ライフサイエンスコーパス: neurological deficit

1 natal outcome (sensorineural hearing loss or neurological deficits).

2 on the specific type of delay or underlying neurological deficit.

3 tration was delayed until after the onset of neurological deficit.

4 with reported nodding and at least one other neurological deficit.

5 perihematomal leukocyte infiltration and the neurological deficit.

6 ss (15.8%) had stable burst fracture without neurological deficit.

7 maller variance of infarct size, and greater neurological deficit.

8 nversely correlated with the severity of the neurological deficit.

9 tion, smaller infarct volumes, and decreased neurological deficit.

10 significant risk of mortality and long-term neurological deficit.

11 of 1 or greater, which represents a moderate neurological deficit.

12 y and secondary brain injuries and permanent neurological deficits.

13 processes exacerbate the extent of permanent neurological deficits.

14 male patient who presented with progressive neurological deficits.

15 R stress, abnormal protein accumulation, and neurological deficits.

16 o-antibodies to Lrp4 should be evaluated for neurological deficits.

17 sis is one of the major causes of poststroke neurological deficits.

18 umulation that leads to liver failure and/or neurological deficits.

19 ther defects in lateralization contribute to neurological deficits.

20 rebral hemorrhage, hypoxia and necrosis, and neurological deficits.

21 reduce CNS axon loss and slow progression of neurological deficits.

22 severely restricted, contributing to chronic neurological deficits.

23 which may result in hemorrhagic strokes and neurological deficits.

24 ned brain regions and cognitive processes or neurological deficits.

25 ideline concussion diagnosis and testing for neurological deficits.

26 ntribute to subsequent neurodegeneration and neurological deficits.

27 .1% to 71.2% without incurring postoperative neurological deficits.

28 educes peri-infact angiogenesis, and worsens neurological deficits.

29 d EPT children with no known brain injury or neurological deficits.

30 l nervous system (CNS) leads to debilitating neurological deficits.

31 Death occurred approximately 48 days due to neurological deficits.

32 one patient was healthy and 12 patients had neurological deficits.

33 lacia (PVL), the leading cause of subsequent neurological deficits.

34 w, such as in cerebral vasospasm, can induce neurological deficits.

35 phenotype, more severe and prolonged post-SD neurological deficits.

36 r, cystamine, on ICH-induced brain edema and neurological deficits.

37 itor, reduces ICH-induced brain swelling and neurological deficits.

38 t damage, which translated to improvement of neurological deficits.

39 hematomas, brain edema formation and marked neurological deficits.

40 afflicted rats died at 30 days due to severe neurological deficits.

41 -/- mice suffer from severe ataxia and other neurological deficits.

42 oms of RTT, including postnatal onset of the neurological deficits.

43 osaposin/saposin deficiencies lead to severe neurological deficits.

44 ls at and below 5 mug/dL are associated with neurological deficits.

45 ubgroups often leave children with life-long neurological deficits.

46 yet poorly understood syndrome of long-term neurological deficits.

47 gnosis and treatment to prevent irreversible neurological deficits.

48 ry macrophages may lead to tissue damage and neurological deficits.

49 tural substrates accounting for these common neurological deficits.

50 a result of the irreversible accumulation of neurological deficits.

51 ndently of IDA, is responsible for long-term neurological deficits.

52 ion imbalance, as well as a range of chronic neurological deficits.

53 e and skeletal and cardiac anomalies without neurological deficits.

54 us system (CNS) leading to demyelination and neurological deficits.

55 se (CHD) are at risk of developing life-long neurological deficits.

56 0.01) reduction of brain infarct volume and neurological deficits.

57 region may provide a mechanism for transient neurological deficits.

58 erfusion injury and the consequent motor and neurological deficits.

59 trategies do not reliably prevent ID-induced neurological deficits.

60 disease would prevent or slow progression of neurological deficits.

61 reduced myelination of the white matter, and neurological deficits.

62 yte death and ameliorated the progression of neurological deficits.

