ライフサイエンスコーパス: levodopa

1 ion of cotemporaneous bursts were reduced by levodopa.

2 ts of citalopram were stronger than those of levodopa.

3 sodes that are not predictably responsive to levodopa.

4 ed with PD patients with stable responses to levodopa.

5 onia and a dramatic long-lasting response to levodopa.

6 son's disease who have motor fluctuations on levodopa.

7 o alleviated dyskinetic behaviors induced by levodopa.

8 ed-release, capsule formulation of carbidopa-levodopa.

9 1) compared with immediate-release carbidopa-levodopa.

10 e abnormalities with STN stimulation but not levodopa.

11 patients were on or off the dopamine prodrug levodopa.

12 ration compared with that achieved with oral levodopa.

13 ation and that address symptoms resistant to levodopa.

14 ly, differences in the long-term response to levodopa.

15 etrahydropyridine (MPTP) and dyskinetic with levodopa.

16 awal of levodopa and after administration of levodopa.

17 ope in patients with Parkinson's disease OFF levodopa (-0.20 degrees /cycle, P = 0.002).

18 ts with early Parkinson's disease to receive levodopa (100 mg three times per day) in combination wit

19 el imaging techniques (6-[fluoride-18]fluoro-levodopa [(18)F-DOPA] PET-CT and glucagon-like peptide 1

20 e conversion with extended-release carbidopa-levodopa, 23 (5%) of 450 patients withdrew because of ad

21 ed to each participant a dopamine precursor (levodopa), a dopamine antagonist (risperidone), and a pl

22 We found that levodopa-a synthetic precursor of dopamine-increases res

23 erial tyrosine decarboxylases at the site of levodopa absorption, proximal small intestine, had a sig

24 ydroxydopamine lesioned model of PD, chronic levodopa administration induced characteristic dyskinesi

25 patients, and PIGD patients before and after levodopa administration.

26 may combine to explain the addictive use of levodopa after loss of midbrain dopamine neurons in some

27 Determining whether levodopa also has a disease-modifying effect could provi

28 doses of co-careldopa were 62.5 mg (50 mg of levodopa and 12.5 mg of carbidopa) and the remaining dos

29 d the remaining doses were 125 mg (100 mg of levodopa and 25 mg of carbidopa).

30 2% (SD 14.91) for extended-release carbidopa-levodopa and 29.79% (15.81) for immediate-release carbid

31 tly seated following overnight withdrawal of levodopa and after administration of levodopa.

32 This patient received levodopa and benserazide (200 and 50 mg, respectively) f

33 ddress gait disorders that respond poorly to levodopa and conventional DBS targets.

34 ptomatic treatment by the dopamine precursor levodopa and dopamine agonists can improve motor symptom

35 Strong evidence supports using levodopa and dopamine agonists for motor symptoms at all

36 se and motor fluctuations who were receiving levodopa and other antiparkinsonian drugs.

37 Levodopa and other dopaminergic treatments have not had

38 siology via aberrant processing of exogenous levodopa and release of dopamine as false neurotransmitt

39 We demonstrate that levodopa and risperidone led to opposite effects in meas

40 combined accumulation of dopamine precursor levodopa and serotonin precursor 5-hydroxytryptophan.

41 tinal pigment epithelial (RPE) cells produce levodopa and their transplantation into the striatum mig

42 years; 11 females) received a single dose of levodopa and then performed a task in which they had to

43 increasing brain dopamine levels (150 mg of levodopa) and blocking dopamine receptors (1.5 mg of hal

44 al lesions were then challenged with l-dopa (levodopa) and various dopamine receptor agonists, and re

45 monotherapy, (2) acute coadministration with levodopa, and (3) chronic coadministration for 1 month.

46 tients treated with dopamine agonists and/or levodopa, and age- and education- matched neurologically

47 able morning off periods, were responsive to levodopa, and were on stable doses of anti-parkinsonian

48 In situ levels of levodopa are compromised by high abundance of gut bacter

49 eloped, current evidence supports the use of levodopa as initial symptomatic treatment in most patien

50 tment of Parkinson's disease, as adjuncts in levodopa based therapy, or for the treatment of schizoph

51 Grafted monkeys were also challenged with levodopa but did not show any greater responses to these

52 te), and had symptoms that responded to oral levodopa but were insufficiently controlled by optimised

53 response of CaMKIIalpha-D2R interactions to levodopa can alleviate levodopa-induced dyskinesia.

