ライフサイエンスコーパス: palsy

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

2 spectrum pathology (progressive supranuclear palsy).

3 th Lewy bodies, and progressive supranuclear palsy).

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

5 associated with increased risks of cerebral palsy.

6 icantly associated with the rate of cerebral palsy.

7 odevelopmental disorders, including cerebral palsy.

8 annot account for pulley displacements in SO palsy.

9 egions examined for progressive supranuclear palsy.

10 IR and MR pulleys were displaced in acquired palsy.

11 system atrophy, and progressive supranuclear palsy.

12 ectus pulleys typically were displaced in SO palsy.

13 ther management of spastic diplegia cerebral palsy.

14 ical patterns of incomitant strabismus in SO palsy.

15 splaced in either unilateral or bilateral SO palsy.

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

17 of the ankle joint in children with cerebral palsy.

18 frequent concerns in children with cerebral palsy.

19 ficial role in select cases of severe Bell's palsy.

20 QoL of adolescents with and without cerebral palsy.

21 seful in cases of bilateral superior oblique palsy.

22 ft and heel strike in children with cerebral palsy.

23 le loss, as seen in progressive supranuclear palsy.

24 r cohort with a diagnosis of ataxic cerebral palsy.

25 its with hypertonia in our model of cerebral palsy.

26 echnique for the prevention of phrenic nerve palsy.

27 e left-sided PVs in those with phrenic nerve palsy.

28 ory deficits in the rabbit model of cerebral palsy.

29 ties are common among children with cerebral palsy.

30 ible for the motor deficits seen in cerebral palsy.

31 rbidity, especially the risk of facial nerve palsy.

32 ent abnormal findings indicative of cerebral palsy.

33 motor alignment in some cases of third nerve palsy.

34 f care for ambulatory children with cerebral palsy.

35 atory muscle weakness but without vocal cord palsy.

36 movement dysfunctions such as abducens nerve palsy.

37 in preterm infants that can lead to cerebral palsy.

38 acteristics such as progressive supranuclear palsy.

39 ns owing to presumed unilateral fourth nerve palsy.

40 ess specifically in progressive supranuclear palsy.

41 tauopathies such as progressive supranuclear palsy.

42 l syndrome, but not progressive supranuclear palsy.

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

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

45 th a significant difference in phrenic nerve palsies (0% RF, 5.8% CB; P=0.002).

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

47 4 controls, 6 AD, 3 progressive supranuclear palsy, 2 cortico basal syndrome) underwent 180-min PET w

48 4 controls, 6 AD, 3 progressive supranuclear palsy, 2 cortico basal syndrome) underwent 180-min PET w

49 gnificant reductions in the risk of cerebral palsy (21% vs. 36%, P=0.03) and the risk of moderate or

50 cant difference in proportions with cerebral palsy (23/295 [8%] and 21/314 [7%], respectively; odds r

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

52 dementia [SD]), 22 progressive supranuclear palsy, 50 Alzheimer disease, 6 Parkinson disease, and 17

53 egeneration: 92.7%; progressive supranuclear palsy: 94.1%) in classifying 58 testing subjects.

54 ditary neuropathy with liability to pressure palsies, a peripheral nerve lesion induced by minimal tr

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

56 guidelines for the acute treatment of Bell's palsy advocate for steroid monotherapy, although controv

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

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

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

60 29/279:10.3%); 150/279 (53.7%) with cerebral palsy and 51/279 (18.2%) acquired brain injury.

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

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

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

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

65 on, Pick's disease, progressive supranuclear palsy and corticobasal degeneration.

66 otemporal dementia, progressive supranuclear palsy and corticobasal syndrome.

67 n foot deformities in children with cerebral palsy and discusses treatment options for each of those

68 neurological symptoms - most often cerebral palsy and epilepsy.

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

70 onset movement disorders, including cerebral palsy and juvenile parkinsonism.

71 Perinatal stroke causes cerebral palsy and lifelong disability.

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

73 Moreover, there was an upgaze supranuclear palsy and slow saccades on vertical plane.

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

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

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

77 e rarely performed in patients with cerebral palsy and there is little proven evidence of genetic cau

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

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

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

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

82 ), 19 patients with progressive supranuclear palsy, and 13 age- and sex-matched controls.

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

84 ria (MDC) (congenital, nonprogressive facial palsy, and abduction deficit) and genetic testing for HO

85 l delay, cardiopulmonary anomalies, cerebral palsy, and aspiration pneumonia and among patients with

86 Optic atrophy, vocal cord palsy, and auditory impairment were observed in 5, 6, an

87 lzheimer's disease, progressive supranuclear palsy, and cases of frontotemporal dementia, but the lin

88 presentation, such as headache, sixth nerve palsy, and cerebrospinal fluid (CSF) opening pressure.

