ライフサイエンスコーパス: migraine

1 osis, parkinsonism, epilepsy, and hemiplegic migraine.

2 relevance to its signature disorders such as migraine.

3 the CGRP receptor, in patients with chronic migraine.

4 ssible effective therapy in the treatment of migraine.

5 de variety of psychiatric comorbidities with migraine.

6 entified 13 independent loci associated with migraine.

7 and functional networks that are involved in migraine.

8 rain barrier has been postulated to occur in migraine.

9 le bowel, functional dyspepsia, or abdominal migraine.

10 et for preventive therapies in patients with migraine.

11 he cortex and is associated with the aura of migraine.

12 minal hypersensitivity, neuropathic pain and migraine.

13 en and adolescents 8 to 17 years of age with migraine.

14 us common neurological conditions, including migraine.

15 epilepsy, paroxysmal movement disorders, and migraine.

16 works of patients in the interictal phase of migraine.

17 tory effect that may underlie its utility in migraine.

18 cs of patients with CEAD IS with and without migraine.

19 works of patients in the interictal phase of migraine.

20 llowed by depression, which is implicated in migraine.

21 a large multicenter cohort of patients with migraine.

22 ventive treatment of high-frequency episodic migraine.

23 a high frequency of migraine and hemiplegic migraine.

24 correlate of aura and a putative trigger for migraine.

25 migraine prevention in adults with episodic migraine.

26 body, in the preventive treatment of chronic migraine.

27 her-order integration systems are altered in migraine.

28 ural thalamic abnormalities in patients with migraine.

29 h variable other symptoms such as vertigo or migraine.

30 evention of headache in adults with episodic migraine.

31 ducing the frequency of chronic and episodic migraine.

32 s with placebo for the prevention of chronic migraine.

33 . irritable bowel syndrome, fibromyalgia, or migraine.

34 to be effective in reducing the frequency of migraine.

35 bodies (CGRP-mAbs) are capable of preventing migraine.

36 ne-related peptide (CGRP) is a key player in migraine.

37 m over lifetime appears to increase risk for migraine.

38 in responder rate in patients with frequent migraine.

39 ischemia, thrombosis, diabetes mellitus, and migraine.

40 ide receptor, for the prevention of episodic migraine.

41 both of which can affect the progression of migraine.

42 g investigated as a preventive treatment for migraine.

43 is involved in the neural pathophysiology of migraines.

44 ivity and the onset of primary headaches and migraines.

45 [OR (95% CI)] 1.49 (0.78, 2.85) for CRS plus migraine, 1.88 (1.08, 3.25) for CRS plus fatigue, 1.95 (

46 e same way that hormonal fluctuations affect migraine activity in patients.

47 Migraine affects approximately 14% of the world's popula

48 sion, asthma, degenerative disk disease, and migraine, all of which were reportedly controlled with m

49 and one PNKD family had familial hemiplegic migraine alone.

50 y 0.2-1 % of children suffers from abdominal migraine (AM).

51 tional studies have suggested a link between migraine and cervical artery dissection (CEAD), any asso

52 vant to common neurological diseases such as migraine and epilepsy.

53 Differences between patients with migraine and healthy subjects were assessed using an ANC

54 PRRT2 mutations included a high frequency of migraine and hemiplegic migraine.

55 We observed co-occurrence of migraine and hypercalcaemia ICD-9 diagnoses (OR = 1.58,

56 Minor cervical traumas, infection, migraine and hypertension are putative risk factors, and

57 ly shown to be associated with lower risk of migraine and increased risk of myocardial infarction.

58 ditions and the complex relationship between migraine and ischemic stroke (IS).

59 the study assessed whether the frequency of migraine and its subtypes (presence or absence of an aur

60 Frequency of migraine and its subtypes in patients with CEAD IS vs no

61 To investigate whether a history of migraine and its subtypes is associated with the occurre

62 findings confirm the multifactorial basis of migraine and might allow new prophylactic options to be

63 enic migraine syndromes, in which hemiplegic migraine and non-hemiplegic migraine with or without aur

64 oreover, the significant association between migraine and OMCNP remained after we adjusted for potent

65 he exact pathophysiologic mechanisms linking migraine and OMCNP.