63 outcome was found to be death (35%), severe neurological deficit (13%), mild neurological deficit (1

64 5%), severe neurological deficit (13%), mild neurological deficit (13%), undefined deficit (4%) and r

65 Brain damage and neurological deficit 24 h after MCAo were exacerbated by

66 cranial pressure (42%), hydrocephalus (30%), neurological deficits (27%; 6% developed during therapy)

67 itment of inflammatory cells, and functional neurological deficits 48 h after MCAO.

68 tions lead to an increased rate of permanent neurological deficits (9%), overall surgical complicatio

69 SS after 24 hours (0-42 [none to most severe neurological deficits; a 4-point difference considered c

70 Albumin treatment improves neurological deficit after ICH but does not affect MRI o

71 ation in cerebral ischemia, and in improving neurological deficit after stroke.

72 lagenase-induced ICH, hemorrhage volumes and neurological deficits after 24 hrs were similar in salin

73 None of these patients had overt neurological deficits after ablation.

74 es vascular sprouting and repair and reduces neurological deficits after cerebral ischemia in mice.

75 Moreover, functional neurological deficits after H/I are significantly improv

76 ited enlarged brain infarction and increased neurological deficits after ischemia-reperfusion compare

77 activation and exacerbates brain injury and neurological deficits after ischemia.

78 that effectively reduces lesion volumes and neurological deficits after ischemic stroke, influences

79 farct risk and volumes, collateral flow, and neurological deficits after pretreatment with olcegepant

80 novel therapeutic target in the treatment of neurological deficits after SAH.

81 HDAC3) decreased infarct size and alleviated neurological deficits after the onset of middle cerebral

82 Similarly, infarct growth and neurological deficits after tMCAO were unaffected by red

83 l haemorrhage, or new/worse persistent focal neurological deficit) after CCM treatment.

84 mide provided significant protection against neurological deficit and axonal degeneration in experime

85 A) directly before reperfusion, and assessed neurological deficit and HT blood volume after 24 hours.

86 Neurological deficit and infarct volume were determined

87 Rats were assessed for neurological deficit and motor function, and their brain

88 showed that TFA-12 significantly ameliorates neurological deficit and severity of myelin oligodendroc

89 rometabolic disease with patients developing neurological deficits and cardiomyopathy in the long-ter

90 mosome 21 in humans (Trisomy 21), leading to neurological deficits and cognitive impairment.

91 y often results in permanent and devastating neurological deficits and disability.

92 ton's disease in vivo before the presence of neurological deficits and huntingtin aggregates.

93 le selected for its binding to MBL, improves neurological deficits and infarct volume when given up t

94 ia in mice; (3) anti-MBL-A antibody improves neurological deficits and infarct volume when given up t

95 ned for changes in physiological parameters, neurological deficits and infarct volume.

96 These SCFA-producers alleviated poststroke neurological deficits and inflammation, and elevated gut

97 Axon regeneration failure causes neurological deficits and long-term disability after spi

98 We conclude that FGF-2 improves neurological deficits and longevity in a transgenic mous

99 induced after severe TBI and contributes to neurological deficits and on-going neurodegenerative pro

100 s most frequently present with pain although neurological deficits and spinal deformity can be presen

101 ect is often difficult because of coexisting neurological deficits and the binaural nature of auditor

102 Clinical examination revealed no neurological deficits and the patient was rated 0 in mRS

103 ute ischaemic stroke with moderate to severe neurological deficits and were treatable by thrombectomy

104 showed significant improvement in survival, neurological deficit, and infarct size at 24 h after mid

105 en are challenging in the absence of a dense neurological deficit, and vary by institutional experien

106 (1) halt progression of disease, (2) reverse neurological deficits, and (3) prevent MS.

107 utcomes for patients include coma, permanent neurological deficits, and death.

108 lesions can cause headache, seizures, focal neurological deficits, and hemorrhagic stroke.

