ライフサイエンスコーパス: palsy

1 or premature or neuroprotection or 'cerebral palsy'].

2 th Lewy bodies, and progressive supranuclear palsy).

3 elated neurological disorders (e.g. cerebral palsy).

4 's disease (AD) and progressive supranuclear palsy.

5 sis, necrotizing enterocolitis, and cerebral palsy.

6 ged 3-9 years with spastic diplegic cerebral palsy.

7 ss in children and adolescents with cerebral palsy.

8 associated with increased risks of cerebral palsy.

9 le loss, as seen in progressive supranuclear palsy.

10 movement dysfunctions such as abducens nerve palsy.

11 nagement of unilateral Superior Oblique (SO) palsy.

12 seful in cases of bilateral superior oblique palsy.

13 ent abnormal findings indicative of cerebral palsy.

14 n of early neuronal connectivity in cerebral palsy.

15 in preterm infants that can lead to cerebral palsy.

16 acteristics such as progressive supranuclear palsy.

17 ns owing to presumed unilateral fourth nerve palsy.

18 ess specifically in progressive supranuclear palsy.

19 tauopathies such as progressive supranuclear palsy.

20 king clinical diagnosis of dystonic cerebral palsy.

21 mporal dementia and progressive supranuclear palsy.

22 l syndrome, but not progressive supranuclear palsy.

23 icantly associated with the rate of cerebral palsy.

24 odevelopmental disorders, including cerebral palsy.

25 annot account for pulley displacements in SO palsy.

26 egions examined for progressive supranuclear palsy.

27 IR and MR pulleys were displaced in acquired palsy.

28 system atrophy, and progressive supranuclear palsy.

29 ectus pulleys typically were displaced in SO palsy.

30 ther management of spastic diplegia cerebral palsy.

31 ical patterns of incomitant strabismus in SO palsy.

32 splaced in either unilateral or bilateral SO palsy.

33 the burden of long-term disability in facial palsy.

34 tively to the diagnosis of dystonic cerebral palsy.

35 with orbital involvement and a cranial nerve palsy.

36 orizontal gaze palsy, and bilateral abducens palsy.

37 o surgery developed a temporary radial nerve palsy.

38 factors, genomic factors may cause cerebral palsy.

39 n participants with progressive supranuclear palsy.

40 in individuals with progressive supranuclear palsy.

41 in patients with severe dyskinetic cerebral palsy.

42 untary toe walking in children with cerebral palsy.

43 novel treatment for progressive supranuclear palsy.

44 eimer's disease and progressive supranuclear palsy.

45 in patients with severe dyskinetic cerebral palsy.

46 currence of cranial nerve (CN)3, CN4, or CN6 palsies.

47 senting within 72 hours of the onset of Bell palsy?

48 auses for dementia (progressive supranuclear palsy = 1, Lewy body disease = 1, vascular brain injury

49 ndon advancements for bilateral fourth nerve palsy: 11 symmetric (</=2 prism diopters [pd] hyperdevia

50 em atrophy, 34 with progressive supranuclear palsy, 15 with corticobasal degeneration, 50 with Alzhei

51 4 controls, 6 AD, 3 progressive supranuclear palsy, 2 cortico basal syndrome) underwent 180-min PET w

52 4 controls, 6 AD, 3 progressive supranuclear palsy, 2 cortico basal syndrome) underwent 180-min PET w

53 ery were frequent (recurrent laryngeal nerve palsy 25.3%; hypoparathyroidism 6%).

54 taset included 551 individuals with cerebral palsy (321 individuals from the PERRIN programme and 230

55 e painful radiculitis (65.9%), cranial nerve palsy (43.4%), and headache (28.3%).

56 ls a total of 65 patients with unilateral SO palsy; 54 congenital and 11 acquired, who met the study

57 se (12.8%; n = 26), progressive supranuclear palsy (6.4%; n = 13), cerebrovascular diseases (1%; n =

58 (46.7% vs 31.9%), recurrent laryngeal nerve palsy (9.5% vs 0.5%), reoperations (18.6% vs 11.0%), 90-

59 f the following: moderate to severe cerebral palsy, a cognitive score less than 85 on the Bayley Scal

60 TX6 are shared with progressive supranuclear palsy, a neurodegenerative disease associated with misfo

61 ls or patients with progressive supranuclear palsy, a type of FTLD-tau.

62 f maternal or fetal birth trauma or cerebral palsy after childbirth.

63 ) is the second most common type of cerebral palsy after spastic forms.

