ライフサイエンスコーパス: cerebral palsy

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

2 in gait-related neurological disorders (e.g. cerebral palsy).

3 n and further management of spastic diplegia cerebral palsy.

4 control of the ankle joint in children with cerebral palsy.

5 lking are frequent concerns in children with cerebral palsy.

6 y of the QoL of adolescents with and without cerebral palsy.

7 es toe lift and heel strike in children with cerebral palsy.

8 nts in our cohort with a diagnosis of ataxic cerebral palsy.

9 rabbit kits with hypertonia in our model of cerebral palsy.

10 and sensory deficits in the rabbit model of cerebral palsy.

11 t deformities are common among children with cerebral palsy.

12 e responsible for the motor deficits seen in cerebral palsy.

13 ronmental factors, genomic factors may cause cerebral palsy.

14 tandard of care for ambulatory children with cerebral palsy.

15 on as a pathogenic mechanism contributing to cerebral palsy.

16 ypical development, such as in children with cerebral palsy.

17 proves gross motor function in children with cerebral palsy.

18 s well as the childhood leukodystrophies and cerebral palsy.

19 chemic brain injury remains a major cause of cerebral palsy.

20 ith a working clinical diagnosis of dystonic cerebral palsy.

21 hildren had been initially misdiagnosed with cerebral palsy.

22 nant injury in the preterm infant leading to cerebral palsy.

23 WMI) in premature babies is a major cause of cerebral palsy.

24 efore preterm birth might reduce the risk of cerebral palsy.

25 out the health and well being of adults with cerebral palsy.

26 the health and well being of adults who have cerebral palsy.

27 mature birth, such as neonatal mortality and cerebral palsy.

28 , and independent living than adults without cerebral palsy.

29 etermined the motor deficits associated with cerebral palsy.

30 ropometric measurements, and the presence of cerebral palsy.

31 d profound mental retardation, epilepsy, and cerebral palsy.

32 time are thought to contribute eventually to cerebral palsy.

33 ual goals in patients with severe dyskinetic cerebral palsy.

34 ng to periventricular leukomalacia (PVL) and cerebral palsy.

35 to involuntary toe walking in children with cerebral palsy.

36 ed in the white-matter injury that occurs in cerebral palsy.

37 published a model in rabbits consistent with cerebral palsy.

38 ature infants and is the major antecedent of cerebral palsy.

39 d substantively to the diagnosis of dystonic cerebral palsy.

40 ent goals in patients with severe dyskinetic cerebral palsy.

41 onset sepsis, necrotizing enterocolitis, and cerebral palsy.

42 hildren aged 3-9 years with spastic diplegic cerebral palsy.

43 ng progress in children and adolescents with cerebral palsy.

44 turn are associated with increased risks of cerebral palsy.

45 te congruent abnormal findings indicative of cerebral palsy.

46 on found in preterm infants that can lead to cerebral palsy.

47 regulation of early neuronal connectivity in cerebral palsy.

48 re significantly associated with the rate of cerebral palsy.

49 k of neurodevelopmental disorders, including cerebral palsy.

50 Epilepsy (52.2% [n = 538,978]) and cerebral palsy (15.9% [n = 164,665]) were the most preva

51 p, had significant reductions in the risk of cerebral palsy (21% vs. 36%, P=0.03) and the risk of mod

52 y significant difference in proportions with cerebral palsy (23/295 [8%] and 21/314 [7%], respectivel

53 mbined dataset included 551 individuals with cerebral palsy (321 individuals from the PERRIN programm

54 There were 1575 VLBW infants born with cerebral palsy; 414 (26%) were of birthweight less than

55 extremely preterm group vs controls were for cerebral palsy (7.0% vs 0.1%; P < .001), for blindness (

56 Cerebral palsy (9179 [14.6%]) and asthma (13 708 [21.8%]

57 of any of the following: moderate to severe cerebral palsy, a cognitive score less than 85 on the Ba

58 Cerebral palsy, a range of non-progressive syndromes of

59 history of maternal or fetal birth trauma or cerebral palsy after childbirth.

