ライフサイエンスコーパス: bradykinesia

1 treatment using tapping speed as an index of bradykinesia.

2 y and the emergence of rigidity, tremor, and bradykinesia.

3 ymptoms of Parkinson disease (PD), including bradykinesia.

4 ge was abnormally narrow and correlated with bradykinesia.

5 aracterized by movement disorders, including bradykinesia.

6 ive supranuclear palsy have criteria-defined bradykinesia.

7 ' and they do not have criteria-defined limb bradykinesia.

8 results in motor symptoms such as tremor and bradykinesia.

9 marily characterized by rigidity, tremor and bradykinesia.

10 h contrasts strongly to coexistent nocturnal bradykinesia.

11 in contralateral tremor (33%, P = 0.016) and bradykinesia (24%, P = 0.013) scores.

12 , bilateral STN DBS improved rigidity (62%), bradykinesia (44%), gait (49%) and postural stability (5

13 wness due to comorbidities misinterpreted as bradykinesia, a tardive syndrome related to undisclosed

14 ted patients with advanced PD, 2 with severe bradykinesia and a declining response to medication, and

15 rmality, severe upward gaze palsy, bilateral bradykinesia and absence of alien limb syndorme separate

16 rst rate was positively correlated with both bradykinesia and axial scores, while the related ratio o

17 disease, and predicts subsequent changes in bradykinesia and cognitive status over 1 year.

18 state, distinguished by increased freezing, bradykinesia and decreased locomotor initiations.

19 ne dopamine D2 receptor gene (drd2) produces bradykinesia and hypothermia.

20 = -0.4, P < 0.02) and between improvement in bradykinesia and increased rCBF in the thalamus (r(s) =

21 ion completely rescued deficits in freezing, bradykinesia and locomotor initiation.

22 example, there is evidence that parkinsonian bradykinesia and rigidity may arise from an oversynchron

23 s (STN) neurons has been correlated with the bradykinesia and rigidity seen in Parkinson's disease.

24 orn off and parkinsonian features, including bradykinesia and rigidity, return) of greater than 1.5 h

25 ale (UPDRS) subscores, kinematic measures of bradykinesia and rigidity, working memory, response inhi

26 orea, and (2) a hypokinetic score, combining bradykinesia and rigidity.

27 ures were the UPDRS III subscores of tremor, bradykinesia and rigidity.

28 e SND phenotype demonstrates the most severe bradykinesia and the OPCA phenotype the more frequent oc

29 a significant difference in the severity of bradykinesia and the presence of cerebellar signs betwee

30 a movement disorder characterized by ataxia, bradykinesia and tremor.

31 STN stimulation reduced bradykinesia and widened this range in all patients, but

32 keys were evaluated clinically (eg, posture, bradykinesia) and behaviorally (open field test), and th

33 Motor dysfunction (e.g., bradykinesia) and motivational deficit (i.e., apathy) ar

34 nian motor signs (tremor, rigidity, akinesia/bradykinesia, and gait dysfunction) and reduced drug-ind

35 , characterized by resting tremor, rigidity, bradykinesia, and postural instability.

36 ymptoms, including resting tremor, rigidity, bradykinesia, and postural instability.

37 sease (PD) include resting tremor, akinesia, bradykinesia, and rigidity, and these motor abnormalitie

38 cardinal parkinsonian signs, such as tremor, bradykinesia, and rigidity-because the hand deformities

39 ed executive function and nonfluent aphasia, bradykinesia, and rigidity.

40 ion criteria: the presence of a rest tremor, bradykinesia, and rigidity; a modified Hoehn and Yahr st

41 sing halorhodopsin in ChIs reduces akinesia, bradykinesia, and sensorimotor neglect.

42 P = .003) were predominantly associated with bradykinesia, and we further discovered associations bet

43 r density, similar effects on brain atrophy, bradykinesia, anxiety, and depression were observed.