66 dence of Headache Reduction in Subjects With Migraine and PFO Using the AMPLATZER PFO Occluder to Med

67 dence of Headache Reduction in Subjects With Migraine and PFO Using the AMPLATZER PFO Occluder to Med

68 explain the pathophysiological links between migraine and psychiatric disorders.

69 , we provide an overview of the link between migraine and several comorbid psychiatric disorders, inc

70 igraine prevention in patients with episodic migraine and support further investigation of AMG 334 in

71 circuitry underlying the association between migraine and the comorbid psychiatric conditions and to

72 led us to investigate the connection between migraine and the glymphatic system.

73 tors in neurological disorders as diverse as migraine and traumatic brain injury (TBI).

74 volved in neurologic disorders as diverse as migraine and traumatic brain injury.

75 and one patient in the AMG 334 70 mg group (migraine and vertigo); these events were judged to be un

76 eased chronic obstructive pulmonary disease, migraine, and affective disorders.

77 ated to episodic ataxia, such as hemiplegia, migraine, and epilepsy.

78 depression, cardiovascular regulation, pain, migraine, and neuroendocrine regulation, including repro

79 ate a link between the glymphatic system and migraine, and suggest a novel mechanism for regulation o

80 understanding the genetic predisposition to migraine, and the discovery of multiple susceptible gene

81 nt of conditions such as multiple sclerosis, migraines, and Alzheimer's disease.

82 nders including age, sex, prior concussions, migraine, anxiety, learning disability, depression, and

83 ts clinical features have led to the view of migraine as a complex, variable disorder of nervous syst

84 The identification of new migraine-associated genes, the visualisation of brain re

85 ht-aversive behavior in mice as a measure of migraine-associated photophobia.

86 -wide association studies have identified 13 migraine-associated variants pointing at genes that clus

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

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

89 re and ocular biometric parameters and acute migraine attack.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

104 did not significantly vary during the acute migraine attacks.

105 ine during acute glyceryl trinitrate-induced migraine attacks.

106 certain brainstem areas are activated during migraine attacks.

107 lonal antibodies can reduce and even prevent migraine attacks.

108 SD is associated with migraine aura and recently recognized as a novel mechani

109 ta help to explain the sensory nature of the migraine aura and reveal that sensory cortices are vulne

110 Migraine aura involves sensory percepts, suggesting that

111 Migraine aura is sparsely studied due to the highly chal

112 ng depression, the experimental correlate of migraine aura, and further evaluated the response of spo

113 preading depression, the neural correlate of migraine aura, closes the paravascular space and impairs

114 reading depression (CSD), an animal model of migraine aura, induces a rapid and nearly complete closu

115 ain the predominant sensory phenomenology of migraine aura.

116 considered as the cellular correlate of the migraine aura.

117 ression (CSD), the putative mechanism of the migraine aura.

118 SD), the electrophysiologic event underlying migraine aura.

119 ase itself or its genetic underpinnings, the migraine brain is altered structurally and functionally.

120 y and the anatomical alterations seen in the migraine brain.

121 cortical and endothelial functioning of the migraine brain.

122 100, with higher scores representing greater migraine burden on functioning).

123 lactic options to be developed, not only for migraine but potentially also for migraine-comorbid diso

124 foramen ovale (PFO) has been associated with migraine, but its role in the disorder remains poorly un

125 e identified Flunarizine - a well-known anti-migraine calcium channel (CC) blocker - being able to di

126 Although migraine can be treated using CGRP antagonists that act

127 ment) was a double-blind study investigating migraine characteristics over 1 year in subjects randomi

128 present data on psychiatric risk factors for migraine chronification.

129 ylaxis of headaches in patients with chronic migraine (CM) involves treatment every 12 weeks.

130 Chronic migraine (CM) is often associated with chronic tendernes

131 period of 3.1 years (range, 1-6 years), the migraine cohort exhibited a greater risk of developing s

132 t only for migraine but potentially also for migraine-comorbid disorders such as epilepsy, depression

133 Secondary endpoints included reduction in migraine days and efficacy in patients with versus witho

134 ) experienced 50% reduction in the number of migraine days at 12 weeks and 9 (29%) at 24 weeks postra

135 The mean change in monthly migraine days at week 12 was -3.4 (SE 0.4) days with AMG

136 imary endpoints were change from baseline in migraine days during the third treatment cycle (weeks 9-

137 e primary endpoint was the change in monthly migraine days from baseline to the last 4 weeks of doubl

138 e primary endpoint was the change in monthly migraine days from baseline to the last 4 weeks of the 1

139 demonstrated a greater decrease in number of migraine days from the baseline period to intervention w

140 The mean number of migraine days per month at baseline was 8.3 in the overa

141 % or greater reduction in the mean number of migraine days per month was achieved for 43.3% of patien

142 rial, patients aged 18-60 years with 4 to 14 migraine days per month were enrolled at 59 headache and

143 ints were a 50% or greater reduction in mean migraine days per month, change in the number of days of

144 to months 4 through 6 in the mean number of migraine days per month.