60 alsy (DCP) is the second most common type of cerebral palsy after spastic forms.

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

62 Using the curves for individuals with cerebral palsy aged 1 year to 21 years, we illustrate ho

63 Adults with cerebral palsy also have less participation in areas suc

64 tatistically significant, the higher rate of cerebral palsy among children who had been exposed to re

65 uction in the frequency of bilateral spastic cerebral palsy among infants of birthweight 1000-1499 g.

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

67 unction and quality of life in children with cerebral palsy and a Gross Motor Function Classification

68 as cognitive abilities, the severity of the cerebral palsy and age all affect participation.

69 matter injury (PWMI) is the leading cause of cerebral palsy and chronic neurological disability in su

70 a large number of survivors with IVH develop cerebral palsy and cognitive deficits.

71 a large number of survivors with IVH develop cerebral palsy and cognitive deficits.

72 ults in neurological dysfunctions, including cerebral palsy and cognitive deficits.

73 or apnea of prematurity reduces the rates of cerebral palsy and cognitive delay at 18 months of age.

74 of brain injuries of the newborn that cause cerebral palsy and cognitive disabilities, as well as mu

75 e matter injury (PWMI) is the major cause of cerebral palsy and cognitive impairment in prematurely b

76 bes common foot deformities in children with cerebral palsy and discusses treatment options for each

77 rders and neurological symptoms - most often cerebral palsy and epilepsy.

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

79 y in Europe, agreed a standard definition of cerebral palsy and inclusion and exclusion criteria.

80 juvenile-onset movement disorders, including cerebral palsy and juvenile parkinsonism.

81 Perinatal stroke causes cerebral palsy and lifelong disability.

82 rth is neuroprotective, reducing the risk of cerebral palsy and major motor dysfunction.

83 y the musculoskeletal issues associated with cerebral palsy and only indirectly discusses the cogniti

84 report a subject presenting with dyskinetic cerebral palsy and partial agenesis of the corpus callos

85 ll participants had a confirmed diagnosis of cerebral palsy and ranged in age from 1 year to 17 years

86 alsy, and probably some spastic quadriplegic cerebral palsy and seizure disorders.

87 al impairment in multiple sclerosis, stroke, cerebral palsy and spinal cord injury.

88 e to motor dysfunction in conditions such as cerebral palsy and spinal cord injury.

89 g to motor dysfunction in conditions such as cerebral palsy and spinal cord injury.SIGNIFICANCE STATE

90 g and registries of birth defects (including cerebral palsy and terminations for defects at any gesta

91 ations are rarely performed in patients with cerebral palsy and there is little proven evidence of ge

92 le evidence for early, accurate diagnosis of cerebral palsy and to summarize best available evidence

93 al questionnaires were used for diagnosis of cerebral palsy and visual and hearing impairments.

94 elopmental delay, cardiopulmonary anomalies, cerebral palsy, and aspiration pneumonia and among patie

95 talisation with asthma, learning disability, cerebral palsy, and death.

96 nical work with patients with schizophrenia, cerebral palsy, and hemispatial neglect.

97 information on strategies for prevention of cerebral palsy, and on the success of these preventive e

98 an important share of congenital hemiplegic cerebral palsy, and probably some spastic quadriplegic c

99 Causes of cerebral palsy, and therefore promising approaches to pr

100 ren with the periventricular leukomalacia of cerebral palsy, another major source of neurological mor

101 ical explanation for why signs of hemiplegic cerebral palsy appear late and progress over the first 2

102 Topography and severity of cerebral palsy are more difficult to ascertain in infanc

103 isability rates and the severity spectrum of cerebral palsy are reduced.

104 analyses of studies of rarer outcomes (e.g., cerebral palsy), are needed to confirm whether such risk

105 cies) in the repeat-corticosteroid group had cerebral palsy as compared with one child (0.5% of pregn

106 and AP4E1 have recently been found to cause cerebral palsy associated with severe intellectual disab

107 ore of less than 70, blindness, deafness, or cerebral palsy at 18 to 22 months corrected age.

108 year of corrected age or moderate or severe cerebral palsy at or beyond 2 years of corrected age.