44 with progression, signs of more generalized bradykinesia appear, which include facial masking, reduc

45 Instead, bradykinesia appeared to result from the inability of Pa

46 tic criterion of Parkinson's disease defines bradykinesia as 'slowness of initiation with progressive

47 Bradykinesia as defined by slowness of initiation of mov

48 In contrast, bradykinesia, assessed as the speed of finger-tapping, h

49 t one extrapyramidal motor sign (EPMS), with bradykinesia being the most common EPMS in both FTD (83%

50 ease dopaminergic drugs especially impact on bradykinesia but less on executive functions.

51 In conclusion, the amelioration of bradykinesia by dopaminergic medication seems to be driv

52 rast to this theory, here we have found that bradykinesia can be completely dissociated from beta osc

53 pattern was compatible with criteria-defined bradykinesia, characterized by slowness with progressive

54 yndrome characterized by rigidity, akinesia, bradykinesia, decreased response to external sensory sti

55 ues in superior STN/zona incerta (quantified bradykinesia), dorsal STN (mood, anxiety), and inferior

56 n the substantia nigra predict the change in bradykinesia following 1 year.

57 bradykinesia OFF treatment and the level of bradykinesia following DBS and medication.

58 otor signs of PD including tremor, rigidity, bradykinesia, gait and balance.

59 the prevalence of four categories of signs--bradykinesia, gait disturbance, rigidity, and tremor--an

60 hyperintensity burden regression effects for bradykinesia had borderline significance.

61 vement in contralateral tremor, rigidity and bradykinesia in all patients followed for 6, 12 and 24 m

62 cal and surgical interventions used to treat bradykinesia in Parkinson's disease.

63 ve finger tapping is commonly used to assess bradykinesia in Parkinson's disease.

64 roved to be effective therapies for treating bradykinesia in Parkinson's disease.

65 e success of medication and DBS at improving bradykinesia in patients with Parkinson's disease, patie

66 ivity in the basal ganglia may contribute to bradykinesia in patients with Parkinson's disease.

67 This observation led to the suggestion that bradykinesia in PD could be due to a reduction in motor

68 We measured bradykinesia in the dominant hand by assessing finger ta

69 tients' medical records, and the severity of bradykinesia in the first year of disease onset and in t

70 Bradykinesia is a prominent phenotype of Parkinson's dis

71 Bradykinesia is associated with abnormal functioning wit

72 Instead, we observed that bradykinesia is causatively regulated by the burst-firin

73 Symptoms of tremor, rigidity, bradykinesia, micrographia, shuffling gait, and difficul

74 This suggests that akinesia and bradykinesia might, in fact, originate from abnormalitie

75 de range of motor deficits such as akinesia, bradykinesia, motor coordination, and sensorimotor negle

76 Thus, the bradykinesia of Parkinson's disease subjects did not see

77 a positive association between the level of bradykinesia OFF treatment and the level of bradykinesia

78 s characterized by resting tremor, rigidity, bradykinesia or slowness, gait disturbance, and postural

79 order characterized by rigidity, tremor, and bradykinesia, originating from degeneration of dopaminer

80 009), postural instability (p = 0.013), body bradykinesia (p = 0.048), and gait disturbance (p = 0.05

81 Our results shift the understanding of bradykinesia pathophysiology from an interactive oscilla

82 rovement was also seen for tremor, rigidity, bradykinesia, percent on time and drug-induced dyskinesi

83 efined as the (1) presence of hypokinesia or bradykinesia plus at least 1 other cardinal sign and/or

84 the combination of symptoms of rigidity and bradykinesia (positive LR, 4.5; negative LR, 0.12); a hi

85 motor impairments involving resting tremor, bradykinesia, postural instability, gait difficulty and

86 r improvement in UPDRS 3 scores in rigidity, bradykinesia, postural stability and gait correlate with

87 of Ink4d- null with Kip1-null mice exhibited bradykinesia, proprioceptive abnormalities, and seizures

88 aracterized by generalized movement slowing (bradykinesia), provides the opportunity to directly expl

89 This difference in S(N) suggests that bradykinesia represents an implicit decision not to move

90 tes alone, and is characterized by rigidity, bradykinesia, resting tremor, and postural instability.