54 patients allocated to immediate-release oral levodopa-carbidopa (difference -1.91 h [95% CI -3.05 to

55 as deep brain stimulation and treatment with levodopa-carbidopa enteral suspension can help individua

56 rom advanced treatments such as therapy with levodopa-carbidopa enteral suspension or deep brain stim

57 ents allocated to the immediate-release oral levodopa-carbidopa group (seven [21%] serious), mainly a

58 We aimed to assess efficacy and safety of levodopa-carbidopa intestinal gel delivered continuously

59 h (SE 0.65) for 35 patients allocated to the levodopa-carbidopa intestinal gel group compared with a

60 ses 35 (95%) of 37 patients allocated to the levodopa-carbidopa intestinal gel group had adverse even

61 dopa plus placebo intestinal gel infusion or levodopa-carbidopa intestinal gel infusion plus oral pla

62 :1) to treatment with immediate-release oral levodopa-carbidopa plus placebo intestinal gel infusion

63 Continuous delivery of levodopa-carbidopa with an intestinal gel offers a promi

64 Most patients benefit dramatically from levodopa/carbidopa, often with further improvement with

65 rary to the model predictions, we found that levodopa caused an increase in the force exerted only in

66 of parkinsonism that is poorly responsive to levodopa, cerebellar ataxia and corticospinal dysfunctio

67 Following levodopa challenge, 5 mg eltoprazine caused a significan

68 an 30, which improved by 33% or more after a levodopa challenge.

69 Parkinson's disease chronically treated with levodopa commonly have delayed or unpredictable onset of

70 y and efficacy of opicapone as an adjunct to levodopa compared with placebo or entacapone in patients

71 and motivation: while the dopamine precursor levodopa, compared with placebo, increased the hedonic e

72 Furthermore, intraperitoneal injection of levodopa could significantly improve the motor dysfuncti

73 arkinson's disease were evaluated ON and OFF levodopa (counterbalanced).

74 ysicians to individually tailor the existing levodopa daily regimen, by potentially reducing the tota

75 t demonstration of the benefit of continuous levodopa delivery in a double-blind controlled study.

76 We found that levodopa did not affect the overall accuracy of choices,

77 mprovement in motor ratings during infusion, levodopa did not alter learning performance or network a

78 Here, we investigated the effects of levodopa (dopamine precursor) on choice performance (iso

79 e to dopaminergic medications (eg, carbidopa-levodopa, dopamine agonists), and slower disease progres

80 tle in the past decade and include carbidopa/levodopa, dopamine agonists, and monoamine oxidase type

81 ks of open-label immediate-release carbidopa-levodopa dose adjustment followed by 6 weeks of open-lab

82 eks of open-label extended-release carbidopa-levodopa dose conversion.

83 men, by potentially reducing the total daily levodopa dose, increasing the dosing interval, and ultim

84 , the expression of which is correlated with levodopa dose, many of which are under the control of ac

85 Identical levodopa doses induced markedly higher striatal synaptic

86 its including decreased off-time and reduced levodopa dosing frequency.

87 fluctuations may be managed by modifying the levodopa dosing regimen or by adding several other medic

88 In the 'OFF' state withdrawn from levodopa, dyskinetic and non-dyskinetic patients had sim

89 (UPDRS item 4) (1.94 [1.33-2.82]), a higher levodopa equivalent daily dose (1.63 [1.09-2.43]), and m

90 NC), age at plasma collection, sex, and the levodopa equivalent daily dose (LEDD), deriving first-pa

91 ies of daily living, and -complications, and levodopa equivalent daily dose (LEDD).

92 on Scale (GDS-15), RBD medication use, total levodopa equivalent daily dose, and dopamine agonist (DA

93 , education, disease duration, language, and levodopa equivalent daily dose.

94 The estimated monthly levodopa equivalent dose changes were 10.9 in the low es

95 we evaluated the longitudinal change in the levodopa equivalent dose per month using a linear mixed

96 ied Parkinson's Disease Rating Scale scores, levodopa equivalent dose, and global Pittsburgh Sleep Qu

97 he independent variable, with adjustment for levodopa equivalent dose, sex, age, disease duration, MD

98 specific T cell responses with age and lower levodopa equivalent dose.

99 independent of cognitive impairment or total levodopa equivalent dose.

