ライフサイエンスコーパス: bradykinesia

1 marily characterized by rigidity, tremor and bradykinesia.

2 treatment using tapping speed as an index of bradykinesia.

3 f these 11 items were subscale components of bradykinesia.

4 ion, was significantly associated with worse bradykinesia.

5 ing and memory and the pole descent task for bradykinesia.

6 greater pulse width and amplitude, relieved bradykinesia.

7 on's disease (PD), clinically manifesting as bradykinesia.

8 rkinson's disease motor symptoms, especially bradykinesia.

9 ubt on prior accounts of how LDRT remediates bradykinesia.

10 nchrony associated with further worsening of bradykinesia.

11 ch correlated significantly with severity of bradykinesia.

12 o motivational deficits (apathy) rather than bradykinesia.

13 h contrasts strongly to coexistent nocturnal bradykinesia.

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

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

16 ge was abnormally narrow and correlated with bradykinesia.

17 aracterized by movement disorders, including bradykinesia.

18 ive supranuclear palsy have criteria-defined bradykinesia.

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

20 results in motor symptoms such as tremor and bradykinesia.

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

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

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

24 sment, and motor function assessment via the BRadykinesia Akinesia INcoordination (BRAIN) tap test.

25 The BRadykinesia Akinesia INcoordination (BRAIN) test is a v

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

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

28 oactivation of this A13 region can alleviate bradykinesia and akinetic features, while increasing tur

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

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

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

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

33 = -0.4, P < 0.02) and between improvement in bradykinesia and increased rCBF in the thalamus (r(s) =

34 Careful studies of PD bradykinesia and LDRT pharmacodynamics offer potential a

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

36 ent disorder, with resting tremor, rigidity, bradykinesia and postural instability being major sympto

37 isorders including resting tremor, rigidity, bradykinesia and postural instability.

38 Bradykinesia and rigidity improvements are associated wi

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

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

41 Beta power was positively associated with bradykinesia and rigidity severity; however, these clini

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

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

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

45 r symptom subscores with a specific focus on bradykinesia and rigidity.

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

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

48 The various clinical aspects related to bradykinesia and the pathophysiological mechanisms under

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

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

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

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

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

54 improvement in motor (eg, tremor, rigidity, bradykinesia) and nonmotor (eg, constipation, cognition,

55 ease, including tremor, slowing of movement (bradykinesia), and rigidity.

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

57 includes motor impairments, such as tremor, bradykinesia, and postural instability.

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

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

60 ing parkinsonism features, including tremor, bradykinesia, and premature death.

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

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

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

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

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

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

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

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

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

70 However, careful behavioural observations of bradykinesia are inconsistent with abnormal computations

71 ep brain stimulation-related improvements in bradykinesia are related to the reduction in beta oscill

72 the pathophysiological mechanisms underlying bradykinesia are, however, still unclear.

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

74 Bradykinesia as defined by slowness of initiation of mov

75 smell test correlated with RBD screening and bradykinesia as measured by BRAIN tap test but not motor

76 ed movement-related symptoms (e.g., walking, bradykinesia) as the most bothersome at all durations wh

77 We found that electrical STN DBS relieved bradykinesia, as measured by movement velocity.

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

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

80 bile Application v2 was developed to measure bradykinesia, bradyphrenia and speech, tremor, gait and

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

82 Levodopa therapy improves bradykinesia, but treatment variably affects the bradyki

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

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

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

86 efine Parkinson's disease as the presence of bradykinesia combined with either rest tremor, rigidity,

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

88 Moreover, the connectivity profile for bradykinesia differed from that for rigidity, tremor, or

89 ich often manifest as tremors, rigidity, and bradykinesia, disrupt this healthy variability.

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

91 Regarding bradykinesia, effective contacts were significantly more

92 are ageing with virally suppressed HIV, with bradykinesia emerging earlier and more frequently than i

93 ykinesia, but treatment variably affects the bradykinesia features and does not significantly modify

94 Correlating bradykinesia features and LDRT pharmacodynamics with our

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

96 as a neural correlate of the progression of bradykinesia following chronic STN DBS.

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

98 this study was to examine whether changes in bradykinesia following long-term subthalamic nucleus (ST

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

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

101 hyperintensity burden regression effects for bradykinesia had borderline significance.