109 halted progression of disease, ii) reversed neurological deficits, and iii) prevented the onset of n

110 enetrated perihematoma brain tissue, reduced neurological deficits, and improved hematoma clearance,

111 n the central nervous system (CNS), enhanced neurological deficits, and reduced survival in vivo.

112 had significantly increased infarct volume, neurological deficits, and serum IL-6 levels three days

113 nfarct volumes, developed significantly less neurological deficits, and showed significantly better o

114 structures surrounding the vertebral column, neurological deficits, and spinal instability.

115 e risk of intracranial haemorrhage and focal neurological deficits, and the factors that might predic

116 Patients with perioperative neurological deficits are 14 times more likely to have h

117 However, neurological deficits are abundant under hypoxic conditi

118 Focal neurological deficits are frequently observed after chim

119 SAC significantly improved neurological deficits assessed by different scoring meth

120 nd thrombogenic responses, brain injury, and neurological deficit associated with experimental stroke

121 Despite the pronounced neurological deficits associated with mental retardation

122 There were no neurological deficits associated with rmTBI 3 day animal

123 understanding the potential role of TAOK2 in neurological deficits associated with the 16p11.2 region

124 ), or proportion of patients with a clinical neurological deficit at 48 h or 30 days.

125 variations in motor behavior as a result of neurological deficit at the different levels of CNS.

126 e depolarisation parallels the expression of neurological deficit at the onset of disease, and during

127 le sclerosis (MS), damage to myelin leads to neurological deficits attributable to demyelination and

128 viously unrecognized patient population with neurological deficits attributed to ARX mutations that a

129 developed severe early onset vision loss and neurological deficits, axonal degeneration without cell

130 uximab, but some die or acquire irreversible neurological deficits before they can respond, and relap

131 activation of A2ARs exacerbated 3-NP-induced neurological deficit behaviors and striatal damage, sele

132 that MT-I,II deficient mice would have more neurological deficits both functionally and anatomically

133 In tumor patients without preoperative neurological deficits, brain areas showing decreased coh

134 Both A438079 and P2X7R siRNA alleviated neurological deficits, brain edema, and BBB disruption a

135 PDGFR-alpha suppression prevented neurological deficits, brain edema, and Evans blue extra

136 Neurological deficits, brain edema, enzyme-linked immuno

137 nx1 depletion (Panx1(-/-)) displayed similar neurological deficits but lesser micturition dysfunction

138 Animals developed contralateral neurological deficits but were ambulatory.

139 Most survivors had mild to moderate neurological deficits, but many reported impaired school

140 nfancy or early childhood and develop severe neurological deficits, but the clinical presentation can

141 atients with relapsing-remitting MS reverses neurological deficits, but these results need to be conf

142 o restore lost motor function to people with neurological deficits by decoding neural activity into c

143 nt ischemic attack (TIA) is defined as focal neurological deficit caused by ischemia resolving within

144 n injury, and the amount of brain damage and neurological deficits caused by a stroke were significan

145 lt mammals and medical treatments to recover neurological deficits caused by axon disconnection are e

146 In 4-month-old Sandhoff mice with neurological deficits, cells staining positively for the

147 er stroke resulted in no salutary effects on neurological deficit, clot burden or lesion volume compa

148 Neurological deficit, clot burden, and lesion volume wer

149 greater in those who presented with a focal neurological deficit, cognitive impairment, cerebral inf

150 Transgenic mice showed less neurological deficit compared with wild-type mice (n=6).

151 ly smaller brain infarctions and less severe neurological deficits compared with controls without an

152 ical worsening as new permanent or transient neurological deficits (compared with presenting signs an

153 enous immunoglobulin (IVIG), and ameliorates neurological deficits, compared to pretreatment status.

