ライフサイエンスコーパス: neurologic deficit

1 nting death and 5 representing no or minimal neurologic deficit).

2 nting death and 5 representing no or minimal neurologic deficit).

3 scharge outcomes (death or survival with new neurologic deficits).

4 on which higher scores indicate more severe neurologic deficits).

5 rithm was strongly predictive of seizure and neurologic deficit.

6 survived to hospital discharge had residual neurologic deficit.

7 operative renal failure, and lower extremity neurologic deficit.

8 l ischemic injury with no differences in the neurologic deficit.

9 s drive the EAE pathogenesis to irreversible neurologic deficit.

10 14 times higher than in individuals without neurologic deficit.

11 rapy in an effort to reduce HIV-1-associated neurologic deficit.

12 t CNS axons is abortive, causing devastating neurologic deficits.

13 severe headaches with or without associated neurologic deficits.

14 nial aneurysm often results in postoperative neurologic deficits.

15 setting is essential to prevent irreversible neurologic deficits.

16 Three developed persistent neurologic deficits.

17 tly influence the severity of CHS-associated neurologic deficits.

18 l, but there is evidence that it may improve neurologic deficits.

19 l cord is a critical determinant of residual neurologic deficits.

20 ke, seizures, recurrent headaches, and focal neurologic deficits.

21 n microhemorrhages, white matter injury, and neurologic deficits.

22 rrelated with the severity of the presenting neurologic deficits.

23 at as many as two thirds of neonates develop neurologic deficits.

24 om other processes that manifest with sudden neurologic deficits.

25 s, increase conduction velocity, and improve neurologic deficits.

26 outcomes from such injuries may be life-long neurologic deficits.

27 to 58% of survivors having permanent severe neurologic deficits.

28 e future opportunities to treat or alleviate neurologic deficits.

29 f neurologic function, and prevention of new neurologic deficits.

30 seven of the survivors had permanent severe neurologic deficits.

31 n that can be removed with a low risk of new neurologic deficits.

32 logic disease often complicated by prolonged neurologic deficits.

33 cell junctions, BBB breakdown, and resulting neurologic deficits.

34 ain causes severe encephalitis and permanent neurologic deficits.

35 leave axons vulnerable, leading to permanent neurologic deficits.

36 ing active RMS, albeit without corresponding neurologic deficits.

37 erosis (Fig 1), albeit without corresponding neurologic deficits.

38 ring early lesion formation and the onset of neurologic deficits.

39 owever, many survivors suffer from long-term neurologic deficits.

40 poreal membrane oxygenation, and significant neurologic deficits.

41 tubated cognitively intact and without focal neurologic deficits.

42 d may include fever, mild renal failure, and neurologic deficits.

43 ren with vs those without acute or long-term neurologic deficits.

44 entangling delirium symptoms from underlying neurologic deficits.

45 plications, including both focal and diffuse neurologic deficits.

46 None of the animals had neurologic deficits.

47 ver, her headache returned and she developed neurologic deficits.

48 with a headache peaking within 1 hour and no neurologic deficits.

49 pper extremity, even in the absence of focal neurologic deficits.

50 brain injury that may lead to a lifetime of neurologic deficits.

51 igh-dose treatment consistently improved all neurologic deficits.

52 There were 18 permanent neurologic deficits (0.8%) in the eversion group and 11

53 urocognitive impairment (30%-40%), and focal neurologic deficits (10%-40%).

54 cribe a patient who presented with bilateral neurologic deficits 4 and 6 weeks after lung transplanta

55 xamined univariately, only the presence of a neurologic deficit (70% vs. 37%; difference, 33%; p < .0

56 d-brain barrier disruption, brain edema, and neurologic deficits, accompanied with phosphorylation of

57 rs of fracture in the elderly included focal neurologic deficit (adjusted odds ratio, 17.7; 95% confi

58 r increase: 1.17; 95% CI: 1.08, 1.28), focal neurologic deficit (adjusted OR: 5.39; 95% CI: 3.90, 7.4

59 ade 1 and 2 deficits on emergence but had no neurologic deficit after 1 hr.

60 There was no incidence of neurologic deficit after stage 2, and early mortality oc

61 ge ET repair was 10/297 (3.4%) and immediate neurologic deficit after the second-stage ET repair was

62 ness, many of the mice developed progressive neurologic deficits after 2 to 4 months of imatinib mesy

63 pothermia is being clinically used to reduce neurologic deficits after cardiac arrest (CA).

64 ay directly contribute to the development of neurologic deficits after demyelination in the Theiler's

65 nflammatory response may still contribute to neurologic deficits after reperfused stroke by using tar

66 Boys with more severe neurologic deficits also had higher levels of CSF GNMPB

67 ilia, eosinophiluria, acute onset of diffuse neurologic deficit, amaurosis fugax, acute renal failure

68 rvive 30 d after the surgery for post-stroke neurologic deficit analyses.

69 and SB 239063 significantly (P<0.05) reduced neurologic deficit and infarct size by at least 30% from

70 Neurologic deficit and MR imaging were utilized at vario

71 category 1 (normal); four of six dogs had no neurologic deficit and normal brain histology.

72 at XXMT treatment significantly improved the neurologic deficit and quality of life of acute ischemic

73 STAT1 mKO was sufficient to reduce long-term neurologic deficits and brain lesion size after TBI.

74 One patient presented with focal neurologic deficits and brain lesions; broad-range molec

75 Neurologic deficits and cerebral apoptosis were assessed

76 hether axonal injury is related to long-term neurologic deficits and cognitive impairment in children

77 hildren with CM is associated with long-term neurologic deficits and cognitive impairment.

