ライフサイエンスコーパス: dyskinesia

1 develop debilitating involuntary movements (dyskinesia).

2 sporter-2 inhibitor-in patients with tardive dyskinesia.

3 ty of valbenazine as a treatment for tardive dyskinesia.

4 such changes correlate with the severity of dyskinesia.

5 ticipate in the expression of L-DOPA induced dyskinesia.

6 e effect of therapy for Parkinson's disease: dyskinesia.

7 n vivo neurotransmitter release in M1 during dyskinesia.

8 op hyperkinetic involuntary movements termed dyskinesia.

9 al responses toward L-DOPA, but develop less dyskinesia.

10 ns is causally related to the development of dyskinesia.

11 ew levodopa formulations will delay onset of dyskinesia.

12 involuntary movements termed l-DOPA-induced dyskinesia.

13 by l-DOPA relieves symptoms of PD but causes dyskinesia.

14 rses aberrant plasticity in levodopa-induced dyskinesia.

15 turbances, weakness on the treated side, and dyskinesia.

16 d dyskinesia, and paroxysmal non-kinesigenic dyskinesia.

17 genital motor dysfunction with hypertonia or dyskinesia.

18 4-dihydroxyphenyl-L-alanine (L-DOPA)-induced dyskinesia.

19 vodopa administration induced characteristic dyskinesia.

20 s (DNAH5; CCDC39) as seen in primary ciliary dyskinesia.

21 d subsequently treated with L-DOPA to induce dyskinesia.

22 mical and electrophysiological substrates of dyskinesia.

23 s to levodopa can alleviate levodopa-induced dyskinesia.

24 the striatum of animals that did not develop dyskinesia.

25 ctively), and time with good mobility and no dyskinesia.

26 osis, and ciliary defects of primary ciliary dyskinesia.

27 io, mimicking the ciliopathy primary ciliary dyskinesia.

28 form of generalized epilepsy and paroxysmal dyskinesia.

29 ficant side effects, including graft-induced dyskinesia.

30 kinson's Disease (PD), and to L-DOPA-induced dyskinesia.

31 supplementation in moderating L-DOPA-induced dyskinesia.

32 limited and mostly confirm the efficacy for dyskinesia.

33 0% of patients known to have primary ciliary dyskinesia.

34 disorder who had moderate or severe tardive dyskinesia.

35 ects of valbenazine in patients with tardive dyskinesia.

36 th LID and OFF time in patients with PD with dyskinesia.

37 symptoms when the medication wears off, and dyskinesias.

38 ation, there is no evidence of graft-induced dyskinesias.

39 e is often limited by wearing off effect and dyskinesias.

40 symptoms and development of levodopa-induced dyskinesias.

41 motor function while reducing l-dopa-induced dyskinesias.

42 Kv3 channel function and VLS-based orofacial dyskinesias.

43 ic approach to the treatment of debilitating dyskinesias.

44 underlies the development of L-DOPA-induced dyskinesias.

45 or symptoms of PD but often causes disabling dyskinesias.

46 referred to as levodopa-induced peak-of-dose dyskinesias.

47 hat herald the emergence of levodopa-induced dyskinesias.

48 icipate in the development of L-DOPA-induced dyskinesias.

49 nic oral eltoprazine to treat l-DOPA-induced-dyskinesias.

50 66.6 +/- 8.8 years old) with L-DOPA-induced dyskinesias.

51 ression of molecular markers associated with dyskinesias.

52 lar changes correlates with the intensity of dyskinesias.

53 e used to define the involvement of DREAM in dyskinesias.

54 es debilitating motor side effects including dyskinesias.

55 plicated by the development of graft-related dyskinesias.