64 Twenty-eight children with cerebral palsy (age 3-14 years), 24 typically-developing children

65 ing the curves for individuals with cerebral palsy aged 1 year to 21 years, we illustrate how this ne

66 Botulism manifests with cranial nerve palsies and flaccid paralysis in children and adults.

67 nd quality of life in children with cerebral palsy and a Gross Motor Function Classification System (

68 umber of survivors with IVH develop cerebral palsy and cognitive deficits.

69 umber of survivors with IVH develop cerebral palsy and cognitive deficits.

70 ver, found on human progressive supranuclear palsy and corticobasal degeneration brain slices.

71 n autopsy-confirmed progressive supranuclear palsy and corticobasal degeneration than in controls, bu

72 lzheimer's disease, progressive supranuclear palsy and corticobasal degeneration, which are character

73 n and tau burden in progressive supranuclear palsy and corticobasal degeneration.

74 Many patients with progressive supranuclear palsy and corticobasal syndrome had language impairments

75 rophy compared with progressive supranuclear palsy and corticobasal syndrome.

76 otemporal dementia, progressive supranuclear palsy and corticobasal syndrome.

77 sive aphasia (PPA), progressive supranuclear palsy and corticobasal syndrome.

78 Incidence rates of cerebral palsy and hazard ratios (HRs) with 95% CIs, adjusted for

79 and postoperative recurrent laryngeal nerve palsy and hypoparathyroidism.

80 Perinatal stroke causes cerebral palsy and lifelong disability.

81 Progressive supranuclear palsy and Parkinson's disease have distinct underlying n

82 subject presenting with dyskinetic cerebral palsy and partial agenesis of the corpus callosum, while

83 icantly reduced in Progressive Supra-nuclear Palsy and Picks' disease, two distinct primary tauopathi

84 ipants had a confirmed diagnosis of cerebral palsy and ranged in age from 1 year to 17 years at basel

85 r dysfunction in conditions such as cerebral palsy and spinal cord injury.

86 r dysfunction in conditions such as cerebral palsy and spinal cord injury.SIGNIFICANCE STATEMENT Acqu

87 The incidence of fourth nerve palsy and the frequency of each etiology were calculated

88 system atrophy, and progressive supranuclear palsy and to accurately distinguish between these diseas

89 ce for early, accurate diagnosis of cerebral palsy and to summarize best available evidence about cer

90 ificantly displaced in superior oblique (SO) palsy and whether displacements account for strabismus p

91 ve to patients with progressive supranuclear palsy and with control subjects, in the hippocampus and

92 ), 19 patients with progressive supranuclear palsy, and 13 age- and sex-matched controls.

93 lzheimer's disease, progressive supranuclear palsy, and a control case to assess the 18F-AV-1451 bind

94 ment, convergent strabismus, horizontal gaze palsy, and bilateral abducens palsy.

95 lzheimer's disease, progressive supranuclear palsy, and chronic traumatic encephalopathy.

96 ataxia, dysarthria, dystonia, vertical gaze palsy, and cognitive decline.

97 lzheimer's disease, progressive supranuclear palsy, and corticobasal degeneration patient brain tissu

98 ple-system atrophy, progressive supranuclear palsy, and corticobasal degeneration was consistently sh

99 ral dementia (FTD), progressive supranuclear palsy, and corticobasal degeneration.

100 ple-system atrophy, progressive supranuclear palsy, and corticobasal degeneration.

101 n with asthma, learning disability, cerebral palsy, and death.

102 lzheimer's disease, progressive supranuclear palsy, and dementia with Lewy bodies, we found that curc

103 k with patients with schizophrenia, cerebral palsy, and hemispatial neglect.

104 ith Lewy bodies) or progressive supranuclear palsy are misdiagnosed as having multiple system atrophy

105 Topography and severity of cerebral palsy are more difficult to ascertain in infancy, and ma

106 rates and the severity spectrum of cerebral palsy are reduced.

107 f IIH such as papilledema and abducens nerve palsy are well recognized, but less common retinal manif

108 of studies of rarer outcomes (e.g., cerebral palsy), are needed to confirm whether such risks are sim

109 gnoses among these children include cerebral palsy, autism spectrum disorder trait, nutritional defic

110 /mental retardation, Down syndrome, cerebral palsy, autism spectrum disorder).

111 to the risk of developing CN3, CN4, and CN6 palsy between cohorts.

112 Cerebral palsy, blindness, and deafness assessed by a pediatricia

113 SF WBC >= 5/muL with blasts or cranial nerve palsies, brain/eye involvement, or hypothalamic syndrome

114 comprised 71% of all children with cerebral palsy, but not for preterm infants.