145 Erenumab 70 mg and 140 mg reduced monthly migraine days versus placebo (both doses -6.6 days vs pl

146 mg and 140 mg reduced the number of monthly migraine days with a safety profile similar to placebo,

147 The mean reductions in monthly migraine days with the 7 mg (-2.2 [SE 0.4]) and the 21 m

148 y efficacy outcome was the monthly number of migraine days within the 3 months following ASD closure

149 up had a reduced mean (SD) number of monthly migraine days within the 3 months following the procedur

150 days per month, of which eight or more were migraine days.

151 The LSM difference in the reduction of migraine-days between the placebo and 225 mg dose groups

152 least square mean (LSM) change in number of migraine-days from baseline to weeks 9-12 was -3.46 days

153 , we randomly assigned patients with chronic migraine (defined as headache of any duration or severit

154 that the initiation of the headache phase of migraine depends on activation of meningeal nociceptors,

155 This is the first identification of an anti-migraine drug that appears to be selective for Adelta-fi

156 Importantly, two clinically effective migraine drugs, the 5-HT1B/D agonist sumatriptan and a C

157 Of these, hemiplegic migraine emerges as a novel PRRT2-associated phenotype.

158 mab for adults aged 18-65 years with chronic migraine, enrolled from 69 headache and clinical researc

159 sorders such as asthma, cardiac arrhythmias, migraine, epilepsy, and depression.

160 INTERPRETATION: In patients with chronic migraine, erenumab 70 mg and 140 mg reduced the number o

161 In patients with IS aged 18 to 45 years, migraine, especially migraine without aura, is consisten

162 This issue provides a clinical overview of migraine, focusing on risk, prevention, diagnosis, treat

163 ose of 70 mg or 140 mg significantly reduced migraine frequency, the effects of migraines on daily ac

164 e temporal and nasal superior sectors in the migraine group (p </= 0.05).

165 to use to prevent the headache of pediatric migraine has not been established.

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

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

168 Migraine headache is uniquely exacerbated by light.

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

170 %) had current CRS symptoms, 1,765 (23%) had migraine headache, and 1,930 (25%) had higher levels of

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

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

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

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

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

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

177 = 0.191, P = 0.03) between serum calcium and migraine headache, indicating that these traits have a g

178 calcium levels were associated with risk of migraine headache.

179 8-65 years) from 62 sites in the USA who had migraine headaches 8-14 days per month.

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

181 es, including depression, anxiety, dementia, migraine, heart disease, peptic ulcers, and arthritis ar

182 ge of 13 years or older, physician-diagnosed migraine history, prior concussion with symptoms lasting

183 RRD) in 7.5% of eyes; classic and ophthalmic migraine in 6.5% of eyes; hypoglycemia in 2.8% of eyes;

184 8125 for the preventive treatment of chronic migraine in a phase 3 trial.

185 y the ability of intravenous CGRP to trigger migraine in humans and the efficacy of CGRP receptor ant

186 Conditions recognised to be comorbid with migraine include asthma, anxiety, depression, and other

187 ne, a diphenylmethylpiperazine used to treat migraine, inhibited HCV cell entry in vitro and in vivo

188 e emerged even if only 1% of headache (2% of migraine) instances were caused by geomagnetic disturban

189 Migraine is a common, multifactorial, disabling, recurre

190 Migraine is a debilitating neurological disorder affecti

191 There is some debate about whether migraine is a disease of vascular dysfunction or a resul

192 The results stress that migraine is a disorder of the CNS in which not only is b

193 Migraine is a highly prevalent and disabling neurologica

194 Migraine is a prevalent and disabling disorder.

195 Migraine is a widespread neurological disease with negat

196 Migraine is among the most common and debilitating neuro

197 Migraine is an unrecognized risk factor for OMCNP develo

198 Migraine is characterized by severe headaches that can b

199 Although migraine is often recognised in women, it is underdiagno

200 The management of patients with migraine is often unsatisfactory because available acute

201 iology of migraine headache, but its role in migraine is still equivocal.

