ライフサイエンスコーパス: dyskinesia

1 develop debilitating involuntary movements (dyskinesia).

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

3 rses aberrant plasticity in levodopa-induced dyskinesia.

4 d dyskinesia, and paroxysmal non-kinesigenic dyskinesia.

5 genital motor dysfunction with hypertonia or dyskinesia.

6 4-dihydroxyphenyl-L-alanine (L-DOPA)-induced dyskinesia.

7 vodopa administration induced characteristic dyskinesia.

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

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

10 ects of valbenazine in patients with tardive dyskinesia.

11 mical and electrophysiological substrates of dyskinesia.

12 s to levodopa can alleviate levodopa-induced dyskinesia.

13 the striatum of animals that did not develop dyskinesia.

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

15 io, mimicking the ciliopathy primary ciliary dyskinesia.

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

17 repeat that in humans causes primary ciliary dyskinesia.

18 roviding new insights into the mechanisms of dyskinesia.

19 inson's disease, also affects L-DOPA-induced dyskinesia.

20 ce of the cAMP/DARPP-32 signaling cascade in dyskinesia.

21 1 (mTORC1) pathways, which are implicated in dyskinesia.

22 it improves motor function without worsening dyskinesia.

23 disorder who had moderate or severe tardive dyskinesia.

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

25 ty of valbenazine as a treatment for tardive dyskinesia.

26 such changes correlate with the severity of dyskinesia.

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

28 n vivo neurotransmitter release in M1 during dyskinesia.

29 op hyperkinetic involuntary movements termed dyskinesia.

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

31 ns is causally related to the development of dyskinesia.

32 involuntary movements termed l-DOPA-induced dyskinesia.

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

34 hat herald the emergence of levodopa-induced dyskinesias.

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

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

37 66.6 +/- 8.8 years old) with L-DOPA-induced dyskinesias.

38 ression of molecular markers associated with dyskinesias.

39 lar changes correlates with the intensity of dyskinesias.

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

41 es debilitating motor side effects including dyskinesias.

42 novel strategy to counteract L-DOPA-induced dyskinesias.

43 n patients with and without levodopa-induced dyskinesias.

44 elopment and maintenance of levodopa-induced dyskinesias.

45 glutamate overactivity in the development of dyskinesias.

46 plicated by the development of graft-related dyskinesias.

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

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

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

50 ic approach to the treatment of debilitating dyskinesias.

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

52 or symptoms of PD but often causes disabling dyskinesias.

53 vs 4 [9%]), somnolence (20 [10%] vs 3 [6%]), dyskinesia (18 [9%] vs 6 [13%]), nausea (17 [9%] vs 5 [1

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

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

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

57 Dyskinesia, a motor complication caused by prolonged adm

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

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

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

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

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

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

64 involuntary movements and postures known as dyskinesia and dystonia.

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

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

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

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

69 kinase on DARPP-32 attenuates l-DOPA-induced dyskinesia and reduces the concomitant activations of ER

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

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

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

73 rapy improves motor function without causing dyskinesia and, as an adjunct to levodopa, it improves m

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

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

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

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

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

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

80 dema, whereas gait problems, disequilibrium, dyskinesia, and falls were reported in both groups.

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

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

83 Ataxia, episodic dyskinesia, and thalamocortical seizures are associated

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

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

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

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

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

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

90 Levodopa-induced dyskinesias are a common complication of long-term thera

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

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

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

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

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

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

97 duced striatal mTOR signaling and diminished dyskinesia, but maintained motor improvement on L-DOPA t

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

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

100 Paroxysmal dyskinesia can be subdivided into three clinical syndrom

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

102 r (anti-NMDAR) encephalitis, which may cause dyskinesias, chorea, ballismus or dystonia (NMDAR antibo

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

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

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

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

107 Dyskinesia could be reduced by local M1 modulation of D1

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

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

110 s associated not only with a reduced risk of dyskinesia development but is also able to rebalance, in

111 sease, being associated to a reduced risk of dyskinesia development.

112 PD patients with dyskinesias display an immediate hypersensitivity of pre

113 verlap between behavioural (ICDs) and motor (dyskinesias) dopaminergic sequelae.

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

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

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

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

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

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

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

121 versely, N/OFQ receptor antagonists worsened dyskinesia expression.