115 system atrophy and progressive supranuclear palsy, but not Parkinson's disease, showed a broad netwo

116 requently observed in children with cerebral palsy, but the mechanisms involved have not been clarifi

117 body mass index (BMI) and rates of cerebral palsy by gestational age and to identify potential media

118 The number of cerebral palsy cases in each BMI category was 64, 1487, 728, 239,

119 nt of damaging de novo mutations in cerebral palsy cases.

120 lzheimer's disease, progressive supranuclear palsy, chronic traumatic encephalopathy, and other tauop

121 nths after surgery in children with cerebral palsy classified as GMFCS levels II and III.

122 k of developing subsequent CN3, CN4, and CN6 palsies compared with the control cohort (HR, 2.67, P <

123 oforms in brains of progressive supranuclear palsy, corticobasal degeneration and familial tauopathy

124 from Pick disease, progressive supranuclear palsy, corticobasal degeneration, and chronic traumatic

125 were calculated for progressive supranuclear palsy, corticobasal degeneration, and neurofibrillary ta

126 heimer tauopathies (progressive supranuclear palsy, corticobasal degeneration, argyrophilic grain dis

127 otemporal dementia, progressive supranuclear palsy, corticobasal syndrome and controls.

128 classifications of progressive supranuclear palsy/corticobasal degeneration (PSP/CBD) or multiple-sy

129 ioceptive deficits in children with cerebral palsy (CP) and linked these with weaker somatosensory co

130 e who survive have a higher rate of cerebral palsy (CP) compared with babies born at term.

131 d body composition in children with cerebral palsy (CP) could be due to differences in energy intake,

132 Individuals with cerebral palsy (CP) have a reduced somatosensory cortical respons

133 Persons with cerebral palsy (CP) have an increased risk for secondary chronic

134 Cerebral Palsy (CP) is a chronic childhood disorder with limited

135 Bayley III), composition scores, or cerebral palsy (CP).

136 t and in children with mild spastic cerebral palsy (CP; n = 15/group; 4-11 y).

137 Dyskinetic cerebral palsy (DCP) is the second most common type of cerebral p

138 s varied widely, and the classic pontobulbar palsy described in BVVL was not constant.

139 Cerebral palsy describes the most common physical disability in c

140 tries, children were followed for a cerebral palsy diagnosis through 2012.

141 Search terms included cerebral palsy, diagnosis, detection, prediction, identification,

142 ammatory bowel disease, infections, cerebral palsy, dilated cardiomyopathy, muscular dystrophy, and s

143 tcome of death, stroke, MI, or cranial nerve palsy during the periprocedural period (OR: 0.75; 95% CI

144 affecting motor function other than cerebral palsy (eg, spina bifida or muscle diseases) were exclude

145 degeneration, nine progressive supranuclear palsy, eight Pick's disease, three frontotemporal dement

146 nts, clinical signs and symptoms of cerebral palsy emerge and evolve before age 2 years; therefore, a

147 sorder, severe learning disability, cerebral palsy, epilepsy, muscle or skeletal disorders, trauma, a

148 Donors with progressive supranuclear palsy exhibited more variation in inhibitor sensitivity,

149 e lifelong drug-resistant epilepsy, cerebral palsy, feeding difficulties, intellectual disability and

150 test to distinguish progressive supranuclear palsy from Lewy body disorders.

151 le of children and adolescents with cerebral palsy from the Netherlands and Canada.

152 dson's syndrome and progressive supranuclear palsy-frontal subtypes) and 20 healthy control subjects

153 Children with cerebral palsy generally showed lower EMG levels than typically-d

154 Like progressive supranuclear palsy, globular glial tauopathy and argyrophilic grain d

155 with mild-moderate crouch gait from cerebral palsy (GMFCS I-II) completed the study.

156 Patients with severe dyskinetic cerebral palsy (Gross Motor Functioning Classification System lev

157 s for children and adolescents with cerebral palsy grouped by GMFCS level.

158 0% of patients with progressive supranuclear palsy had corticobasal syndrome-like features.

159 mporal dementia and progressive supranuclear palsy had impaired response inhibition, with longer stop

160 wenty-four children with unilateral cerebral palsy had physiological and anatomical measures of the m

161 system atrophy and progressive supranuclear palsy have elevated free-water in the substantia nigra.

