ライフサイエンスコーパス: migraine

1 nt was effective for preventive treatment of migraine.

2 atic structural brain lesions in people with migraine.

3 and efficacy for the preventive treatment of migraine.

4 agonist under investigation for treatment of migraine.

5 mended indications, such as heart disease or migraine.

6 development for the preventive treatment of migraine.

7 chanisms of cortical spreading depression in migraine.

8 debilitating symptom reported by people with migraine.

9 with women with migraine without aura or no migraine.

10 ion of 48 hours for the premonitory phase of migraine.

11 these forebrain regions in the regulation of migraine.

12 ment can reduce future stroke in people with migraine.

13 fficacy and safety in the acute treatment of migraine.

14 ocessing of ipRGC signals for photophobia in migraine.

15 t under investigation for acute treatment of migraine.

16 f the role of the channel in nociception and migraine.

17 r has been implicated in the pathogenesis of migraine.

18 thway inhibitors are emerging treatments for migraine.

19 explain why only TRESK-MT is associated with migraine.

20 tment and to compare it with other drugs for migraine.

21 of CGRP in a cohort of patients with chronic migraine.

22 periodontal inflammation and CGRP in chronic migraine.

23 ular risk factor at baseline, in addition to migraine.

24 s have not played a role in the treatment of migraine.

25 gain, and sensory processing dysfunctions in migraine.

26 sensory neuron excitability and is linked to migraine.

27 t therapeutic outcomes in different types of migraine.

28 herapeutic target for headache disorders and migraine.

29 circuit in a mouse model of a rare monogenic migraine.

30 and sex-matched individuals free of headache/migraine.

31 a clinical candidate for acute treatment of migraine.

32 ibility and shared biology underlying BP and migraine.

33 ant with placebo for preventive treatment of migraine.

34 ed and heralds a new era in the treatment of migraine.

35 f pathological conditions such as stroke and migraine.

36 ough complex partial seizures with postictal migraines.

37 Among the 418,965 patients with migraine, 1060 (0.25%) were subsequently diagnosed with

38 High levels of comorbidity included migraine (33), irritable bowel syndrome (17), functional

39 % CI = 2.16-8.65) and men (OR = 2.47 for any migraine, 95% CI = 1.32-4.61; OR = 3.61 for MA, 95% CI =

40 ion emerged in both women (OR = 2.97 for any migraine, 95% CI = 1.61-5.47; OR = 4.32 for MA, 95% CI =

41 In the acute treatment of migraine, a single 75 mg dose of rimegepant in an orally

42 Among adults with migraine, acute treatment with ubrogepant compared with

43 h adult gender expression only), depression, migraines (adult gender expression only), and physical l

44 d clinically efficacious plasma exposure for migraine also suggests a reduced potential for hepatotox

45 ck also seems to be increased in people with migraine, although this issue has not been extensively i

46 d 18-75 years), with a history (>=1 year) of migraine and 4-14 migraine days per month, were randomly

47 ly fremanezumab (month 1: 225 mg in episodic migraine and 675 mg in chronic migraine; months 2 and 3:

48 al disorders, primarily for the treatment of migraine and action tremor (mainly essential tremor), wo

49 The effect of PFO on the association between migraine and CIS was analyzed with logistic regression i

50 se to assess independent association between migraine and CIS.

51 Non-invasive neuromodulation therapies for migraine and cluster headache are a practical and safe a

52 tinct common pathophysiological mechanism in migraine and coronary heart disease such as endothelial

53 el syndrome, functional dyspepsia, abdominal migraine and functional abdominal pain not otherwise spe

54 insurance claims database for patients with migraine and matched control subjects without migraine b

55 Significant interaction between history of migraine and menopausal status for the prediction of VMS

56 Any migraine and migraine with (MA) and migraine without aur

57 nel is a potential pharmacological target in migraine and neuropathic pain.

58 EMENT Occipital headaches are common in both migraine and non-migraine headaches.

59 marrow, a finding of potential relevance to migraine and other neuroinflammatory brain disorders.

