ライフサイエンスコーパス: migraine attack

1 imescale compatible with the duration of the migraine attack.

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

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

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

5 re and ocular biometric parameters and acute migraine attack.

6 n nociception and associated symptoms of the migraine attack.

7 areas when examined during a fully developed migraine attack.

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

9 certain brainstem areas are activated during migraine attacks.

10 lonal antibodies can reduce and even prevent migraine attacks.

11 auditory, and olfactory stimuli can trigger migraine attacks.

12 did not significantly vary during the acute migraine attacks.

13 tification spectra, experienced during their migraine attacks.

14 operidol is very effective in aborting acute migraine attacks.

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

16 ine during acute glyceryl trinitrate-induced migraine attacks.

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

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

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

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

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

22 37 patients did not treat a migraine attack and were excluded from outcome analyses.

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

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

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

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

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

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

29 Migraine attacks are associated with the development of

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

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

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

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

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

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

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

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

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

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

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

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

42 Migraine attacks consist of head pain and hypersensitivi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

58 The migraine attack is characterized by alterations in senso

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

74 Migraine attacks with auras are sometimes associated wit

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

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

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