154 to-Kakizaki (GK) rats develop greater HT and neurological deficit despite smaller infarcts after tran

155 before the age of 3 y can lead to long-term neurological deficits despite prompt diagnosis of ID ane

156 Delayed ischemic neurological deficit (DIND) contributes to poor outcome

157 Delayed ischemic neurological deficit (DIND) is a major driver of adverse

158 Patients with lesion-induced neurological deficits displayed decreased connectivity e

159 emorrhage or persistent or progressive focal neurological deficit due to the cerebral cavernous malfo

160 acute ischemic stroke and moderate to severe neurological deficits due to proximal artery occlusion a

161 eversible axonal dysfunction at the onset of neurological deficits during an acute central nervous sy

162 sed BBB leakage, reduced brain infection and neurological deficits during JEV infection, and prolonge

163 ouse model, fingolimod reduced infarct size, neurological deficit, edema, and the number of dying cel

164 rain injury can initiate an array of chronic neurological deficits, effecting executive function, lan

165 Post-assessments, including neurological deficits, Fluoro-Jade C staining, brain ede

166 clinical presentation with ICH or new focal neurological deficit (FND) without brain imaging evidenc

167 The neurological deficit following MCAO was lower and oxidat

168 ive for retarding tissue damage and reducing neurological deficits following a clinically relevant co

169 protected from excitotoxic brain damage and neurological deficits following experimental stroke, usi

170 WMI) caused by hypoxia is a leading cause of neurological deficits following premature birth.

171 y, and also can contribute to improvement in neurological deficits following such injury.

172 Secondary outcomes included neurological deficits following treatment, hospitalisati

173 recurrent intracranial haemorrhage or focal neurological deficit from a CCM is greater than the risk

174 er risk of intracranial haemorrhage or focal neurological deficit from cerebral cavernous malformatio

175 In several PML cases, viral persistence and neurological deficits have continued for several years,

176 r cause of birth defects that include severe neurological deficits, hearing and vision loss, and intr

177 se of birth defects, including microcephaly, neurological deficits, hearing impairment, and vision lo

178 DMF treatment reduced neurological deficit, immune cell infiltration, and demy

179 re often not visually evident, and may cause neurological deficits, impacting survival.

180 arct volume, oxidative stress parameters and neurological deficit in ischemic rats treated with vehic

181 Outcomes at hospital discharge included neurological deficits in 453 (74%) patients and death in

182 e dose of emboli (P(50) in mg) that produces neurological deficits in 50% of the rabbits.

183 effective stroke dose (P(50)) that produces neurological deficits in 50% of the rabbits.

184 ng or depleting MCAM in vivo reduces chronic neurological deficits in active, transfer, and spontaneo

185 hemia significantly reduces brain injury and neurological deficits in an animal model of ischemic str

186 enase-bright stem cells, capable of reducing neurological deficits in animal models.

187 ear cells (MNCs) from the bone marrow reduce neurological deficits in animal stroke models.

188 can be done to improve our understanding of neurological deficits in CHD.

189 s associated with anaemia, developmental and neurological deficits in children, and increased mortali

190 Cerebral damage and neurological deficits in experimental stroke were increa

191 al factors modulate susceptibility to SD and neurological deficits in FHM1 mutant mice, providing a p

192 Many of these neurological deficits in FXS probably involve the prefro

193 hippocampus may contribute to Abeta-induced neurological deficits in hAPP mice and, possibly, also i

194 al morbidities are associated with long term neurological deficits in life and have also been associa

195 R) robustly reduces infarctions and improves neurological deficits in mice.

196 l dysfunction is a major cause of reversible neurological deficits in neuroinflammatory disease, such

197 t that dendritic pathology may contribute to neurological deficits in patients with Angelman syndrome

198 The neurological deficits in these mice were associated with

199 Neurological deficits included flaccid limb weakness (n=

200 stroke is responsible for a large number of neurological deficits including memory impairment.

201 birth, but displayed severe and progressive neurological deficits including seizures and, ultimately

202 tant mice were viable, but exhibited complex neurological deficits including seizures, tremors, and g

203 c transmission, producing early and lifelong neurological deficits, including childhood absence epile

204 Heart failure is associated with neurological deficits, including cognitive dysfunction.

205 ilson's disease can present with hepatic and neurological deficits, including dystonia and parkinsoni

206 eficient reporter mice displayed progressive neurological deficits, including impaired motor function

207 Patients with FXS exhibit a range of neurological deficits, including motor skill deficits.

208 es, promoted worsening paralysis and induced neurological deficits, including optic neuritis.