102 cography recordings revealed that tremor and bradykinesia had nearly opposite neural signatures, whil

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

104 halamic deep brain stimulation may alleviate bradykinesia in Parkinson patients.

105 nt speed, and loss of these neurons leads to bradykinesia in Parkinson's disease (PD).

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

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

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

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

110 ic circuits are associated with rigidity and bradykinesia in patients with Parkinson's disease.

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

112 tive, I consider the leading prior models of bradykinesia in PD and argue that a more functionally re

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

114 A dominant pathophysiological model of bradykinesia in PD has existed for approximately 30 year

115 nsmission error and present a novel model of bradykinesia in PD that incorporates this evidence.

116 thological bilateral network contributing to bradykinesia in PD.

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

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

119 Bradykinesia is a prominent phenotype of Parkinson's dis

120 Bradykinesia is associated with abnormal functioning wit

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

122 In Parkinson's disease, bradykinesia is characterized by slowness, the reduced a

123 Bradykinesia is one of the cardinal motor symptoms of Pa

124 occurs early in Parkinson's disease (PD) and bradykinesia is required for diagnosis.

125 Bradykinesia is the major cardinal motor sign of Parkins

126 ning and most LDRT responsive feature of PD, bradykinesia, is a complex phenomenon exhibiting impairm

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

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

129 correlated with motor UPDRS (p < 0.005) and bradykinesia motor (p < 0.05) and ADL (p < 0.005) UPDRS

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

131 Upper-limb bradykinesia occurs early in Parkinson's disease (PD) an

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

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

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

135 Bradykinesia, or slowness of movement, is a defining fea

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

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

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

139 A better understanding of bradykinesia pathophysiology will serve as the new start

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

141 review clinical and experimental studies on bradykinesia performed in patients with Parkinson's dise

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

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

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

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

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

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

148 We also found an increase in bradykinesia ratings associated with increased acetylcho

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

150 tia nigra pars compacta and characterised by bradykinesia, rest tremor and rigidity.

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

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

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

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

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

156 When stimulation ceases abruptly, bradykinesia returns gradually.

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

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

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

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

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

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

163 Deep Brain Stimulation can improve tremor, bradykinesia, rigidity, and axial symptoms in patients w

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

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

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

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

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

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

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

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

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

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

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

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

176 t GPi bursts were stronger and correlated to bradykinesia-rigidity severity.

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

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

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

180 frequency was negatively correlated with the bradykinesia scores.

181 Whereas bradykinesia seems to be mitigated by stimulation of the

182 Bradykinesia should be interpreted as arising from netwo

183 , which leads to motor dysfunctions, such as bradykinesia (slowed movement), rigidity, and tremors.

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

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

186 symptoms, i.e., tremor at rest, rigidity and bradykinesia, studies suggest that PD is associated with

187 sphere associated with increased severity of bradykinesia sub-score derived from MDS-UPDRS part III (

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

189 thways, leading to transient improvements in bradykinesia that can persist beyond stimulation cessati

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

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

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

193 Although bradykinesia, tremor and rigidity are the hallmark motor

194 Stimulation effectiveness in reducing bradykinesia, tremor, and rigidity was evaluated for eac

195 th PD, including motor deficits (progressive bradykinesia, tremor, hypomimia) and altered DA neurotra

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

197 nerative disorder with motor symptoms (e.g., bradykinesia, tremors) and non-motor symptoms (e.g., cog

198 quantitative motor task to decode tremor and bradykinesia - two cardinal motor signs of PD - and rela

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

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

201 Bradykinesia was more markedly improved in the cZI group

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

203 The observed change in bradykinesia was related to the change in interhemispher

204 in the subthalamic nucleus (STN), tremor and bradykinesia were better decoded from distinct subregion

205 whether stimulation-related improvements in bradykinesia were contingent on reduction of beta power

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

207 Akinesia and bradykinesia were strongly ameliorated by discrete inact

208 ng the hallmark slowness of movement, termed bradykinesia, were described more than 100 years ago.

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

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

211 task, a validated quantitative assessment of bradykinesia, while local field potentials were recorded

212 Examination typically demonstrates bradykinesia with tremor, rigidity, or both.

213 Behaviourally, the analysis revealed bradykinesia, with hand movement cycle width increasing

214 precursor L-DOPA reversed reserpine-induced bradykinesia without restoring fast dopamine dynamics, a

215 Bradykinesia worsened off therapy over time.