ライフサイエンスコーパス: tremor

1 es of deep brain stimulation (DBS; essential tremor).

2 modality that can be used to treat essential tremor.

3 thin the tremor physiologic range may worsen tremor.

4 that relate to clinical features of dystonic tremor.

5 thy invariably associated with a distinctive tremor.

6 patients with dystonic tremor and essential tremor.

7 neurosurgery for treatment of drug-resistant tremor.

8 r and the majority had additional upper-limb tremor.

9 t unerupted, teeth; and cerebellar intention tremor.

10 roving severe, refractory multiple sclerosis tremor.

11 the lithium group tended to experience more tremor.

12 is anterior muscle and the onset of hindlimb tremor.

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

14 surgery has been applied in the treatment of tremor.

15 the treatment of patients with pathological tremor.

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

17 copies of the LINGO1 gene also present with tremor.

18 stic biomarkers for functional myoclonus and tremor.

19 nuclei was sufficient to generate an action tremor.

20 around 10 Hz, thereby reducing physiological tremor.

21 ent problems such as rigidity, slowness, and tremor.

22 radykinesia (slowed movement), rigidity, and tremors.

23 s were encephalopathy (57%), headache (42%), tremor (38%), aphasia (35%) and focal weakness (11%).

24 arkinson disease) = 303; n(dystonia) = 64; n(tremor) = 39; n(treatment-resistant depression/anorexia

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

26 weakness, followed by the emergence of hand tremor, a prodromal sign of the disease.

27 neuromuscular reflex-related phenotype (e.g. tremors accompanied by clonus) of Amish nemaline myopath

28 de muscle weakness, atrophy, contracture and tremors accompanied by clonus.

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

30 Tremor alleviation was related to connections with the i

31 Finally, we manipulated tremor amplitude by switching DBS ON and OFF to examine

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

33 was performed in 1 patient, and quantitative tremor analysis was carried out in 2 patients.

34 cell connectivity as a neural substrate for tremor and a gateway for signals that mediate the diseas

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

36 ant clinical presentation, e.g. paralysis or tremor and additional symptomatology such as cognitive s

37 patients produced exacerbation of grip-force tremor and associated changes in functional activation.

38 the effect of visual feedback on grip-force tremor and associated functional network-level activatio

39 portant problem in neurology, distinguishing tremor and ataxia using quantitative methods.

40 rat model of Purkinje cell loss resulting in tremor and ataxia.

41 ntial (VsEP) responses to jerk stimuli, head tremor and deficits in balance beam tests that are consi

42 dard of care in Parkinson disease, essential tremor and dystonia, and is also under active investigat

43 tosomal dominant familial cortical myoclonic tremor and epilepsy (FCMTE), a syndrome not yet official

44 that differs substantially between dystonic tremor and essential tremor and should be further explor

45 remor during the grip-force task in dystonic tremor and essential tremor cohorts.

46 functional connectivity networks in dystonic tremor and essential tremor groups relative to controls.

47 activation and connectivity between dystonic tremor and essential tremor patient cohorts to better un

48 Patients with dystonic tremor and essential tremor were characterized by distin

49 vity z-scores were able to classify dystonic tremor and essential tremor with 89% area under the curv

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

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

52 n and connectivity in patients with dystonic tremor and essential tremor.

53 y body disease; resting tremor, pill-rolling tremor and hallucinations were more frequent in Lewy bod

54 s show abnormal gait and locomotor activity, tremor and memory deficits, but human disorders related

55 -activated K(+) (BK) channels also result in tremor and motor disorders.

56 and crying, jerky myoclonic postural/action tremor and polyminimyoclonus) and seven disability miles

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

58 stonic tremor can resemble that of essential tremor and present a diagnostic confound for clinicians.

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

60 ts in WT alphaS mice and the PD-like resting tremor and progressive motor decline of 3K alphaS mice.