56 patient-reported ON-time without troublesome dyskinesia (1.6, 3.3, and 1.5 hours, respectively) and q

57 Most common were increased on-medication dyskinesias (20 events, 11 patients) and on-off phenomen

58 psy (41.7%; n = 602), paroxysmal kinesigenic dyskinesia (38.7%; n = 560) and infantile convulsions an

59 is for the initial episode was biliary colic/dyskinesia (65.3%), acute cholecystitis (26.6%), choledo

60 One such condition is dyskinesia, a serious adverse effect of medical and surg

61 cholecystectomy for biliary colic or biliary dyskinesia, acute cholecystitis, or chronic cholecystiti

62 of LID in parkinsonian mice with established dyskinesia after chronic L-DOPA treatment.

63 ing in the basal ganglia is thought to cause dyskinesia, alterations in primary motor cortex (M1) act

64 rder of respiratory cilia is primary ciliary dyskinesia, an inherited disorder that leads to impaired

65 Chronic L-DOPA treatment, which induced dyskinesia and aberrant FosB expression, restored spine

66 with ciliopathies, including primary ciliary dyskinesia and Bardet-Biedl syndrome, also suffer from i

67 f infection, 33% of Hu-NSG mice exhibited LV dyskinesia and dyssynchrony.

68 ations of human DNAAF2 can result in ciliary dyskinesia and identify Dnaaf2 as an essential component

69 verexpression plays a role in L-dopa-induced dyskinesia and in drug addiction.

70 suggest that D5R can modulate L-DOPA induced dyskinesia and is a critical activator of CINs via pERK

71 The rates of dyskinesia and levodopa-related fluctuations in motor re

72 ith side effects in the form of drug-induced dyskinesia and motor fluctuations and surgical therapies

73 targets are considered for treating tardive dyskinesia and negative and cognitive symptoms.

74 form of dyskinesias that resembled diphasic dyskinesia and persisted in the off-medication state.

75 tions to improve on time without troublesome dyskinesia and reduce wearing off.

76 a rodent model of PD, that treatment-induced dyskinesia and striatal ERK activation are bidirectional

77 wo patients with PD who experienced frequent dyskinesia and studied them both at rest and during volu

78 the cylinder test after the establishment of dyskinesia and the molecular changes by immunohistochemi

79 Thirteen PD patients with dyskinesias and 13 PD patients without dyskinesias recei

80 non-motor behavioural side-effects, such as dyskinesias and impulse control disorders also known as

81 avioral complications, such as fluctuations, dyskinesias and impulse-control disorders.

82 intronic to PNKD (paroxysmal non-kinesigenic dyskinesia) and TMBIM1 (transmembrane BAX inhibitor moti

83 is revealed that quirky mice display ataxia, dyskinesia, and absence epilepsy.

84 vation of DREAM potentiated the intensity of dyskinesia, and DREAM(-/-) mice exhibited an increase in

85 choreoathetosis, paroxysmal exercise-induced dyskinesia, and paroxysmal non-kinesigenic dyskinesia.

86 spiratory distress syndrome, primary ciliary dyskinesia, and pulmonary hypertension.

87 Ataxia, episodic dyskinesia, and thalamocortical seizures are associated

88 s with aging, PD progression, development of dyskinesias, and cognitive decline were observed.

89 sy, addiction, anxiety, schizophrenia, pain, dyskinesias, and melanoma, a large number of drugs are b

90 ome, faciobrachial dystonic spells or facial dyskinesias, and mesial temporal sclerosis abnormality o

91 s, including myoclonus, tongue and orofacial dyskinesias, and opsoclonus.

92 episodic movement disorders, the paroxysmal dyskinesias, and study of the causative genes and protei

93 ienced worsening of parkinsonism with severe dyskinesias, and underwent subthalamic nucleus deep brai

94 s in animal models of PD have suggested that dyskinesias are associated with the overactivation of G

95 change in motor on-time without troublesome dyskinesia as a prespecified key secondary outcome.

96 ircuit-level mechanism for the generation of dyskinesia as well as a promising control signal for clo

97 ounteracted both l-DOPA-induced rotation and dyskinesia as well as AMPA receptor phosphorylation.