109 rking diagnoses among these children include cerebral palsy, autism spectrum disorder trait, nutritio

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

111 variety of neurological disorders, including cerebral palsy, autism spectrum disorders, schizophrenia

112 on of neuroinflammation in disorders such as cerebral palsy, autism, multiple sclerosis, Alzheimer di

113 ntal outcomes, defined as either disability (cerebral palsy, bilateral blindness, or bilateral hearin

114 e matter disorders and of ischemic stroke in cerebral palsy; birth asphyxia, congenital malformations

115 Cerebral palsy, blindness, and deafness assessed by a pe

116 >or=85) and were free of major disabilities (cerebral palsy, blindness, or deafness), and full-term (

117 Data for children with cerebral palsy born in the years 1980-96 were pooled.

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

119 king is frequently observed in children with cerebral palsy, but the mechanisms involved have not bee

120 pregnancy body mass index (BMI) and rates of cerebral palsy by gestational age and to identify potent

121 changes in the frequency and distribution of cerebral palsy by sex and neurological subtype in infant

122 e first to report that the ataxic subtype of cerebral palsy can be caused by de novo dominant point m

123 The number of cerebral palsy cases in each BMI category was 64, 1487,

124 enrichment of damaging de novo mutations in cerebral palsy cases.

125 ce the risk of pathological fractures in the cerebral palsy child.

126 the 24 months after surgery in children with cerebral palsy classified as GMFCS levels II and III.

127 In the past few years, the cerebral palsy community has learned that the evidence o

128 Cerebral palsy consistent with kernicterus occurred in 3

129 Cerebral palsy consistent with kernicterus occurred only

130 d by the persistence of cognitive delays and cerebral palsy (CP) affecting nearly one in eight surviv

131 a number of neurological diseases, including cerebral palsy (CP) and autism.

132 and proprioceptive deficits in children with cerebral palsy (CP) and linked these with weaker somatos

133 Misdiagnoses of cerebral palsy (CP) are common.

134 The early antecedents of cerebral palsy (CP) are unknown but are suspected to be

135 and those who survive have a higher rate of cerebral palsy (CP) compared with babies born at term.

136 Altered body composition in children with cerebral palsy (CP) could be due to differences in energ

137 Individuals with cerebral palsy (CP) have a reduced somatosensory cortica

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

139 elopment of the hypertonic motor deficits of cerebral palsy (CP) in premature and full-term infants w

140 onitis is associated with increased risk for cerebral palsy (CP) in term infants.

141 Cerebral Palsy (CP) is a chronic childhood disorder with

142 Cerebral palsy (CP) is a chronic condition about which l

143 Cerebral palsy (CP) is a common, clinically heterogeneou

144 Cerebral palsy (CP) is a permanent, nonprogressive disor

145 Cerebral palsy (CP) is caused by either hypoxia-ischemia

146 Cerebral palsy (CP) is defined as motor impairment that

147 Children with Down syndrome (DS) and cerebral palsy (CP) often have reduced visual acuity (VA

148 Cerebral palsy (CP) results from an upper motoneuron (UM

149 ngs have been reported for specific clinical cerebral palsy (CP) subgroups or lesion types but not in

150 Children with cerebral palsy (CP) tend to be either excluded from stud

151 hemic stroke (PAS) experience development of cerebral palsy (CP), epilepsy, and cognitive impairment,

152 rements (ERs) of preschool-age children with cerebral palsy (CP), the knowledge of which is essential

153 SB) levels thought to place them at risk for cerebral palsy (CP).

154 re to PFASs increases the risk of congenital cerebral palsy (CP).

155 comes were death, IQ<70, and moderate/severe cerebral palsy (CP).

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

157 nt of periventricular leukomalacia (PVL) and cerebral palsy (CP).

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

159 Dyskinetic cerebral palsy (DCP) is the second most common type of c

160 Cerebral palsy describes the most common physical disabi

161 iculomegaly and an echolucent lesion) and of cerebral palsy diagnoses at age 2 years.

162 nal registries, children were followed for a cerebral palsy diagnosis through 2012.