60 ral CGRP signaling in the pathophysiology of migraine and propose a model where dural CGRP-based mech

61 used to investigate the association between migraine and risk of all RAO, central RAO (CRAO), branch

62 Migraine and stroke are two common and heterogeneous neu

63 as a primary location of action for CGRP in migraine and suggest that female-specific mechanisms dow

64 sure (BP) was inconsistently associated with migraine and the mechanisms of BP-lowering medications i

65 brogepant against other acute treatments for migraine and to evaluate the long-term safety of ubrogep

66 ned adults with at least a 1-year history of migraine and two to eight migraine attacks of moderate o

67 or to placebo in the preventive treatment of migraine and was safe and well tolerated in patients for

68 ticonvulsant drug that is also used to treat migraines and bipolar disorder.

69 irth also reported more chronic headaches or migraines and joint pain, but experienced similar levels

70 ng been implicated in the pathophysiology of migraine, and CGRP-based therapeutics are efficacious fo

71 valence of obesity, smoking, hyperlipidemia, migraine, and gestational hypertension.

72 implicated; this includes pain, motivation, migraine, and the microbiome.

73 Although migraine appears to be associated with haemorrhagic stro

74 ral therapies used in the treatment of acute migraine are thought to be associated with medication ov

75 In a model of chronic migraine-associated pain using the human migraine trigge

76 mg doses, and absence of the most bothersome migraine-associated symptom at 2 hours only with the 50-

77 tial dose and absence of the most bothersome migraine-associated symptom at 2 hours.

78 tive at 2 h post-dose for acute treatment of migraine at all oral doses tested.

79 ra compared with migraine without aura or no migraine at baseline.

80 wer than 15 headache days per month; chronic migraine, at least eight migraine headache days per mont

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

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

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

84 25 mg (n = 561), or placebo (n = 563) for a migraine attack of moderate or severe pain intensity.

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

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

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

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

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

90 Because migraine attacks are hardly predictable and thereby the

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

92 1-year history of migraine and two to eight migraine attacks of moderate or severe intensity per mon

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

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

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

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

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

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

99 f the premonitory phase in spontaneous human migraine attacks.

100 the conceptual model for the progression of migraine attacks.

101 SD is the basis of migraine aura and is increasingly associated with many o

102 n the cortical spreading depression model of migraine aura in conditional knockout mice.

103 be associated with haemorrhagic stroke, the migraine aura status has a small influence on this relat

104 neuronal depolarization thought to underlie migraine aura.

105 polarization (SD), the phenomenon underlying migraine aura.

106 study has shown that a TRESK mutation causes migraine because it leads to the formation of a dominant

107 igraine and matched control subjects without migraine between 2007 and 2016.

108 trigeminal nerve endings in the mechanism of migraine, blockade of neuropeptide release by anti-migra

109 While mammalian studies indicate that the migraine brain is hyperexcitable due to enhanced excitat

110 alpha2-Na/K ATPase cause familial hemiplegic migraine, but the mechanisms by which alpha2-Na/K ATPase

111 Heterogeneity in chronic migraine (CM) presents significant challenge for diagnos

112 ble to treatment and have associated chronic migraine compared with primary CH.

113 o (HR) for incident all RAO in patients with migraine compared with those without migraine was 3.48 (

114 We found that all migraine coordinates (11/11, 100%) were negatively conne

115 area with the most specific connectivity to migraine coordinates compared to control coordinates (vo

116 ferences between two commonly used models of migraine, CSD induction and systemic CGRP infusion.

117 e studies when focusing on this phase of the migraine cycle.

118 um in migraineurs, which oscillates over the migraine cycle.

119 outcome was change from baseline in monthly migraine days across 12 weeks of treatment using a modif

120 om baseline in the monthly average number of migraine days during the 12-week treatment period.

121 We explored the validity of imputing migraine days on migraine-locked entries, and estimated

122 iated with a significant decrease in monthly migraine days over 12 weeks compared with placebo.

123 rom the observation period in mean number of migraine days per month during weeks 9-12 was -4.3 days

124 ary endpoint of change in the mean number of migraine days per month during weeks 9-12.

125 eek observation period in the mean number of migraine days per month in the last 4 weeks of the doubl

126 th a history (>=1 year) of migraine and 4-14 migraine days per month, were randomly assigned 2:1:2:2:

127 an (SE) change from baseline in mean monthly migraine days versus placebo: atogepant 10 mg once daily

128 ients demonstrated significant clustering of migraine days.

