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1  outcome now perceived as shifted toward the involuntary movement.
2 brain activity in healthy subjects during an involuntary movement.
3 ontal projections, resulting in breakthrough involuntary movements.
4 r, may be effective in reversing established involuntary movements.
5  dystonia experienced abnormal posturing and involuntary movements.
6 s underwent a pallidotomy that abolished his involuntary movements.
7  of opioid agents in the management of these involuntary movements.
8 ting stable stimuli, our eyes undergo small, involuntary movements.
9 ia physiological biases in cortically-evoked involuntary movements.
10 characterized by the execution of repetitive involuntary movements.
11 onia is a movement disorder characterized by involuntary movements.
12 may be transferred from voluntary actions to involuntary movements.
13 bnormal motor drive that ultimately triggers involuntary movements.
14 ny subjective boundary between voluntary and involuntary movements.
15 ults with focal or segmental distribution of involuntary movements.
16 tained muscle contractions, postures, and/or involuntary movements.
17 ponsiveness to dopamine and the emergence of involuntary movements.
18 e, and various other disorders with abnormal involuntary movements.
19 1 status and the presence of phasic or tonic involuntary movements.
20 time course of improvement of L-dopa-induced involuntary movements.
21  sleep breath disturbance, and sleep-related involuntary movements.
22 6/9), hypotonia (7/9), hypertonia (6/9), and involuntary movements (3/9).
23                  The development of abnormal involuntary movements (a measure of LID) as well as rota
24 can mimic the full range of organic abnormal involuntary movements, affect gait and speech, or presen
25 ability, its reversal, and the exhibition of involuntary movements after levodopa administration.
26  we examined cylinder behaviour and abnormal involuntary movement (AIM), respectively.
27 ats that developed levodopa-induced abnormal involuntary movements (AIMs) after three weeks of drug t
28   Therefore, following induction of abnormal involuntary movements (AIMs), 6-OHDA rats were injected
29  following the second injection for abnormal involuntary movements (AIMs), analogous to dyskinesia ob
30 rly genes only in rats experiencing abnormal involuntary movements (AIMs).
31                               Total abnormal involuntary movements (AIMs, a measure of LID) were sign
32  monotherapy the agonists delay the onset of involuntary movements, although at the expense of poorer
33 magnetic resonance imaging (fMRI) during the involuntary movement and during a matched voluntary move
34 e then tested whether the combination of the involuntary movement and tone alone might now suffice to
35 characterized by onset in the fourth decade, involuntary movements and abnormalities of voluntary mov
36        Neurological signs, including ataxia, involuntary movements and cognitive impairment developed
37 od of 6 months ataxia developed, followed by involuntary movements and cognitive impairment.
38 y onset torsion dystonia is characterized by involuntary movements and distorted postures and is usua
39 likely to be important in the development of involuntary movements and epilepsy.
40 tests, including different types of abnormal involuntary movements and hypersensitivity of rotational
41 e include fluctuating levodopa responses and involuntary movements and postures known as dyskinesia a
42        However, long-term treatment leads to involuntary movements and response fluctuations which ad
43 evodopa causes motor complications including involuntary movements and response fluctuations.
44 whereas adenosine A1 receptor-null mice show involuntary movements and seizure at stimulation intensi
45  a condition defined by the presence of semi-involuntary movements and sounds.
46 op adverse events in the form of dyskinesia (involuntary movements) and fluctuations in motor respons
47  Myoclonus is characterized by sudden, brief involuntary movements, and its presence is debilitating.
48          One influential model proposes that involuntary movements are driven by an imbalance in the
49 e loops during resting and their relation to involuntary movements are not well characterized.
50                                          The involuntary movements are paroxysmal at early ages, incr
51 esigenic dyskinesia (PNKD) to assess whether involuntary movements are related to aberrant activity i
52               During quiet resting behavior, involuntary movements are suppressed.
53                                              Involuntary movements arise from disturbed striatal rest
54 omy there was a significant reduction in the involuntary movement associated with these disorders and
55                                     Abnormal involuntary movements associated with LID were measured
56                                 The abnormal involuntary movements associated with this disease are b
57 tains decorrelation and induces intermittent involuntary movements at high rate.
