ライフサイエンスコーパス: tremor

1 erase (ChAT) neurons reduces tacrine-induced tremor.

2 roving severe, refractory multiple sclerosis tremor.

3 pha desynchronization occurring in essential tremor.

4 udies show a high heritability for essential tremor.

5 with PD, with a greater effect on PIGD than tremor.

6 ator PPARGC1A were associated with essential tremor.

7 the differential diagnosis of patients with tremor.

8 s of indeterminate senile tremor or dystonic tremor.

9 the lithium group tended to experience more tremor.

10 ures suggested a dose-dependent reduction of tremor.

11 d not confirm the association with essential tremor.

12 ticentre cohort of patients with orthostatic tremor.

13 cluding stiffness, slowness of movement, and tremor.

14 toms, with three patients manifesting action tremor.

15 Age was the strongest predictor of tremor.

16 n phase difference between postural and rest tremor.

17 nput to antagonistic motoneuron pools on the tremor.

18 ical tremor of the hand-kinetic and postural tremor.

19 G recorded during postural, but not kinetic, tremor.

20 is anterior muscle and the onset of hindlimb tremor.

21 ad]) for the treatment of multiple sclerosis tremor.

22 surgery has been applied in the treatment of tremor.

23 the treatment of patients with pathological tremor.

24 osis of well-known causes, such as essential tremor.

25 Clinically, these mice exhibit ataxia and tremors.

26 llum plays an important role in pacing those tremors.

27 re, seizure disorders, gait disturbance, and tremors.

28 rease in FA and clinical improvement in hand tremor 3 months after lesion inducement (P < .001).

29 athisia, the most common adverse events were tremor (42 [79%] patients in the quetiapine-ER group vs

30 mon adverse events with stepwise dosing were tremor (48%), pyrexia (44%), fatigue (26%), and edema (2

31 a genome-wide association study of essential tremor, a common movement disorder characterized mainly

32 Tremor accelerometry was shown to be coherent with the c

33 p brain stimulation to a particular phase of tremor afforded clinically significant tremor relief (up

34 of Parkinson's disease (PD) include resting tremor, akinesia, bradykinesia, and rigidity, and these

35 c neurons leads to early lethality, obesity, tremor, altered anxiety-like behaviors, and impaired aco

36 stion that blood lead may be associated with tremor among the younger men in our cohort.

37 n's disease cohort were associated with rest tremor amplitude (beta = -0.106, P < 0.05), rest tremor

38 cerebral activity associated with changes in tremor amplitude (using peripheral EMG measures as a pro

39 cerebral activity associated with changes in tremor amplitude drives network activity through the bas

40 and essential postural tremor severity (i.e. tremor amplitude) differed in their relative tolerance t

41 The relationship between the tremor amplitudes and plume height changes considerably

42 patients presented with isolated orthostatic tremor and 13.2% had additional neurological features.

43 lectrophysiological diagnosis of orthostatic tremor and a minimum follow-up of 5 years is presented.

44 are tremors generally present with an action tremor and a variable combination of postural and kineti

45 Moreover, severe motor impairment, resting tremor and abnormal gait and posture, phenotypes reminis

46 has to be balanced considering the increased tremor and adverse drug reactions.

47 Finally, the coincidence of tremor and coherence was significantly higher in tremor

48 , which can discriminate Parkinson's disease tremor and essential tremor with high diagnostic accurac

49 fication performance for Parkinson's disease tremor and essential tremor, in both test and validation

50 and ammonium ions, which could contribute to tremor and increase susceptibility to epilepsy, respecti

51 Earth tides modulate tremor and low-frequency earthquakes (LFEs) on faults in

52 y for movement disorders including essential tremor and Parkinson's disease.

53 examine the association between genotype and tremor and postural instability and gait difficulty (PIG

54 parkinsonian syndromes (PS), from essential tremor and probable dementia with Lewy bodies (DLB) from

55 r, peripheral trauma-induced tremor, tardive tremor and rabbit syndrome, paroxysmal tremors (heredita

56 1 in dopamine D1R-containing neurons exhibit tremor and rotational responses toward L-DOPA, but devel

57 , it permits the amplitudes of physiological tremor and stretch reflex to be decoupled.