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

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

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

92 tic encephalopathy, progressive supranuclear palsy, and corticobasal degeneration.

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

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

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

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

97 al degeneration and progressive supranuclear palsy, are characterized by aggregates of the microtubul

98 th nerve and pupil-sparing partial 3rd nerve palsies as well as progressive neurological findings.

99 s (11.2%) were associated with phrenic nerve palsy as determined by radiographic screening; 25 of the

100 ss than 70, blindness, deafness, or cerebral palsy at 18 to 22 months corrected age.

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

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

103 roinflammation in disorders such as cerebral palsy, autism, multiple sclerosis, Alzheimer disease, an

104 he 13 patients with progressive supranuclear palsy (baseline area under the receiver operating charac

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

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

107 ve colitis with colonic perforation and Bell Palsy (both possibly related).

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

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

110 al contributors to the development of Bell's palsy, but the precise cause remains unclear.

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

112 t can be differentiated from trochlear nerve palsy by the direction of ocular torsion and the change

113 o report that the ataxic subtype of cerebral palsy can be caused by de novo dominant point mutations,

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

115 Third nerve palsy causes disfiguring, incomitant strabismus with lim

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

117 In the past few years, the cerebral palsy community has learned that the evidence of benefit

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

119 Cerebral palsy consistent with kernicterus occurred in 3 infants

120 Cerebral palsy consistent with kernicterus occurred only in infan

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

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

123 rotein 43 (TDP-43), progressive supranuclear palsy, corticobasal degeneration, dementia with Lewy bod

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

125 of neurological diseases, including cerebral palsy (CP) and autism.

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

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

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

129 Cerebral palsy (CP) is a chronic condition about which little is

130 Cerebral palsy (CP) is a common, clinically heterogeneous group o

131 s thought to place them at risk for cerebral palsy (CP).

132 Ss increases the risk of congenital cerebral palsy (CP).

133 e death, IQ<70, and moderate/severe cerebral palsy (CP).

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

135 Twelve patients with lateral rectus palsy demonstrated symmetric, highly significant 40% red

136 Cerebral palsy describes the most common physical disability in c

137 aused by lateral rectus superior compartment palsy despite an intact lateral rectus inferior compartm

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

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

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

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

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

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

144 The syndrome of cerebral palsy encompasses a large group of childhood movement an

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

146 in the prevalence of post-neonatal cerebral palsy, especially in developing countries, should be pos

147 d 18 patients with unilateral lateral rectus palsy fixated monocularly on a target placed in central

148 oebius syndrome is bilateral horizontal gaze palsy from pontine abducens nuclear defects, rather than

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

150 Sixteen children with cerebral palsy (Gross Motor Classification System I:6, II:6, III:

151 Outcomes included cerebral palsy, gross motor functional limitation, behavioral sco

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

153 Adolescents with cerebral palsy had significantly lower QoL than did those in the

154 Six patients with lateral rectus palsy had similar significant but asymmetric reductions

155 psychiatric disorders, e.g. stroke or facial palsy, had a physical basis requiring the attention of a

156 8 controls, who had progressive supranuclear palsy, had IgLON5 antibodies.

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

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

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

160 ditary neuropathy with liability to pressure palsies (HNPP) caused by PMP22 deficiency.

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

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

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

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

165 reterm delivery reduces the risk of cerebral palsy in early childhood, although its effects into scho

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

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

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

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

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

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

172 c paraplegia to tetraplegia and pseudobulbar palsy in the seventh decade.

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

174 al degeneration and progressive supranuclear palsy, in particular, might be identifiable at a single

175 Bell's palsy is a common cranial neuropathy causing acute unila

176 Cerebral palsy is a lifelong disorder; approaches to intervention

177 Facial nerve palsy is a potentially devastating condition that can ar

178 Cerebral palsy is a sporadic disorder with multiple likely aetiol

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

180 ility/developmental delay (n = 28), cerebral palsy-like encephalopathy (n = 11), autism spectrum diso

181 velop a devastating progressive supranuclear palsy-like syndrome approximately 5 years after onset, p

182 had evolved into a progressive supranuclear palsy-like syndrome; they showed a combination of severe

183 with clinical lateral rectus palsy may have palsy limited to the superior compartment.

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 set of patients with clinical lateral rectus palsy may have palsy limited to the superior compartment

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

188 Mortality, cerebral palsy, motor function, IQ, basic academic skills, attent

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

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

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

192 Adolescents with cerebral palsy need particular help to maintain and develop peer

193 d lesion was observed, neither phrenic nerve palsy nor severe PV stenosis was seen in any dogs.

