ライフサイエンスコーパス: movement disorder

1 udies had motor symptoms (either weakness or movement disorder).

2 ENT Dystonia is a common and often disabling movement disorder.

3 ion and a treatment-resistant choreoathetoid movement disorder.

4 epilepsy, intellectual disability (ID), and movement disorder.

5 pain in conjunction with bloating and bowel movement disorder.

6 dominant manner to onset of a characteristic movement disorder.

7 cognitive function in addition to causing a movement disorder.

8 s disease (PD), the most common degenerative movement disorder.

9 essential tremor than in subjects without a movement disorder.

10 's disease is a debilitating, age-associated movement disorder.

11 se (PD), the most frequent neurodegenerative movement disorder.

12 se (PD) is the most common neurodegenerative movement disorder.

13 remor is currently ranked as the most common movement disorder.

14 rom the phenomenological presentation with a movement disorder.

15 lly variable form of pediatric-onset spastic movement disorder.

16 (often with regression), and a hyperkinetic movement disorder.

17 etic protoporphyria, and a neurodegenerative movement disorder.

18 when prescribing medications that can induce movement disorders.

19 ing number of medications can induce various movement disorders.

20 importance of the ERK/MAPK pathway in human movement disorders.

21 tual disability, postnatal microcephaly, and movement disorders.

22 sed to alleviate the symptoms of a number of movement disorders.

23 drug abuse, as well as neuropsychiatric and movement disorders.

24 data needed to understand human movement and movement disorders.

25 new therapeutic strategies for certain human movement disorders.

26 how disturbances in neural activity produce movement disorders.

27 ial tremor (ET) is one of the most prevalent movement disorders.

28 s are very efficient to control epilepsy and movement disorders.

29 lia and cerebellum in the pathophysiology of movement disorders.

30 contribute to both epilepsy and hyperkinetic movement disorders.

31 treatments for chorea and other hyperkinetic movement disorders.

32 ity can contribute to the pathophysiology of movement disorders.

33 buting to the development and progression of movement disorders.

34 ncluding varying therapeutic efficacy across movement disorders.

35 resenting a target for clinical treatment of movement disorders.

36 henotype detection in experimental models of movement disorders.

37 the pathophysiology of basal-ganglia-related movement disorders.

38 these changes in patients with hyperkinetic movement disorders.

39 ssential tremor (ET) are the two most common movement disorders.

40 type-genotype overlap among these paroxysmal movement disorders.

41 for many patients with advanced PD and other movement disorders.

42 tter can also cause psychiatric symptoms and movement disorders.

43 graines and a variety of ocular motility and movement disorders.

44 , autism, depression, anxiety, addiction and movement disorders.

45 ment is impaired in patients with functional movement disorders.

46 se and essential tremor, the two most common movement disorders.

47 ed to model sensory processing in functional movement disorders.

48 nforming therapeutic approaches for treating movement disorders.

49 outcomes for many patients with drug-induced movement disorders.

50 ements and is a primary site of pathology in movement disorders.

51 cause epilepsy, intellectual disability, and movement disorders.

52 deficits, often accompanied by exotropia and movement disorders.

53 Two adults had encephalopathy with movement disorder, 1 had encephalitis, and 1 had Guillai

54 n 30 patients with GLUT1-DS with predominant movement disorders, 18 patients with movement disorders

55 Thirty-one studies treated movement disorders, 22 treated disorders of consciousnes

56 exercise intolerance (25%) and hyperkinetic movement disorders (41%), including dystonia and myoclon

57 77.4%-95.0%, respectively) and subjects with movement disorders (67.0%-97.9% and 71.4%-98.4%, respect

58 In patients with paroxysmal movement disorders 68 families had mutations (47%) out o

59 Twelve children had encephalopathy (1 with movement disorder), 8 had encephalitis, and 1 had mening

60 haracteristic of the G1D syndrome, including movement disorders, absence epilepsy (typical and atypic

61 the literature to delineate the spectrum of movement disorder aetiologies associated with SIBs.