58 owed signs of movement poverty and slowness, tremor and subtle cognitive deficits.

59 ransporter levels correlate with severity of tremor and symptoms of fatigue, depression, and sleep di

60 Parkinson's disease, essential and dystonic tremor and tremor related to multiple sclerosis (MS) and

61 nd dysmetric ataxia, truncal sway, intention tremors and absent menace responses, with positional hor

62 ene expression in oligodendrocytes developed tremors and ataxia and died before reaching maturity.

63 Here, we demonstrate that parkinsonian tremors and ETs result from distinct patterns of interac

64 layed severe neurological symptoms including tremors and hind-limb paralysis.

65 papillitis, inflammatory myelitis, postural tremor, and cerebellar ataxia.

66 ement disorders such as Parkinson's disease, tremor, and dystonia involves the placement of focal les

67 contrast, Nefl(N98S/+) mice had a noticeable tremor, and most animals showed a hindlimb clasping phen

68 ort an association between lead exposure and tremor, and suggest no association with cumulative lead

69 association between blood lead and essential tremor, and that this association is modified by polymor

70 d 20 postural tremor recordings in essential tremor, and validated on a second, independent cohort co

71 ts transient adverse effects include pallor, tremor, anxiety, and palpitations.

72 hysiological (as distinct from pathological) tremor are an unavoidable component of human motor contr

73 While the origins of physiological tremor are known to depend on muscle afferentation, it i

74 side effect rate of lesional treatments for tremor are presented separately alongside this article.

75 molecular genetic determinants of essential tremor are unknown.

76 e essential clinical features of orthostatic tremor are well established, little is known about the n

77 ts (FEMs; including microsaccades, drift and tremor) are thought to improve visibility during fixatio

78 other movement disorders, such as essential tremor, are relatively unexplored.

79 Modulation of physiological tremor as a function of muscle stretch differs from that

80 Here we measure hand tremor at different levels of gravitational field streng

81 g Olig2-Cre results in mice displaying rapid tremors at postnatal day 10, followed by death at postna

82 Fragile X-associated tremor ataxia syndrome (FXTAS) is a neurodegenerative di

83 sclerosis/frontotemporal dementia, fragile X tremor ataxia syndrome, myotonic dystrophy type 1, spino

84 ized by progressive development of intention tremor, ataxia, parkinsonism and neuropsychological prob

85 e development of hand stereotypies, anxiety, tremor, ataxia, respiratory dysrhythmias, and seizures.

86 taneous mouse mutation, nm2719, which causes tremors, ataxia, and loss of cerebellar Purkinje neurons

87 Fragile X-associated tremor/ataxia syndrome (FXTAS) is a late-onset neurodege

88 Fragile X-associated tremor/ataxia syndrome (FXTAS) is a late-onset neurodege

89 Fragile X-associated tremor/ataxia syndrome (FXTAS) is a neurodegenerative di

90 Fragile X-associated tremor/ataxia syndrome (FXTAS) is a neurological disorde

91 Fragile X-associated tremor/ataxia syndrome (FXTAS) is one such condition, re

92 In Fragile X-associated tremor/ataxia syndrome (FXTAS), a CGG repeat expansion i

93 FMR1 overexpression and Fragile X-associated tremor/ataxia syndrome (FXTAS), a late-onset neurodegene

94 rodegenerative disorder fragile X-associated tremor/ataxia syndrome (FXTAS), primary ovarian insuffic

95 common in patients with fragile X-associated tremor/ataxia syndrome (FXTAS), with no targeted treatme

96 ated region that causes fragile X-associated tremor/ataxia syndrome (FXTAS).

97 expanded CGG repeats in fragile X-associated tremor/ataxia syndrome is initiated at an upstream ACG n

98 CGG repeats that cause fragile X-associated tremor/ataxia syndrome, revealing similarities and diffe

99 The review includes fragile X-associated tremor/ataxia syndrome, spinocerebellar ataxia type 12,

100 sorders such as ALS and fragile X-associated tremor/ataxia syndrome.

101 CGG repeats that cause fragile X-associated tremor/ataxia syndrome.

102 creased incidence of low executive function, tremors, below-average IQ, and FXTAS.