209 s treatments the zebrafish were analyzed for neurological deficits, including tactile response, swimm

210 d carbenoxolone both failed to attenuate the neurological deficits induced by SAH, and they did not r

211 Delayed ischemic neurological deficit is the most common cause of neurolo

212 The susceptibility to SD and neurological deficits is affected by allele dosage and i

213 gh the mechanism(s) involved with persistent neurological deficits is not fully known, mitochondrial

214 On day 7 post-MCAO, neurological deficit-matched rats were assigned to a tre

215 The presence of severe neurological deficits may, however, give clinicians the

216 eductions, compared with control animals, in neurological deficit (mean+/-SD neuroscores of 21.5+/-21

217 led infarct volumes (p < 0.001) and worsened neurological deficits (median score = 9 vs 5 with vehicl

218 Twenty-one of 37 (56.7%) suffered residual neurological deficits (most commonly memory/cognition im

219 l twice a day for 7 days) on infarct volume, neurological deficit (neurological score, grip test, foo

220 can lead to encephalopathy, seizures, focal neurological deficits, neurological disability, and deat

221 cal management when there are no significant neurological deficits, neuroradiologic arterial evaluati

222 eyond which therapeutic ultrasound can cause neurological deficits not detectable by standard histolo

223 mposite of intracranial haemorrhage or focal neurological deficits (not including epileptic seizure)

224 Collectively, these data suggest that the neurological deficits observed in AS patients and in AS

225 The pathological mechanisms underlying neurological deficits observed in individuals born prema

226 ring brain development is illustrated by the neurological deficits observed in infants with mitochond

227 No neurological deficit occurred in either group.

228 In contrast to monkeys, neurological deficits occurred acutely in mice brain and

229 cic Surgeons (STS) criteria as any confirmed neurological deficit of abrupt onset that did not resolv

230 r how a loss of MeCP2 function generates the neurological deficits of Rett.

231 subsequent intracranial haemorrhage or focal neurological deficit (one [2%] of 61 vs 29 [12%] of 239,

232 hat constitutive deletion of Scly results in neurological deficits only when mice are challenged with

233 (using the Cre/loxP strategy) did not affect neurological deficit or striatal damage after the acute

234 ain parenchyma, which may eventually lead to neurological deficits or cognitive decline in the long t

235 Neurological deficits or lower-limb injuries can lead to

236 performance category score of 1 (mild or no neurological deficit) or 2 (moderate cerebral disability

237 ymptoms, such as headache, seizure, or focal neurological deficit, or have no symptoms and the lesion

238 bid speech and language disorder caused by a neurological deficit other than stroke, required treatme

239 infection, CD1(-/-) mice had an increase in neurological deficits over those observed in wild-type m

240 ng virus in plasma to non-detectable levels, neurological deficits persist.

241 And 138 cases (82.1%) had developed neurological deficits preoperatively with the average tu

242 l column and the spinal cord., It results in neurological deficits ranging from bladder and bowel inv

243 The cause of these neurological deficits remains unresolved.

244 Arousal was quantified using the neurological deficit scale (NDS).

245 olume (37.4%, 40.1%, and 39.9% vs 49.7%) and neurological deficit score (2.2, 2.6, and 2.8 vs 3.7), t

246 ter resuscitation was monitored using serial Neurological Deficit Score (NDS) calculation and qEEG an

247 ductions in both infarct volume (P<0.01) and neurological deficit score (P<0.05).

248 europrotection (31.0% infarct volume and 1.6 neurological deficit score) was found in stroke animals

249 educed cerebral infarct volume, and improved neurological deficit score.