62 ease (PD) is a progressive neurodegenerative movement disorder affecting over 10 million people world

63 se (PD) is the most common neurodegenerative movement disorder, affecting 1% of the population over 6

64 Essential tremor (ET) is the most prevalent movement disorder, affecting millions of people in the U

65 rt, is often professed to be the most common movement disorder, affecting up to one percent of adults

66 Cranial movement disorders--affecting the eyes, face, jaw, tongu

67 r understanding of the mechanisms underlying movement disorders allows improved diagnostic and treatm

68 Patients with functional movement disorders also had significantly slower respons

69 he parasite-brain interactions and epilepsy, movement disorders, Alzheimer's disease, and cancer.

70 syndrome, was the most common extrapyramidal movement disorder among pediatric patients with mitochon

71 analyzed a cohort of patients with atypical movement disorder and identified 2 DAT coding variants,

72 s the most common cause of neurodegenerative movement disorder and the second most common cause of de

73 mination task in 36 patients with functional movement disorders and 36 control subjects.

74 neurologic disorders, most often related to movement disorders and disorders of consciousness.

75 of tailored approaches to the management of movement disorders and enable the optimization of precli

76 The etiology of many severe childhood movement disorders and epilepsies remains uncharacterize

77 n (DBS) is an effective treatment for common movement disorders and has been used to modulate neural

78 Both patients with eye movement disorders and healthy participants whose oculom

79 rofile of lumateperone with reduced risk for movement disorders and hyperprolactinemia.

80 ry queues or reduce symptoms associated with movement disorders and increasingly for psychological an

81 been shown to be an effective treatment for movement disorders and it is now being extended to the t

82 rial at the University of Florida Center for Movement Disorders and Neurorestoration clinic (Gainesvi

83 egions of the brain, resulting in paroxysmal movement disorders and seizure phenotypes.

84 progressive neurological symptoms, including movement disorders and spasticity.

85 plete knowledge about the pathophysiology of movement disorders and their influence on normal motor d

86 hich is a necessary first step to understand movement disorders and to create patient-specific surgic

87 dominated by dementia, psychiatric changes, movement disorders and upper motor neuron signs.

88 dy, study participants were identified at 33 movement-disorder and neuropaediatric specialty centres

89 ding central visual impairment, hyperkinetic movement disorder, and epilepsy or electroencephalograph

90 sease (PD) is the most prevalent hypokinetic movement disorder, and symptomatic PD pathogenesis has b

91 STN effectively alleviate motor symptoms in movement disorders, and cholinergic stimulation boosts t

92 e seizure types, severe developmental delay, movement disorders, and elevated risk of sudden unexpect

93 s of infancy, including epilepsy, paroxysmal movement disorders, and migraine.

94 al delay, intellectual disability, epilepsy, movement disorders, and neurodegeneration, among others.

95 disorders such as schizophrenia, functional movement disorders, and Parkinson's disease.

96 x, address the basic clinical definitions of movement disorders, and then place diseases within an an

97 evere intellectual deficiency, microcephaly, movement disorders, and/or early-onset intractable epile

98 The signs and symptoms of movement disorders appear to result largely from signatu

99 Developmental disability and movement disorder are key features.

100 Drug-induced movement disorders are disabling but are often under-rec

101 cits we observed in patients with functional movement disorders are likely to stem from abnormal allo

102 Extrapyramidal movement disorders associated with mitochondrial disease

103 arious combinations of cognitive impairment, movement disorders, ataxia and upper motor neuron signs.

104 , using the search terms Parkinson's disease,movement disorders, ataxia, dystonia, chorea, and Creutz

105 ominant movement disorders, 18 patients with movement disorders attributed to other genetic defects,

106 various other features including hypotonia, movement disorders, behavior problems, corpus callosum h

107 ogical conditions (most notably epilepsy and movement disorders), but widespread use is limited by co

108 clinically recognized to treat parkinsonian movement disorders, but its mechanisms remain elusive.

109 tial tremor (ET) is among the most prevalent movement disorders, but its origins are elusive.

110 Hyperkinetic states are common in human movement disorders, but their neural basis remains uncer

111 cally similar to those of subjects without a movement disorder by reducing excess sensorimotor cortic

112 delay the deterioration of motor function in movement disorders by blocking aberrant motor learning.