98 in a series of 145 families with paroxysmal dyskinesias as well as in a series of 53 patients with f

99 insonian motor features) without troublesome dyskinesia, as assessed from diary data.

100 apid onset and offset, frequency dependence, dyskinesia at higher stimulation intensity, and associat

101 periods"), medication-resistant tremor, and dyskinesias, benefit from advanced treatments such as th

102 ion in increased ON time without troublesome dyskinesias between the active and control groups was 3.

103 dopa-independent continuous form of diphasic dyskinesias, but insufficient to provide an antiparkinso

104 atients who later developed levodopa-induced dyskinesias, but not patients without dyskinesias, showe

105 Paroxysmal dyskinesia can be subdivided into three clinical syndrom

106 Defects in CCDC103 lead to primary ciliary dyskinesia caused by the loss of outer dynein arms.

107 treated rats gradually expressed more severe dyskinesia compared with L-DOPA alone over time.

108 d choreoathetosis and paroxysmal kinesigenic dyskinesia, confirming a common disease spectrum that ha

109 ents in the opicapone vs placebo groups were dyskinesia, constipation, and dry mouth.

110 ed and tailored for patients on the basis of dyskinesia control and tolerability.

111 ose that was tolerable and provided adequate dyskinesia control, based on investigator judgement, wit

112 Dyskinesia could be reduced by local M1 modulation of D1

113 Although levodopa-induced dyskinesias could be elicited postoperatively, GIDs were

114 sms underlying impulse control disorders and dyskinesias could provide crucial insights into other be

115 PD patients with dyskinesias display an immediate hypersensitivity of pre

116 ted in a patient diary of moderate to severe dyskinesia during waking hours.

117 designate this locus as Episodic Kinesigenic Dyskinesia (EKD3).

118 or 45 minutes after levodopa intake or until dyskinesias emerged.

119 genic dyskinesia, paroxysmal non-kinesigenic dyskinesia, episodic ataxia and myotonia and we identifi

120 opa revealed, in some cases, the presence of dyskinesias even in the absence of L-dopa.

121 /OFQ receptor synthetic agonist also reduced dyskinesia expression in 1-methyl-4-phenyl-1,2,3,6-tetra

122 like NOP antagonists, which appear to worsen dyskinesia expression, these NOP partial agonists did no

123 estion the utility of pERK as a biomarker of dyskinesia expression.

124 partial agonists did not attenuate or worsen dyskinesia expression.

125 given systemically (0.01-1 mg/Kg) attenuated dyskinesias expression in 6-hydroxydopamine hemilesioned

126 In primary ciliary dyskinesia, factors leading to disease heterogeneity are

127 nously enhancing M1 inhibition may attenuate dyskinesia, findings that are in agreement with function

128 e to Parkinson's disease pathophysiology and dyskinesia from chronic L-3,4-dihydroxyphenylalanine (L-

129 e been carried out on each of the paroxysmal dyskinesia genes, to date there has been no large study

130 Rodent models of graft-induced dyskinesias (GIDs) have been proposed, but their accurac

131 Patients aged 18-80 years with tardive dyskinesia (>/=3 months before screening) were randomly

132 Orthostatic hypotension, syncope, dyskinesia, hallucinations, prolongation of the QT inter

133 ME is highly associated with Primary Ciliary Dyskinesia, implicating significant contributions of cil

134 ated kinases in striatal neurons, leading to dyskinesia in animals treated with L-DOPA or D1 receptor

135 f caffeine with a low dose of l-DOPA reduces dyskinesia in animals with striatopallidal knock-out to

136 REAM decreases development of L-DOPA-induced dyskinesia in mice and reduces L-DOPA-induced expression

137 ngton's disease, dystonia and l-DOPA-induced dyskinesia in Parkinson's disease are all characterized

138 e-compulsive disorders, and levodopa induced dyskinesia in Parkinson's disease.