103 yndrome, paroxysmal tremors (hereditary chin tremor, bilateral high-frequency synchronous discharges,

104 g inclusion criteria: the presence of a rest tremor, bradykinesia, and rigidity; a modified Hoehn and

105 (DBS) in motor thalamus (Mthal) ameliorates tremor but not akinesia in Parkinson's disease.

106 y is associated with the severity of resting tremor but not non-motor symptoms.

107 ed ultrasound (FUS) thalamotomy in essential tremor, but its effectiveness and safety for managing tr

108 trated improvements in medication-refractory tremor by CRST assessments, even in the setting of a pla

109 Quantification of physiological tremor by manipulation of joint angle may be a useful ex

110 ance characterizes the temporal evolution of tremor by quantifying the range of frequencies over whic

111 tolerances predicted stronger entrainment of tremor by stimulation, providing good evidence that the

112 ion was observed between experience and anti-tremor - C2 (rho = 0.026), P3 (rho = 0.015), P4 (rho = 0

113 Lastly, it suggests that physiological tremor can be used as a simple, non-invasive measure of

114 jects with Parkinson's disease and essential tremor can produce movements that are kinematically simi

115 nything, the peak frequency of physiological tremor can reveal about the operation of the nervous sys

116 g post-mortem cerebellar tissue of essential tremor cases and controls.

117 ia syndrome, spinocerebellar ataxia type 12, tremors caused by autosomal recessive cerebellar ataxias

118 scular atrophy, progressive gait ataxia with tremor, cerebellar vermis atrophy, and optic-nerve thinn

119 movement disorders (parkinsonism, dystonia, tremor, chorea, and restless legs syndrome) were include

120 n activation within established nodes of the tremor circuit: sensorimotor cortex, thalamus, contralat

121 or and coherence was significantly higher in tremor clusters.

122 or amplitude (beta = -0.106, P < 0.05), rest tremor constancy (beta = -0.109, P < 0.05), and index of

123 r availability was also associated with rest tremor constancy (beta = -0.380, P < 0.05) and index of

124 subscore from the Clinical Rating Scale for Tremor (CRST).

125 These patterns are reflected in the tremors' derived frequency tolerance, a novel measure re

126 ression) in selected patients with essential tremor despite delivering less than half the energy of c

127 ng multiple sclerosis tremor or other severe tremor disorders.

128 ced differences in neural activation between tremor dominant (TD) and postural instability/gait diffi

129 We classified 235 subjects by motor subtype: tremor dominant (TD), intermediate (I), or postural inst

130 tudinally, EDS in PD was associated with non-tremor dominant phenotype, autonomic dysfunction, depres

131 ut its effectiveness and safety for managing tremor-dominant Parkinson disease (TDPD) is unknown.

132 ication design on two independent cohorts of tremor-dominant Parkinson patients sampled brain activit

133 hort comprising 16 rest tremor recordings in tremor-dominant Parkinson's disease and 20 postural trem

134 ventional and incisionless interventions for tremor due to Parkinson's disease, essential and dystoni

135 We measured physiological tremor during tonic, isometric plantarflexion torque at

136 Pathologies such as Parkinson's disease and tremor emerge when brain regions controlling movement ca

137 rrower frequency-amplitude tolerance so that tremor entrainment through extrinsic driving is necessar

138 in which transient activity at the onset of tremor episodes (assessed using EMG) drove network activ

139 tested: (1) whether activity at the onset of tremor episodes drives tremulous network activity throug

140 rgery, compared with patients with essential tremor (ET) and isolated dystonia (ID).

141 Parkinson's disease (PD) and essential tremor (ET) are the two most common movement disorders.

142 Essential tremor (ET) is a common movement disorder with an estima

143 Essential tremor (ET) is one of the most prevalent movement disord

144 Essential tremor (ET) is the most prevalent movement disorder, aff

145 Essential tremor (ET), a movement disorder characterised by an unc

146 The pathophysiology of essential tremor (ET), the most common movement disorder, is not f

147 matter microstructural changes in essential tremor (ET).

148 efficacy in treating patients with essential tremor (ET).