91 he presentation of clinical symptoms such as bradykinesia, resting tremor, and rigidity.

92 neurodegenerative disorder characterized by bradykinesia, resting tremor, muscular rigidity, and pos

93 he key clinical features of PD, rigidity and bradykinesia, result from neurotransmitter imbalance, pa

94 rs that produced improvement in rigidity and bradykinesia resulted in changes in the pattern and powe

95 When stimulation ceases abruptly, bradykinesia returns gradually.

96 wed a severe parkinsonian syndrome featuring bradykinesia, rigidity (axial > appendicular), and po

97 psilateral improvement was also observed for bradykinesia, rigidity and drug-induced dyskinesias.

98 egenerative disease characterized by tremor, bradykinesia, rigidity and postural instability.

99 ee of the cardinal symptoms of parkinsonism: bradykinesia, rigidity and postural instability.

100 enerative disorder with clinical features of bradykinesia, rigidity and resting tremor resulting from

101 mised motor system performance as evinced by bradykinesia, rigidity and tremor, suggesting that netwo

102 proves three of the cardinal features of PD: bradykinesia, rigidity, and postural instability.

103 e neurodegenerative disease characterized by bradykinesia, rigidity, and resting tremor, is the most

104 Signs of gait disturbance, bradykinesia, rigidity, and tremor were assessed proxima

105 oss of substantia nigra neurons resulting in bradykinesia, rigidity, and tremor.

106 l motor symptoms due to combinations of mild bradykinesia, rigidity, and tremor.

107 ated to gait impairment (p < 0.001), but not bradykinesia, rigidity, or tremor.

108 ypical levodopa-responsive parkinsonism with bradykinesia, rigidity, resting tremor, and impaired pos

109 ia characterized by motor symptoms including bradykinesia, rigidity, resting tremor, and postural ins

110 mals developed progressive parkinsonism with bradykinesia, rigidity, tremor, and an abnormal posture,

111 the globus pallidus can substantially reduce bradykinesia, rigidity, tremor, and gait difficulties in

112 global parkinsonism or component measures of bradykinesia, rigidity, tremor, and gait impairment that

113 correlated with the degree of improvement in bradykinesia-rigidity as did local STN activity at 300-4

114 The cardinal symptoms (bradykinesia, rigor, tremor, and postural instability) a

115 ency of hospitalizations, inability to walk, bradykinesia, scoliosis, gastrostomy feeding, age of sei

116 -water values predicted the 1 year change in bradykinesia scores (r = 0.74, P < 0.001) and 1 year cha

117 frequency was negatively correlated with the bradykinesia scores.

118 ntrol and enable more selective targeting of bradykinesia-specific mechanisms to improve PD therapy.

119 nic toe curling, action tremor, masked face, bradykinesia, stooped posture, and rigidity), together w

120 at 5 and 8 years, mostly driven by axial and bradykinesia subscores.

121 Primary motor underactivity may explain the bradykinesia that these patients exhibit and, if inhibit

122 parkin larvae displayed a marked bradykinesia that was caused by a reduction in both the

123 rcuits have long been the leading theory for bradykinesia, the slow movements that are cardinal sympt

124 e), potential prediagnostic motor (hypo- and bradykinesia, tremor, rigidity, postural imbalance, post

125 otor symptoms of Parkinson's disease such as bradykinesia typically improve under dopaminergic medica

126 ction in parkin mutants induces Parkinsonian bradykinesia via a neuronal energy deficit and resulting

127 Bradykinesia was more markedly improved in the cZI group

128 Bradykinesia was present in all cases, rigidity in 96%,

129 Serial quantitative assessments of bradykinesia were performed during a defined period foll

130 Akinesia and bradykinesia were strongly ameliorated by discrete inact

131 Parkinson's disease subjects displayed bradykinesia when performing maximal speed reaches to th

132 In addition to bradykinesia, which is a core symptom, different types o