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

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

124 2% and 22%), and higher incidence of tardive dyskinesia for chlorpromazine versus clozapine (risk dif

125 concurrently identified, and primary ciliary dyskinesia, for which causative genes have been previous

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

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

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

129 main reasons underlying the reduced risk of dyskinesia have not yet been fully characterized.

130 was the change in on time without bothersome dyskinesia (ie, good quality on time) at 3 months as rec

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

132 set: esotropia in 54%, exotropia in 26%, and dyskinesia in 10%.

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

134 Here we show that levodopa-induced dyskinesia in hemiparkinsonian rats is strongly associat

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

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

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

138 g proteins may be useful in the treatment of dyskinesia in Parkinson's patients.

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

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

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

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

146 ted with the development of levodopa-induced dyskinesias in animal models of Parkinsonism.

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

148 have a place in the management of disabling dyskinesias in Parkinson's disease.

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 Tardive dyskinesia is a persistent movement disorder induced by

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

160 -3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia is an incapacitating complication of L-DOPA t

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

162 Although dyskinesia is associated with dynamic changes in primary

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

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

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

166 he drug regimen the usual course of onset of dyskinesias is observed.

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

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

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

170 -3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID) in Parkinson's disease (PD), boosting M

171 -3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID) in Parkinson's disease shed light, nota

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

173 4-Dihydroxyphenyl-L-alanine (L-DOPA)-induced dyskinesia (LID) is a debilitating side effect of long-t

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

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

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

177 -3,4-dihydroxyphenylalanine (l-DOPA)-induced dyskinesia (LID), a common motor complication of current

178 L-DOPA-induced dyskinesia (LID), a detrimental consequence of dopamine

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

180 ptor (D1R) is associated with L-DOPA-induced dyskinesia (LID), a major complication of L-DOPA treatme

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

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

187 icial effects are hindered by L-DOPA-induced dyskinesia (LID).

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

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

190 rging strategies for managing L-dopa-induced dyskinesias (LIDs) in patients with Parkinson disease ha

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 croinjections revealed that N/OFQ attenuated dyskinesias more potently and effectively when microinje

195 Primary ciliary dyskinesia most often arises from loss of the dynein mot

196 Dyskinesias, motor fluctuations and demands in dopaminer

197 rsor levodopa gradually induces involuntary "dyskinesia" movements.

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

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

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

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

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

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

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

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

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

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

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

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

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 genetically heterogeneous recessiv

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

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

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

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

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

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

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

222 tion (CD) similar to that of primary ciliary dyskinesia (PCD) may contribute to increased respiratory

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

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

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

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

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

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

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

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

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

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

233 y conserved organelles cause primary ciliary dyskinesia (PCD).

234 Cilia motility defects cause primary ciliary dyskinesia (PCD, MIM244400), a disorder affecting 1:15,0

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

236 lies with epilepsy and paroxysmal exertional dyskinesia (PED).

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

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

239 When dyskinesia persists during therapeutic deep brain stimul

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

241 nd ciliary motility, causing primary ciliary dyskinesia phenotypes that include hydrocephalus and lat

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

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

244 Paroxysmal non-kinesigenic dyskinesia (PNKD) is a rare autosomal dominant movement

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

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 tral apparatus that includes primary ciliary dyskinesia protein 1 (Pcdp1).

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

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 N) or internal globus pallidus (GPi) reduces dyskinesias remain largely unknown.

264 Tardive dyskinesia results from exposure to dopamine receptor an

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

266 rogressive, chronic disease characterized by dyskinesia, rigidity, instability, and tremors.

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

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

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

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

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

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

278 ntral gyrus compared to the patients without dyskinesias, suggesting that dyskinetic patients may hav

279 Tardive dyskinesia (TD) has no well-accepted treatments or known

280 by chronic haloperidol as a model of tardive dyskinesia (TD) in rats, we confirmed the antidyskinetic

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

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

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

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

285 L-DOPA-induced dyskinesia, the rate-limiting side effect in the therapy

286 iling hypothesis that links levodopa-induced dyskinesia to an altered sensitivity to dopamine only in

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

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

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

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

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

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 ttachment factor that causes primary ciliary dyskinesia when mutated.

296 ts were ineffective in striatum but worsened dyskinesias when given in SN.

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

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

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

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