149 hat cerebral activity related to Parkinson's tremor first arises in the GPi and is then propagated to

150 f the ET network support oscillations at the tremor frequency and the application of a DBS-like input

151 rce upon hand acceleration, we conclude that tremor frequency can be almost completely explained by a

152 disorder with increased disability although tremor frequency is unchanged over time.

153 There was no change in orthostatic tremor frequency over time.

154 A reduction in tremor frequency produced by adding an inertial mass to

155 k exhibited oscillatory behaviour within the tremor frequency range, as did our electrophysiological

156 relative tolerance to spontaneous changes in tremor frequency when stimulation was not applied.

157 r than resonance are involved in determining tremor frequency.

158 t is imperative to distinguish physiological tremor from pathological tremor types.

159 Rare tremors generally present with an action tremor and a va

160 Yet, the mechanisms underlying tremor generation remain largely unknown.

161 l input and spinal afferents is relevant for tremor generation.

162 Physiological hand tremor has a clear peak between 6 and 12 Hz, which has b

163 frequency thalamic stimulation in essential tremor has a narrower frequency-amplitude tolerance so t

164 Human physiological hand tremor has a resonant component.

165 Parkinson's resting tremor has been linked to pathophysiological changes bot

166 rdive tremor and rabbit syndrome, paroxysmal tremors (hereditary chin tremor, bilateral high-frequenc

167 not suggest dystonic tremor or indeterminate tremor in any of them.

168 he prevalence and the clinical correlates of tremor in patients with adult-onset primary dystonia.

169 bal p11 knockout (KO) mice develop fewer jaw tremors in response to tacrine.

170 for Parkinson's disease tremor and essential tremor, in both test and validation datasets.

171 to examine the relationship between lead and tremor, including modification by ALAD, in a prospective

172 The amplitude of physiological tremor increased as calf muscles shortened in contrast t

173 se younger than the median age (68.9 years), tremor increased significantly with blood lead (p = 0.03

174 , plantarflexion contractions, physiological tremor increases as the ankle joint becomes plantarflexe

175 d 5.0 mg/kg) attenuated the increase in oral tremor induced by coadministration of TBZ (0.75 mg/kg) w

176 nt, Ia afferents provided significant common tremor input due to passive stretch.

177 They also indicated that the common tremor input is always shared by the antagonistic motone

178 In addition, when the supraspinal tremor input to one muscle was weak or absent, Ia affere

179 by the relative strength of the supraspinal tremor input to the motoneuron pools.

180 e spastic ataxia with frequent occurrence of tremor, involvement of the central sensory tracts and de

181 vealed that the peak frequency of human hand tremor is 99% predictable on the basis of a resonant mec

182 Here we show that tremor is a common feature of patients with adult-onset

183 Tremor is a common neurological condition in clinical pr

184 Orthostatic tremor is a progressive disorder with increased disabili

185 Orthostatic tremor is a rare condition characterised by high-frequen

186 neuronal oscillators on human physiological tremor is controversial.

187 Tremor is one of the most common neurological signs, yet

188 Dystonic tremor is presumably under-reported, and we aimed to ass

189 Since treatment of tremors is disease specific, accurate and early diagnosi

190 ients who initially had isolated orthostatic tremor later developed further neurological signs.

191 postural and kinetic components with resting tremors less frequently seen.

192 gest that thalamic deep brain stimulation in tremor likely exerts its effects through modulation of b

193 high-frequency synchronous discharges, head tremor, limb-shaking transient ischaemic attack), bobble

194 d early diagnosis plays an important role in tremor management.

195 Amplitude of physiological tremor may be altered as a function of reflex pathway ga

196 ying the range of frequencies over which the tremor may be considered stable.

197 nson's disease, but also occurs in essential tremor, most prominently for the coupling of alpha to ga

198 Parkinson's disease (n = 11), with essential tremor (n = 9) and without a movement disorder (n = 6).

199 e resonant characteristics of the underlying tremor network.

200 he different manifestations of physiological tremor of the hand-kinetic and postural tremor.

201 aracterized mainly by a postural and kinetic tremor of the upper extremities.

202 rse effects, including a Parkinson-like hand tremor, often limit its use.

203 investigated the dependence of physiological tremor on muscle length in healthy individuals.