139 y valbenazine significantly improved tardive dyskinesia in participants with underlying schizophrenia

140 to reduce medication usage and drug-induced dyskinesia in patients with severe PD refractory to medi

141 inic M3 receptor (rM3Ds) induced appreciable dyskinesia in PD mice.

142 ic approaches for alleviating L-DOPA-induced dyskinesia in PD patients.

143 and tolerability in the treatment of tardive dyskinesia in phase 2 studies.

144 Rats showed greater dyskinesia in response to l-DOPA and SKF81297 after repe

145 evodopa treatment leads to the appearance of dyskinesia in the majority of Parkinson's disease patien

146 se events in the active-treatment group were dyskinesia in the off-medication state in 6 patients and

147 receptors effectively blocks L-DOPA-induced dyskinesias in animal models of dopamine depletion, just

148 ty as a neural signature of levodopa-induced dyskinesias in humans.

149 A/B receptor agonist, against L-DOPA-induced dyskinesias in patients with Parkinson's disease.

150 (fMRI) to map the emergence of peak-of-dose dyskinesias in patients with PD.

151 underlying the emergence of levodopa-induced dyskinesias in vivo are still poorly understood.

152 mycin with L-DOPA counteracts L-DOPA-induced dyskinesias in wild-type mice, but not in mice lacking p

153 e most frequently reported adverse event was dyskinesia (in 40 [14.6%] vs 15 [5.5%] and as a severe e

154 The most common adverse events were dyskinesia (in five patients in the placebo group, ten i

155 ey also show fewer abnormal motor behaviors (dyskinesias) in response to l-3,4-dihydroxyphenylalanine

156 such as cystic fibrosis and primary ciliary dyskinesia, in which mucociliary dysfunction predisposes

157 Mean on-time without troublesome dyskinesia increased by 4.11 h (SE 0.75) in the intestin

158 is involved in the development of orofacial dyskinesias, involuntary chewing-like movements that oft

159 Primary ciliary dyskinesia is a genetically and clinically heterogeneous

160 Tardive dyskinesia is a persistent movement disorder induced by

161 A putative source of dyskinesia is abnormally high levels of phosphorylated e

162 -3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia is an incapacitating complication of L-DOPA t

163 We show that dyskinesia is associated with a narrowband gamma oscilla

164 Although dyskinesia is associated with dynamic changes in primary

165 esent study demonstrates that l-DOPA-induced dyskinesia is associated with increased M1 inhibition an

166 is movement disorder, the molecular basis of dyskinesia is not understood.

167 ity in striatum, we investigated whether the dyskinesia is related to morphological changes in MSNs.

168 nt models of PD (PD mice) and L-DOPA-induced dyskinesia (LID mice).

169 Levodopa-induced dyskinesia (LID) develops after repeated levodopa (l-DOP

170 Medical treatment of levodopa-induced dyskinesia (LID) in Parkinson disease (PD) is an unmet n

171 -3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID) in Parkinson's disease (PD), boosting M

172 -3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID) in Parkinson's disease shed light, nota

173 s, and side effects including l-DOPA-induced dyskinesia (LID) increase, affecting up to 78% of patien

174 4-Dihydroxyphenyl-L-alanine (L-DOPA)-induced dyskinesia (LID) is a debilitating side effect of long-t

175 Levodopa-induced dyskinesia (LID) is a persistent behavioral sensitizatio

176 Levodopa-induced dyskinesia (LID) poses a significant health care challen

177 ctive medical management of levodopa-induced dyskinesia (LID) remains an unmet need for patients with

178 involuntary movements termed L-DOPA-induced dyskinesia (LID), a clinically significant obstacle for

179 -3,4-dihydroxyphenylalanine (l-DOPA)-induced dyskinesia (LID), a common motor complication of current

180 urons reduces the severity of l-DOPA-induced dyskinesia (LID), a finding that correlates with lowered

181 4-dihydroxy-l-phenylalanine (L-DOPA)-induced dyskinesia (LID), a motor complication affecting Parkins

182 -3,4-dihydroxyphenylalanine (L-Dopa)-induced dyskinesia (LID), the debilitating side-effects of chron

183 , the immediate early gene of L-dopa induced dyskinesia (LID), was mitigated in the striatum by the c

184 plicated by the appearance of L-DOPA-induced dyskinesia (LID).