194 Phrenic nerve palsy occurred in 1 of 50 (2%) patients.

195 Phrenic nerve palsy occurred in 3% (3/100) of the patients.

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

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

198 TBI might additionally lead to ocular motor palsies, optic neuropathies, and orbital pathologies.

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

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

201 e they had abduction deficits without facial palsy or facial palsy with full ocular motility.

202 rimary outcome was survival without cerebral palsy or neurosensory impairment, or a Bayley III develo

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

204 gia with choking, vertical supranuclear gaze palsy or slowing, balance difficulties with falls and ur

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

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

208 .4% male), 3029 were diagnosed with cerebral palsy over a median 7.8 years of follow-up (risk, 2.13 p

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

210 cognitive disability (P < .01), and cerebral palsy (P = .02).

211 9 to 2.13 cases of recurrent laryngeal nerve palsy per 100 operations.

212 In 3 cases, phrenic nerve palsy persisted beyond the end of the procedure, with al

213 9%), paresthesias (32.5%), peripheral facial palsy (PFP) (36.4%), meningeal signs (19.5%), and parese

214 ditary neuropathy with liability to pressure palsy/PMP22 deletion.

215 tic vein can aid in preventing phrenic nerve palsy (PNP) during cryoballoon ablation for atrial fibri

216 (P < 0.001) but not progressive supranuclear palsy, presumably because of the overlap ( approximately

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

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

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

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

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

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

223 ion of CBD with top progressive supranuclear palsy (PSP) GWAS single-nucleotide polymorphisms (SNPs)

224 Progressive supranuclear palsy (PSP) has been conceptualized as a large-scale net

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

226 Progressive supranuclear palsy (PSP) is a movement disorder characterized by tau

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

228 Because progressive supranuclear palsy (PSP) is linked to tau pathology, davunetide could

229 Progressive supranuclear palsy (PSP) is usually sporadic, but few pedigrees with

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

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

232 beta pathology, and progressive supranuclear palsy (PSP), a primary tauopathy characterised by deposi

233 omes (APSs) such as progressive supranuclear palsy (PSP), multiple system atrophy (MSA) and corticoba

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

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

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

237 dementia (FTD), and progressive supranuclear palsy (PSP).

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

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

240 g the cohort to the Danish National Cerebral Palsy Register, and we randomly selected 550 controls us

241 omly selected from population-based cerebral palsy registers in nine European regions.

242 generation- and the progressive supranuclear palsy-related metabolic topographies.

243 reviously validated progressive supranuclear palsy-related pattern provided excellent specificity (co

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

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

246 Phrenic nerve palsy remains the most frequent complication associated

247 %, and 2.8 % for cranial nerves VI, III, IV palsies respectively.

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

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

250 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

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

252 hout life are what individuals with cerebral palsy seek, not improved physical function for its own s

253 is characterized by progressive pontobulbar palsy, sensorineural hearing loss and respiratory insuff

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

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

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

257 The progressive supranuclear palsy subtype of FTLD-tau consistently caused prominent

258 mporal dementia and progressive supranuclear palsy syndrome.

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

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

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

262 system atrophy and progressive supranuclear palsy (the two most common atypical parkinsonian syndrom

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

264 recent childhood forms of progressive bulbar palsy to be genetically defined.

265 n to relate QoL of adolescents with cerebral palsy to impairments (cross-sectional analysis) and to c

266 from pediatric leukodystrophies and cerebral palsy, to multiple sclerosis and white matter stroke.

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

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

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

270 lf-reported QoL of adolescents with cerebral palsy varies with impairment and compares with the gener

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

272 Cerebral palsy was judged to be consistent with kernicterus if ma

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

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

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

276 atic sample or the presence of cranial nerve palsy) was present.

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

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

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

280 Motor deficits in cerebral palsy were associated with loss of unmyelinated WM tract

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

282 Optic atrophy and vocal cord palsy were observed in patients with severe disability a

283 Comparable low rates of phrenic nerve palsy were recorded (1.1% versus 1.7%; P=0.64).

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

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

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

287 anatomy and pathophysiology of facial nerve palsy, while also exploring different treatment options.

288 Children with cerebral palsy who can self-report have similar quality of life (

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

290 s of 6 consecutive patients with third nerve palsy who underwent adjustable nasal transposition of th

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

292 trophy, and 13 with progressive supranuclear palsy) who were followed up for 5 to 9 years.

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

294 rome, especially in patients who have facial palsy with full ductions.

295 tion deficits without facial palsy or facial palsy with full ocular motility.

296 1, n=17, 43%) was bilateral horizontal gaze palsy with intact vertical range.

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

298 2 (n=10, 26%) was bilateral horizontal gaze palsy with variable vertical limitations.

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