162 onnaires were used for diagnosis of cerebral palsy, hearing and vision impairments, and cognition for

163 the Psychomotor Development Index), cerebral palsy, hearing or visual impairment, and anthropometric

164 ditary neuropathy with liability to pressure palsies (HNPP).

165 in patients with severe dyskinetic cerebral palsy; however, the current level of evidence for the ef

166 LS (HR, 1.0 [reference]), progressive bulbar palsy (HR, 1.48; 95% CI, 0.58-3.75; P = .41), and upper

167 ondition, GM hemorrhage can lead to cerebral palsy, hydrocephalus, and mental retardation.

168 pplied to a neonatal mouse model of cerebral palsy (Hypoxic-Ischaemic Encephalopathy).

169 wy body disease and progressive supranuclear palsy if a patient developed orthostatic hypotension or

170 incidence of isolated, presumed fourth nerve palsy in a defined population, and to report the frequen

171 n between maternal BMI and rates of cerebral palsy in full-term children was mediated through asphyxi

172 literature about early diagnosis of cerebral palsy in MEDLINE (1956-2016), EMBASE (1980-2016), CINAHL

173 It is uncertain whether risk of cerebral palsy in offspring increases with maternal overweight an

174 identify all cases of isolated fourth nerve palsy in Olmsted County, Minnesota, USA diagnosed over a

175 For cerebral palsy in survivors, magnesium sulphate treatment had a s

176 , and increased for progressive supranuclear palsy in the putamen, caudate, thalamus, and vermis, and

177 eimer's disease and progressive supranuclear palsy in vivo would help to develop biomarkers for these

178 Children with cerebral palsy, in contrast, continue to co-contract agonist and

179 ementia and 18 with progressive supranuclear palsy, including both Richardson's syndrome and progress

180 Progressive supranuclear palsy is a rare neurodegenerative disease associated wit

181 Cerebral palsy is the most frequent cause of severe physical disa

182 obasal syndrome had progressive supranuclear palsy-like features and 30% of patients with progressive

183 We speculate that children with cerebral palsy maintain a co-contraction activation pattern when

184 lude that at least some subtypes of cerebral palsy may be caused by de novo genetic mutations and pat

185 Bilateral fourth nerve palsy may be symmetric or asymmetric with combined verti

186 on owing to presumed unilateral fourth nerve palsy, measuring 14-25 prism diopters (PD) in straight-a

187 stem atrophy (MSA), progressive supranuclear palsy (MSP)).

188 system atrophy from progressive supranuclear palsy (multiple system atrophy versus progressive supran

189 ntly diagnosed with progressive supranuclear palsy (n = 16, seven males, age at death 68.9 +/- 6.0 ye

190 volume loss in both progressive supranuclear palsy (n = 340 regions; beta 0.155; 95% CI: 0.061, 0.248

191 ), a false aneurysm (n=1), and phrenic nerve palsy (n=1) were observed.

192 n severity, in both progressive supranuclear palsy [n = 340 regions; beta 0.036; 95% confidence inter

193 set of 70 patients (progressive supranuclear palsy, n = 22; corticobasal syndrome, n = 13; behavioura

194 inflamed controls (ie, individuals with Bell palsy, normal pressure hydrocephalus, or Tourette syndro

195 5% CI, -3.3% to 9.6%; P = .47), and cerebral palsy occurred in 18/419 (4.3%) vs 25/443 (5.6%), for a

196 Phrenic nerve palsy occurred in a patient in whom phrenic pacing was i

197 Individuals with cerebral palsy often exhibit crouch gait, a debilitating and inef

198 In unilateral SO palsy, on average the medial rectus (MR) pulley was disp

199 ditary neuropathy with liability to pressure palsies or demyelinating forms of Charcot-Marie-Tooth di

200 al impairment was defined as severe cerebral palsy or a composite motor or composite cognitive score

201 not differ between isotropic and anisotropic palsy or between patients with cyclotropia of less than

202 entia (AUC=92.13%), progressive supranuclear palsy or corticobasal syndrome (AUC=88.47%), and Parkins

203 The incidence of cerebral palsy or other major neurological impairments was not si

204 nifesting with developmental delay, cerebral palsy or seizures.

205 : 0.45; 95% CI: 0.27 to 0.75); cranial nerve palsy (OR: 0.07; 95% CI: 0.04 to 0.14); and the composit

206 19.5, P < 0.01) and progressive supranuclear palsy (OR: 3.1, 95% CI: 1.1-8.9, P = 0.032).

207 24.2, P < 0.01) and progressive supranuclear palsy (OR: 4.8, 95% CI: 1.7-13.6, P < 0.01).

