ライフサイエンスコーパス: involuntary movement

1 outcome now perceived as shifted toward the involuntary movement.

2 brain activity in healthy subjects during an involuntary movement.

3 dystonia experienced abnormal posturing and involuntary movements.

4 s underwent a pallidotomy that abolished his involuntary movements.

5 of opioid agents in the management of these involuntary movements.

6 sleep breath disturbance, and sleep-related involuntary movements.

7 may be transferred from voluntary actions to involuntary movements.

8 bnormal motor drive that ultimately triggers involuntary movements.

9 ults with focal or segmental distribution of involuntary movements.

10 tained muscle contractions, postures, and/or involuntary movements.

11 ponsiveness to dopamine and the emergence of involuntary movements.

12 e, and various other disorders with abnormal involuntary movements.

13 1 status and the presence of phasic or tonic involuntary movements.

14 characterized by the execution of repetitive involuntary movements.

15 time course of improvement of L-dopa-induced involuntary movements.

16 ontal projections, resulting in breakthrough involuntary movements.

17 r, may be effective in reversing established involuntary movements.

18 The development of abnormal involuntary movements (a measure of LID) as well as rota

19 can mimic the full range of organic abnormal involuntary movements, affect gait and speech, or presen

20 ability, its reversal, and the exhibition of involuntary movements after levodopa administration.

21 we examined cylinder behaviour and abnormal involuntary movement (AIM), respectively.

22 ats that developed levodopa-induced abnormal involuntary movements (AIMs) after three weeks of drug t

23 Therefore, following induction of abnormal involuntary movements (AIMs), 6-OHDA rats were injected

24 following the second injection for abnormal involuntary movements (AIMs), analogous to dyskinesia ob

25 rly genes only in rats experiencing abnormal involuntary movements (AIMs).

26 Total abnormal involuntary movements (AIMs, a measure of LID) were sign

27 monotherapy the agonists delay the onset of involuntary movements, although at the expense of poorer

28 magnetic resonance imaging (fMRI) during the involuntary movement and during a matched voluntary move

29 e then tested whether the combination of the involuntary movement and tone alone might now suffice to

30 characterized by onset in the fourth decade, involuntary movements and abnormalities of voluntary mov

31 characterized by onset in the fourth decade, involuntary movements and abnormalities of voluntary mov

32 Neurological signs, including ataxia, involuntary movements and cognitive impairment developed

33 od of 6 months ataxia developed, followed by involuntary movements and cognitive impairment.

34 y onset torsion dystonia is characterized by involuntary movements and distorted postures and is usua

35 tests, including different types of abnormal involuntary movements and hypersensitivity of rotational

36 e include fluctuating levodopa responses and involuntary movements and postures known as dyskinesia a

37 However, long-term treatment leads to involuntary movements and response fluctuations which ad

38 evodopa causes motor complications including involuntary movements and response fluctuations.

39 whereas adenosine A1 receptor-null mice show involuntary movements and seizure at stimulation intensi

40 a condition defined by the presence of semi-involuntary movements and sounds.

41 op adverse events in the form of dyskinesia (involuntary movements) and fluctuations in motor respons

42 Myoclonus is characterized by sudden, brief involuntary movements, and its presence is debilitating.

43 e loops during resting and their relation to involuntary movements are not well characterized.

44 The involuntary movements are paroxysmal at early ages, incr

45 During quiet resting behavior, involuntary movements are suppressed.

46 Involuntary movements arise from disturbed striatal rest

47 omy there was a significant reduction in the involuntary movement associated with these disorders and

48 The abnormal involuntary movements associated with this disease are b

49 tains decorrelation and induces intermittent involuntary movements at high rate.

50 n synchronizes striatal dynamics, leading to involuntary movements at low rate.

51 Comparable involuntary movements caused by magnetic brain stimulati

52 shing feature of the disease is uncontrolled involuntary movements (chorea) accompanied by progressiv

53 e disorder that is characterized by abnormal involuntary movements (chorea), intellectual impairment

54 opment of fluctuations in motor response and involuntary movements commonly complicate the treatment

55 dramatically reduced l-dopa-induced abnormal involuntary movements compared with control mice.

56 parkin PD gene leads to exaggerated abnormal involuntary movements compared with wild-type mice.

57 tive for some types of dystonia in relieving involuntary movements, correcting abnormal posture, prev

58 to 22% of secondary movement disorders, and involuntary movements develop after 1-4% of strokes.

59 Myoclonus, one of the most common involuntary movement disorders, poses particular challen

60 ing levodopa eventually develop debilitating involuntary movements (dyskinesia).

61 Assessments included abnormal involuntary movements, extrapyramidal signs, psychiatric

62 limited by gradual development of disabling involuntary movements for which the underlying causes ar

63 hree patients assigned to sham stimulation), involuntary movements (ie, dyskinesia or worsening of dy

64 f agency but, with repeated association, the involuntary movement in itself comes to produce some key

65 ralysis typically develop a wide spectrum of involuntary movements in muscles receiving innervation c

66 essential to motor behavior and may lead to involuntary movements in pathologic conditions.