204 and social abnormalities but did not rescue tremor or anxiety.

205 probably been cases of indeterminate senile tremor or dystonic tremor.

206 case note analysis did not suggest dystonic tremor or indeterminate tremor in any of them.

207 and effective in treating multiple sclerosis tremor or other severe tremor disorders.

208 tom cluster including memory loss and finger tremor (OR 14, 95% CI: 3.5, 57).

209 d to akinetic-rigid patients with no resting tremor (P < 0.05).

210 e tremor, Wilson's disease, slow orthostatic tremor, peripheral trauma-induced tremor, tardive tremor

211 s with Parkinson disease, RBD predicts a non-tremor-predominant subtype, gait freezing, and an aggres

212 al diagnosis of PS, non-PS (mainly essential tremor), probable DLB, and non-DLB (mainly Alzheimer dis

213 Tremor rates and adverse drug reactions favoured the pla

214 t of their tremor with the Tolosa-Fahn-Marin Tremor Rating Scale (TRS) during optimised VIM or VO lea

215 One hundred seconds of tremor recording were selected for analysis in each pati

216 dominant Parkinson's disease and 20 postural tremor recordings in essential tremor, and validated on

217 assessed in a test cohort comprising 16 rest tremor recordings in tremor-dominant Parkinson's disease

218 rt, cheap, widely available and non-invasive tremor recordings, and is independent of operator or pos

219 tremulous Parkinson's disease and essential tremor recordings.

220 h a clinical diagnosis of multiple sclerosis tremor refractory to previous medical therapy.

221 s disease, essential and dystonic tremor and tremor related to multiple sclerosis (MS) and midbrain l

222 Out findings suggest that Parkinson's tremor-related activity first arises in the basal gangli

223 using peripheral EMG measures as a proxy for tremor-related neuronal activity) drove network activity

224 bello-thalamo-cortical loop is driven into a tremor-related state by virtue of its connectivity with

225 se of tremor afforded clinically significant tremor relief (up to 87% tremor suppression) in selected

226 those circuits in initiating and maintaining tremor remains unclear.

227 In most cases, orthostatic tremor represents an isolated syndrome.

228 Observations and models of slow slip and tremor require the presence of near-lithostatic pore-flu

229 l thalamus, timed according to the patient's tremor rhythm.

230 Changes in tremor, rigidity, akinesia, and gait scores were also as

231 ns that control motor function, resulting in tremor, rigidity, and gait abnormalities.

232 r early symptoms, comprising motor features (tremor, rigidity, balance impairments, neck pain or stif

233 prediagnostic motor (hypo- and bradykinesia, tremor, rigidity, postural imbalance, postural abnormali

234 s disease (n=4769) had a higher incidence of tremor (RR 13.70, 95% CI 7.82-24.31), balance impairment

235 sis of Parkinson's disease, the incidence of tremor (RR 7.59, 95% CI 1.11-44.83) and constipation (2.

236 association between bone lead and change in tremor score over time.

237 A tremor score was created based on an approach using hand

238 the associations between lead biomarkers and tremor score.

239 between quintiles of all lead biomarkers and tremor scores (p-values < 0.13), which did not persist i

240 On-medication median tremor scores improved 62% (IQR, 22%-79%) from a baselin

241 aster progression in PIGD scores, but not in tremor scores.

242 mf11, which causes reduced body size, evoked tremor, seizures, muscle stiffness, and morbidity by pos

243 (beta = -0.109, P < 0.05), and index of rest tremor severity (beta = -0.104, P < 0.05).

244 (beta = -0.380, P < 0.05) and index of rest tremor severity (beta = -0.322, P < 0.05).

245 Parkinsonian rest and essential postural tremor severity (i.e. tremor amplitude) differed in thei

246 plasma concentrations as well as effects on tremor severity across the 5 dose levels.

247 VOP/ZI DBS produced a mean reduction in tremor severity of 80.75% based on Bain's tremor severit

248 in tremor severity of 80.75% based on Bain's tremor severity scale, with significant reductions in al

249 y underwent blinded assessments using Bain's tremor severity scale.

