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1 , the majority of which are intermittent and hyperkinetic.
2 se domain(8,9) of Shaker's K(V)beta subunit, Hyperkinetic(10,11).
3  that one of the potassium channel subunits, Hyperkinetic, alters the firing properties of sleep-prom
4 onal territories leads to territory-specific hyperkinetic and hyperbehavioral symptoms.
5 rule-in physical signs that are specific for hyperkinetic and hypokinetic functional motor symptoms.
6 inesia (n=5), parkinsonism (n=4), or a mixed hyperkinetic and hypokinetic movement disorder (n=2).
7                         The presence of both hyperkinetic and hypokinetic movement disorders such as
8                    These animals also show a hyperkinetic and impulsive-like phenotype, reminiscent o
9                              Dyskinesias are hyperkinetic and involuntary movements that may result f
10 homologues of two HERG-interacting proteins, Hyperkinetic and K channel regulator 1 (KCR1), modify un
11 w neurological decline with the emergence of hyperkinetic and/or hypokinetic movement disorder, cogni
12 nesia (PNKD) is characterized by spontaneous hyperkinetic attacks that are precipitated by alcohol, c
13  in DNAH11, the only PCD gene known to cause hyperkinetic beat.
14                 Behavioral symptoms included hyperkinetic behavior (100%), and a majority exhibited h
15 omozygous Kcnma1(H444Q/H444Q) mice displayed hyperkinetic behavior.
16  attenuated prepulse inhibition (males); and hyperkinetic behavior.
17 ling complexes in budding yeast and detected hyperkinetic behaviors for chromatin-bound molecules tha
18                        The sheep developed a hyperkinetic cardiovascular response concomitant with a
19 failure, there is a sympathetically mediated hyperkinetic cardiovascular response to exercise that li
20                                 Another with hyperkinetic ciliary beat had 2 mutations in DNAH11, the
21 sterone activation, and inflammation lead to hyperkinetic circulation, volume overload, and vascular
22 ent key components to the development of the hyperkinetic clinical phenotype observed in myoclonus dy
23 lve (48%) patients suffered life-threatening hyperkinetic crises.
24  hyperkinetic symptoms and prevented further hyperkinetic crises.
25 on deficit hyperactivity disorder (ADHD) and hyperkinetic disorder (HKD) are made on the basis of phe
26 genic mice raising the possibility that this hyperkinetic disorder has a unique pharmacogenetic profi
27 ion-deficit hyperactivity disorder (ADHD) or hyperkinetic disorder is currently unknown.
28 n ADHD diagnosis was defined as diagnosis of hyperkinetic disorder or receipt of dispensed ADHD medic
29 /hyperactivity disorder (ADHD; also known as hyperkinetic disorder) is a common neurodevelopmental co
30 ars, who met diagnostic criteria for ADHD or hyperkinetic disorder, but not schizophrenia and autism,
31  attention-deficit/hyperactivity disorder or hyperkinetic disorder.
32 y (odds ratio, 2.71 [95% CI, 1.29-5.70]) and hyperkinetic disorders (2.19 [1.13-4.25]) were higher am
33 ]), which was associated with an increase in hyperkinetic disorders (RR, 1.13; CI, 1.09-1.18) and anx
34 or of VMAT2 that is used in the treatment of hyperkinetic disorders associated with Huntington diseas
35         We also identified two patients with hyperkinetic disorders carrying the smallest SHANK3-span
36 se changes have been detected in humans with hyperkinetic disorders either via direct recordings from
37 ptor ligands for treatment of both hypo- and hyperkinetic disorders of basal ganglia origin, such as
38 ical and preclinical studies have shown that hyperkinetic disorders such as Huntington's disease, dys
39  increased risk for substance use disorders, hyperkinetic disorders, and mental retardation.
40 relative paucity of comprehensive reviews of hyperkinetic disorders, even though they are equally or
41 eedback-controlled neurostimulation to treat hyperkinetic disorders.