61 Tremor and quality of life were assessed before, 1 month

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

63 tially between dystonic tremor and essential tremor and should be further explored in implementing ap

64 cluding seizures, encephalopathy, myoclonus, tremor and spasticity, with immunotherapy responsiveness

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

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

67 ervical dystonia patients with dystonic head tremor and the majority had additional upper-limb tremor

68 It is currently FDA approved for essential tremor and tremor dominant Parkinson's disease.

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

70 le and female subjects affected by essential tremor and undergoing deep brain stimulation surgery, ve

71 The evidence of these tremors and electrical conductivity anomalies along the

72 ased on limb-specific paresis and paralysis, tremors and seizures, and other clinical signs, along wi

73 Rigidity, tremor, and dysarthric side effects seem to be influence

74 rs off ("off periods"), medication-resistant tremor, and dyskinesias, benefit from advanced treatment

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

76 people worldwide, leading to incoordination, tremor, and falls.

77 tion effectiveness in reducing bradykinesia, tremor, and rigidity was evaluated for each electrode co

78 headache, decreased level of consciousness, tremor, and seizures were most commonly observed.

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

80 f the tremor, which we classify as "myogenic tremor." ANN NEUROL 2019.

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

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

83 Lesions causing Holmes tremor are part of a single connected brain circuit that

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

85 t expert consensus labelled the incidence of tremor as a core feature of dystonia that can affect bod

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

87 analysis of the mechanisms defining cortical tremor, as seen in FCMTE.

88 of these currents and may contribute to the tremor associated with increased LINGO1 levels.

89 ive diseases, including fragile X-associated tremor ataxia syndrome (FXTAS), ALS, and frontotemporal

90 roughput small-molecule screen for fragile X tremor ataxia syndrome.

91 Fragile X associated tremor/ataxia syndrome (FXTAS) is a late adult-onset neu

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

93 Fragile X-associated Tremor/Ataxia Syndrome (FXTAS) is a neurodegenerative di

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

95 Fragile X-associated tremor/ataxia syndrome (FXTAS) is an adult-onset neurode

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

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

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

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

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

101 to neurodegeneration in fragile X-associated tremor/ataxia syndrome.

102 been hypothesized as the prime generator of tremor because of the pacemaker properties of ION neuron

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

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

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

106 cleus neurons, which might produce an action tremor by causing signal oscillations during movement.

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

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

109 atible with a role in reducing physiological tremor by suppressing oscillations around 10 Hz.

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

111 Lesions causing Holmes tremor can occur in multiple different brain locations,

112 the same time, clinical features of dystonic tremor can resemble that of essential tremor and present

113 Case reports of Holmes tremor caused by focal brain lesions were identified thr

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

115 is consistent with observations of thalamic tremor cells in ET patients.

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

117 This Holmes tremor circuit was then compared to neurosurgical treatm

118 subthalamic nucleus fell outside our Holmes tremor circuit, whereas the globus pallidus target was c

119 inical features included progressive ataxia, tremor, cognitive decline, dysphagia, optic atrophy, dys

120 -force task in dystonic tremor and essential tremor cohorts.

121 tatement of the Movement Disorder Society on tremor coined a new term: essential tremor-plus (ET-plus

122 ly anterolaterally, to fibers beneficial for tremor control as published by Al-Fatly et al in 2019.

123 ve programming strategies to achieve optimal tremor control without speech impairment in essential tr

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

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

126 ale fault marked by clusters of non-volcanic tremors directly beneath the southern Central Range.

127 Essential tremor (ET) is the most common tremor disorder globally and is characterized by kinetic

128 sm that may underlie the prevalent essential tremor disorder.

129 e nucleus of the thalamus is a treatment for tremor disorders.

130 ng multiple sclerosis tremor or other severe tremor disorders.

131 understanding of ET and other cerebellar and tremor disorders.

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

133 rently FDA approved for essential tremor and tremor dominant Parkinson's disease.

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

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

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

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

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

139 We quantified tremor during postural tasks using accelerometry and dys

140 visual feedback similarly exacerbated force tremor during the grip-force task in dystonic tremor and

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

142 ulate the progressive motor dysfunction with tremor, dystonia and ataxia seen in H-ABC.

