ライフサイエンスコーパス: migraine aura

1 ain the predominant sensory phenomenology of migraine aura.

2 considered as the cellular correlate of the migraine aura.

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

4 SD), the electrophysiologic event underlying migraine aura.

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

6 the neurovascular unit in the development of migraine aura.

7 iac and extracardiac right-to-left shunts to migraine aura.

8 neuronal depolarization thought to underlie migraine aura.

9 opagating slow depolarization that underlies migraine aura.

10 e of neuroglial depolarization implicated in migraine aura.

11 uronal activity, is the most likely cause of migraine aura.

12 g rCBF changes may help our understanding of migraine aura.

13 of the cerebral disturbances which subserve migraine aura.

14 ion (CSD) may be the underlying mechanism of migraine aura.

15 ents during spontaneous and visually induced migraine aura.

16 be similar to those in human patients during migraine aura.

17 l focal ischaemia, and may also underlie the migraine aura.

18 at occurs in the setting of brain injury and migraine aura.

19 (SD) is an intense depolarization underlying migraine aura.

20 ation associated with acute brain injury and migraine aura.

21 pression (CSD), a physiological correlate of migraine aura, also decreased cortical neurite growth, w

22 posed as the pathophysiological substrate of migraine aura and as an endogenous trigger of headache p

23 Here we establish a link between migraine aura and headache by demonstrating that cortica

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

25 rious acute neurological settings, including migraine aura and ischemic stroke.

26 we critically examine the pathophysiology of migraine aura and migraine headache, exploring evidence

27 elationship of spreading depolarization with migraine aura and migraine headache.

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

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

30 sion, the electrophysiological surrogate for migraine aura, and develop severe and prolonged motor de

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

32 rlying the initiation and propagation of the migraine aura, and the visual percept that is produces,

33 epolarization (the phenomenon that underlies migraine aura), but mechanisms underlying this migraine-

34 The visual percept of migraine aura changes depending on the region of the occ

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

36 vents menstrually related migraine (MRM) and migraine aura frequency.

37 ish a mechanism linking microembolization to migraine aura in an experimental animal model.

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

39 (CSD) as the pathophysiological mechanism of migraine aura in human beings, whereas novel animal stud

40 e detailed drawings of his visual percept of migraine aura in real time during more than 1000 attacks

41 and temporal lobe involvement contributes to migraine aura in some instances.

42 ds were measured during spontaneous onset of migraine auras in 4 migraine patients, and compared with

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

44 Migraine aura involves sensory percepts, suggesting that

45 Migraine aura is sparsely studied due to the highly chal

46 (CSD), the electrophysiological substrate of migraine aura, is enhanced in mice expressing a vascular

47 Migraine aura - manifesting as transient, neurological d

48 If translatable to humans, a subset of migraine auras may belong to a spectrum of hypoperfusion

49 ves in women with migraine in the absence of migraine aura or other risk factors.

50 ctivated in spontaneous and visually induced migraine aura patients.

51 ered various diagnoses, including persistent migraine aura, post-hallucinogen flashback, or psychogen

52 ing of the visual disturbance (36%), whereas migraine aura (seven patients) and consumption of illici

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

54 on-like neuroelectric event occurring during migraine aura that can arise spontaneously or be visuall

55 visual disturbance clinically distinct from migraine aura that can be disabling for patients.

56 ression (CSD), the proposed mechanism of the migraine aura, to shape the cortical activity that under

57 n real time during more than 1000 attacks of migraine aura without headache over 18 years.