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1 ars, with spasticity of perinatal origin (11 hemiplegic, 11 quadriplegic, 16 with Rett syndrome) and
2  cartilage-bone margin, were similar between hemiplegic and non-hemiplegic knees (p > 0.05).
3                                              Hemiplegic and non-hemiplegic knees of 48 stroke patient
4 ciated with knee pain are comparable between hemiplegic and non-hemiplegic knees of stroke patients.
5 hophysiological explanation for why signs of hemiplegic cerebral palsy appear late and progress over
6                         Subjects with severe hemiplegic cerebral palsy have increased ipsilateral cor
7                          Fifty children with hemiplegic cerebral palsy participated and were asked to
8 e underlies an important share of congenital hemiplegic cerebral palsy, and probably some spastic qua
9 is is the first reported association between hemiplegic cerebral palsy, placental thrombosis, and fac
10 ause of in utero cerebrovascular disease and hemiplegic cerebral palsy.
11 opmental syndrome characterized by recurrent hemiplegic episodes and distinct neurological manifestat
12 y early-onset, recurrent, often alternating, hemiplegic episodes; seizures and non-paroxysmal neurolo
13 ase 1 delta (CK1delta) was identified in non-hemiplegic familial migraine with aura and advanced slee
14              Median nerve stimulation of the hemiplegic hand showed reproducible early-latency ipsila
15 imary sensorimotor area) for movement of the hemiplegic hand than for movement of the normal hand.
16 ask practice and behavioral shaping with the hemiplegic hand) or usual and customary care (n = 116; r
17 unaided walking, voluntary grasping with the hemiplegic hand, and speaking through Bayesian multivari
18 ning hemisphere with passive movement of the hemiplegic hand.
19 es had residual sensorimotor function in the hemiplegic hand.
20 pastic cerebral palsy, which was unilateral (hemiplegic) in 336 (24%).
21                      The previously isolated hemiplegic, induction-negative, repression-positive muta
22 pes anserinus tendinosis had greater risk of hemiplegic knee pain (HKP) when compared to stroke patie
23 s reported more often in hemiplegic than non-hemiplegic knees (n = 16 vs. n = 6, p = 0.021).
24 gin, were similar between hemiplegic and non-hemiplegic knees (p > 0.05).
25 rtilage thickness were more prevalent in the hemiplegic knees compared to the healthy control knees (
26                           Hemiplegic and non-hemiplegic knees of 48 stroke patients as well as both k
27 ue arthritic changes associated with pain in hemiplegic knees of stroke patients in our environment.
28 in are comparable between hemiplegic and non-hemiplegic knees of stroke patients.
29 -subunit, have been associated with familial hemiplegic migraine (ATP1A2), alternating hemiplegia of
30 genetic susceptibility of both rare familial hemiplegic migraine (FHM) and more common types of migra
31 HC) is typically distinguished from familial hemiplegic migraine (FHM) by infantile onset of the char
32                                     Familial hemiplegic migraine (FHM) has been related to mutations
33                                     Familial hemiplegic migraine (FHM) is a rare subtype of migraine
34                                     Familial hemiplegic migraine (FHM) is an autosomal dominant disor
35                                     Familial hemiplegic migraine (FHM) is an autosomal dominant subty
36 emory difficulties observed in some familial hemiplegic migraine (FHM) patients, we examined hippocam
37 neurons (FS INs) in mouse models of familial hemiplegic migraine (FHM) suggested the hypothesis that
38 ortical synapses in mouse models of familial hemiplegic migraine (FHM) suggested the hypothesis that
39                                     Familial hemiplegic migraine (FHM), a migraine subtype that also
40 thin a candidate region at 1q23 for familial hemiplegic migraine (FHM).
41 o several human diseases, including familial hemiplegic migraine (FHM).
42  and has previously been related to familial hemiplegic migraine (MIM#602481) and alternating hemiple
43 venous sinus thrombosis and seizure (n = 3), hemiplegic migraine (n = 1), and hyperacute arterial inf
44 odic ataxia and one PNKD family had familial hemiplegic migraine alone.