163 Search terms included cerebral palsy, diagnosis, detection, prediction, identi

164 hma, inflammatory bowel disease, infections, cerebral palsy, dilated cardiomyopathy, muscular dystrop

165 number of neurological disorders, including cerebral palsy, dystonia, Parkinson's disease, stroke, a

166 nditions affecting motor function other than cerebral palsy (eg, spina bifida or muscle diseases) wer

167 In infants, clinical signs and symptoms of cerebral palsy emerge and evolve before age 2 years; the

168 The syndrome of cerebral palsy encompasses a large group of childhood mo

169 ors will develop neurologic sequelae such as cerebral palsy, epilepsy or cognitive deficits.

170 tivity disorder, severe learning disability, cerebral palsy, epilepsy, muscle or skeletal disorders,

171 Reduction in the prevalence of post-neonatal cerebral palsy, especially in developing countries, shou

172 describe self-reported QoL of children with cerebral palsy, factors that influence it, and how it co

173 experience lifelong drug-resistant epilepsy, cerebral palsy, feeding difficulties, intellectual disab

174 arge sample of children and adolescents with cerebral palsy from the Netherlands and Canada.

175 Children with cerebral palsy generally showed lower EMG levels than ty

176 Novel cerebral palsy genes will probably be identified as more

177 9 years) with mild-moderate crouch gait from cerebral palsy (GMFCS I-II) completed the study.

178 Sixteen children with cerebral palsy (Gross Motor Classification System I:6, I

179 Patients with severe dyskinetic cerebral palsy (Gross Motor Functioning Classification S

180 Outcomes included cerebral palsy, gross motor functional limitation, behav

181 ajectories for children and adolescents with cerebral palsy grouped by GMFCS level.

182 Twenty-four children with unilateral cerebral palsy had physiological and anatomical measures

183 Adolescents with cerebral palsy had significantly lower QoL than did thos

184 Children with cerebral palsy had similar QoL to children in the genera

185 r behavioural deficits that could also model cerebral palsy has not been tested.

186 Adults with cerebral palsy have a high prevalence of comorbid and se

187 Subjects with severe hemiplegic cerebral palsy have increased ipsilateral corticospinal

188 Past efforts to prevent cerebral palsy have not had the benefits sought, but rec

189 al questionnaires were used for diagnosis of cerebral palsy, hearing and vision impairments, and cogn

190 sed with the Psychomotor Development Index), cerebral palsy, hearing or visual impairment, and anthro

191 dystonia in patients with severe dyskinetic cerebral palsy; however, the current level of evidence f

192 eonatal condition, GM hemorrhage can lead to cerebral palsy, hydrocephalus, and mental retardation.

193 ing was applied to a neonatal mouse model of cerebral palsy (Hypoxic-Ischaemic Encephalopathy).

194 enotype of other neurological disorders (eg, cerebral palsy, hypoxic ischaemic encephalopathy, paroxy

195 base provide evidence that the prevalence of cerebral palsy in children of birthweight less than 1500

196 of very preterm delivery reduces the risk of cerebral palsy in early childhood, although its effects

197 roup of 16 European centres, Surveillance of Cerebral Palsy in Europe, agreed a standard definition o

198 ssociation between maternal BMI and rates of cerebral palsy in full-term children was mediated throug

199 uch as multiple sclerosis (MS) in adults and cerebral palsy in infants.

200 ched the literature about early diagnosis of cerebral palsy in MEDLINE (1956-2016), EMBASE (1980-2016

201 It is uncertain whether risk of cerebral palsy in offspring increases with maternal over

202 The major neuropathological correlate of cerebral palsy in premature infants is periventricular l

203 The major brain abnormality underlying cerebral palsy in premature infants is periventricular l

204 malacia (PVL), the major disorder underlying cerebral palsy in premature infants.

205 population-based registers of children with cerebral palsy in six European countries and 743 (63%) a

206 cause of chronic neurological disability and cerebral palsy in survivors of premature birth, the cell

207 For cerebral palsy in survivors, magnesium sulphate treatmen

208 a (PVL), the major pathological substrate of cerebral palsy in the premature infant.

