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1 ngulate cortex (possibly as a consequence of cortical spreading depression).
2 centage of neurons that showed activation by cortical spreading depression.
3 nisms such as an increased susceptibility to cortical spreading depression.
4 sels in the trigemino-vascular system and in cortical spreading depression.
5 cortical neuronal excitability that leads to cortical spreading depression.
6 na, including hearing, vision, epilepsy, and cortical spreading depression.
7 or the first time it has been shown that the cortical spreading depression activated the trigeminovas
8 an cause neurovascular dysfunction and evoke cortical spreading depression, an event that is widely t
9 e significance to migraine of events such as cortical spreading depression and activation of the trig
10 e the typical hypoperfusion responses during cortical spreading depression and alpha-chloralose anaes
11 g evidence for the occurrence of spontaneous cortical spreading depression and peri-infarct depolariz
12 under isoflurane anesthesia showed that both cortical spreading depression and terminal anoxic depola
13 that these gain-of-function effects lead to cortical spreading depression, aura, and potentially mig
14 shold (central) trigeminovascular neurons by cortical spreading depression, but not their activation
15 se results are the first to demonstrate that cortical spreading depression can be blocked in vivo usi
19 blood flow (rCBF) changes that occur during cortical spreading depression (CSD) are considered to be
20 dentified, although, animal models highlight cortical spreading depression (CSD) as a potential candi
21 onal imaging has confirmed the importance of cortical spreading depression (CSD) as the pathophysiolo
22 to detect and characterize complex waves of cortical spreading depression (CSD) evoked with KCL plac
28 during intensive care and were classified as cortical spreading depression (CSD) if they took place i
41 ession and, if so, the threshold for evoking cortical spreading depression (CSD), a process sharing c
42 n, insufficient to cause infarcts, triggered cortical spreading depression (CSD), a propagating slow
43 2Q mutation exhibit increased propensity for cortical spreading depression (CSD), a propagating wave
45 injected mice, we show that a single wave of cortical spreading depression (CSD), an animal model of
46 V 2.1 channels and are highly susceptible to cortical spreading depression (CSD), the electrophysiolo
49 ocytes during somatosensory stimulations and cortical spreading depression (CSD), the putative mechan
51 rpose of this study was to determine whether cortical spreading depression (CSD)--an event believed t
52 spontaneous and evoked activity in naive and cortical spreading depression (CSD)-sensitized trigemino
54 nal groups (with [n=7] or without [n=7] HH), cortical spreading depressions (CSD) were elicited to as
56 we tested the effect of fremanezumab on the cortical spreading depression-evoked activation of mecha
57 g multiwavelength optical intrinsic imaging, cortical spreading depression has been shown to have a t
59 aine aura and headache by demonstrating that cortical spreading depression, implicated in migraine vi
60 to focal cerebral ischaemia, and blocking of cortical spreading depression improved stroke outcome in
61 uncture wound, global cerebral ischemia, and cortical spreading depression in C57BL6 mice; 1 day afte
63 netic stimulation blocked the propagation of cortical spreading depression in two of eight animals.
65 ral activity in reducing the total number of cortical spreading depressions induced by potassium chlo
66 derlying mechanism for the susceptibility of cortical spreading depression initiation in migraine dis
73 des demonstrated significant activity in the cortical spreading depression model of migraine as we re
76 observed spontaneous, recurring episodes of cortical spreading depression (SD) as early as 20 min po
78 emale hormone levels in these mice modulated cortical spreading depression susceptibility in much the
79 or R192Q mutation are highly susceptible to cortical spreading depression, the electrophysiological
83 ephalic cat cortices, when administered post-cortical spreading depression, transcranial magnetic sti
84 ascular function, one during the propagating cortical spreading depression wave and a second much lon
85 The direct current shift associated with the cortical spreading depression wave was accompanied by ma
86 potassium concentration increased during the cortical spreading depression wave, but recovered and re
89 bited both mechanical and chemically-induced cortical spreading depression when administered immediat
90 excitability, and enhanced susceptibility to cortical spreading depression, which is the electrophysi
91 l, mild, and transient ischaemia can trigger cortical spreading depression without an enduring tissue
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