45 med on 7 family members, 5 with a history of hemiplegic migraine and 2 without history of migraine.
46  variant was identified in two families with hemiplegic migraine and in one patient with migraine wit
47 h controls the PCr/Pi ratio in patients with hemiplegic migraine and in patients with persistent aura
48          Studies of linkage between familial hemiplegic migraine and marker 19p13 in 13 extended fami
49  a gain-of-function and associated with both hemiplegic migraine and migraine with aura in patients.
50  rare monogenic migraine syndromes, in which hemiplegic migraine and non-hemiplegic migraine with or
51 ered to provide an understanding of familial hemiplegic migraine and possibly, by extrapolation, may
52                          We suggest that the hemiplegic migraine attacks and the cerebellar degenerat
53                                    Of these, hemiplegic migraine emerges as a novel PRRT2-associated
54                                     Familial hemiplegic migraine is an episodic neurological disorder
55                                     Familial hemiplegic migraine is associated with at least 13 diffe
56                                     Familial hemiplegic migraine is caused by mutations in the calciu
57                                     Familial hemiplegic migraine knock-in mice expressing the S218L o
58 aptic transmission resulting from a familial hemiplegic migraine mutation (S218L).
59         Two PRRT2 mutations were in familial hemiplegic migraine or episodic ataxia, one SLC2A1 famil
60 and was significantly lower in patients with hemiplegic migraine than in patients with non-motor aura
61 3 patients with familial episodic ataxia and hemiplegic migraine to investigate the mutation frequenc
62                                     Familial hemiplegic migraine type 1 (FHM1) arises from missense m
63                                     Familial hemiplegic migraine type 1 (FHM1) is a subtype of migrai
64                                     Familial hemiplegic migraine type 1 (FHM1) is an autosomal domina
65             Patients suffering from familial hemiplegic migraine type 1 (FHM1) may have a disproporti
66                                     Familial hemiplegic migraine type 1 (FHM1), a monogenic migraine
67 aV2.1 channels, are associated with familial hemiplegic migraine type 1 (FHM1), a rare monogenic subt
68                                     Familial hemiplegic migraine type 1 (FHM1), a severe migraine wit
69 minant form of this common disease, familial hemiplegic migraine type 1 (FHM1), arises from missense
70 se Episodic Ataxia type 2 (EA2) and Familial Hemiplegic Migraine type 1 (FHM1).
71 -gated calcium channels can lead to familial hemiplegic migraine type 1 (FHM1).
72  mutations that are associated with familial hemiplegic migraine type 1 (FHM1).
73 tation analogous to the one causing familial hemiplegic migraine type 1 in humans, showed markedly re
74                                  In familial hemiplegic migraine type 1 mice, olcegepant 1mg/kg incre
75                                  In familial hemiplegic migraine type 1 mutant mice expressing human
76 into subcortical structures in both familial hemiplegic migraine type 1 mutants.
77 rization in mice carrying the human familial hemiplegic migraine type 1 R192Q missense mutation as we
78                                     Familial hemiplegic migraine type 1, a monogenic migraine variant
79 ttene et al. study a mouse model of familial hemiplegic migraine type 1, and provide evidence for the
80 (NTG)-induced rat migraine model, a familial hemiplegic migraine type 2 (FHM2) mouse model, and a tra
81  we show that awake mice carrying a familial hemiplegic migraine type 2 (FHM2) mutation have slower c
82          The neurological disorders familial hemiplegic migraine type 2 (FHM2), alternating hemiplegi
83  severe human pathologies including Familial Hemiplegic Migraine type 2, Alternating Hemiplegia of Ch
84                                     Familial hemiplegic migraine type 3 (FHM3) is a severe autosomal
85 enic subtype of migraine with aura, familial hemiplegic migraine type 3 (FHM3).