113 gical approaches might benefit children with movement disorders by modifying synaptic function.

114 ital neutropenia, progressive brain atrophy, movement disorder, cataracts, and 3-methylglutaconic aci

115 cephalopathy with progressive brain atrophy, movement disorder, cataracts, and early death.

116 ility in DYT1 dystonia, a neurodevelopmental movement disorder caused by a loss-of-function (LOF) mut

117 and the etiology of DYT1 primary dystonia, a movement disorder caused by a single glutamate deletion

118 ia parkinsonism (XDP) is a neurodegenerative movement disorder caused by a single mutation: SINE-VNTR

119 DYT1 is a debilitating movement disorder caused by loss-of-function mutations i

120 Myoclonus dystonia (DYT11) is a movement disorder caused by loss-of-function mutations i

121 Myoclonus-dystonia (M-D) is a very rare movement disorder, caused in approximately 30-50% of cas

122 nal study of 44 participants at 17 different movement disorder centers who were in the Consortium on

123 45 participants in two cohorts from tertiary movement disorder centres.

124 Essential tremor (ET), a movement disorder characterised by an uncontrollable sha

125 Myoclonus-dystonia (M-D) is a rare movement disorder characterized by a combination of non-

126 Parkinson's disease (PD) is a movement disorder characterized by a progressive loss of

127 Dystonia is a movement disorder characterized by involuntary and repet

128 Dystonia is a movement disorder characterized by involuntary muscle co

129 Dystonia is a movement disorder characterized by sustained or intermit

130 Progressive supranuclear palsy (PSP) is a movement disorder characterized by tau neuropathology wh

131 Parkinson's disease (PD) is a major movement disorder characterized by the loss of dopamine

132 ase (PD) is a progressive, neurodegenerative movement disorder characterized by the loss of dopaminer

133 ociation study of essential tremor, a common movement disorder characterized mainly by a postural and

134 ep-disordered breathing (SDB), sleep-related movement disorders, circadian rhythm sleep-wake disorder

135 re recruited for 18F-DTBZ PET scans from the Movement Disorders Clinic in the Chang Gung Memorial Hos

136 nd PD patients collected systematically in a movement disorders clinic over 3 years.

137 A cross-sectional study at an academic movement disorders clinic that included a predominantly

138 rs of the A53T SNCA mutation from specialist Movement Disorders clinics in Athens, Greece, and Salern

139 iopathic Parkinson's disease (cohort 1) from Movement Disorders clinics in London, UK, and retrieved

140 The cohorts were from 2 movement disorders clinics in Montreal, Quebec, Canada (

141 rom 1549 patients with PD recruited across 5 movement disorders clinics located in Europe, Israel, an

142 solated dystonia), in combination with other movement disorders (combined dystonia), or in the contex

143 s a progressive and devastating degenerative movement disorder commonly associated with loss of cereb

144 acid-responsive epilepsy (one patient) and a movement disorder compatible with AADC deficiency (one p

145 disability often associated with early-onset movement disorders comprising cerebellar ataxia and/or e

146 etraction syndrome (DRS) is a congenital eye-movement disorder defined by limited outward gaze and re

147 ing a disorder characterized by a dyskinetic movement disorder, developmental delay, and autism.

148 have been described in other childhood-onset movement disorders, different forms of seizures, headach

149 Many movement disorders disrupt motor unit contractile dynami

150 tic factors are associated with drug-related movement disorders (DRMD), in an attempt to provide a sy

151 from two families affected by a hyperkinetic movement disorder due to homozygous mutations c.320A>G (

152 UBB6, one of which (TUBB4) is mutated in the movement disorder dystonia type 4 (DYT4).

153 In DCP, two major movement disorders, dystonia and choreoathetosis, are pr

154 sidered in patients with undiagnosed complex movement disorders even in the absence of a family histo

155 tandard is the clinical evaluation made by a movement disorders expert.

156 were scored blindly and independently by two movement-disorders experts.