58 n synchronizes striatal dynamics, leading to involuntary movements at low rate.
59                                   Comparable involuntary movements caused by magnetic brain stimulati
60 shing feature of the disease is uncontrolled involuntary movements (chorea) accompanied by progressiv
61 e disorder that is characterized by abnormal involuntary movements (chorea), intellectual impairment
62 opment of fluctuations in motor response and involuntary movements commonly complicate the treatment
63 dramatically reduced l-dopa-induced abnormal involuntary movements compared with control mice.
64 parkin PD gene leads to exaggerated abnormal involuntary movements compared with wild-type mice.
65 tive for some types of dystonia in relieving involuntary movements, correcting abnormal posture, prev
66  to 22% of secondary movement disorders, and involuntary movements develop after 1-4% of strokes.
67            Myoclonus, one of the most common involuntary movement disorders, poses particular challen
68 ing levodopa eventually develop debilitating involuntary movements (dyskinesia).
69    Levodopa-induced dyskinesias are abnormal involuntary movements experienced by the majority of per
70                Assessments included abnormal involuntary movements, extrapyramidal signs, psychiatric
71  limited by gradual development of disabling involuntary movements for which the underlying causes ar
72 hree patients assigned to sham stimulation), involuntary movements (ie, dyskinesia or worsening of dy
73 f agency but, with repeated association, the involuntary movement in itself comes to produce some key
74 ralysis typically develop a wide spectrum of involuntary movements in muscles receiving innervation c
75 may be a key mechanism for the generation of involuntary movements in other disorders.SIGNIFICANCE ST
76  essential to motor behavior and may lead to involuntary movements in pathologic conditions.
77 n of the globus pallidus internus alleviates involuntary movements in patients with dystonia.
78 uring periods of rest, relief with movement, involuntary movements in sleep (viz., periodic leg movem
79 rt disease or neuropsychiatric behaviors and involuntary movements in Sydenham chorea.
80 ative disorder characterized by hyperkinetic involuntary movements, including motor restlessness and
81 e a suitable therapeutic strategy to control involuntary movements induced by nonselective DA agonist
82                      This is demonstrated by involuntary movements induced by STN lesions and the suc
83 al RGS9-2 overexpression diminishes both the involuntary movement intensity and the anti-parkinsonian
84  injection into the striatum--diminishes the involuntary movement intensity without lessening the ant
85 isease leads to the development of disabling involuntary movements named dyskinesias that are related
86            Tremor, defined as a rhythmic and involuntary movement of any body part, is the most preva
87 g for differences in patient positioning and involuntary movement of internal organs, often necessita
88                 Oculomotor synkinesis is the involuntary movement of the eyes or eyelids with a volun
89 luntary action was always associated with an involuntary movement of the other hand.
90 movements (CMM), a disorder characterized by involuntary movements of one hand that mirror intentiona
91              The jitter was not due to small involuntary movements of the eyes, because it only occur
92 logical disorder characterized by sustained, involuntary movements of the head and neck.
93 emergency department with a 2-day history of involuntary movements of the right upper and lower extre
94  movements (MM) disorder is characterized by involuntary movements on one side of the body that mirro
95                         Mirror movements are involuntary movements on one side of the body that occur
96 nt, is associated with debilitating abnormal involuntary movements or dyskinesias, for which few trea
97 ere is no clear explanation for the onset of involuntary movements or for the priming process that in
98 ts in other disorders.SIGNIFICANCE STATEMENT Involuntary movements, or dyskinesias, are part of many
99                                     Abnormal involuntary movements, or dyskinesias, are seen in many
100 elopmental disorder commonly associated with involuntary movements, or tics.