86 3V) missense mutation, which causes familial hemiplegic migraine type 3 in heterozygous family member
87 sistent with mild gain of function, familial hemiplegic migraine type 3 variants induce a larger effe
88 tional studies of both epilepsy and familial hemiplegic migraine type 3 variants reveal alterations o
89 were related to Dravet syndrome and familial hemiplegic migraine type 3 variants.
90  between SCN1A-related epilepsy and familial hemiplegic migraine type 3, and identifies sodium channe
91  SCN1A variants are associated with familial hemiplegic migraine type 3.
92           The neurological disorder familial hemiplegic migraine type II (FHM2) is caused by mutation
93 (rapid-onset dystonia parkinsonism, familial hemiplegic migraine type-2), as well as reduction in Na,
94 n mutations of NaV1.1 (SCN1A) cause familial hemiplegic migraine type-3 (FHM3), a subtype of migraine
95 dromes, in which hemiplegic migraine and non-hemiplegic migraine with or without aura are part of a w
96                                     Familial hemiplegic migraine, a rare Mendelian form of MA, can be
97 with neurological disorders, such as ataxia, hemiplegic migraine, and epilepsy.
98 e ion pump alpha2-Na/K ATPase cause familial hemiplegic migraine, but the mechanisms by which alpha2-
99 gical and developmental disorders, including hemiplegic migraine, epilepsy, developmental delay, and
100           The recent discovery that familial hemiplegic migraine, episodic ataxia type 2, and spinoce
101 type voltage-gated calcium channel (familial hemiplegic migraine, episodic ataxia type 2, spinocerebe
102 such human neurological diseases as familial hemiplegic migraine, episodic ataxia-2, and spinocerebel
103 um channel gene are associated with familial hemiplegic migraine, episodic or progressive ataxia, com
104  linkage and association studies of familial hemiplegic migraine.
105 teral sclerosis, parkinsonism, epilepsy, and hemiplegic migraine.
106 ns included a high frequency of migraine and hemiplegic migraine.
107 mechanism for enhanced CSD susceptibility in hemiplegic migraine.
108 ified a novel PNKD gene deletion in familial hemiplegic migraine.
109 rders is much broader than strictly familial hemiplegic migraine.
110 human neurologic diseases including familial hemiplegic migraine.
111  myoclonic epilepsy of infancy, and familial hemiplegic migraine.
112 cium channel gene associated with ataxia and hemiplegic migraine.
113                                        These hemiplegic mutations identify amino acid residues that,
114 tation of motor and cognitive impairments in hemiplegic or paraplegic patients by offering on-line fe
115                Clinical trials involving two hemiplegic patients and a tetraplegic patient demonstrat
116 icantly slower than a control group of aware hemiplegic patients in performing the inhibition task wi
117                       A group of anosognosic hemiplegic patients was significantly slower than a cont
118 ning in awareness in patients with AHP: Four hemiplegic patients with and four without anosognosia we
119                                 In contrast, hemiplegic patients without neglect will reach across an
120 tients should undergo ultrasonography of the hemiplegic shoulder to define the nature and extent of s
121 rmed to sonographically evaluate post-stroke hemiplegic shoulders and explore possible relationship(s
122                                              Hemiplegic shoulders exhibited significantly higher numb
123                                              Hemiplegic shoulders have significantly higher number of
124         The most frequent pathologies in the hemiplegic shoulders were the following: tendinosis of t
125 he long head of bicep tendon was commoner in hemiplegic shoulders with poor motor status than those w
126 al abnormalities were found in all 45 (100%) hemiplegic shoulders, 25 (55.6%) unaffected shoulders of
127 pecialty-specific operation complicated by a hemiplegic stroke and respiratory failure.
128                         Rehabilitation after hemiplegic stroke has typically relied on the training o
129                                              Hemiplegic stroke patients should undergo ultrasonograph
130 erapy significantly improves gait in chronic hemiplegic stroke patients.
131 ird of patients presenting with a unilateral hemiplegic stroke, yet its neurophysiological basis rema
132 consistent and reliable clinical features of hemiplegic stroke.
133              Pain was reported more often in hemiplegic than non-hemiplegic knees (n = 16 vs. n = 6,

 
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