67 n of the globus pallidus internus alleviates involuntary movements in patients with dystonia.

68 uring periods of rest, relief with movement, involuntary movements in sleep (viz., periodic leg movem

69 rt disease or neuropsychiatric behaviors and involuntary movements in Sydenham chorea.

70 ative disorder characterized by hyperkinetic involuntary movements, including motor restlessness and

71 e a suitable therapeutic strategy to control involuntary movements induced by nonselective DA agonist

72 This is demonstrated by involuntary movements induced by STN lesions and the suc

73 al RGS9-2 overexpression diminishes both the involuntary movement intensity and the anti-parkinsonian

74 injection into the striatum--diminishes the involuntary movement intensity without lessening the ant

75 isease leads to the development of disabling involuntary movements named dyskinesias that are related

76 Tremor, defined as a rhythmic and involuntary movement of any body part, is the most preva

77 g for differences in patient positioning and involuntary movement of internal organs, often necessita

78 luntary action was always associated with an involuntary movement of the other hand.

79 movements (CMM), a disorder characterized by involuntary movements of one hand that mirror intentiona

80 The jitter was not due to small involuntary movements of the eyes, because it only occur

81 emergency department with a 2-day history of involuntary movements of the right upper and lower extre

82 Mirror movements are involuntary movements on one side of the body that occur

83 nt, is associated with debilitating abnormal involuntary movements or dyskinesias, for which few trea

84 ere is no clear explanation for the onset of involuntary movements or for the priming process that in

85 er she was discharged from the hospital, the involuntary movements progressively decreased over the n

86 es were analyzed in relationship to abnormal involuntary movement ratings.

87 ion in Parkinson's disease, it often elicits involuntary movements, referred to as levodopa-induced p

88 e precise physiopathology of these disabling involuntary movements remains to be fully elucidated.

89 th the motor subset of the modified Abnormal Involuntary Movement Scale (AIMS) by raters blind to pre

90 pared with the placebo group on the Abnormal Involuntary Movement Scale (AIMS) dyskinesia score (item

91 ary efficacy endpoint was change in Abnormal Involuntary Movement Scale (AIMS) score from baseline to

92 l efficacy was determined using the Abnormal Involuntary Movement Scale (AIMS).

93 The Abnormal Involuntary Movement Scale and research diagnostic crite

94 nt disorders were assessed with the Abnormal Involuntary Movement Scale and Simpson-Angus Rating Scal

95 ues, weight, metabolic indices, and Abnormal Involuntary Movement Scale score.

96 ngus Scale, Barnes Akathisia Scale, Abnormal Involuntary Movement Scale) were not significantly chang

97 he Assessment of Negative Symptoms, Abnormal Involuntary Movement Scale, and a 40-item side effect ch

98 ed adverse events, vital signs, the Abnormal Involuntary Movement Scale, the Barnes Akathisia Scale,

99 ardive dyskinesia symptoms with the Abnormal Involuntary Movement Scale.

100 y movements were assessed using the Abnormal Involuntary Movement Scale.

101 ssessments performed were clinical (Abnormal Involuntary Movements Scale, Barnes Akathisia Scale, and

102 in the putamen scored higher on the Abnormal Involuntary Movements Scale.

103 r neuropathy, ophthalmological disturbances, involuntary movements, seizures, cognitive dysfunction,

104 showed activation of the putamen whereas the involuntary movement showed much greater activation of t

105 hronic levodopa treatment can produce severe involuntary movements (so-called dopa-induced dyskinesia

106 e l-DOPA and eventually develop hyperkinetic involuntary movements termed dyskinesia.

107 omplicated by eventual debilitating abnormal involuntary movements termed L-DOPA-induced dyskinesia (

108 PA almost always leads to the development of involuntary movements termed l-DOPA-induced dyskinesia.

109 n's disease (PD) often leads to debilitating involuntary movements, termed L-dopa-induced dyskinesia

110 mice are more susceptible to L-dopa-induced involuntary movements than unilateral 6-OHDA-lesioned RG

111 hetosis (PDC) is characterized by attacks of involuntary movements that last up to several hours and

112 Dyskinesias are hyperkinetic and involuntary movements that may result from any of a numb

113 e conjectures of earlier authors, during the involuntary movement there was widespread activation of

114 This shift required involuntary movements to have been previously associated

115 The involuntary movement was driven by an involuntary postur

116 ale and the Barnes Akathisia Scale; abnormal involuntary movements were assessed using the Abnormal I

117 In contrast, involuntary movements were associated with a distinctive

118 persisted in DYT1 dystonia patients in whom involuntary movements were suppressed by sleep.

119 osure, extrapyramidal symptoms, and abnormal involuntary movements were used as covariates.

120 rt that RGS9 knock-out mice develop abnormal involuntary movements when inhibition of dopaminergic tr

121 rther postulated that the particular type of involuntary movement which develops also depends on the

122 cross two experiments, repeatedly pairing an involuntary movement with a voluntary action induced key

123 The transgenic mice developed abnormal involuntary movements with dystonic-appearing, self-clas