hours and even days.

91 interfere with processes that contribute to migraine attack generation or attack frequency.

92 rom migraine with aura, experienced frequent migraine attacks, had previously failed > or = 2 classes

93 The acute treatment of migraine attacks has been limited to the use of analgesi

94 of brainstem structures in the initiation of migraine attacks has been proposed based on functional m

95 For long the initial changes during a migraine attack have been shown to occur in the occipita

96 bilaterally at several time points during a migraine attack in a 42-year-old male.

97 We found that loss of appetite during the migraine attack in humans coincided strongly with the on

98 d develop gradually during the course of the migraine attack in more than 70% of patients.

99 bolic and activation parameters during acute migraine attacks in humans.

100 rformed using 100 000 permutations of random migraine attacks in migraine patients.

101 sensory hypersensitivities and that trigger migraine attacks in response to sensory stimuli might he

102 lammation with a time course consistent with migraine attacks in susceptible individuals.

103 red, whereas the second patient, who had had migraine attacks in the past, had a brief throbbing head

104 Studies of the clinical features of a migraine attack, in combination with imaging and electro

105 ding cumulative data of 27 spontaneous human migraine attacks including scans before, during, and aft

106 patients were assessed during a spontaneous migraine attack, including headache characteristics and

107 The migraine attack is characterized by alterations in senso

108 that eventually progresses into a full-blown migraine attack is common.

109 The occurrence of new-onset migraine attacks is a complication of transcatheter atri

110 with selection of subjects with long-lasting migraine attacks is not sufficient to overcome high plac

111 patients were required to have a history of migraine attacks lasting at least 4 hours.

112 associated symptoms, the true beginning of a migraine attack lies in the premonitory phase.

113 nd more severe (OR, 1.17; 95% CI, 1.13-1.21) migraine attacks, lower frequency of nonmigraine headach

114 However, recent studies suggest that migraine attacks may be associated with pathologic chang

115 ndings of hypothalamic abnormalities between migraine attacks may form part of the neuroanatomical su

116 receptor antagonists as a novel therapy for migraine attacks may represent a new era in the acute ma

117 er rate (defined as 50% reduction in monthly migraine attacks), mean reduction in monthly migraine at

118 The VIP-induced migraine attacks mimicked patients' spontaneous attacks.

119 ould be altered by the proximity of the last migraine attack not just during pre-ictal periods, but i

120 remediable risk factors include frequency of migraine attacks, obesity, excessive use of medications

121 ess, sleep, diet, and physical activity) and migraine attack occurrence.

122 ucted to dose at home within 4 h of onset of migraine attack of at least moderate intensity and not i

123 cipants who took the study medication, had a migraine attack of moderate or severe pain intensity at

124 participants who took study medication for a migraine attack of moderate or severe pain intensity, an

125 5 mg rimegepant or placebo to treat a single migraine attack of moderate or severe pain intensity.

126 r matching placebo and self-treated a single migraine attack of moderate or severe pain intensity.

127 25 mg (n = 561), or placebo (n = 563) for a migraine attack of moderate or severe pain intensity.

128 or placebo and instructed to treat a single migraine attack of moderate or severe pain intensity.

129 1-year history of migraine and two to eight migraine attacks of moderate or severe intensity per mon

130 We tested a simple Markov model of migraine attacks on headache diary data and estimated tr

131 ne, resulted in a lower monthly frequency of migraine attacks over 3 months.

132 attack onset, a sound theoretical model of a migraine attack, paired with a uniform standard for coun

133 r without aura and a history of two to eight migraine attacks per month with moderate to severe heada

134 ine with or without aura experiencing 2 to 8 migraine attacks per month.

135 a history of two to eight moderate or severe migraine attacks per month.

136 10 mg or placebo to treat up to 3 vestibular migraine attacks per participant.

137 CI, 2.17-14.00), and faster reappearance of migraine attacks post partum (OR, 3.19; 95% CI, 2.40-4.2

138 The severity of migraine attacks progressively decreased over time; no m

139 n to approximate the progression of observed migraine attacks satisfactorily, and imputing on migrain

140 ts with migraine precipitates the onset of a migraine attack several hours after completion of the in

141 central sensitization mechanisms involved in migraine attacks.SIGNIFICANCE STATEMENT A crucial unsolv

142 A 2-hour infusion of VIP caused migraine attacks, suggesting an important role of VIP in

143 depression (CSD) has long been implicated in migraine attacks that begin with visual aura.

144 In 31 patients, we studied 34 migraine attacks that were associated with allodynia at

145 ne therapy experiencing a moderate to severe migraine attack, treatment with intravenous eptinezumab

146 and during acute glyceryl trinitrate-induced migraine attacks using positron emission tomography with

147 tients with moderately or severely disabling migraine attacks vs 37% [7 patients] in the placebo grou

148 The frequency of migraine attacks was lower in patients in the last DPI t

149 Using nitroglycerine to trigger migraine attacks, we investigated whether cranial allody

150 ial allodynia accompanying their spontaneous migraine attacks were significantly more likely to have

151 a vasoactive peptide that is known to induce migraine attacks when administered by intravenous infusi

152 r glyceryl trinitrate (GTN) provokes delayed migraine attacks when infused into migraineurs and also

153 tive and well tolerated for the treatment of migraine attacks when taken during the prodrome.

154 l patients who were randomly assigned, had a migraine attack with pain of moderate or severe intensit

155 ve confirmed the primary neural basis of the migraine attack with secondary vascular changes, reconci

156 Treatment of a migraine attack with the oral calcitonin gene-related pe

157 Migraine attacks with auras are sometimes associated wit

158 t a dose of 100 mg for treatment of a single migraine attack, with the option to take a second dose.

159 y entries of potential migraine triggers and migraine attacks within 12 and 24 hours after trigger ex

160 A total of 27 patients (15.8%) had new-onset migraine attacks within the 3 months following ASD closu

161 Sildenafil has been shown to induce migraine attack without dilation of cerebral blood vesse

162 In addition, as the monthly frequency of migraine attacks worsens, the strength of the connectivi

163 ose in the clopidogrel group had less-severe migraine attacks (zero patients with moderately or sever