185 triatum of rodents expressing l-DOPA-induced dyskinesia (LID).

186 Parkinson's disease (PD) and L-DOPA-induced dyskinesia (LID).

187 ts, known in their complex as L-DOPA-induced dyskinesia (LID).

188 , treatment is complicated by L-dopa-induced dyskinesias (LID).

189 neurons of rats exhibiting levodopa-induced dyskinesia [LID; a side-effect to dopamine replacement s

190 Levodopa-induced dyskinesias (LIDs) are the most common and disabling adv

191 es dyskinesias referred to as L-DOPA-induced dyskinesias (LIDs).

192 e striatal circuits change in l-DOPA-induced dyskinesias (LIDs).

193 comotor effects while markedly enhancing the dyskinesia-like effects of acute or chronic L-DOPA treat

194 Dyskinesia, motor fluctuations and activities of daily l

195 Dyskinesias, motor fluctuations and demands in dopaminer

196 rsor levodopa gradually induces involuntary "dyskinesia" movements.

197 se Parkinson's disease with levodopa-induced dyskinesias (n = 12), correlated with lower (11)C-IMA107

198 Levodopa-induced dyskinesias occur in up to 80% of patients with Parkinso

199 Transient post-gene therapy dyskinesia occurred in all patients but was resolved wit

200 ed a significant reduction of L-DOPA-induced dyskinesias on area under the curves of Clinical Dyskine

201 eurodegeneration PD models, without inducing dyskinesias on chronic daily treatment.

202 e clinical syndromes: paroxysmal kinesigenic dyskinesia or choreoathetosis, paroxysmal exercise-induc

203 ham stimulation), involuntary movements (ie, dyskinesia or worsening of dystonia; five vs one), and d

204 e DA deficit and improve symptoms but induce dyskinesias over time, and neuroprotective therapies are

205 P<0.001), and time with good mobility and no dyskinesia (P=0.01).

206 ndividual patient would subsequently develop dyskinesias (p < 0.001) as well as severity of their day

207 as severity of their day-to-day symptomatic dyskinesias (p < 0.001).

208 phenotypes including paroxysmal kinesigenic dyskinesia, paroxysmal non-kinesigenic dyskinesia, episo

209 s of cilia motility in human primary ciliary dyskinesia patients is not fully associated with scolios

210 nical phenotype of childhood primary ciliary dyskinesia (PCD) and ultrastructural defects and genotyp

211 ard approach to diagnosis of primary ciliary dyskinesia (PCD) in the United Kingdom consists of asses

212 Primary ciliary dyskinesia (PCD) is a ciliopathy characterized by airway

213 Primary ciliary dyskinesia (PCD) is a genetic disorder characterized by

214 Primary ciliary dyskinesia (PCD) is a genetic disorder in which impaired

215 Primary ciliary dyskinesia (PCD) is a genetically heterogeneous recessiv

216 Primary ciliary dyskinesia (PCD) is a genetically heterogeneous recessiv

217 Primary ciliary dyskinesia (PCD) is a genetically heterogeneous syndrome

218 Primary ciliary dyskinesia (PCD) is a genetically heterogeneous, autosom

219 Primary ciliary dyskinesia (PCD) is an autosomal recessive disease cause

220 Primary ciliary dyskinesia (PCD) is an autosomal recessive disorder freq

221 Primary ciliary dyskinesia (PCD) is an inherited chronic respiratory obs

222 Primary ciliary dyskinesia (PCD) is caused when defects of motile cilia

223 Primary ciliary dyskinesia (PCD) is characterized by dysfunction of resp

224 Primary ciliary dyskinesia (PCD) originates from dysfunction of motile c

225 some of which are typical of primary ciliary dyskinesia (PCD), a condition caused by motile cilia def