250 p phenomena, including recent discoveries of tremor, slow-slip and low-frequency earthquakes, are les

251 adults have varying degrees of physiological tremor so it is imperative to distinguish physiological

252 tionship at Pavlof arose from changes in the tremor source related to volcanic vent erosion.

253 ere encephalopathy and aphasia (each 9%) and tremor, speech disorder, dizziness, somnolence, and diso

254 The tremor stability index can aid in the differential diagn

255 The tremor stability index is derived from kinematic measure

256 Tremor stability index maximum sensitivity, specificity

257 Tremor stability index with a cut-off of 1.05 gave good

258 a robust new neurophysiological measure, the tremor stability index, which can discriminate Parkinson

259 Examination revealed a bilateral jerky tremor, stimulus-sensitive myoclonus, and difficulty wit

260 t 3 months in the on-medication treated hand tremor subscore from the Clinical Rating Scale for Tremo

261 significant reductions in all five component tremor subscores: rest, postural, kinetic, proximal and

262 nce as evinced by bradykinesia, rigidity and tremor, suggesting that network function might actually

263 nically significant tremor relief (up to 87% tremor suppression) in selected patients with essential

264 ght to be the active substance that mediates tremor suppression.

265 f patients reported worsening of orthostatic tremor symptoms.

266 fy the available literature for each unusual tremor syndrome.

267 recognition and treatment of various unusual tremor syndromes in the adult and paediatric populations

268 ommentary on this article.Misdiagnosis among tremor syndromes is common, and can impact on both clini

269 rthostatic tremor, peripheral trauma-induced tremor, tardive tremor and rabbit syndrome, paroxysmal t

270 jects with Parkinson's disease and essential tremor than in subjects without a movement disorder.

271 re condition characterised by high-frequency tremor that appears on standing.

272 ed the early-onset twisting, stiff limbs and tremor that is observed in dystonia, a debilitating move

273 ivated in developing Schwann cells displayed tremor that progressed to hindlimb paralysis, which corr

274 The eruption generated strong tremor that was recorded by seismic and remote low-frequ

275 edicted that without a voluntary drive (rest tremor) the neural drives would be more likely in phase,

276 , and 10.0 mg/kg) increased TBZ-induced oral tremor (tremulous jaw movements), and decreased locomoto

277 guish physiological tremor from pathological tremor types.

278 ifferential diagnosis of the two most common tremor types.

279 s intermedius thalamic nucleus for essential tremor underwent functional magnetic resonance imaging d

280 Furthermore, patients exhibit resting tremor, unstable gait, and impaired balance, which may b

281 treatments of refractory multiple sclerosis tremor using lesioning or deep brain stimulation (DBS) h

282 Tremor was assessed using accelerometry, digital spiral

283 Tremor was associated with higher tracer binding in the

284 Essential tremor was present in persons either heterozygous or hom

285 Furthermore, tremor was selectively entrained by transcranial alterna

286 atients with medication-refractory essential tremor were enrolled in a HIPAA-compliant pilot study an

287 yrexia, nasopharyngitis, sleep disorder, and tremor were the most frequent adverse events in patients

288 of eight consecutive patients with post-ABI tremor were treated with DBS of the ventro-oralis poster

289 story of jerks when brushing her teeth and a tremor when carrying drinks.

290 y of SCN4A with the development of essential tremor, which adds ET to the growing list of neurologica

291 to the occurrence of non-motor symptoms and tremor, which are only partially explained by dopamine l

292 em in rodents, in which STOs were related to tremor, whisking, and licking, fueled a debate over whet

293 bellar ataxias, myorhythmia, isolated tongue tremor, Wilson's disease, slow orthostatic tremor, perip

294 arkinson patients sampled brain activity and tremor with concurrent EMG-fMRI.

295 ate Parkinson's disease tremor and essential tremor with high diagnostic accuracy.

296 drive to produce increases in physiological tremor with muscle shortening - while successfully repli

297 llowed by blinded safety assessment of their tremor with the Tolosa-Fahn-Marin Tremor Rating Scale (T

298 remarkable increase in research on essential tremor, with consequent advances in our understanding of

299 ctivity in Parkinson's disease and essential tremor, with the greatest high-beta desynchronization oc

300 while a concurrent voluntary input (postural tremor) would lead more frequently to an out-of-phase pa