42 resently in use for symptomatic treatment of hyperkinetic disorders.
43  in the GPi is important in the mechanism of hyperkinetic disorders.
44 antibodies should be tested in patients with hyperkinetic encephalitis and neuropsychiatric prodrome
45           Previous studies have demonstrated hyperkinetic endocardial motion of noninfarcted myocardi
46 alpha4 subunit associated with sleep-related hyperkinetic epilepsy.
47    Both age groups (<=4 and >4 years) showed hyperkinetic features (21.1% vs 32.1%), contrary to prev
48                      Cholecystectomy for the hyperkinetic gallbladder appears to be an emerging pheno
49 ecystectomy for pediatric dyskinesia and the hyperkinetic gallbladder population.
50 c population, the emerging phenomenon of the hyperkinetic gallbladder, and suggestions for addressing
51 iary orientation and had an asynchronous and hyperkinetic (GAS2L2-deficient = 19.8 Hz versus control
52 w that the Drosophila beta subunit homologue Hyperkinetic (Hk) associates with members of the ether g
53                                   Drosophila Hyperkinetic (Hk) mutations alter a gene encoding a homo
54                  Mutants of the Shaker (Sh), Hyperkinetic (Hk), and ether a go-go (eag) genes, which
55 tassium (K(+)) channel beta-subunit (Kvbeta) Hyperkinetic (Hk).
56 tiated by a beta modulatory subunit coded by Hyperkinetic (Hk).
57 s will receive l-DOPA and eventually develop hyperkinetic involuntary movements termed dyskinesia.
58  neurodegenerative disorder characterized by hyperkinetic involuntary movements, including motor rest
59 nipulations elicited anxiety-like behaviors, hyperkinetic locomotion, age-dependent motor deficits, a
60 thesized that dlBST could play a role in LID hyperkinetic manifestations.
61        These results are consistent with the hyperkinetic model, which suggests that hemiballismus re
62  variants of CAMK4 found in individuals with hyperkinetic movement disorder and comorbid neurological
63            Early-onset torsion dystonia is a hyperkinetic movement disorder caused by a deletion of o
64 lonus dystonia syndrome is a childhood onset hyperkinetic movement disorder characterized by predomin
65  individuals from two families affected by a hyperkinetic movement disorder due to homozygous mutatio
66                         A common form of the hyperkinetic movement disorder dystonia is caused by mut
67 isorder progresses, a complex hypertonic and hyperkinetic movement disorder is a common phenotype.
68                               The paroxysmal hyperkinetic movement disorder phenocopies a form of dys
69                                  Chorea is a hyperkinetic movement disorder resulting from dysfunctio
70 et torsion dystonia is an autosomal dominant hyperkinetic movement disorder that has recently been li
71      Myoclonus dystonia is a childhood-onset hyperkinetic movement disorder with a combined motor and
72 sion dystonia (ITD) is an autosomal dominant hyperkinetic movement disorder with incomplete penetranc
73 se in the first years of life to late-onset, hyperkinetic movement disorder with poor fine motor skil
74 atures, including central visual impairment, hyperkinetic movement disorder, and epilepsy or electroe
75 mental delay and/or intellectual disability, hyperkinetic movement disorder, transient elevation of t
76                   Dystonia is a debilitating hyperkinetic movement disorder, which can be transmitted
77 a residue that is mutated in patients with a hyperkinetic movement disorder.
78 pmental delay (often with regression), and a hyperkinetic movement disorder.
79 ormal, but developed ataxia and a paroxysmal hyperkinetic movement disorder.
80 ologically dystonia most closely resembles a hyperkinetic movement disorder.
81 lanine has been described in patients with a hyperkinetic movement disorder.
82 recently identified in a family with a novel hyperkinetic movement disorder.
83 ment (49%) to exercise intolerance (25%) and hyperkinetic movement disorders (41%), including dystoni
84 spose some individuals to the development of hyperkinetic movement disorders and seizures.