202 Migraine is two to three times more prevalent in women t

203 nt underlying numerous pathologies including migraine, ischemic stroke, aneurysmal subarachnoid hemor

204 enic-migraine-syndrome gene mutations showed migraine-like features, increased glutamatergic neurotra

205 rain and the periphery of the mouse to cause migraine-like photophobia by apparently distinct mechani

206 ing a transcortical approach, in preclinical migraine models.

207 Two cohorts were selected: patients with migraine (n = 138 907) and propensity score-matched cont

208 that some conditions, such as depression and migraine, negatively affect seizure outcome and quality

209 tion or severity on >/=15 days per month and migraine on >/=8 days per month) in a 1:1:1 ratio to rec

210 lity loci, we carried out a genetic study of migraine on 59,674 affected subjects and 316,078 control

211 y reduced migraine frequency, the effects of migraines on daily activities, and the use of acute migr

212 PRRT2 mutations were in familial hemiplegic migraine or episodic ataxia, one SLC2A1 family had episo

213 tions during, rather than in the absence of, migraine or in control subjects, and that the associatio

214 ter inclusion of additional risk factors for migraine (OR = 1.23, P = 2 x 10-3).

215 e was associated with an increase in risk of migraine (OR = 1.80, 95% CI: 1.31-2.46, P = 2.5 x 10-4),

216 elated peptide (CGRP) is a central player in migraine pathogenesis, yet its site(s) of action remains

217 The understanding of migraine pathophysiology is advancing rapidly.

218 or calcitonin gene-related peptide (CGRP) in migraine pathophysiology.

219 iceptive information and plays a key role in migraine pathophysiology.

220 lated peptide (CGRP) pathway is important in migraine pathophysiology.

221 utic approach may not be effective for every migraine patient.SIGNIFICANCE STATEMENT Calcitonin gene-

222 ve, cross-sectional and comparative study 38 migraine patients and 44 age and sex matched controls we

223 cular thickness measurements were thinner in migraine patients but the difference between groups was

224 Impaired DPMS in migraine patients can be normalized after effective trea

225 fference in intraocular pressure between the migraine patients during acute migraine attacks (15.07 m

226 pressure and ocular biometric parameters in migraine patients during acute migraine attacks and comp

227 tral corneal thickness, and pupil size of 40 migraine patients during acute migraine attacks and pain

228 liminary imaging studies in small cohorts of migraine patients have suggested a role of the thalamus

229 Five migraine patients were studied during various forms of a

230 est that there is sectorial RNFL thinning in migraine patients without aura and pulsative choroidal b

231 Migraine patients without aura have normal OPA values, n

232 acular thickness and visual field testing in migraine patients without aura.

233 rons, and why it may not be effective in all migraine patients.SIGNIFICANCE STATEMENT Recently, we re

234 Subjects had 6 to 14 days of migraine per month, had failed at least 3 migraine preve

235 st that patients' experience with colour and migraine photophobia could originate in cone-driven reti

236 rment and everyday-activities domains of the Migraine Physical Function Impact Diary (scale transform

237 for CRS plus fatigue, 1.95 (1.18, 3.21) for migraine plus fatigue, and 1.84 (1.08, 3.14) for all thr

238 ociations with known comorbidities including migraines, postoperative nausea and vomiting (PONV), ver

239 lerability of simvastatin plus vitamin D for migraine prevention in adults with episodic migraine.

240 G 334 70 mg might be a potential therapy for migraine prevention in patients with episodic migraine a

241 In migraine prevention, the most promising new approaches a

242 onal antibody against the CGRP receptor, for migraine prevention.

243 at erenumab could be a potential therapy for migraine prevention.

244 of migraine per month, had failed at least 3 migraine preventive medications, and had significant rig

245 matic brain injury (mTBI) with posttraumatic migraines (PTMs) and those without PTMs on the basis of

246 Complete migraine remission for 1 year occurred in 10 patients (8

247 ezumab as a preventive treatment for chronic migraine resulted in a lower frequency of headache than

248 rphisms (SNPs) significantly associated with migraine risk (P < 5 x 10(-8)) that mapped to 38 distinc

249 ex hormones as a major factor in determining migraine risk and characteristics, which accounts for se

250 d to investigate the mechanisms that lead to migraine sensory hypersensitivities by measuring brain r

251 east a moderate level or days in which acute migraine-specific medication [triptans or ergots] was us

252 es on daily activities, and the use of acute migraine-specific medication over a period of 6 months.

