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1 we identified a novel PNKD gene deletion in familial hemiplegic migraine.
2 ated disorders is much broader than strictly familial hemiplegic migraine.
3 umber of human neurologic diseases including familial hemiplegic migraine.
4 7) severe myoclonic epilepsy of infancy, and familial hemiplegic migraine.
5 dies, and linkage and association studies of familial hemiplegic migraine.
9 ly engineered to provide an understanding of familial hemiplegic migraine and possibly, by extrapolat
10 KA) alpha-subunit, have been associated with familial hemiplegic migraine (ATP1A2), alternating hemip
11 ons of the ion pump alpha2-Na/K ATPase cause familial hemiplegic migraine, but the mechanisms by whic
13 onal P/Q-type voltage-gated calcium channel (familial hemiplegic migraine, episodic ataxia type 2, sp
14 to cause such human neurological diseases as familial hemiplegic migraine, episodic ataxia-2, and spi
15 ame calcium channel gene are associated with familial hemiplegic migraine, episodic or progressive at
16 s to the genetic susceptibility of both rare familial hemiplegic migraine (FHM) and more common types
17 ldhood (AHC) is typically distinguished from familial hemiplegic migraine (FHM) by infantile onset of
22 ive and memory difficulties observed in some familial hemiplegic migraine (FHM) patients, we examined
23 at intracortical synapses in mouse models of familial hemiplegic migraine (FHM) suggested the hypothe
24 ing interneurons (FS INs) in mouse models of familial hemiplegic migraine (FHM) suggested the hypothe
32 n tissues and has previously been related to familial hemiplegic migraine (MIM#602481) and alternatin
40 e-gated CaV2.1 channels, are associated with familial hemiplegic migraine type 1 (FHM1), a rare monog
42 rare, dominant form of this common disease, familial hemiplegic migraine type 1 (FHM1), arises from
46 arry a mutation analogous to the one causing familial hemiplegic migraine type 1 in humans, showed ma
50 ng depolarization in mice carrying the human familial hemiplegic migraine type 1 R192Q missense mutat
52 euron, Tottene et al. study a mouse model of familial hemiplegic migraine type 1, and provide evidenc
53 glycerin (NTG)-induced rat migraine model, a familial hemiplegic migraine type 2 (FHM2) mouse model,
54 imaging, we show that awake mice carrying a familial hemiplegic migraine type 2 (FHM2) mutation have
56 s lead to severe human pathologies including Familial Hemiplegic Migraine type 2, Alternating Hemiple
59 SCN1A(L263V) missense mutation, which causes familial hemiplegic migraine type 3 in heterozygous fami
60 itude consistent with mild gain of function, familial hemiplegic migraine type 3 variants induce a la
63 echanisms between SCN1A-related epilepsy and familial hemiplegic migraine type 3, and identifies sodi
66 isoforms (rapid-onset dystonia parkinsonism, familial hemiplegic migraine type-2), as well as reducti
67 f-function mutations of NaV1.1 (SCN1A) cause familial hemiplegic migraine type-3 (FHM3), a subtype of