101 er she was discharged from the hospital, the involuntary movements progressively decreased over the n
102 es were analyzed in relationship to abnormal involuntary movement ratings.
103 ion in Parkinson's disease, it often elicits involuntary movements, referred to as levodopa-induced p
104 e precise physiopathology of these disabling involuntary movements remains to be fully elucidated.
105 th the motor subset of the modified Abnormal Involuntary Movement Scale (AIMS) by raters blind to pre
106 pared with the placebo group on the Abnormal Involuntary Movement Scale (AIMS) dyskinesia score (item
107 cy endpoints included the change in Abnormal Involuntary Movement Scale (AIMS) score (items 1 to 7) f
108 ary efficacy endpoint was change in Abnormal Involuntary Movement Scale (AIMS) score from baseline to
109 l efficacy was determined using the Abnormal Involuntary Movement Scale (AIMS).
110                                 The Abnormal Involuntary Movement Scale and research diagnostic crite
111 nt disorders were assessed with the Abnormal Involuntary Movement Scale and Simpson-Angus Rating Scal
112 ues, weight, metabolic indices, and Abnormal Involuntary Movement Scale score.
113 ngus Scale, Barnes Akathisia Scale, Abnormal Involuntary Movement Scale) were not significantly chang
114 he Assessment of Negative Symptoms, Abnormal Involuntary Movement Scale, and a 40-item side effect ch
115 ed adverse events, vital signs, the Abnormal Involuntary Movement Scale, the Barnes Akathisia Scale,
116 ardive dyskinesia symptoms with the Abnormal Involuntary Movement Scale.
117 y movements were assessed using the Abnormal Involuntary Movement Scale.
118 ssessments performed were clinical (Abnormal Involuntary Movements Scale, Barnes Akathisia Scale, and
119 in the putamen scored higher on the Abnormal Involuntary Movements Scale.
120 ment was assessed using traditional abnormal involuntary movement scores and head-mounted inertial se
121 r neuropathy, ophthalmological disturbances, involuntary movements, seizures, cognitive dysfunction,
122 showed activation of the putamen whereas the involuntary movement showed much greater activation of t
123 hronic levodopa treatment can produce severe involuntary movements (so-called dopa-induced dyskinesia
124 e l-DOPA and eventually develop hyperkinetic involuntary movements termed dyskinesia.
125 omplicated by eventual debilitating abnormal involuntary movements termed L-DOPA-induced dyskinesia (
126 PA almost always leads to the development of involuntary movements termed l-DOPA-induced dyskinesia.
127 n's disease (PD) often leads to debilitating involuntary movements, termed L-dopa-induced dyskinesia
128  mice are more susceptible to L-dopa-induced involuntary movements than unilateral 6-OHDA-lesioned RG
129 bnormal electrical activity in the brain and involuntary movement that can lead to physical injury an
130 nongenetic disorders and is characterized by involuntary movements that impair precision and motor rh
131 hetosis (PDC) is characterized by attacks of involuntary movements that last up to several hours and
132             Dyskinesias are hyperkinetic and involuntary movements that may result from any of a numb
133 e conjectures of earlier authors, during the involuntary movement there was widespread activation of
134                          This shift required involuntary movements to have been previously associated
135                                          The involuntary movement was driven by an involuntary postur
136 ale and the Barnes Akathisia Scale; abnormal involuntary movements were assessed using the Abnormal I
137                                 In contrast, involuntary movements were associated with a distinctive
138  persisted in DYT1 dystonia patients in whom involuntary movements were suppressed by sleep.
139 osure, extrapyramidal symptoms, and abnormal involuntary movements were used as covariates.
140 rt that RGS9 knock-out mice develop abnormal involuntary movements when inhibition of dopaminergic tr
141 rther postulated that the particular type of involuntary movement which develops also depends on the
142 cross two experiments, repeatedly pairing an involuntary movement with a voluntary action induced key
143       The transgenic mice developed abnormal involuntary movements with dystonic-appearing, self-clas

 
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