100 n, UPDRS III scores off and on medication or levodopa equivalent doses between the two techniques.

101 isease, rates of pre-existing depression and Levodopa equivalent doses of anti-Parkinson's medication

102 However, almost all patients receiving levodopa eventually develop debilitating involuntary mov

103 agonist buspirone prior to levodopa reduced levodopa-evoked striatal synaptic dopamine increases and

104 dyskinesias received 200mg fast-acting oral levodopa following prolonged withdrawal from their norma

105 nd watch strategy, and establish whether new levodopa formulations will delay onset of dyskinesia.

106 g-term treatment with the dopamine precursor levodopa gradually induces involuntary "dyskinesia" move

107 mization by an average of 5.2 letters in the levodopa group and by 3.8 letters in the placebo group (

108 and only 12% in the Parkinson's disease OFF levodopa group.

109 een-group difference at week 80 implies that levodopa had no disease-modifying effect.

110 Although levodopa had no effect in controls, it acquired 2 promin

111 For several decades, the dopamine precursor levodopa has been the primary therapy for Parkinson's di

112 Dopaminergic therapies such as levodopa have provided benefit for millions of patients

113 ase (PD), and the subsequent introduction of levodopa have revolutionalized the field of PD therapeut

114 Levodopa improved consistent micrographia accompanied by

115 Levodopa improves consistent micrographia by restoring t

116 t group) or placebo for 40 weeks followed by levodopa in combination with carbidopa for 40 weeks (del

117 over the course of 80 weeks, treatment with levodopa in combination with carbidopa had no disease-mo

118 mitigated by the outcomes of the PD MED and Levodopa in Early Parkinson's Disease (LEAP) studies.

119 rmulation versus immediate-release carbidopa-levodopa in patients with Parkinson's disease and motor

120 and efficacy of tozadenant as an adjunct to levodopa in patients with Parkinson's disease who have m

121 ntrolled trial of opicapone as an adjunct to levodopa in patients with Parkinson's disease with end-o

122 upport safinamide as an effective adjunct to levodopa in patients with PD and motor fluctuations to i

123 is sensitive to long-term administration of levodopa in PD rats.

124 stine, had a significant impact on levels of levodopa in the plasma of rats.

125 , nor interactions between movement type and levodopa in the STN, nor in the coherence between STN an

126 iological interaction analysis revealed that levodopa increased effective connectivity between the po

127 low level of dopamine sufficient to cause a levodopa-independent continuous form of diphasic dyskine

128 In parallel, levodopa induced an increase in CaMKIIalpha-D2R interact

129 anxiety, obsessive-compulsive disorders, and levodopa induced dyskinesia in Parkinson's disease.

130 sioned 6-hydroxydopamine rats that developed levodopa-induced abnormal involuntary movements (AIMs) a

131 This novel, levodopa-induced difference in the neural responses betw

132 logy, few neuroimaging studies have examined levodopa-induced differences in neural activation betwee

133 Levodopa-induced dyskinesia (LID) develops after repeate

134 Medical treatment of levodopa-induced dyskinesia (LID) in Parkinson disease (

135 Levodopa-induced dyskinesia (LID) is a persistent behavi

136 Levodopa-induced dyskinesia (LID) poses a significant he

137 Effective medical management of levodopa-induced dyskinesia (LID) remains an unmet need

138 duced in striatal neurons of rats exhibiting levodopa-induced dyskinesia [LID; a side-effect to dopam

139 Here we show that levodopa-induced dyskinesia in hemiparkinsonian rats is

140 sion of the prevailing hypothesis that links levodopa-induced dyskinesia to an altered sensitivity to

141 neurons and reverses aberrant plasticity in levodopa-induced dyskinesia.

142 a-D2R interactions to levodopa can alleviate levodopa-induced dyskinesia.

143 Levodopa-induced dyskinesias (LIDs) are the most common

144 ale scores in those Parkinson's disease with levodopa-induced dyskinesias (n = 12), correlated with l

145 Although levodopa-induced dyskinesias could be elicited postopera

146 rtical connectivity as a neural signature of levodopa-induced dyskinesias in humans.

147 eural mechanisms underlying the emergence of levodopa-induced dyskinesias in vivo are still poorly un

148 Levodopa-induced dyskinesias occur in up to 80% of patie

149 n revealed that patients who later developed levodopa-induced dyskinesias, but not patients without d

150 sease (PD) motor symptoms and development of levodopa-induced dyskinesias.