85 at endogenous mu agonists may play a role in hyperkinetic movement disorders by inducing sustained ac
86   The dystonias are a heterogeneous group of hyperkinetic movement disorders characterised by involun
87 s are still lacking, effective management of hyperkinetic movement disorders demands that physicians
88 therapy for the treatment of hypokinetic and hyperkinetic movement disorders has, however, led to an
89                                              Hyperkinetic movement disorders include tremors, dystoni
90  manifest in parkinsonism or a wide range of hyperkinetic movement disorders including chorea, ballis
91 man mutations in the PDE10A gene manifest in hyperkinetic movement disorders that phenocopy many feat
92 native diagnoses but atypical presentations (hyperkinetic movement disorders).
93 nt for medication-refractory hypokinetic and hyperkinetic movement disorders, and it is being explore
94 azine, show therapeutic efficacy in managing hyperkinetic movement disorders, including Huntington's
95  on studies in animal models and humans with hyperkinetic movement disorders, it is postulated that d
96 elated differences in PD and the most common hyperkinetic movement disorders, namely, essential tremo
97  treat medically intractable hypokinetic and hyperkinetic movement disorders, the course of the palli
98 e of pathogenic DRD2 variants in early-onset hyperkinetic movement disorders.
99 ectrum of antibodies accompanying autoimmune hyperkinetic movement disorders.
100 een shown to contribute to both epilepsy and hyperkinetic movement disorders.
101 lly targeted treatments for chorea and other hyperkinetic movement disorders.
102 ed to reverse these changes in patients with hyperkinetic movement disorders.
103 ovel therapeutic target for the treatment of hyperkinetic movement disorders.
104 , has been extended to the treatment of many hyperkinetic movement disorders.
105 e receptor blocker, is used to treat several hyperkinetic movement disorders.
106 n the subthalamic nucleus (STN) results in a hyperkinetic movement syndrome, similar to the HD phenot
107 ment disorder was observed in 3/21 patients: hyperkinetic movements (1), truncal ataxia (1) and dysto
108 : altered mental status (all), seizures (4), hyperkinetic movements (4), psychiatric features (3), me
109 ording of seizure activity in a patient with hyperkinetic movements during the seizure.
110              The occurrence of non-epileptic hyperkinetic movements in the context of developmental e
111 orphism, progressive psychomotor disability, hyperkinetic movements, and axial hypotonia with variabl
112 opathy, seizures, autonomic instability, and hyperkinetic movements.
113       The dichotomy between the hypo- versus hyperkinetic nature of Parkinson's disease (PD) and dyst
114 indicate that SHANK3 overexpression causes a hyperkinetic neuropsychiatric disorder.
115                                          The hyperkinetic phase causes a drop in slo gene expression
116                          Women had a greater hyperkinetic response than men in the noninfarct zone (S
117 ormation is stored in the oxidation state of Hyperkinetic's nicotinamide adenine dinucleotide phospha
118  test, and 2 subscores were extracted: (1) a hyperkinetic score, combining dystonia and chorea, and (
119 es, typical frontal lobe features, including hyperkinetic seizures, are observed even in very young c
120 temperature and using hyperactivity mutants (Hyperkinetic, Shaker) demonstrates that the rate of this
121 ells also requires the K(+) channel subunits Hyperkinetic, Shaker, and ether-a-go-go.
122                                              Hyperkinetic states are common in human movement disorde
123 nt such as Parkinson's disease as well as to hyperkinetic states such as those induced by stimulant d
124               Deep brain stimulation reduced hyperkinetic symptoms and prevented further hyperkinetic
125 ticipants of any age with a clinical ADHD or hyperkinetic syndrome diagnosis were included.
126                            Here we show that Hyperkinetic, the beta-subunit of the K(V)1 channel Shak
127  patients (18%) were classified as "mismatch-hyperkinetic." The mean LVEF for these patients signific
128 rons, which register this rise by converting Hyperkinetic to the NADP(+)-bound form.

 
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