143 inetic movement disorders, namely, essential tremor, dystonia, Huntington disease and other chorea sy

144 tions such as Parkinson's disease, essential tremor, dystonia, obsessive-compulsive disorder, and epi

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

146 Essential tremor (ET) is among the most prevalent movement disorde

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

148 Essential tremor (ET) is the most common tremor disorder globally

149 ials and Methods Participants with essential tremor (ET) or Parkinson disease (PD) undergoing thalamo

150 reened 662 subjects comprising 462 essential tremor (ET) subjects (285 sporadic, 125 with family hist

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

152 In addition to redefining essential tremor (ET), the 2018 consensus statement of the Movemen

153 including Parkinson's disease and essential tremor (ET).

154 matter microstructural changes in essential tremor (ET).

155 nal sign of ataxia, from tremor in essential tremor (ET).

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

157 with Parkinson's disease (PD) and Essential Tremor (ET).

158 uding Parkinson's Disease (PD) and Essential Tremor (ET).

159 The clinical tremor features observed in all mutation carriers, toget

160 analyses such data to simultaneously predict tremor, fine-motor impairment and PD.

161 ortical myoclonus spectrum, and how cortical tremor fits into it.

162 Second, even for trials with tremor-free trajectories to the target, ET exhibited gre

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

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

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

166 facilitate sustained oscillatory activity at tremor frequency throughout the network as well as a rob

167 These results suggest a mechanism for tremor generation under cerebellar dysfunction, which ma

168 ge cycling as the first muscle-based step in tremor genesis.

169 cts were far more widespread in the dystonic tremor group as changes in functional connectivity were

170 The dystonic tremor group included primarily cervical dystonia patien

171 ty networks in dystonic tremor and essential tremor groups relative to controls.

172 s, such as Parkinson's disease and essential tremor, has encouraged its application to a wide range o

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

174 This is consistent with deep, non-volcanic tremors identified in the same area.

175 n motor thalamus FA 1 day after ablation and tremor improvement (ET: R = -0.52 [P = .03]; PD: R = -0.

176 e dysmetria, a cardinal sign of ataxia, from tremor in essential tremor (ET).

177 t we can quantify dysmetria independently of tremor in ET.

178 cell output in the cerebellar nuclei reduced tremor in freely moving mice.

179 cing cerebellar Purkinje cell output blocked tremor in mice that were given the tremorgenic drug harm

180 ould identify and distinguish dysmetria from tremor in non-DBS ET.

181 ned Purkinje cell activity drives a powerful tremor in otherwise normal mice.

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

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

184 A unique pattern for dystonic tremor included widespread reductions in functional conn

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

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

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

188 Essential tremor is a common brain disorder affecting millions of

189 Tremor is a common neurological condition in clinical pr

190 Holmes tremor is a debilitating movement disorder with limited

191 Cortical tremor is a fine rhythmic oscillation involving distal u

192 how in awake behaving mice that the onset of tremor is coincident with rhythmic Purkinje cell firing,

193 Cortical tremor is considered a rhythmic variant of cortical myoc

194 Tremor is currently ranked as the most common movement d

195 Such tremor is especially problematic for dexterous hand move

196 Cortical tremor is the hallmark feature of autosomal dominant fam

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

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

199 ily for the treatment of migraine and action tremor (mainly essential tremor), worldwide.

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

201 t whether lesion locations that cause Holmes tremor map to a connected brain circuit and whether this

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

203 the traditional harmaline-induced essential tremor model.

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

205 e resonant characteristics of the underlying tremor network.

206 ctoriness to intravenous immunoglobulin, and tremor of possible cerebellar origin.

207 der globally and is characterized by kinetic tremor of the upper limbs, although other clinical featu

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

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

210 onvert to NIID up to 4 decades after initial tremor onset.

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

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

213 radykinesia differed from that for rigidity, tremor, or dysarthria.

214 Using a promising animal model for action tremor, our results thus characterized a synaptic circui

215 Third, activating DBS reduced tremor (p < 0.01) but had no effect on dysmetria (p > 0.

216 tivity between dystonic tremor and essential tremor patient cohorts to better understand disease-spec

217 his study demonstrates that SID in essential tremor patients is associated with both motor cortex and

218 Prior work using this paradigm in essential tremor patients produced exacerbation of grip-force trem

219 ed worsening of intelligibility in essential tremor patients with bilateral thalamic deep brain stimu

220 ntrol without speech impairment in essential tremor patients with thalamic DBS.

