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1 ns included a high frequency of migraine and hemiplegic migraine.
2 mechanism for enhanced CSD susceptibility in hemiplegic migraine.
3 ified a novel PNKD gene deletion in familial hemiplegic migraine.
4 rders is much broader than strictly familial hemiplegic migraine.
5 human neurologic diseases including familial hemiplegic migraine.
6 myoclonic epilepsy of infancy, and familial hemiplegic migraine.
7 cium channel gene associated with ataxia and hemiplegic migraine.
8 linkage and association studies of familial hemiplegic migraine.
9 teral sclerosis, parkinsonism, epilepsy, and hemiplegic migraine.
12 med on 7 family members, 5 with a history of hemiplegic migraine and 2 without history of migraine.
13 variant was identified in two families with hemiplegic migraine and in one patient with migraine wit
14 h controls the PCr/Pi ratio in patients with hemiplegic migraine and in patients with persistent aura
16 a gain-of-function and associated with both hemiplegic migraine and migraine with aura in patients.
17 rare monogenic migraine syndromes, in which hemiplegic migraine and non-hemiplegic migraine with or
18 ered to provide an understanding of familial hemiplegic migraine and possibly, by extrapolation, may
20 -subunit, have been associated with familial hemiplegic migraine (ATP1A2), alternating hemiplegia of
22 e ion pump alpha2-Na/K ATPase cause familial hemiplegic migraine, but the mechanisms by which alpha2-
24 gical and developmental disorders, including hemiplegic migraine, epilepsy, developmental delay, and
26 type voltage-gated calcium channel (familial hemiplegic migraine, episodic ataxia type 2, spinocerebe
27 such human neurological diseases as familial hemiplegic migraine, episodic ataxia-2, and spinocerebel
28 um channel gene are associated with familial hemiplegic migraine, episodic or progressive ataxia, com
29 genetic susceptibility of both rare familial hemiplegic migraine (FHM) and more common types of migra
30 HC) is typically distinguished from familial hemiplegic migraine (FHM) by infantile onset of the char
35 emory difficulties observed in some familial hemiplegic migraine (FHM) patients, we examined hippocam
36 ortical synapses in mouse models of familial hemiplegic migraine (FHM) suggested the hypothesis that
37 neurons (FS INs) in mouse models of familial hemiplegic migraine (FHM) suggested the hypothesis that
45 and has previously been related to familial hemiplegic migraine (MIM#602481) and alternating hemiple
47 venous sinus thrombosis and seizure (n = 3), hemiplegic migraine (n = 1), and hyperacute arterial inf
49 and was significantly lower in patients with hemiplegic migraine than in patients with non-motor aura
50 3 patients with familial episodic ataxia and hemiplegic migraine to investigate the mutation frequenc
56 aV2.1 channels, are associated with familial hemiplegic migraine type 1 (FHM1), a rare monogenic subt
58 minant form of this common disease, familial hemiplegic migraine type 1 (FHM1), arises from missense
62 tation analogous to the one causing familial hemiplegic migraine type 1 in humans, showed markedly re
66 rization in mice carrying the human familial hemiplegic migraine type 1 R192Q missense mutation as we
68 ttene et al. study a mouse model of familial hemiplegic migraine type 1, and provide evidence for the
69 (NTG)-induced rat migraine model, a familial hemiplegic migraine type 2 (FHM2) mouse model, and a tra
70 we show that awake mice carrying a familial hemiplegic migraine type 2 (FHM2) mutation have slower c
72 severe human pathologies including Familial Hemiplegic Migraine type 2, Alternating Hemiplegia of Ch
75 3V) missense mutation, which causes familial hemiplegic migraine type 3 in heterozygous family member
76 sistent with mild gain of function, familial hemiplegic migraine type 3 variants induce a larger effe
77 tional studies of both epilepsy and familial hemiplegic migraine type 3 variants reveal alterations o
79 between SCN1A-related epilepsy and familial hemiplegic migraine type 3, and identifies sodium channe
82 (rapid-onset dystonia parkinsonism, familial hemiplegic migraine type-2), as well as reduction in Na,
83 n mutations of NaV1.1 (SCN1A) cause familial hemiplegic migraine type-3 (FHM3), a subtype of migraine
84 dromes, in which hemiplegic migraine and non-hemiplegic migraine with or without aura are part of a w