226 are the most common cause of primary ciliary dyskinesia (PCD), a congenital disorder of ciliary beati

227 aused a phenotype resembling primary ciliary dyskinesia (PCD), a disorder characterized by chronic ai

228 and 9 have been linked with primary ciliary dyskinesia (PCD), a disorder characterized by ciliary dy

229 embly are the major cause of primary ciliary dyskinesia (PCD), an inherited disorder of ciliary and f

230 example in cystic fibrosis, primary ciliary dyskinesia (PCD), and select immunodeficiencies(3).

231 lia and sperm flagella cause primary ciliary dyskinesia (PCD), characterized by chronic airway diseas

232 efects of motile cilia cause primary ciliary dyskinesia (PCD), characterized by recurrent respiratory

233 ts in the pediatric syndrome primary ciliary dyskinesia (PCD).

234 results in diseases such as primary ciliary dyskinesia (PCD).

235 sensitive to lung disease in primary ciliary dyskinesia (PCD).

236 ead to a ciliopathy known as primary ciliary dyskinesia (PCD).

237 ted to cilia defects such as primary ciliary dyskinesia (PCD; OMIM: 612518).

238 ured in Parkinson's disease patients without dyskinesia (PD), cervical dystonia (CD) and writer's cra

239 ian nonhuman primate model of l-DOPA-induced dyskinesia (PD-LID).

240 functional abdominal pain, sphincter of Oddi dyskinesia, pelvic floor dysfunction, and extra-intestin

241 o experienced at least 1 hour of troublesome dyskinesia per day with at least mild functional impact.

242 When dyskinesia persists during therapeutic deep brain stimul

243 microdeletions and a paroxysmal kinesigenic dyskinesia phenotype have been reported.

244 Paroxysmal kinesigenic dyskinesia (PKD) is characterized by recurrent and brief

245 tile seizures (BFIS), paroxysmal kinesigenic dyskinesia (PKD), and their combination-known as infanti

246 Paroxysmal nonkinesigenic dyskinesia (PNKD) is an autosomal dominant episodic move

247 receptor D1 (D1R) stimulation is involved in dyskinesias prompted us to perform electrophysiological

248 nating disorders with atypical symptoms (eg, dyskinesias, psychosis) may have anti-NMDAR encephalitis

249 Paroxysmal dyskinesias (PxD) refer to a rare group of clinically an

250 ting Scale [-1.02(1.49); P = 0.004] and Rush Dyskinesia Rating Scale [-0.15(0.23); P = 0.003]; and ma

251 inesias on area under the curves of Clinical Dyskinesia Rating Scale [-1.02(1.49); P = 0.004] and Rus

252 les; area under the curve scores on Clinical Dyskinesia Rating Scale for 3 h post-dose and maximum ch

253 0.15(0.23); P = 0.003]; and maximum Clinical Dyskinesia Rating Scale score [-1.14(1.59); P = 0.005].

254 ng Scale score, area under the curve of Rush Dyskinesia Rating Scale score for 3 h post-dose, mood pa

255 east-squares mean (SE) change in the Unified Dyskinesia Rating Scale score was -15.9 (1.6) for ADS-51

256 ectives included effects on maximum Clinical Dyskinesia Rating Scale score, area under the curve of R

257 Higher Unified Dyskinesia Rating Scale scores in those Parkinson's dise

258 f the area under the curve and peak Clinical Dyskinesia Rating Scale scores.