221 ome resembling the core symptom of essential tremor patients.

222 reased burst durations relative to essential tremor patients.

223 polar reviews were conducted in 14 essential tremor patients.

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

225 itional central loop modulating the clinical tremor phenomenology.

226 own to segregate perfectly with the myopathy/tremor phenotype in the respective families.

227 n cerebellar nuclei, which also reversed the tremor phenotype in the traditional harmaline-induced es

228 J-background, Lyst-mutant mice exhibit overt tremor phenotypes associated with loss of cerebellar Pur

229 Pathological Hand Tremor (PHT), which is considered among the most common

230 d incoordination, and frequencies within the tremor physiologic range may worsen tremor.

231 in all mutation carriers, together with the tremor physiology studies performed in family 2, suggest

232 han patients with Lewy body disease; resting tremor, pill-rolling tremor and hallucinations were more

233 ciety on tremor coined a new term: essential tremor-plus (ET-plus).

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

235 than HC and dysmetria did not correlate with tremor (R(2) < 0.01).

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

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

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

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

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

241 tremulous Parkinson's disease and essential tremor recordings.

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

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

244 alamic high-frequency stimulation suppressed tremor-related activity in thalamus but increased the os

245 Tremor-related oscillations initiated in small neural po

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

247 Better tremor relief in ET was associated with lower fractional

248 ability-gait impairment and with predominant tremor revealed asymmetries for step length in both coho

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

250 omatic, focused on improvement in motor (eg, tremor, rigidity, bradykinesia) and nonmotor (eg, consti

251 ion typically demonstrates bradykinesia with tremor, rigidity, or both.

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

253 nce problems (RR, 8.9; 95% CI, 2.3 to 34.8); tremors (RR, 7.5; 95% CI, 1.9 to 29.9); weakness in legs

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

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

256 recurrent inhibition may function to reduce tremor.SIGNIFICANCE STATEMENT We present the first direc

257 ore motor features of the disease, including tremor, slowing of movement (bradykinesia), and rigidity

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

259 The tremor stability index can aid in the differential diagn

260 The tremor stability index is derived from kinematic measure

261 Tremor stability index maximum sensitivity, specificity

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

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

264 on), characteristic movement difficulty (eg, tremor, stiffness, slowness), and psychological or cogni

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

266 rage research into the creation of essential tremor subsets that are defined with respect to differen

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

268 parvalbumin neurons in mice caused an action tremor syndrome resembling the core symptom of essential

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

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

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

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

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

274 ifferential diagnosis of the two most common tremor types.

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

276 dysmetria can be quantified independently of tremor using fast, reverse-at-target goal-directed movem

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

278 FAME) is characterised by cortical myoclonic tremor usually from the second decade of life and overt

279 Tremor was associated with higher tracer binding in the

280 The tremor was rescued by completely blocking synaptic trans

281 ure that endpoint accuracy was unaffected by tremor, we quantified dysmetria in selected trials manif

282 data acquired during treatments of essential tremor, we verified that our simulation framework can be

283 Patients with dystonic tremor and essential tremor were characterized by distinct functional activat

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

285 is often associated with non-specific action tremor, which is usually treated with propranolol.

286 stent with a unique sarcomeric origin of the tremor, which we classify as "myogenic tremor." ANN NEUR

287 We identified 36 lesions causing Holmes tremor, which were scattered across multiple different b

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

289 le to classify dystonic tremor and essential tremor with 89% area under the curve, whereas combining

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

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

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

293 This term is uncertainly defined as tremor with the characteristics of ET, with additional n

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

295 unctional connectivity compared to essential tremor within higher-level cortical, basal ganglia, and

296 migraine and action tremor (mainly essential tremor), worldwide.

297 commonly used for parkinsonism and essential tremor, worsened incoordination, and frequencies within

298 n help individuals with medication-resistant tremor, worsening symptoms when the medication wears off

299 It remains unclear, though, how tremor would relate to a dysfunction of cerebellar conne

300 combining functional connectivity with force tremor yielded 94%.