208 otemporal dementia, progressive supranuclear palsy, or Alzheimer's disease.

209 mental impairment (cognitive delay, cerebral palsy, or hearing or vision loss) at 22 to 26 months of

210 Alzheimer disease, progressive supranuclear palsy, or multiple system atrophy.

211 efined as any of cognitive deficit, cerebral palsy, or severe visual or hearing impairment.

212 stem atrophy versus progressive supranuclear palsy: OR: 11.2, 95% CI: 3.2-39.2, P < 0.01].

213 stem atrophy versus progressive supranuclear palsy: OR: 3.4, 95% CI: 1.2-9.7, P = 0.023).

214 .4% male), 3029 were diagnosed with cerebral palsy over a median 7.8 years of follow-up (risk, 2.13 p

215 One patient (1%) had fourth nerve palsy owing to a known intracranial neoplasm.

216 tic and dynamic validated scoring for facial palsy patients, and complications.

217 sidential care than progressive supranuclear palsy patients, whereas patients with Lewy body disease

218 9 to 2.13 cases of recurrent laryngeal nerve palsy per 100 operations.

219 9%), paresthesias (32.5%), peripheral facial palsy (PFP) (36.4%), meningeal signs (19.5%), and parese

220 PIck's disease and Progressive supranuclear palsy Prevalence and INcidence study (PiPPIN).

221 e confers long-term benefits beyond cerebral palsy prevention with sex-specific differences in respon

222 Progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) are neur

223 Studies of progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) suggest

224 ential diagnosis of progressive supranuclear palsy (PSP) and Lewy body disorders, which include Parki

225 s disease (PD) from progressive supranuclear palsy (PSP) and multiple system atrophy (MSA), which hav

226 al in patients with progressive supranuclear palsy (PSP) and multiple system atrophy (MSA).

227 in samples from two progressive supranuclear palsy (PSP) cases and a MAPT P301L mutation carrier.

228 o tau aggregates in progressive supranuclear palsy (PSP) have yielded mixed results.

229 Progressive supranuclear palsy (PSP) is a neurodegenerative disorder characterize

230 Progressive supranuclear palsy (PSP) is a rare and progressive neurodegenerative

231 phasia (nfvPPA) and progressive supranuclear palsy (PSP) or corticobasal degeneration (CBD) proved by

232 in 17 patients with progressive supranuclear palsy (PSP) Richardson's syndrome.

233 ubcortical-dominant progressive supranuclear palsy (PSP) tau topologies.

234 m atrophy (MSA) and progressive supranuclear palsy (PSP) than in Parkinson disease (PD), we hypothesi

235 stem atrophy (MSA), progressive supranuclear palsy (PSP), and corticobasal syndrome (CBS) have signs

236 Progressive supranuclear palsy (PSP), previously believed to be a common cause of

237 eneration (CBD) and progressive supranuclear palsy (PSP), tau also aggregates in astrocytes and oligo

238 m atrophy (MSA) and progressive supranuclear palsy (PSP), the most common atypical parkinsonian look-

239 ants of survival in progressive supranuclear palsy (PSP).

240 er disease (AD) and progressive supranuclear palsy (PSP).

241 not specific versus progressive supranuclear palsy (PSP).

242 rognostic factor in progressive supranuclear palsy (PSP).

243 ins of AD (AD-tau), progressive supranuclear palsy (PSP-tau), and corticobasal degeneration (CBD-tau)

244 e (PD; n = 32), and progressive supranuclear palsy (PSP; n = 31), were included in our cohort for dia

245 and died with FTLD (progressive supranuclear palsy [PSP], n = 10; corticobasal degeneration [CBD], n

246 (GMFM-66) and seven domains of the Cerebral Palsy Quality of Life Questionnaire ([CP-QoL] social wel

247 eimer's disease and progressive supranuclear palsy relative to controls [main effect of group, F(2,41

248 y, in patients with progressive supranuclear palsy, relative to patients with Alzheimer's disease, 18

249 %, and 2.8 % for cranial nerves VI, III, IV palsies respectively.

250 linically diagnosed progressive supranuclear palsy (Richardson's syndrome), 24 patients with clinical

251 Cerebral palsy risk genes in enriched pathways were shown to regu

252 Candidate cerebral palsy risk genes overlapped with neurodevelopmental diso

253 roidism, transient recurrent laryngeal nerve palsy (RLNP), reoperations for bleeding, inadvertently r

254 isk [RR], 2.2; 95% CI, 1.2-4.1) and cerebral palsy (RR, 2.6; 95% CI, 1.1-6.2) were found.