259 ange from baseline to week 12 in the Unified Dyskinesia Rating Scale total score for ADS-5102 vs plac

260 with dyskinesias and 13 PD patients without dyskinesias received 200mg fast-acting oral levodopa fol

261 anine (L-DOPA), but its prolonged use causes dyskinesias referred to as L-DOPA-induced dyskinesias (L

262 Dyskinesia-related oscillations are minimally affected b

263 Tardive dyskinesia results from exposure to dopamine receptor an

264 The bidirectional modulation of dyskinesia reveals a central role for CK2 in striatal ph

265 PD pathogenesis and/or motor dysfunction and dyskinesia: RGSs 4, 6, 9, and 10.

266 e Abnormal Involuntary Movement Scale (AIMS) dyskinesia score (items 1-7), as assessed by blinded cen

267 mean change from baseline to week 6 in AIMS dyskinesia score was -3.2 for the 80 mg/day group, compa

268 AIMS dyskinesia score was also reduced in the 40 mg/day group

269 t common adverse events in these groups were dyskinesia (seven [8%] of 84 patients in the placebo gro

270 en elucidated, however a correlation between dyskinesia severity and pERK expression in cholinergic c

271 nous compensatory response designed to limit dyskinesia severity and that potentiating this response

272 Individual dyskinesia severity was predicted by levodopa-induced mo

273 trials, PD patients who would later develop dyskinesias showed an abnormal gradual increase of activ

274 nduced dyskinesias, but not patients without dyskinesias, showed a linear increase in connectivity be

275 microdialysis revealed that N/OFQ prevented dyskinesias simultaneously with its neurochemical correl

276 g MDs that look like seizure (eg, paroxysmal dyskinesia, status dystonicus) and seizures that look li

277 nin 1A receptor agonist +/-8-OH-DPAT reduces dyskinesia, suggesting it may exhibit efficacy through t

278 rtex (M1) activity are also prominent during dyskinesia, suggesting that the cortex may represent a t

279 amidal side effects (EPS), including tardive dyskinesia (TD).

280 rexia (16 [16%] of 101 events) and orofacial dyskinesia (ten [10%]).

281 d in more pronounced rotational behavior and dyskinesia than in their WT counterparts.

282 tify patients with a form of primary ciliary dyskinesia that has been difficult to diagnose.

283 e, the grafts were associated with a form of dyskinesias that resembled diphasic dyskinesia and persi

284 e disorder is referred to as primary ciliary dyskinesia, the most common motile ciliopathy.

285 evidence-based treatment for primary ciliary dyskinesia; therapies aim at relieving symptoms and redu

286 an develop uncontrollable movements known as dyskinesia upon treatment with L-DOPA.

287 uations that quickly progressed to disabling dyskinesias, warranting discontinuation of l-DOPA.

288 change in daily on time without troublesome dyskinesia was +1.42 (2.80) hours for safinamide, from a

289 In daDREAM mice, L-DOPA-induced dyskinesia was decreased throughout the entire treatment

290 ons into M1 demonstrated that l-DOPA-induced dyskinesia was reduced by M1 infusion of a D1 antagonist

291 s cholinergic interneurons in L-DOPA induced dyskinesia, we used D5R knockout mice that were rendered

292 l-3,4-dihydroxyphenylalanine-mediated dyskinesias were also significantly attenuated.

293 Dyskinesias were evaluated twice a week in mice with 6-h

294 The form, intensity, and frequency of these dyskinesias were quite variable, but their manifestation

295 restin2 overexpression significantly reduced dyskinesias while maintaining the therapeutic effect of

296 provided a significant reduction in tardive dyskinesia, with favourable safety and tolerability.

297 have been reported to cause primary ciliary dyskinesia, with many other genes likely to be discovere

298 otility deficiencies lead to primary ciliary dyskinesia, with upper-airways recurrent infections, lef

299 with good symptom control and no troublesome dyskinesias, with no increase in anti-parkinsonian medic

300 AM may be useful to alleviate L-DOPA-induced dyskinesia without interfering with the therapeutic moto