ライフサイエンスコーパス: cluster headache

1 cation of eight genetic loci associated with cluster headache.

2 sal effect of cigarette smoking intensity on cluster headache.

3 ed understanding of the clinical features of cluster headache.

4 d the pathophysiological pathways underlying cluster headache.

5 of eptinezumab for the treatment of chronic cluster headache.

6 t specific preventive treatment for episodic cluster headache.

7 athophysiologic, and therapeutic features of cluster headache.

8 uster headache is the most disabling form of cluster headache.

9 e only available guidelines for migraine and cluster headache.

10 established treatment option in migraine and cluster headache.

11 to similarly affected patients with chronic cluster headache.

12 ut was present in two of three patients with cluster headache.

13 be similarly effective in both migraine and cluster headache.

14 ested a pivotal role for the hypothalamus in cluster headache.

15 tter as the key area for the basic defect in cluster headache.

16 d peptide, may be a preventive treatment for cluster headache.

17 of cervical hypersensitivity in migraine and cluster headache.

18 vel avenue for the treatment of migraine and cluster headache.

19 the structure of the brains of patients with cluster headache.

20 ent as has been reported in acute attacks of cluster headache.

21 anglion stimulation for treatment of chronic cluster headache.

22 the primum movens in the pathophysiology of cluster headache.

23 che attacks in nine patients who had chronic cluster headache.

24 in persons suffering from both migraine and cluster headache.

25 the primum movens in the pathophysiology of cluster headache.

26 rnative approach to the treatment of chronic cluster headache.

27 or factor in headache attacks in migraine or cluster headache.

28 cerebral blood flow (rCBF) in patients with cluster headache.

29 l injection and tearing (SUNCT syndrome) and cluster headache.

30 hysiology of migraine and to a lesser extent cluster headache.

31 in the same pattern previously described in cluster headache.

32 lectively explaining 7.2% of the variance of cluster headache.

33 munological processes in the pathogenesis of cluster headache.

34 enetic variants that confer genetic risk for cluster headache.

35 as been implicated in the pathophysiology of cluster headaches.

36 junctival injection and tearing (SUNCT; 5%), cluster headache (4%), hemicrania continua (1%) and prim

37 Cluster headache, a primary headache disorder, consists

38 aged 18-75 years with a diagnosis of chronic cluster headache according to the International Classifi

39 the weekly frequency of attacks of episodic cluster headache across weeks 1 through 3 after the init

40 l (Eptinezumab in Participants With Episodic Cluster Headache [ALLEVIATE]) was conducted between Dece

41 tween migraine and controls was 89%, and for cluster headache and controls it was 98%.

42 f what is known about the pathophysiology of cluster headache and discuss the existing treatment opti

43 rovides insights into the pathophysiology of cluster headache and highlight areas for future research

44 There is growing evidence that cluster headache and hypnic headache are chronobiologica

45 lysis gives clues to the biological basis of cluster headache and indicates that smoking is a causal

46 dertaken to identify susceptibility loci for cluster headache and obtain insights into relevant disea

47 ontext of the differential diagnosis between cluster headache and paroxysmal hemicrania leads to a co

48 The trigeminal-autonomic cephalgias include cluster headache and paroxysmal hemicranias, in which he

49 derstanding the pathophysiology of migraine, cluster headache and subarachnoid haemorrhage.

50 or depressive disorder, Alzheimer's disease, cluster headaches and aggressive behaviours.

51 It is known that cluster headaches and hypnic headache are associated wit

52 a model to explain the pain in migraine and cluster headache, and has been used to characterize the

53 ventive effect was not replicated in chronic cluster headache, and the European Medicines Agency did

54 at depression, addiction, anxiety disorders, cluster headaches, and many other neuropsychiatric disor

55 e neuromodulation therapies for migraine and cluster headache are a practical and safe alternative to

56 cross a cohort of 708 patients evaluated for cluster headache at the National Hospital for Neurology

57 nge from baseline in the weekly frequency of cluster headache attacks across weeks 1 through 3 after

58 he mean reduction in the weekly frequency of cluster headache attacks across weeks 1 through 3 was 8.

59 e of at least 50% in the weekly frequency of cluster headache attacks at week 3.

60 aptic activity, during nitroglycerin-induced cluster headache attacks in nine patients who had chroni

61 Cluster headache attacks involve severe unilateral pain

62 The mean (+/-SD) number of cluster headache attacks per week in the baseline period

63 ter headache, who reported a minimum of four cluster headache attacks per week that were unsuccessful

64 substrate that differentiates migraine from cluster headache attacks with their distinct clinical fe

65 etter than placebo in the acute treatment of cluster headache but not in the acute management of migr

66 Eight patients who had cluster headache but were not in the bout acted as a con

67 state and was not seen in patients who have cluster headache but were out of the bout.

68 ociation study, where 852 UK and 591 Swedish cluster headache cases were compared with 5,614 and 1,13

69 is a treatment option for refractory chronic cluster headache (CCH).

70 connectivity pathways involved in migraine, cluster headache (CH), paroxysmal hemicrania (PH), hemic

71 (CGRP) is involved in the pathophysiology of cluster headache (CH).