129 on migraine frequencies-e.g. the fraction of migraine-days of the observed days-without paying attent

130 y contain single, migraine-free days between migraine-days, and we argue here that such 'migraine-loc

131 Instead, people with migraine demonstrate an enhanced response to integrated

132 Chronically, patients with vestibular migraine develop abnormal responsiveness to both vestibu

133 sted of 467 women with a self-reported prior migraine diagnosis and 2,466 women without prior migrain

134 aine diagnosis and 2,466 women without prior migraine diagnosis who were assessed longitudinally duri

135 uding CRAO, BRAO, and other RAO, after first migraine diagnosis.

136 Our results indicate that people with migraine do not differ from headache-free controls in th

137 ne, blockade of neuropeptide release by anti-migraine drugs, and activation and sensitisation of trig

138 ts were female, 628 (76%) were white, median migraine duration was 17.5 years (IQR 10.0-28.0), and 23

139 ache days per month; high frequency episodic migraine, eight to 14 migraine headache days per month a

140 is hypothesis led to a transformation in the migraine field and understanding of key concepts surroun

141 d migraine frequency (low frequency episodic migraine, four to fewer than eight migraine headache day

142 patients' diaries frequently contain single, migraine-free days between migraine-days, and we argue h

143 Many studies report on migraine frequencies-e.g. the fraction of migraine-days

144 timated the effect of imputation on observed migraine frequencies.

145 eb-response system stratified by country and migraine frequency (low frequency episodic migraine, fou

146 ement of pupil responses was not seen in the migraine group, nor were group differences found in surv

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

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

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

150 .11 (galcanezumab) vs -0.53+/-0.11 (placebo) migraine headache days indicated onset at week 1.

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

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

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

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

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

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

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

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

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

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

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

162 lipidemia, diabetes, coronary heart disease, migraine, hypotension, and obstructive sleep apnea syndr

163 fective for acute treatment of patients with migraine in a phase 3 double-blind randomized controlled

164 peutics are efficacious for the treatment of migraine in humans.

165 flecting one that is relevant to spontaneous migraine in many migraineurs, whose symptoms of cranial

166 s, leading to neuronal hyperexcitability and migraine in rodents.

167 raine without aura and 24 246 [87.0%] had no migraine in the year prior to baseline).

168 otential marker for the premonitory phase of migraine in this unique dataset, our data corroborated a

169 ation contribute to the higher prevalence of migraine in women.

170 nd understanding of key concepts surrounding migraine, including the role of neuropeptides and their

171 There is growing evidence that migraine increases the overall risk of cerebrovascular d

172 Familial hemiplegic migraine is an episodic neurological disorder characteri

173 Migraine is associated with a higher risk of OAG for pat

174 Migraine is associated with increased risk of all types

175 We sought to determine if migraine is associated with increased risk of retinal ar

176 The premonitory phase of migraine is characterized by a well-described complex of

177 Although migraine is defined by the headache and headache-associa

178 Migraine is linked to endothelial dysfunction and is con

179 Migraine is one of the most prevalent and disabling dise

180 This effect of migraine is selective for ratings of visual discomfort,

181 Whether migraine is simply a concomitant condition in glaucoma p

182 e found that ischaemic stroke in people with migraine is strongly associated with migraine with aura,

183 Migraine is the second leading cause for disability worl

184 s (70%) developed headache exacerbation with migraine-like features after CGRP, compared with 6 patie

185 e in incidence of headache exacerbation with migraine-like features and (2) difference in area under

186 The most common PTH phenotypes are migraine-like headache and tension-type-like headache.

187 al sensory neuron excitability, leading to a migraine-like phenotype in rodents.

188 cally heterogeneous neuroimaging findings of migraine localize to a common brain network.

189 aine attacks satisfactorily, and imputing on migraine-locked days was consistent with the conceptual

190 migraine-days, and we argue here that such 'migraine-locked days' should routinely be interpreted as

191 ed the validity of imputing migraine days on migraine-locked entries, and estimated the effect of imp

192 est that the origin of occipital and frontal migraine may differ.

193 n non-occipital headaches and that occipital migraines may be associated more closely with cerebellar

194 ating inflammation in the pathophysiology of migraine meningeal symptoms.

195 eviously been related to familial hemiplegic migraine (MIM#602481) and alternating hemiplegia of chil

196 ebrain regions may play an important role in migraine modulation.