250 Neurological deficit scores and survival time were obser

251 insult reduced brain infarct percentage and neurological deficit scores in C57BL/6 J mice, these eff

252 ollowing ischemic reperfusion, and decreased neurological deficit scores in treated animals, supporti

253 rculation, myocardial ejection fraction, and neurological deficit scores were observed in the hypothe

254 Postresuscitation myocardial function, neurological deficit scores, and 72-hour survival were s

255 group had better overall performance, final neurological deficit scores, and histological damage sco

256 etter postresuscitation myocardial function, neurological deficit scores, and longer duration of surv

257 abilize the PNJs and prevent the progressive neurological deficits seen in mutants lacking TBs; and 2

258 iated with AVF were recorded: heart failure, neurological deficit/seizure, and hemorrhage.

259 The risk of long-term neurological deficit should be discussed with prospectiv

260 ociated with severe brain swelling, but with neurological deficits, suggesting hypoxic injury in surv

261 gnificantly smaller brain infarcts and fewer neurological deficits than littermate controls.

262 mutant mice were more susceptible to SD and neurological deficits than males.

263 ucing cerebral infarct volume and alleviated neurological deficits than sTM after cerebral ischemia/r

264 mice showed larger infarct volumes and worse neurological deficits than the wild-type mice after isch

265 icient mice showed smaller infarcts and less neurological deficits than wild-type animals after a 90

266 ts who presented with urinary retention as a neurological deficit that was attributable to lateral me

267 HI) on P10 and the structural and functional neurological deficits that appear in the adult mouse as

268 arly in life, but also leads to a pattern of neurological deficits that are reminiscent of HD.

269 eased cerebral blood flow and development of neurological deficits that commonly follow SAH.

270 rtality, that Thiopental created exaggerated neurological deficits that were revealed through limb pl

271 protocols do not normally produce long-term neurological deficits, the rapid expansion of potential

272 al network pathology underlying a particular neurological deficit, thereby opening the way for strati

273 ting in subdural hematoma with no associated neurological deficits; this was managed conservatively.

274 ity rates, patients often suffer an array of neurological deficits throughout life.

275 e stroke, stratified by severity of baseline neurological deficit, to establish the very early time c

276 r number of strokes (45 vs 12, p<0.0001) and neurological deficits unrelated to stroke (14 vs 1, p=0.

277 PDA ligation and congenital mydriasis but no neurological deficit up to age 41.

278 The neurological deficit was closely correlated with spinal

279 Neurological deficit was greater in diabetic rats.

280 Infarct volume was reduced and I/R-induced neurological deficit was improved in immunodeficient Rag

281 ebral ischemia induction, infarct volume and neurological deficit were significantly increased at D1

282 Neurological deficits were evaluated after reperfusion.

283 Neurological deficits were examined at 3, 24, and 48 h a

284 before and 3 and 7 days post-surgery whilst neurological deficits were monitored daily.

285 follow-up of 42 months, no complications or neurological deficits were noted in either patient cohor

286 Neurological deficits were present and comparable in all

287 Observed neurological deficits were quantitatively, temporally, a

288 Infarct volume, edema, and neurological deficits were significantly reduced in grou

289 The total infarct volume and neurological deficits were significantly reduced in red

290 arction size was significantly enlarged, and neurological deficits were significantly worsened after

291 only partially prevent chronically worsening neurological deficits, which are largely attributable to

292 an increased risk of permanent postoperative neurological deficits, which should be taken into consid

293 ve imaging modalities may reduce the risk of neurological deficit while improving completeness of res

294 of care for patients with moderate to severe neurological deficits who present within 4.5 hours of sy

295 atio for individual studies of patients with neurological deficit with changes in SSEPs was 14.39 (95

296 hemia vera who developed a progressive focal neurological deficit with white matter abnormalities on

297 er tissues, culminating in stroke and severe neurological deficits with 100% penetrance.

298 OD1 dual transgenic mice develop accelerated neurological deficits, with a mean survival of 36 days,

299 igraine with multiple auras, transient focal neurological deficits without headache, coma triggered b

300 rative development of a severe headache, new neurological deficits without infarction, seizure or int