255 ities (RR, 10.6; 95% CI, 5.5-20.2), cerebral palsy (RR, 4.8; 95% CI, 2.3-10.0), epilepsy (RR, 4.9; 95

256 g clinical manifestations of horizontal gaze palsy, scoliosis, and intellectual disability.

257 ion sensitivity for progressive supranuclear palsy seeds by ~10(6) Hofmeister analysis also improved

258 system atrophy and progressive supranuclear palsy shared several symptoms and signs, ataxia and stri

259 tients with a clinical diagnosis of cerebral palsy should be genetically investigated before causatio

260 -developing children, children with cerebral palsy showed no age-related decline in tibialis anterior

261 while patients with progressive supranuclear palsy showed, relative to controls, increased 18F-AV-145

262 lower GMFCS levels (ie, less severe cerebral palsy) showed higher developmental limits that were reac

263 arize best available evidence about cerebral palsy-specific early intervention that should follow ear

264 ccur commonly in conditions such as cerebral palsy, stroke, muscular dystrophy, Charcot-Marie-Tooth d

265 obasal syndrome and progressive supranuclear palsy syndrome were identified out of the 943 citations

266 mporal dementia and progressive supranuclear palsy syndrome.

267 of binding sites on progressive supranuclear palsy tau deposits for 11C-PBB3 than 18F-AV-1451.

268 rates of periprocedural MI and cranial nerve palsy than CEA.

269 and in no case was an isolated fourth nerve palsy the presenting sign of an intracranial tumor.

270 In a clinical trial of cerebral palsy, the level of plasma interleukin-8 (IL-8) was incr

271 ns owing to presumed unilateral fourth nerve palsy, there appears no clear advantage of 2-muscle surg

272 In children with unilateral cerebral palsy (uCP), the corticospinal tract (CST)-wiring patter

273 perative follow-up in patients with abducens palsy undergoing IRT shows a significant improvement in

274 mal results in subgroups of patients with SO palsy: unilateral versus bilateral, congenital versus ac

275 injury in children with unilateral cerebral palsy (USCP).

276 o oral corticosteroids for treatment of Bell palsy was associated with a higher proportion of people

277 Cerebral palsy was observed in 9.5% of extremely preterm children

278 kinson's disease or progressive supranuclear palsy was observed.

279 The whole spectrum of severity of cerebral palsy was represented in terms of motor function, using

280 or 3 patients (4%) the cause of fourth nerve palsy was undetermined.

281 study, the majority of isolated fourth nerve palsies were presumed congenital, even though they prese

282 rmal-weight mothers, adjusted HR of cerebral palsy were 1.22 (95% CI, 1.11-1.33) for overweight, 1.28

283 s of granulation tissue, otalgia, and facial palsy were 90.9%, 31.8%, and 9.1%, respectively.

284 the following subgroups of patients with SO palsy were compared with normal results in subgroups of

285 k of obesity at age 5 y and risk of cerebral palsy were similar between planned repeat CS or unschedu

286 But patients with progressive supranuclear palsy were strongly biased towards a pro-saccade decisio

287 ed more frequently in children with cerebral palsy when compared to typically-developing children and

288 d MR pulleys were displaced in congenital SO palsy, whereas the IR and MR pulleys were displaced in a

289 easurements data from children with cerebral palsy who had been prescribed fixed ankle-foot orthoses

290 records of patients with chronic sixth nerve palsy who underwent dual augmented VRT with or without m

291 smus practice with a complete lateral rectus palsy who underwent IRT were studied.

292 l records of all patients with unilateral SO palsy who underwent one of the aforementioned IO weakeni

293 countries, 2 in 3 individuals with cerebral palsy will walk, 3 in 4 will talk, and 1 in 2 will have

294 robable or possible progressive supranuclear palsy with a score of 20 or greater on the Mini-Mental S

295 Contralateral eye muscle in third nerve palsy with aberrant innervation offers the advantage of

296 onal study on patients with oculomotor nerve palsy with aberrant innervation who had contralateral ey

297 bduction associated with chronic sixth nerve palsy with low rate of induced vertical deviation.

298 rome, Kallmann syndrome, and horizontal gaze palsy with progressive scoliosis.

299 Displacements were similar in bilateral SO palsy, with the SR pulley additionally displaced 0.9 mm

300 terns of incomitant strabismus typical of SO palsy, without requiring any abnormality of SO or inferi