151 ia connectivity that herald the emergence of levodopa-induced dyskinesias.

152 on in parkinsonian patients with and without levodopa-induced dyskinesias.

153 namic causal modelling was applied to assess levodopa-induced modulation of effective connectivity be

154 ividual dyskinesia severity was predicted by levodopa-induced modulation of striato-cortical feedback

155 otor disability, activities of daily living, levodopa-induced motor complications (as assessed with t

156 .001), activities of daily living (P<0.001), levodopa-induced motor complications (P<0.001), and time

157 an earlier age at onset, and less asymmetry, levodopa-induced motor complications, dysautonomia, and

158 advanced Parkinson's disease who have severe levodopa-induced motor complications.

159 licits involuntary movements, referred to as levodopa-induced peak-of-dose dyskinesias.

160 ep brain stimulation (n = 14) or intravenous levodopa infusion (n = 14).

161 e studied the subjects during an intravenous levodopa infusion titrated to achieve a motor response e

162 n the putamen and primary motor cortex after levodopa intake during movement suppression.

163 on-making tasks, following either placebo or levodopa intake in a double blind within-subject protoco

164 The scan was continued for 45 minutes after levodopa intake or until dyskinesias emerged.

165 ), placebo, or entacapone (200 mg with every levodopa intake) for 14-15 weeks.

166 After levodopa intake, the PIGD patients had significantly inc

167 Immediately before and after levodopa intake, we performed fMRI, while patients produ

168 ty emerged during the first 20 minutes after levodopa intake.

169 ew extended release formulation of carbidopa/levodopa (IPX066), safinamide which inhibits MAO-B, dopa

170 role allows levodopa to be delayed, but once levodopa is added to the drug regimen the usual course o

171 Levodopa is the main treatment for symptoms of Parkinson

172 Levodopa is the most effective medical treatment for Par

173 Although levodopa is the most effective medication available for

174 Levodopa is the most effective therapy for Parkinson's d

175 inson's disease using the dopamine precursor levodopa is unfortunately limited by gradual development

176 The optimization of levodopa is, in most cases, the most powerful therapeuti

177 out causing dyskinesia and, as an adjunct to levodopa, it improves motor function without worsening d

178 By boosting dopamine levels using levodopa (l-DOPA) as human subjects made economic decisi

179 ced dyskinesia (LID) develops after repeated levodopa (l-DOPA) exposure in Parkinson disease patients

180 l sensitization that develops after repeated levodopa (l-DOPA) exposure in Parkinson disease patients

181 A clinical trial of levodopa (L-DOPA) in AS is ongoing, although the underly

182 The dopamine precursor levodopa (L-DOPA) increased the task-based learning rate

183 Levodopa (L-DOPA) is widely used for symptomatic managem

184 This study examined whether carbidopa/levodopa (L-DOPA) monotherapy increased dopamine availab

185 t of a single dose of the dopamine precursor levodopa (l-DOPA) on mesostriatal fractional amplitude o

186 reversals would occur on haloperidol than on levodopa (l-DOPA) or placebo.

187 Restoration of dopamine transmission by levodopa (L-DOPA) relieves motor symptoms of PD but ofte

188 Dopamine replacement with levodopa (L-DOPA) represents the mainstay of Parkinson's

189 Levodopa (L-dopa) therapy in PD patients has been shown

190 certain catecholamines viz., dopamine (DA), levodopa (l-Dopa), epinephrine (EP) and norepinephrine (

191 tabolizes the Parkinson's disease medication Levodopa (l-dopa), potentially reducing drug availabilit

192 bacteria from the gut microbiota metabolize Levodopa (L-dopa), reducing bioavailability of the drug

193 dopamine function and sometimes remedied by levodopa (L-DOPA).

194 e precursor and standard anti-Parkinson drug levodopa (l-DOPA).

195 armacological dopamine (DA) replacement with Levodopa [L-dihydroxyphenylalanine (L-DOPA)] is the gold

196 iO(2) nanoparticles for the determination of levodopa (LD) and carbidopa (CD) was described.

197 The dopamine precursor levodopa led to a dose-dependent (inverted U-shape) pers

198 Plasma levodopa levels were determined with and without nalbuph

199 nti-PD effect of levodopa or changing plasma levodopa levels.

