ライフサイエンスコーパス: neurological deficit

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

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

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

4 perihematomal leukocyte infiltration and the neurological deficit.

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

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

7 and 20 (A2b2), when the animals demonstrated neurological deficit.

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

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

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

11 which may result in hemorrhagic strokes and neurological deficits.

12 ideline concussion diagnosis and testing for neurological deficits.

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

14 .1% to 71.2% without incurring postoperative neurological deficits.

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

16 e and skeletal and cardiac anomalies without neurological deficits.

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

18 Death occurred approximately 48 days due to neurological deficits.

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

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

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

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

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

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

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

26 tural substrates accounting for these common neurological deficits.

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

28 hematomas, brain edema formation and marked neurological deficits.

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

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

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

32 osaposin/saposin deficiencies lead to severe neurological deficits.

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

34 0.01) reduction of brain infarct volume and neurological deficits.

35 erfusion injury and the consequent motor and neurological deficits.

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

37 ccessful strategies for delaying or avoiding neurological deficits.

38 ognitive function without inducing permanent neurological deficits.

39 ischemia-induced brain damage and associated neurological deficits.

40 The rats were scored post-reperfusion for neurological deficits.

41 ause meningitis, encephalitis, and long-term neurological deficits.

42 d pressure differentials, and 17% have focal neurological deficits.

43 , MK2(-/-) mice had significant reduction in neurological deficits.

44 disease would prevent or slow progression of neurological deficits.

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

46 yte death and ameliorated the progression of neurological deficits.

47 processes exacerbate the extent of permanent neurological deficits.

48 male patient who presented with progressive neurological deficits.

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

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

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

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

53 ther defects in lateralization contribute to neurological deficits.

54 a result of the irreversible accumulation of neurological deficits.

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

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

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

58 5%), severe neurological deficit (13%), mild neurological deficit (13%), undefined deficit (4%) and r

59 strokes (4.8%), and 6 episodes of transient neurological deficit (14.3%).

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

61 s (59%), headaches (35%), seizures and focal neurological deficits (24%) are common.

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

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

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

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

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

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

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

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

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

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

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

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

74 al blood flow and the development of delayed neurological deficits after SAH.

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

76 ral ischemia was increased, infarct size and neurological deficits after transient focal cerebral isc

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

78 In-hospital complications (neurological deficits, altered mental status, myocardial

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

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

81 Neurological deficit and infarct volume were determined

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

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

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

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

86 cking a functional Olig1 gene develop severe neurological deficits and die in the third postnatal wee

87 tributes to the development of non-remitting neurological deficits and disability in multiple scleros

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

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

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

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

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

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

94 , cerebral cortex and cerebellum, as well as neurological deficits and premature death.

95 strated significantly earlier improvement in neurological deficits and shortened latency of adhesive

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

111 However, neurological deficits are abundant under hypoxic conditi

112 Neurological deficits are observed in patients with cong

113 SAC significantly improved neurological deficits assessed by different scoring meth

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

115 Despite the pronounced neurological deficits associated with mental retardation

116 This mechanism may contribute to neurological deficits associated with n-3 fatty acid def

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

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

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

120 gnificantly reduced the mean (SD) scores for neurological deficit at both the peak of disease (Flec:

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

122 plus MP showed significantly less motor and neurological deficits at day 1, but thereafter displayed

123 nction and impulse conduction may exacerbate neurological deficits at subsequent disease stages.

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

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

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

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

128 d by episodic acute onset of irritability or neurological deficits between 2 months and 3.5 years of

129 injury produced a significant attenuation of neurological deficits (blocked by coadministration of MK

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

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

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

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

134 Neurological deficits, brain edema, enzyme-linked immuno

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

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

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

138 to 2 mg/kg significantly improved the motor neurological deficit by 3.8- to 3.2-fold and reduced inf

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

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

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

142 to focal or generalised seizure disorders or neurological deficits caused by compression of adjacent

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

144 tion and inflammation both contribute to the neurological deficits characteristic of multiple scleros

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

146 Neurological deficit, clot burden, and lesion volume wer

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

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

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

150 ficantly (P<0.05) reduced infarct volume and neurological deficits compared with saline-treated rats.

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

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

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

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

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

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

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

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

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

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

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

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

163 The neurological deficit following MCAO was lower and oxidat

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

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

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

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

168 Secondary outcomes included neurological deficits following treatment, hospitalisati

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

170 ccounts for 20% of all stroke-related sudden neurological deficits, has the highest morbidity and mor

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

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

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

174 olesterol and sphingolipid storage, onset of neurological deficits, histopathological lesions, Purkin

175 In addition to neurological deficits, Huntington's disease (HD) patient

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

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

178 There was a trend toward less improvement in neurological deficit in patients with secondary injury v

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

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

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

182 he role of testosterone during recovery from neurological deficits in a rat focal ischemia model.

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

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

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

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

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

188 toplasmic domain mutations may contribute to neurological deficits in CRASH.

189 Cerebral damage and neurological deficits in experimental stroke were increa

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

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

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

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

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

195 nts since this is likely to be the basis for neurological deficits in surviving infants.

196 The neurological deficits in these mice were associated with

197 al cord neurons are critical determinants of neurological deficits in various pathological conditions

198 Neurological deficits included flaccid limb weakness (n=

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

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

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

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

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

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

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

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

207 as pulse or blood pressure differentials and neurological deficits increase the likelihood of disease

208 The presence of pulse deficits or focal neurological deficits increases the likelihood of an acu

209 Neurological deficits induced by ischemia were also redu

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

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

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

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

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

215 cause significant pathology with associated neurological deficits, mental disorders, and cognitive i

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

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

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

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

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

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

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

223 No neurological deficit occurred in either group.

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

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

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

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

228 )Atrn(mg) animals, we observe no evidence of neurological deficit or neuropathology in md/md mice.

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

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

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

232 tions are haemorrhage, seizures, progressive neurological deficit, or headache.

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

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

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

236 The cause of these neurological deficits remains unresolved.

237 % (p < 0.05) and 23% (p < 0.05) reduction in neurological deficits, respectively.

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

239 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

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

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

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

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

244 All animals (n = 52) developed high-grade neurological deficits (score 11 of 12) during ischemia,

245 Neurological deficit scores and survival time were obser

246 ia) reduced brain infarct sizes and improved neurological deficit scores assessed 6, 24, and 72 h aft

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

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

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

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

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

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

253 he REST transcription factor and some of the neurological deficits seen in Down's syndrome.

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

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

256 aemorrhage and can lead to delayed ischaemic neurological deficit (stroke).

257 cal conversion disorders refer to functional neurological deficits such as paralysis, anaesthesia or

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

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

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

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

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

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

264 c symptoms and high prevalence of associated neurological deficits that become increasingly obvious w

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

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

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

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

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

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

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

272 The neurological deficit was closely correlated with spinal

273 Neurological deficit was greater in diabetic rats.

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

275 In addition to neurological deficits, we find widespread ultrastructura

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

277 Neurological deficits were also more severe in hBACE1 an

278 At 2 and 24 h post-MCAO, neurological deficits were assessed.

279 Neurological deficits were evaluated after reperfusion.

280 Residual neurological deficits were evident.

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

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

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

284 Neurological deficits were present and comparable in all

285 Observed neurological deficits were quantitatively, temporally, a

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

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

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

289 Neurological deficits were similar between groups (oestr

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

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

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

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

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

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

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

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

298 t clear TMEV infection and develop prominent neurological deficits within 6 wk.

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