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 turn are associated with increased risks of cerebral palsy.

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

5 tandard of care for ambulatory children with cerebral palsy.

6 on as a pathogenic mechanism contributing to cerebral palsy.

7 te congruent abnormal findings indicative of cerebral palsy.

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

9 proves gross motor function in children with cerebral palsy.

10 s well as the childhood leukodystrophies and cerebral palsy.

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

12 hildren had been initially misdiagnosed with cerebral palsy.

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

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

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

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

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

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

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

20 , and independent living than adults without cerebral palsy.

21 etermined the motor deficits associated with cerebral palsy.

22 ropometric measurements, and the presence of cerebral palsy.

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

24 time are thought to contribute eventually to cerebral palsy.

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

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

27 published a model in rabbits consistent with cerebral palsy.

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

29 above average always had the lowest risk of cerebral palsy.

30 esults in chronic neurologic disability from cerebral palsy.

31 n preterm infants and a common antecedent to cerebral palsy.

32 py for the treatment of spastic quadriplegic cerebral palsy.

33 and inflammation contributes to the risk of cerebral palsy.

34 e of the five deaths, the cause of death was cerebral palsy.

35 tection against H-I brain injury, a model of cerebral palsy.

36 irth contributes approximately 6% of spastic cerebral palsy.

37 re significantly associated with the rate of cerebral palsy.

38 k of neurodevelopmental disorders, including cerebral palsy.

39 n and further management of spastic diplegia cerebral palsy.

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

41 lking are frequent concerns in children with cerebral palsy.

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

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

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

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

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

47 t deformities are common among children with cerebral palsy.

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

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

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

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

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

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

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

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

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

57 The gestational-age-specific prevalence of cerebral palsy after fetal death of the co-twin is much

58 Cerebral palsy after preterm birth is hypothesized to be

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

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

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

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

63 y absent from epidemiological studies of the cerebral palsies and rarely diagnosed, presumably becaus

64 Three of the 102 had cerebral palsy and 12 had other cerebral impairment.

65 Of the 241 respondents, 23 had cerebral palsy and 28 had other cerebral impairment.

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

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

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

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

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

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

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

75 t chorioamnionitis is a risk factor for both cerebral palsy and cPVL.

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 hronic problem in 80 to 90% of children with cerebral palsy and in children with neurodevelopmental d

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

81 riventricular leukomalacia (PVL)] results in cerebral palsy and is the leading cause of brain injury

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

83 Perinatal stroke causes cerebral palsy and lifelong disability.

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

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

86 ix children (24 boys, 12 girls) with spastic cerebral palsy and PVL and 21 age-matched control subjec

87 The charts of children with spastic cerebral palsy and PVL documented on brain magnetic reso

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

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

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

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

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

93 pose very preterm and more mature infants to cerebral palsy and that antenatal exposure to steroids m

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

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

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

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

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

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

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

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

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

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

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

105 Diseases that have been misdiagnosed as cerebral palsy are presented here to provide the clinici

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

107 WDS falls clearly within the cerebral palsies as a syndrome that includes motor impai

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

109 a 16-year-old girl with spastic quadriplegic cerebral palsy associated with premature birth and typic

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

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

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

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

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

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

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

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

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

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

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

121 n registers for 4503 singleton children with cerebral palsy born between 1976 and 1990 with the numbe

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

123 s has been implicated in the pathogenesis of cerebral palsy, but most studies have not reported a sig

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

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

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

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

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

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

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

131 Cerebral palsy consistent with kernicterus occurred in 3

132 Cerebral palsy consistent with kernicterus occurred only

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

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

135 Misdiagnoses of cerebral palsy (CP) are common.

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

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

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

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 Half of all cases of cerebral palsy (CP) occur in term infants, for whom risk

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

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

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

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

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

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

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

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

158 ntal retardation without autism (n = 60), or cerebral palsy (CP, n = 63) and of control children (n =

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

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

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

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

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

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

172 Studies evaluating risk of cerebral palsy following maternal fever, urinary tract i

173 Novel cerebral palsy genes will probably be identified as more

174 9 years) with mild-moderate crouch gait from cerebral palsy (GMFCS I-II) completed the study.

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

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

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

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

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

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

181 ic diplegia and was initially diagnosed with cerebral palsy, has also shown clinical improvement.

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

183 Subjects with severe hemiplegic cerebral palsy have increased ipsilateral corticospinal

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

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

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

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

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

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

190 artum magnesium sulfate exposure and risk of cerebral palsy in a case-control study of low birth weig

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

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

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

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

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

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

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

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

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

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

201 is a major cause of developmental delay and cerebral palsy in prematurely born infants.

202 acia (cPVL) is believed to be a precursor of cerebral palsy in preterm infants.

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

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

205 For cerebral palsy in survivors, magnesium sulphate treatmen

206 Risk factors for cerebral palsy in term or near-term children include int

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

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

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

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

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

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

213 Cerebral palsy is a lifelong disorder; approaches to int

214 Cerebral palsy is a sporadic disorder with multiple like

215 Cerebral palsy is caused by injury or developmental dist

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

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

218 Cerebral palsy is the most frequent cause of severe phys

219 The risk of cerebral palsy, like the risk of perinatal death, is low

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

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

222 randomized clinical trials of magnesium and cerebral palsy may shed more definitive light on this re

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

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

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

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

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

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

229 lassified as having static encephalopathies (cerebral palsy), often attributed to perinatal or prenat

230 ) or histologic (n = 7) chorioamnionitis and cerebral palsy or cPVL in both preterm and full-term inf

231 cts that discussed prenatal risk factors for cerebral palsy or cPVL.

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 Patients with mental retardation, cerebral palsy, or congenital esophageal anomalies were

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

238 1.8]; 51.4% male), 3029 were diagnosed with cerebral palsy over a median 7.8 years of follow-up (ris

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

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

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

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

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

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

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

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

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

248 on between exposure to magnesium sulfate and cerebral palsy risk (odds ratio = 0.9; 95% confidence in

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

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

251 nitis was significantly associated with both cerebral palsy (RR, 1.9; 95% CI, 1.4-2.5) and cPVL (RR,

252 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.

253 found between clinical chorioamnionitis and cerebral palsy (RR, 4.7; 95% CI, 1.3-16.2).

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

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

256 Cerebral palsy seems to be more common in term babies wh

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

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

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

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

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

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

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

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

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

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

267 tandards) were 4-6 times more likely to have cerebral palsy than were children in a reference band be

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

269 omponent of the brain injury associated with cerebral palsy, the most common human birth disorder.

270 Cerebral palsy-the most common physical disability of ch

271 eonatal H-I brain injury in mice (a model of cerebral palsy), there was evidence of apoptotic changes

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

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

274 ple children affected by symmetrical spastic cerebral palsy, to locate recessive genes responsible fo

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

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

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

278 The RR of histologic chorioamnionitis and cerebral palsy was 1.6 (95% CI, 0.9-2.7) in preterm infa

279 n who survived to infancy, the prevalence of cerebral palsy was 106 (95% CI 70-150) per 1000 and prev

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

281 The prevalence of cerebral palsy was 29 (95% CI 6-83) per 1000 and of othe

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

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

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

285 Cerebral palsy was judged to be consistent with kernicte

286 Cerebral palsy was observed in 9.5% of extremely preterm

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

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

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

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

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

296 n = 97) included all singleton children with cerebral palsy who were born in 1985-1989 in Atlanta, Ge

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