157 Functional movement disorders (FMD) are proposed to reflect a speci

158 Functional movement disorders (FMDs), part of the wide spectrum of

159 d therapeutic intervention for patients with movement disorders following spinal cord injury.

160 is involved in several neuropsychiatric and movement disorders for which a dysfunctional signaling o

161 ease (PD) is a progressive neurodegenerative movement disorder frequently associated with a wide vari

162 entional MR imaging-guided DBS placement for movement disorders from September 2013 to August 2014 fo

163 lopmental delay; hypotonia; autistic traits; movement disorders; growth abnormalities; and facial dys

164 or psychogenic) motor symptoms (weakness and movement disorder) has not been systematically reviewed.

165 ed therapeutic modality for the treatment of movement disorders, has recently shown potential benefic

166 ng of gait compared to lesions causing other movement disorders (hemichorea or asterixis).

167 Parkinson's disease is a neurodegenerative movement disorder; however, peripheral symptoms can aris

168 In addition, the nonepileptic paroxysmal movement disorder hyperekplexia has not previously been

169 sonism was the most prevalent extrapyramidal movement disorder in adults and was commonly associated

170 ing many features with our patients: the eye movement disorder in Ahr-/- mice appears early in develo

171 se (PD) is the most common neurodegenerative movement disorder in humans.

172 of a congenital intellectual disability and movement disorder in humans.

173 ing rates that, when dysfunctional, causes a movement disorder in patients and flies.

174 Movement disorders in children are causally and clinical

175 The diagnosis and management of movement disorders in children can be improved by unders

176 e mechanisms that underlie some of the major movement disorders in children.

177 the pathophysiological mechanisms underlying movement disorders in humans.

178 e findings reveal that gut bacteria regulate movement disorders in mice and suggest that alterations

179 the secondary motor cortex, can also reverse movement disorders in mice.

180 l as radiological findings in the context of movement disorders in mitochondrial disease.

181 e >/=20 years) from two clinics for tertiary movement disorders in the UK.

182 ed with the mutant human ATG5 exhibit severe movement disorder, in contrast to flies expressing the w

183 The sensory aspects of movement disorders include intrinsic sensory abnormaliti

184 rimental to the cerebellum and can result in movement disorders including ataxias.

185 is an established neurosurgical therapy for movement disorders including essential tremor and Parkin

186 of individuals with age-related neurological movement disorders including Parkinson's Disease (PD) an

187 expression of RGMa resulted in a progressive movement disorder, including motor coordination and imba

188 nosis for both infantile- and juvenile-onset movement disorders, including cerebral palsy and juvenil

189 Tardive dyskinesia is a persistent movement disorder induced by dopamine receptor blockers,

190 l to transfer the expanding knowledge of the movement disorders into the development of novel symptom

191 revention of the development of drug-induced movement disorders is an important consideration when pr

192 The pathophysiology of both movement disorders is largely unknown.

193 l drugs to provide symptomatic relief of the movement disorders is limited by adverse effects and the

194 expanded, appreciation of cranial functional movement disorders is still insufficient.

195 Parkinson disease (PD), the most common movement disorder, is a progressive neurodegenerative di

196 inson's disease, the most common age-related movement disorder, is a progressive neurodegenerative di

197 s disease (PD), the most common degenerative movement disorder, is caused by a preferential loss of m

198 gy of essential tremor (ET), the most common movement disorder, is not fully understood.

199 Seizures and movement disorders (MDs) are distinct neurological condi

200 novel autosomal dominant neurodevelopmental movement disorders mirroring phenotypes previously descr

201 with essential tremor (n = 9) and without a movement disorder (n = 6).

202 ences in PD and the most common hyperkinetic movement disorders, namely, essential tremor, dystonia,

203 Isolated focal dystonia is a debilitating movement disorder of unknown pathophysiology.

204 in two control groups (patients with organic movement disorders (OMD) and healthy volunteers).

205 a 3-year-old boy who presented with a mixed movement disorder (opsoclonus, ataxia, and chorea) as we

206 opriate clinical management of patients with movement disorders or dementia.

207 ildren and adults with cognitive impairment, movement disorder, or epilepsy.