200 Treatment with levodopa limited this evolution leading to a relative in

201 double-blind with extended-release carbidopa-levodopa (mean 3.6 doses per day [SD 0.7]) had greater r

202 ouble-blind with immediate-release carbidopa-levodopa (mean 5.0 doses per day [1.2]).

203 .79% (15.81) for immediate-release carbidopa-levodopa (mean difference -5.97, 95% CI -9.05 to -2.89;

204 hioneine, and significantly higher levels of levodopa metabolites and biliverdin than those of normal

205 Extended-release carbidopa-levodopa might be a useful treatment for patients with P

206 In this study, PD patients using Levodopa (n = 25), Deep Brain Stimulation (DBS; n = 6),

207 tients allocated immediate-release carbidopa-levodopa), nausea (six [3%] vs three [2%]), and falls (s

208 Neither Levodopa nor DBS therapy led to significant improvements

209 The effects of levodopa on both local and distant synchronization at 60

210 ibitor citalopram and the dopamine precursor levodopa on decisions to inflict pain on oneself and oth

211 finger movements and of the dopamine prodrug levodopa on induced power in the contralateral primary m

212 ) without compromising the anti-PD effect of levodopa or changing plasma levodopa levels.

213 We gave 31 healthy older adults 150 mg of levodopa or placebo (double-blinded, randomised) 1 hour

214 Sixteen weeks of oral levodopa or placebo administered 3 times daily while pat

215 rmeability, following separate injections of levodopa or saline.

216 and efficacy of CVT-301, a self-administered levodopa oral inhalation powder, for the treatment of pa

217 amic nucleus stimulation (p < 0.005) but not levodopa (p = 0.25).

218 re from off to on state after use of an oral levodopa plus a dopa-decarboxylase inhibitor combination

219 Their pharmacotherapy included oral levodopa plus benserazide or carbidopa in a regimen that

220 tment with either low- or high-dose Sinemet (levodopa plus carbidopa) for 2 weeks and compared their

221 level II) documented visual improvement with levodopa plus carbidopa.

222 ended-release or immediate-release carbidopa-levodopa plus matched placebos.

223 ves pharmacologic approaches (typically with levodopa preparations prescribed with or without other m

224 striato-cortical connectivity in response to levodopa produces an aberrant reinforcement signal produ

225 The implantation of such levodopa-producing cells can concurrently decrease the e

226 k activity by striatal implantation of human levodopa-producing retinal pigment epithelial (hRPE) cel

227 by early disease onset, moderate response to levodopa, rapid progression leading to loss of autonomy

228 Extended-release carbidopa-levodopa reduced daily off-time by, on average, an extra

229 arm aversion for both self and others, while levodopa reduced hyperaltruism.

230 receptor type 1A agonist buspirone prior to levodopa reduced levodopa-evoked striatal synaptic dopam

231 lly, administration of the dopamine prodrug, levodopa, reduced the frequency and duration of periods

232 talopram enhancing behavioral inhibition and levodopa reducing slowing related to being responsible f

233 s reflected in the long-duration response to levodopa, reinterpreted here as the correction of aberra

234 The rates of dyskinesia and levodopa-related fluctuations in motor response did not

235 c therapy, and strategies to delay and treat levodopa-related motor complications and nonmotor Parkin

236 ne agonists) may be initiated first to avoid levodopa-related motor complications.

237 Although levodopa remains the most effective oral pharmacotherapy

238 subjects and trials (p = 0.01), although the levodopa response was not significant.

239 D who may have PD on the basis of a positive levodopa response, clinical progression, imaging and/or

240 These include fluctuating levodopa responses and involuntary movements and posture

241 cant dissociation of vasomotor and metabolic levodopa responses was seen in the striatum/globus palli

242 tase deficiency (SRD) is an under-recognized levodopa-responsive disorder.

243 nsideration of SRD not only in patients with levodopa-responsive motor disorders, but also in patient

244 s had mild developmental delay and developed levodopa-responsive parkinsonism between the ages of 25

245 A 55-year-old levodopa-responsive woman with PD received bilateral put

246 rogression, early postural instability, poor levodopa responsiveness and symmetric involvement) were

247 Levodopa resulted in a strong trend towards impairing ti

248 ence of benefits for galantamine, modafinil, levodopa, rotigotine, clozapine, duloxetine, clonazepam,

249 Thus, increasing dopamine levels with levodopa selectively boosted striatal and substantia nig

250 ation of levodopa, which led to misconceived levodopa-sparing strategies, have been largely mitigated

251 While levodopa therapy alleviates basal ganglia dysfunction in

252 ings reported in patients with PD undergoing levodopa therapy and other symptomatic interventions.