197 g in episodic migraine and 675 mg in chronic migraine; months 2 and 3: 225 mg in both migraine subgro

198 everaging large-scale summary statistics for migraine (N(cases)/N(controls) = 59,674/316,078) and BP

199 Our findings help unify migraine neuroimaging literature and offer a migraine-sp

200 Inconsistent findings from migraine neuroimaging studies have limited attempts to l

201 , back, and joint pain; chronic headaches or migraines; obesity; asthma; gestational and nongestation

202 Compared with nonmigraineurs, any migraine (odds ratio [OR] = 2.48, 95% confidence interva

203 age, with episodic or chronic migraine, with migraine onset before the age of 50 years, who had a doc

204 nts and of suffering from associated chronic migraine (OR 10.35, 95% CI 3.96 to 28.82).

205 ) for women with migraine without aura or no migraine (P < .001).

206 ks including scans before, during, and after migraine pain as well as interictal scans.

207 ostoperative, inflammatory, neuropathic, and migraine pain, as well as opioid-induced hyperalgesia.

208 he view that there is more than one truth to migraine pathophysiology and that it is unlikely that on

209 of calcitonin gene-related peptide (CGRP) in migraine pathophysiology was identified over 30 years ag

210 monetary incentive delay task in 29 episodic migraine patients and 41 headache-free controls.

211 Our findings reveal that vestibular migraine patients exhibited abnormally elevated reflexiv

212 Migraine patients showed decreased activation in one clu

213 acy of surgical trigger site deactivation in migraine patients.

214 ich alpha2-Na/K ATPase mutations lead to the migraine phenotype remain incompletely understood.

215 rs), and absence of symptoms associated with migraine (photophobia, phonophobia, and nausea) at 2 hou

216 the mechanism of action of anti-CGRP-mAbs in migraine prevention.SIGNIFICANCE STATEMENT The current s

217 documented failure to two to four classes of migraine preventive medications in the past 10 years.

218 usly not responded to two to four classes of migraine preventive medications.

219 ously not responded to up to four classes of migraine preventive medications.

220 Many patients who require migraine preventive treatment have not been able to tole

221 vative therapy targets the central theory of migraine propagation.

222 rrently no direct evidence to support that a migraine prophylactic treatment can reduce future stroke

223 the mechanisms of BP-lowering medications in migraine prophylaxis are unknown.

224 ons to treat hyperhidrosis, facial wrinkles, migraine prophylaxis, spasticity, and spasms, had a sign

225 , phase II-a study in patients with episodic migraine receiving galcanezumab 150 mg or placebo biweek

226 of CM, we utilized data reduction methods on migraine-related clinical dataset.

227 natural clusters in 100 CM patients using 14 migraine-related clinical variables.

228 rn of clinical features positively loaded by migraine-related disability, depression, poor sleep qual

229 self-efficacy and exercise levels had lower migraine-related disability, depression, sleep quality,

230 nt featured highest levels of depression and migraine-related disability.

231 on is associated with loss of function and a migraine relevant cellular phenotype.

232 tion suggesting that carriers of the reduced migraine risk allele have reduced sensitivity to cold st

233 cold thermosensor is associated with reduced migraine risk.

234 of neurological adverse reactions including, migraine, several peripheral neuropathies, and visual an

235 Common triggers were: migraine/severe headache (15), stroke (12), surgery or i

236 rebellar abnormalities than in non-occipital migraines.SIGNIFICANCE STATEMENT Occipital headaches are

237 l reflecting negative affect associated with migraine, SNC80 was only effective in loxP controls and

238 migraine neuroimaging literature and offer a migraine-specific target for neuromodulatory treatment.

239 diseases worldwide, but until recently, few migraine-specific therapies had been developed.

240 The mechanism behind the migraine-stroke association is unknown.

241 nic migraine; months 2 and 3: 225 mg in both migraine subgroups), or matched monthly placebo for 12 w

242 , the determination of success or failure of migraine surgery is based on whether there is greater or

243 A detailed analysis of outcomes after migraine surgery suggests an anatomic etiology of pain,

244 e findings support a critical role of DBP in migraine susceptibility and shared biology underlying BP

245 ng studies have limited attempts to localize migraine symptomatology.

246 the underlying neural mechanism of cephalic migraine symptoms, central sensitization, also predictin

247 an mediate the underlying neurophysiology of migraine symptoms, with nitrergic-induced changes reflec

248 [1.15-1.25]/10 mmHg; P = 5.57 x 10(-25)) on migraine than SBP (1.05 [1.03-1.07]/10 mmHg; P = 2.60 x

249 urability and safety of ubrogepant for acute migraine treatment and to compare it with other drugs fo

250 elated peptide receptor antagonist for acute migraine treatment.