208 eports on RAD51-associated congenital mirror movement disorders, our results point to an important ro

209 transferase BCAT-1 and the neurodegenerative movement disorder Parkinson's disease (PD).

210 and with 1 or more predefined extrapyramidal movement disorders (parkinsonism, dystonia, tremor, chor

211 The recognition of the particular movement disorder phenotype, coupled with information ab

212 Psychogenic movement disorders (PMDs) may be difficult to differenti

213 sia (PNKD) is an autosomal dominant episodic movement disorder precipitated by coffee, alcohol, and s

214 tual disability to severe global disability; movement disorders (present in 44%) included choreoathet

215 neurodegenerative diseases characterized by movement disorders, psychiatric disturbances and cogniti

216 phalopathy, refractory seizures, and a mixed movement disorder rather than limbic encephalitis.

217 e been used to a greater extent for mood and movement disorders, recent work has explored brain stimu

218 ype associations and deep phenotyping of the movement disorders related to mitochondrial disease.

219 er isolated or combined) with coexisting non-movement disorder-related neurological symptoms (100 [45

220 eless, the real impact of sex differences in movement disorders remains under-recognized.

221 Functional movement disorders require attention to manifest yet pat

222 Chorea is a hyperkinetic movement disorder resulting from dysfunction of striatal

223 available evidence suggests that the varied movement disorders resulting from dysfunction of this ci

224 the brainstem were associated with increased Movement Disorder Score-Unified Parkinson's Disease Rati

225 ch is characterised by progressive dementia, movement disorders, seizures and premature death.

226 ant presented with an early onset dyskinetic movement disorder, severe motor delay, and profound cogn

227 range of neurological conditions, including movement disorders, sex-related differences are emerging

228 The investigation of paroxysmal movement disorders should always include the analysis of

229 In movement disorders, SIBs are typically associated with t

230 ndrial homeostasis and the pathogenesis of a movement disorder similar to Parkinson's disease.

231 have been in fact reported in the setting of movement disorders, sleep disorders and even internal me

232 NMS defined by a score of >=4 points on the Movement Disorder Society - Unified PD Rating Scale-I (M

233 /- 4.0 y; Hoehn and Yahr stage, 2.1 +/- 0.6; Movement Disorder Society [MDS]-revised Unified Parkinso

234 nd PSP phenotype (with reference to the 2017 Movement Disorder Society criteria).

235 or (ET), the 2018 consensus statement of the Movement Disorder Society on tremor coined a new term: e

236 The Movement Disorder Society Task Force criteria were used

237 tcome was a 2 min walk, with motor symptoms (Movement Disorder Society Unified Parkinson's Disease Ra

238 ire [RBDSQ], Geriatric Depression Scale, and Movement Disorder Society Unified Parkinson's Disease Ra

239 of neurological examinations, including the Movement Disorder Society Unified Parkinson's Disease Ra

240 NMS were rated using the Movement Disorder Society Unified Parkinson's Disease Ra

241 ange from predose to 30 min post-dose in the Movement Disorder Society Unified Parkinson's Disease Ra

242 (mean (SD) 1.8 (1.9) vs 0.8 (1.2); p=0.01), Movement Disorder Society Unified Parkinson's Disease Ra

243 higher disease burden scores, measured with Movement Disorder Society Unified Parkinson's Disease Ra

244 We collected demographic data, Movement Disorder Society Unified Parkinson's Disease Ra

245 verity and phenotype were assessed using the Movement Disorder Society Unified PD Rating Scale (UPDRS

246 The NMSs were assessed by Movement Disorder Society-sponsored revision of the Unif

247 pared with the placebo group (differences in Movement Disorder Society-sponsored revision of the Unif

248 GBA genotype and motor progression, with the Movement Disorder Society-sponsored version of the Unifi

249 l rate of change in combined scores from the Movement Disorder Society-Unified Parkinson's Disease Ra

250 dual-task TUG (DT-TUG), motor section of the Movement Disorder Society-Unified Parkinson's Disease Ra

251 the change from baseline to 4 months in the Movement Disorder Society-Unified Parkinson's Disease Ra