253 Levodopa therapy improves bradykinesia, but treatment va

254 d-of-dose motor fluctuations associated with levodopa therapy in patients with Parkinson disease (PD)

255 picapone compared with placebo as adjunct to levodopa therapy in patients with PD experiencing end-of

256 rs4680 polymorphism modulated the effect of levodopa therapy on planning-related activations in the

257 disadvantages of delaying the initiation of levodopa therapy, the role of dopamine agonists, particu

258 OFF levodopa, this link with acceptance was weakened.

259 hway and BUP1, was able to convert exogenous Levodopa to 3 +/- 4 mg/L codeine via a 14-step bioconver

260 sts such as pramipexole or ropinirole allows levodopa to be delayed, but once levodopa is added to th

261 erion for noninferiority of early receipt of levodopa to delayed receipt.

262 d bacteria in their ability to decarboxylate levodopa to dopamine via tyrosine decarboxylases.

263 tyrosine decarboxylases efficiently convert levodopa to dopamine, even in the presence of tyrosine,

264 dopaminergic and nondopaminergic actions) in levodopa-treated patients with motor fluctuations.

265 dose-finding clinical trial of tozadenant in levodopa-treated patients with Parkinson's disease who h

266 nificant reduction in mean daily off-time in levodopa-treated patients with PD and motor fluctuations

267 We studied 24 patients with levodopa-treated, moderate to advanced Parkinson's disea

268 can explain the increased dosage regimen of levodopa treatment in Parkinson's disease patients.

269 The addition of opicapone 50 mg to levodopa treatment in patients with Parkinson's disease

270 Levodopa treatment is the major pharmacotherapy for Park

271 Chronic levodopa treatment leads to the appearance of dyskinesia

272 ver, motor complications uniquely related to levodopa treatment may emerge that may be difficult to m

273 rk alterations were not seen with open-label levodopa treatment or during disease progression.

274 nic kainic acid lesion of the STN or chronic levodopa treatment reliably suppressed the giant GABAerg

275 Older age at diagnosis and poorer levodopa treatment response were the other factors assoc

276 der age at diagnosis, male sex, poor initial levodopa treatment response, and postural instability an

277 re acquired in each animal before initiating levodopa treatment, and again following the period of da

278 mice, together with the beneficial effect of levodopa treatment, strongly suggest that dysfunction of

279 egulated in direct pathway SPNs upon chronic levodopa treatment.

280 of a parkinsonian lesion followed by chronic levodopa treatment.

281 hese power peaks increased with movement and levodopa treatment.

282 ations in the primary motor cortex following levodopa treatment.

283 motor abnormalities and are not improved by levodopa treatment.

284 letion, which are reduced by apomorphine and levodopa treatments.

285 a variable combination of autonomic failure, levodopa-unresponsive parkinsonism, cerebellar ataxia an

286 ed propensity for falls are interrelated and levodopa-unresponsive symptoms in patients with Parkinso

287 atients allocated extended-release carbidopa-levodopa vs two [1%] of 192 patients allocated immediate

288 Treatment with levodopa was associated with worsening, whereas treatmen

289 Nalbuphine coadministered with levodopa was well tolerated and did not cause sedation.

290 Levodopa was well tolerated during aDBS and led to furth

291 with Parkinson's disease who were receiving levodopa were enrolled and treated at 44 sites in 15 cou

292 No serious adverse effects from levodopa were reported during treatment.

293 m levels, and abnormal reinforcing effect of levodopa when PD+HS patients are confronted with erotic

294 te hypersensitivity of preSMA and putamen to levodopa, which heralds the failure of neural networks t

295 cations arising from the early initiation of levodopa, which led to misconceived levodopa-sparing str

296 idual amblyopia after patching therapy, oral levodopa while continuing to patch 2 hours daily does no

297 duration 9.4 years +/- 2.5) both OFF and ON levodopa while they had to decide whether to engage in a

298 an sites among patients with PD treated with levodopa who experienced at least 1 hour of troublesome

299 d patients with moderate to severe PD taking levodopa who were experiencing motor fluctuations.

300 B permeability are simultaneously induced by levodopa within areas of active microvascular remodeling