253 ebo), and the number of days of use of acute migraine-specific medication was reduced by 1.1 days in

254 change in the number of days of use of acute migraine-specific medication, and change in scores on th

255 Migraine-specifically migraine with aura-has been identi

256 miplegic migraine type 1 (FHM1), a monogenic migraine subtype, is caused by gain-of-function of volta

257 However, different migraine subtypes showed no significant differences.

258 a postulated brainstem site of action during migraine, suggesting that dihydroergotamine is not able

259 ever, the mechanism underlying increased CSD/migraine susceptibility remains unclear.

260 Transgenic mouse models with human monogenic-migraine-syndrome gene mutations showed migraine-like fe

261 e identified in patients with rare monogenic migraine syndromes, in which hemiplegic migraine and non

262 ul new approaches for the treatment of acute migraine target calcitonin gene-related peptide (CGRP) a

263 eatments based on the distinct mechanisms of migraine that affect individual patients.

264 ues, consistent with a predominant theory of migraine that highlights vascular etiologies.

265 In migraine, the nature of aura symptoms suggests that sens

266 egabalin (Lyrica) shows clinical promise for migraine therapy, although its efficacy and mechanism of

267 advances that have led to novel targets for migraine therapy.

268 Among patients with migraines, those in the clopidogrel group had less-sever

269 with familial episodic ataxia and hemiplegic migraine to investigate the mutation frequency and type

270 mimics, such as transient ischemic attacks, migraine, Todd paralysis, and Uhthoff phenomenon.

271 As a new approach to migraine treatment, humanized anti-CGRP monoclonal antib

272 transient ischaemic attack from epilepsy and migraine, two important transient ischaemic attack mimic

273 Familial hemiplegic migraine type 1 (FHM1) is a subtype of migraine with aur

274 Familial hemiplegic migraine type 1 (FHM1), a monogenic migraine subtype, is

275 In familial hemiplegic migraine type 1 mutant mice expressing human mutations (

276 mice carrying the human familial hemiplegic migraine type 1 R192Q missense mutation as well as in wi

277 an pathologies including Familial Hemiplegic Migraine type 2, Alternating Hemiplegia of Childhood, Ra

278 Among unexpected observations, we found that migraine, typically classified as a disease of the centr

279 For general adult populations, chronic migraine was 10% (5-20); chronic tension-type headache w

280 Chronic migraine was defined as 15 or more headache days per mon

281 Migraine was more common in the CEAD IS group (103 [30.8

282 Medical records of patients with migraine who were entered in the National Health Insuran

283 Future management of migraine will have the capacity to tailor treatments bas

284 ly specific strategy treating CSD associated migraine with a likely better safety profile.

285 lated disability in childhood and adolescent migraine with amitriptyline, topiramate, or placebo over

286 of magnetic stimulation in the treatment of migraine with and without aura.

287 n to be effective for the acute treatment of migraine with and without aura.

288 ing headaches of intracranial origin such as migraine with aura and why this therapeutic approach may

289 legic migraine type 1 (FHM1) is a subtype of migraine with aura caused by a gain-of-function mutation

290 In a young man with migraine with aura including hemiplegia, we identified a

291 Compared with migraine with aura, migraine without aura was independen

292 Migraine-specifically migraine with aura-has been identified as a risk factor

293 which hemiplegic migraine and non-hemiplegic migraine with or without aura are part of a wider clinic

294 of percutaneous PFO closure as a therapy for migraine with or without aura.

295 of the treatment considerations for treating migraine with psychiatric comorbidities.

296 o determine the most effective treatment for migraine with psychiatric comorbidity.

297 = .01), and the difference was mainly due to migraine without aura (80 [24.0%] vs 335 [15.6%], P < .0

298 ending pain modulatory system (DPMS) between migraine without aura (MwoA) patients and healthy contro

299 Compared with migraine with aura, migraine without aura was independently associated with

300 IS aged 18 to 45 years, migraine, especially migraine without aura, is consistently associated with C