209 eterm labor may aid in primary prevention of cerebral palsy in very preterm infants.

210 describe the distribution and prevalence of cerebral palsy in VLBW infants.

211 s do not support use of HBO as a therapy for cerebral palsy in young children who did not have neonat

212 Children with cerebral palsy, in contrast, continue to co-contract ago

213 holistic approaches for their children with cerebral palsy includes the widespread adoption of compl

214 underlying pathophysiological mechanisms of cerebral palsy increases, so will the possibility of dev

215 Cerebral palsy is a lifelong disorder; approaches to int

216 Cerebral palsy is a sporadic disorder with multiple like

217 Cerebral palsy is caused by injury or developmental dist

218 Cerebral palsy is estimated to affect nearly 1 in 500 ch

219 A growing body of evidence suggests that cerebral palsy is probably caused by multiple genetic fa

220 Cerebral palsy is the most frequent cause of severe phys

221 ual disability/developmental delay (n = 28), cerebral palsy-like encephalopathy (n = 11), autism spec

222 We speculate that children with cerebral palsy maintain a co-contraction activation patt

223 We conclude that at least some subtypes of cerebral palsy may be caused by de novo genetic mutation

224 can in the neonatal intensive care unit, and cerebral palsy, microcephaly, and a low score on a Bayle

225 Mortality, cerebral palsy, motor function, IQ, basic academic skill

226 Adolescents with cerebral palsy need particular help to maintain and deve

227 following domains: neuromotor (nonambulatory cerebral palsy), neurosensory (blindness, deafness, or n

228 f 3.2% (95% CI, -3.3% to 9.6%; P = .47), and cerebral palsy occurred in 18/419 (4.3%) vs 25/443 (5.6%

229 ified secondary analysis, moderate or severe cerebral palsy occurred significantly less frequently in

230 Individuals with cerebral palsy often exhibit crouch gait, a debilitating

231 velopmental impairment was defined as severe cerebral palsy or a composite motor or composite cogniti

232 duce the combined risk of moderate or severe cerebral palsy or death, although the rate of cerebral p

233 The primary outcome was survival without cerebral palsy or neurosensory impairment, or a Bayley I

234 in 6 h of asphyxia improves survival without cerebral palsy or other disability by about 40% and redu

235 The incidence of cerebral palsy or other major neurological impairments w

236 mmonly manifesting with developmental delay, cerebral palsy or seizures.

237 rodevelopmental impairment (cognitive delay, cerebral palsy, or hearing or vision loss) at 22 to 26 m

238 bility, defined as any of cognitive deficit, cerebral palsy, or severe visual or hearing impairment.

239 Although likely a rare cause of cerebral palsy, our findings indicate a critical role fo

240 1.8]; 51.4% male), 3029 were diagnosed with cerebral palsy over a median 7.8 years of follow-up (ris

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

242 ously thought, including multiple sclerosis, cerebral palsy (periventricular leukomalacia), and spina

243 amethasone confers long-term benefits beyond cerebral palsy prevention with sex-specific differences

244 As adolescents with cerebral palsy progress to adulthood, they decrease thei

245 n Measure (GMFM-66) and seven domains of the Cerebral Palsy Quality of Life Questionnaire ([CP-QoL] s

246 velopmental outcomes at follow-up, including cerebral palsy (range of significant odds ratios [ORs],

247 by linking the cohort to the Danish National Cerebral Palsy Register, and we randomly selected 550 co

248 were randomly selected from population-based cerebral palsy registers in nine European regions.

249 vivors, cooling resulted in reduced risks of cerebral palsy (relative risk, 0.67; 95% CI, 0.47 to 0.9

250 ularly birth asphyxia, the specific cause of cerebral palsy remains unknown in most individuals.

251 Cerebral palsy risk genes in enriched pathways were show

252 Candidate cerebral palsy risk genes overlapped with neurodevelopme

253 udies indicate that mild hypothermia lessens cerebral palsy risk in term infants with moderate neonat

254 ogy, and genetic variants also contribute to cerebral palsy risk.