252 The Movement Disorders Society PSP diagnostic criteria inclu

253 PD-MCI was classified using Movement Disorders Society Task Force level I (Montreal

254 y outcome was the adjusted difference in the Movement Disorders Society Unified Parkinson's Disease R

255 Motor sign severity was assessed using the Movement Disorders Society Unified Parkinson's Disease R

256 measures of visuoperceptual function and the Movement Disorders Society Unified Parkinson's Disease R

257 Models considered adjustment for age, sex, Movement Disorders Society Unified Parkinson's Disease R

258 d significantly increased mean scores on the Movement Disorders Society Unified Parkinson's Disease R

259 or Disorder screening questionnaire (RBDsq), Movement Disorders Society Unified Parkinson's Disease R

260 All cases were classified by a movement disorder specialist using defined criteria thro

261 A movement-disorder specialist reviewed medical records to

262 A movement-disorders specialist reviewed the medical recor

263 -blind, placebo-controlled study was done by movement disorder specialists at 32 sites in the USA and

264 s with Parkinson's disease were diagnosed by movement disorder specialists in accordance with the UK

265 .9 y; age range, 21-80 y) were referred from movement disorder specialists.

266 r imaging, subjects were followed by blinded movement disorders specialists for an average of 2.2 y b

267 uals with familial PD enrolled from academic movement disorder specialty clinics across the United St

268 ining expanded glutamine stretches cause the movement disorder spinocerebellar ataxia type 1 (SCA1) t

269 the positive features of cranial functional movement disorders such as convergence and unilateral pl

270 xtensive efforts, half of patients with rare movement disorders such as hereditary spastic paraplegia

271 that it may contribute to motor symptoms in movement disorders such as Parkinson's disease (PD).

272 Modern functional neurosurgery for movement disorders such as Parkinson's disease, tremor,

273 ibutes to the motor symptoms of a variety of movement disorders such as Parkinson's disease.

274 Given the involvement of sodium pumps in movement disorders, such as amyotrophic lateral sclerosi

275 he general cortical neurophysiology of other movement disorders, such as essential tremor, are relati

276 c target for deep brain stimulation (DBS) in movement disorders, such as Parkinson's disease.

277 The most frequently described signs were movement disorders, such as parkinsonism (12%) and dysto

278 ore the single neuron's role in epilepsy and movement disorders, surgical anesthesia, and in cognitiv

279 ese well-known aetiologies, a range of other movement disorder syndromes may also present with SIBs,

280 en January 1, 2004, and April 30, 2009, by a movement disorder team at a university hospital that rep

281 Dystonia is a neurological movement disorder that forces the body into twisting, re

282 arkinson's disease (PD), a neurodegenerative movement disorder that inflicts millions worldwide.

283 hlight the most relevant clinical aspects of movement disorders that differ between men and women.

284 in the PDE10A gene manifest in hyperkinetic movement disorders that phenocopy many features of early

285 nsights into a fascinating group of episodic movement disorders, the paroxysmal dyskinesias, and stud

286 of deep brain stimulation (DBS) for treating movement disorders, there is growing interest in using D

287 In subjects with movement disorders, this effect was observed to an even

288 what the field has uncovered thus far about movement disorders through DBS.

289 disease were diagnosed by a neurologist with movement disorder training, in accordance with the UK Pa

290 iatal cholinergic dysfunction in dystonia, a movement disorder typically resulting in twisted posture

291 2016, in a tertiary care center's memory and movement disorders units.

292 sis as reference standard, and subjects with movement disorders versus dementia.

293 age range, 20-81 years]) with extrapyramidal movement disorders were identified.

294 Movement disorders, which include disorders such as Park

295 Essential tremor (ET) is a common movement disorder with an estimated prevalence of 5% of

296 Parkinson's disease is a movement disorder with characteristic motor features tha

297 Holmes tremor is a debilitating movement disorder with limited treatment options.

298 se of a progressive, pediatric-onset spastic movement disorder with variable clinical presentation.

299 and MCP-1 separates iNPH from cognitive and movement disorders with good diagnostic sensitivity and

300 he basal ganglia (BG) are implicated in many movement disorders, yet how they contribute to movement