251 nic migraine-associated pain using the human migraine trigger, nitroglycerin, we observed increased e

252 In familial hemiplegic migraine type 1 mice, olcegepant 1mg/kg increased infarc

253 at awake mice carrying a familial hemiplegic migraine type 2 (FHM2) mutation have slower clearance du

254 tant form of the TRESK ion channel linked to migraine undergoes alternative translation to produce an

255 Vestibular migraine (VM) is the most common cause of spontaneous ve

256 ts with migraine compared with those without migraine was 3.48 (95% confidence interval [CI] 3.07-3.9

257 eas only 335 (0.08%) of the patients without migraine were diagnosed with RAO.

258 episodic (269 [58%]) or chronic (193 [42%]) migraine were randomly assigned and received at least on

259 Adults with at least a 1-year history of migraine were recruited.

260 onnection with primary rewards or in chronic migraine where the pain experience is (almost) constant.

261 te longitudinal associations between VMS and migraine while adjusting for baseline and time-varying d

262 pitcher plant extract injections for chronic migraine, while her identical twin sister has normal iri

263 ts aged 18-70 years with episodic or chronic migraine who had documented failure to two to four class

264 tonin gene-related peptide, in patients with migraine who had not benefited from preventive medicatio

265 ly humanised CGRP antibody, in patients with migraine who had previously not responded to two to four

266 olerated in patients with difficult-to-treat migraine who had previously not responded to up to four

267 There were 418,965 patients with migraine who met the study criteria and were included in

268 t extract injections to her face for chronic migraine, who later developed bilateral depigmentation o

269 Any migraine and migraine with (MA) and migraine without aura (MO) were i

270 pression (CSD) underlies the neurobiology of migraine with aura (MWA).

271 4.7 [7.1] years), among whom 1435 (5.2%) had migraine with aura and 26 423 (94.8%) did not (2177 [7.8

272 ld-type mice, providing a novel mechanism in migraine with aura and, by extension, the other neurolog

273 Self-reported migraine with aura compared with migraine without aura o

274 essionals aged at least 45 years, women with migraine with aura had a higher adjusted incidence rate

275 Patients with migraine with aura had a higher risk for incident RAO co

276 Migraine with aura is a common but poorly understood sen

277 with increased risk of all types of RAO and migraine with aura is associated with increased risk of

278 Migraine with aura is known to increase the risk of card

279 cremental increase in the incidence rate for migraine with aura ranged from 1.01 additional cases per

280 The absolute contribution of migraine with aura to CVD incidence in relation to other

281 was 3.36 (95% CI, 2.72-3.99) for women with migraine with aura vs 2.11 (95% CI, 1.98-2.24) for women

282 The incidence rate for women with migraine with aura was significantly higher than the adj

283 of the higher risk of stroke in people with migraine with aura, it is important to identify and modi

284 le with migraine is strongly associated with migraine with aura, young age, female sex, use of oral c

285 ]) were significantly higher than those with migraine with aura.

286 1), we find positive genetic correlations of migraine with diastolic BP (DBP, r(g) = 0.11, P = 3.56 x

287 Participants were adults with migraine with or without aura experiencing 2 to 8 migrai

288 and 20 each with interictal photophobia from migraine with or without visual aura.

289 nflammatory marker in extra-axial tissues in migraine with visual aura.

290 lvarial bone overlying the occipital lobe in migraine with visual auras.

291 18-75 years of age, with episodic or chronic migraine, with migraine onset before the age of 50 years

292 We assigned adults with migraine, with or without aura, in a 1:1:1 ratio to rece

293 sk for incident RAO compared with those with migraine without aura (HR 1.58 [95% CI 1.40-1.79]; P < .

294 Any migraine and migraine with (MA) and migraine without aura (MO) were identified by a screener

295 and 26 423 (94.8%) did not (2177 [7.8%] had migraine without aura and 24 246 [87.0%] had no migraine

296 a vs 2.11 (95% CI, 1.98-2.24) for women with migraine without aura or no migraine (P < .001).

297 lf-reported migraine with aura compared with migraine without aura or no migraine at baseline.

298 cidence rate of CVD compared with women with migraine without aura or no migraine.

299 ted with increased risk of RAO compared with migraine without aura.

300 seems to be more apparent among people with migraine without traditional risk factors.