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

256 g disabilities (RR, 10.6; 95% CI, 5.5-20.2), cerebral palsy (RR, 4.8; 95% CI, 2.3-10.0), epilepsy (RR

257 on throughout life are what individuals with cerebral palsy seek, not improved physical function for

258 ns and patients with a clinical diagnosis of cerebral palsy should be genetically investigated before

259 typically-developing children, children with cerebral palsy showed no age-related decline in tibialis

260 als with lower GMFCS levels (ie, less severe cerebral palsy) showed higher developmental limits that

261 d to summarize best available evidence about cerebral palsy-specific early intervention that should f

262 or perinatal white matter injury leading to cerebral palsy), spinal cord injury, multiple sclerosis

263 ent groups: amputation or limb deficiencies, cerebral palsy, spinal cord-related disability, visual i

264 ered glutamate-mediated damage, as occurs in cerebral palsy, stroke and spinal cord injury, the actio

265 h as periventricular leukomalacia leading to cerebral palsy, stroke, and secondary ischemia after spi

266 acture, occur commonly in conditions such as cerebral palsy, stroke, muscular dystrophy, Charcot-Mari

267 numerous neurological conditions, including cerebral palsy, stroke, spinal cord injury, stiff-person

268 owed that gross motor function (p<0.001) and cerebral palsy subtype (p<0.05) were associated with cha

269 ptor protein-4 complex in forms of inherited cerebral palsy, suggesting a role for components of the

270 eived erythromycin or co-amoxiclav developed cerebral palsy than did those born to mothers who receiv

271 The risk of cerebral palsy, the commonest physical disability of chi

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

273 Cerebral palsy-the most common physical disability of ch

274 d with fetal injury, and efforts to decrease cerebral palsy through better antenatal biophysical test

275 regression to relate QoL of adolescents with cerebral palsy to impairments (cross-sectional analysis)

276 ranging from pediatric leukodystrophies and cerebral palsy, to multiple sclerosis and white matter s

277 In children with unilateral cerebral palsy (uCP), the corticospinal tract (CST)-wiri

278 or system injury in children with unilateral cerebral palsy (USCP).

279 ed how self-reported QoL of adolescents with cerebral palsy varies with impairment and compares with

280 ajor disability among survivors; the rate of cerebral palsy was 15 of 77 (19 percent) in the hypother

281 iod of the Register and, at two years of age cerebral palsy was diagnosed in 22% of infants; half of

282 The frequency of cerebral palsy was higher in male than female babies in

283 The risk of cerebral palsy was increased by either antibiotic, altho

284 Cerebral palsy was judged to be consistent with kernicte

285 Cerebral palsy was observed in 9.5% of extremely preterm

286 ent, and 34 percent, respectively; disabling cerebral palsy was present in 30 children (12 percent).

287 erebral palsy or death, although the rate of cerebral palsy was reduced among survivors.

288 The whole spectrum of severity of cerebral palsy was represented in terms of motor functio

289 ren of normal-weight mothers, adjusted HR of cerebral palsy were 1.22 (95% CI, 1.11-1.33) for overwei

290 Motor deficits in cerebral palsy were associated with loss of unmyelinated

291 nine children aged 3 to 8 years with spastic cerebral palsy were randomized to 40 treatments of HBO (

292 Risk of obesity at age 5 y and risk of cerebral palsy were similar between planned repeat CS or

293 as observed more frequently in children with cerebral palsy when compared to typically-developing chi

294 1426 (94%) had spastic cerebral palsy, which was unilateral (hemiplegic) in 336

295 Children with cerebral palsy who can self-report have similar quality

296 epeated-measurements data from children with cerebral palsy who had been prescribed fixed ankle-foot

297 of young children with primary motor delay (cerebral palsy) who need a clinical trial of L-dopa.

298 ured that most children aged 8-12 years with cerebral palsy will have similar QoL to other children.

299 gh-income countries, 2 in 3 individuals with cerebral palsy will walk, 3 in 4 will talk, and 1 in 2 w

300 The increased risk of cerebral palsy with decreasing gestational age categorie