72 ckade is a short-term preventive therapy for cluster headache (CH).

73 Cluster headache, characterised by attacks of severe, re

74 Cluster headache, characterized by bouts of excruciating

75 Owing to the low prevalence of cluster headache, continued collaboration through multic

76 including depression, anxiety, migraine and cluster headaches, drug abuse, and post-traumatic stress

77 Among adults with episodic cluster headache, eptinezumab did not significantly redu

78 therapeutic rationale to plant migraine and cluster headache firmly in the brain as neurological pro

79 aged 18-75 years) with a history of episodic cluster headache for 1 or more years (with bouts lasting

80 An association was found with cluster headache for 4 independent loci (r(2) < 0.1) wit

81 For distinguishing cluster headache from migraine patients, the MRI classif

82 e derive a succinct latent representation of cluster headache from non-linear dimensionality reductio

83 nagement include new treatments for episodic cluster headache (galcanezumab and non-invasive vagus ne

84 Cluster headache has the longest attack duration and rel

85 Patients with chronic cluster headache have unremitting illness that necessita

86 tions supporting a genetic predisposition in cluster headache in a genome-wide association study invo

87 Cluster headache is a debilitating primary headache diso

88 Episodic cluster headache is a disabling neurologic disorder that

89 Cluster headache is a form of primary headache that feat

90 Cluster headache is a form of primary neurovascular head

91 Cluster headache is a strictly unilateral headache that

92 Chronic cluster headache is an uncommon but highly debilitating

93 m non-headache indications, so management of cluster headache is challenging.

94 Cluster headache is characterized by recurrent, unilater

95 Cluster headache is included with the shorter-lasting he

96 Cluster headache is one such idiopathic headache with ma

97 Chronic cluster headache is the most common of these disorders,

98 Chronic cluster headache is the most disabling form of cluster h

99 ncluding migraine, tension-type headache and cluster headache, is the currently accepted view that th

100 story of myocardial infarction (MI), stroke, cluster headache, malignant cancer, or hospice service w

101 The case illustrates that cluster headache may be generated primarily from within

102 psychiatric disorders, including depression, cluster headaches, migraines, anxiety, and obsessive-com

103 disruption and a diseased control group with cluster headache (n = 35).

104 e human retina in acute migraine (n = 8) and cluster headache (n = 5) using fluorescein or indocyanin

105 control study in the Dutch Leiden University Cluster headache neuro-Analysis program (LUCA) study pop

106 Cluster headache, one of the most severe pain syndromes

107 Cluster headache, one of the most severe pain syndromes

108 eminal autonomic cephalalgias, which include cluster headache, paroxysmal hemicrania, short-lasting u

109 ur at night or during sleep, with a focus on cluster headaches, paroxysmal hemicrania, short-lasting

110 However, as our understanding of cluster headache pathophysiology has evolved on the basi

111 biomarkers that differentiate migraine from cluster headache patients and imaging features that are

112 ant MRI features in classifying migraine and cluster headache patients from controls.

113 Compared to migraine, cluster headache patients showed decreased functional in

114 I data were obtained from 20 migraineurs, 20 cluster headache patients, and 15 healthy controls.

115 RCVS patients in the remission stage and in cluster headache patients, suggesting that these meninge

116 erential expression of POLR1B and TMEM87B in cluster headache patients.

117 ive MRI feature in classifying migraine from cluster headache patients.

118 and PAG networks, are shared by migraine and cluster headache patients.

119 baseline assessment, as well as a history of cluster headache periods lasting at least 6 weeks, and r

120 iagnosis include the redefinition of chronic cluster headache (remission periods lasting less than th

121 that the current view of the neurobiology of cluster headache requires complete revision and that thi

122 egian sample of 144 cases from the Trondheim Cluster headache sample and 1,800 controls from the Nord

123 Occipital nerve stimulation in cluster headache seems to offer a safe, effective treatm

124 From a physiological viewpoint, therefore, cluster headache should be described as a neurovascular

125 genes prioritized as potentially causal for cluster headache showed enrichment to artery and brain t

126 tion to, for example, treatment response and cluster headache subtypes, could provide unprecedented i

127 independent analysis identified 2 replicable cluster headache susceptibility loci on chromosome 2.

128 structure within the phenotypic landscape of cluster headache that enables prediction of treatment re

129 enomewide association study meta-analysis of cluster headache, to identify genetic risk variants, and

130 ide polymorphism (SNP)-based heritability of cluster headache was 14.5%.

131 Cluster headache was genetically correlated with cigaret

132 patients with medically intractable chronic cluster headache were implanted in the suboccipital regi

133 n and 1,429 women) with clinically diagnosed cluster headache were recruited from 10 European and 1 E

134 In total, 217 patients (182 RCVS, 35 cluster headache) were analyzed and separated into 2 gro

135 patients aged 22 years or older with chronic cluster headache, who reported a minimum of four cluster

136 Device-specific guidelines for migraine and cluster headache will be soon available, but adherence t

137 ntified and replicated genetic risk loci for cluster headache with effect sizes larger than those typ

138 well tolerated in participants with chronic cluster headache, with a similar safety profile as previ