78 occasionally present with new or progressive neurologic deficits and detectable HIV-1 RNA in the cere

79 WT) and DP1(-/-) mice were subjected ICH and neurologic deficits and hemorrhagic lesion outcomes were

80 rity of patients with WMLs develop permanent neurologic deficits and imaging changes.

81 GD2.CARTs exhibited transient improvement of neurologic deficits and increased circulating cytokines/

82 year survival of 92% in patients with 0 or 1 neurologic deficits and magnetic resonance imaging (MRI)

83 ng ISM are associated with fewer late severe neurologic deficits and more extensive resection, and th

84 nge, 2-14 years) with HbSS genotype, without neurologic deficits and no history of stroke, were enrol

85 with resultant midline CS tenderness and/or neurologic deficits and were undergoing CT of the CS.

86 air, 0 of 103 patients experienced immediate neurologic deficit, and 10 of 103 (9.7%) died within 30

87 nt of patients presented with a preoperative neurologic deficit, and 5% developed a new cerebrovascul

88 Age, neurologic deficit, and history of childhood febrile sei

89 Fifty-six of 269 patients (21 %) developed a neurologic deficit, and in 9% the neurologic deficit per

90 antly greater myocardial impairment, greater neurologic deficit, and lesser duration of survival.

91 rologic and CT findings, 43% by new onset of neurologic deficits, and 23% by physical examination (ne

92 eased rates of anemia, osteoporosis, cancer, neurologic deficits, and additional autoimmune disorders

93 n cause delayed development, epilepsy, focal neurologic deficits, and mental retardation.

94 n half of the patients had developmental and neurologic deficits, and one-fourth had a diagnosis of e

95 but slow recovery; two were left with severe neurologic deficits; and one died after return to the re

96 acial/cervical-spinal fractures; unexplained neurologic deficit; anisocoria; lateral neck soft tissue

97 MEV infection of the central nervous system, neurologic deficits appear to result either from the abs

98 No new neurologic deficits appeared more than 28 months after r

99 er inoculation and approximately 62 d before neurologic deficits appeared.

100 Permanent neurologic deficits are common in patients that survive,

101 ile the associated neuroinflammation and the neurologic deficits are dramatically exacerbated.

102 +) T cells as a potential mechanism by which neurologic deficits are induced after demyelination.

103 ith low back pain when severe or progressive neurologic deficits are present or when serious underlyi

104 use of norepinephrine, absence of reflexes, neurologic deficit as cause of death, and absence of car

105 characterized by long-term motor and sensory neurologic deficits as a consequence of an external phys

106 perforin-deficient mice showed only minimal neurologic deficits as indicated by clinical disease sco

107 lammation, brain edema, iron deposition, and neurologic deficits associated with delayed hematoma cle

108 associated with MS and often precedes other neurologic deficits associated with MS.

109 cant challenges due to the increased risk of neurologic deficits associated with treatment.

110 imilar modified Rankin Scale and severity of neurologic deficit at 14 days but higher (worse) modifie

111 composite of death from any cause or severe neurologic deficit at 30 days.

112 tory of stroke and hypertension, severity of neurologic deficit at admission, Acute Physiology and Ch

113 Neurologic deficit at admission, MCA recanalization, sym

114 of CT or MRI was associated with white race, neurologic deficit at baseline, sciatica, poor functiona

115 ent of an adverse clinical outcome (death or neurologic deficit at discharge).

116 with spinal tuberculosis, 54/133 (40.6%) had neurologic deficits at admission and 17.3% presented wit

117 Ten of 42 (24%) survived with new neurologic deficits at discharge and 8 (19%) died.

118 ts survived, but 15 of them (12 percent) had neurologic deficits at discharge.

119 ogic involvement, 17 survivors (40%) had new neurologic deficits at hospital discharge, and 11 patien

120 rations were associated with the presence of neurologic deficits at hospital discharge, and at 6, 12,

121 0 to 42, with higher scores indicating worse neurologic deficit) at 12 hours, and no receipt of rescu

122 ta, and outcomes (death or survival with new neurologic deficits) at hospital discharge.

123 Adverse events included a transient neurologic deficit attributed to a magnetic resonance im

124 Critically, blockade of either reduces neurologic deficit, blood-brain barrier disruption and p

125 stroke (AIS), while an ischemic episode with neurologic deficits but without acute infarction defines

126 sessment Method for the ICU in patients with neurologic deficits, but novel tools designed for such p

127 We assessed neurologic deficits by neurobehavioral tests and blood-b

128 4 hrs, and she was discharged home with mild neurologic deficit (Cerebral Performance Category 2) on

129 cy are typical in SAMD9, whereas progressive neurologic deficits characterize SAMD9L.

130 iencing fevers, syncope or presyncope, focal neurologic deficits, chest pain, nausea, vomiting, unint

131 increase in survival (P < 0.05), and reduced neurologic deficit compared with ICAM-1 +/+ controls.

132 s confirmed that only the frequency of a new neurologic deficit differed significantly in the two gro

133 The neurologic deficits do not necessarily correlate with bl

134 Three patients had transient neurologic deficits during BAE.

135 for obtaining the HCT (mental status change, neurologic deficit, fever, seizures), coagulation profil

136 of the elderly patients (56.33%) had a mild neurologic deficit (GCS score, 13-15), whereas most of t

137 d increased odds of presenting with a severe neurologic deficit (GCS score, 3-8) at each of the follo

138 f the younger patients (63.28%) had a severe neurologic deficit (GCS score, 3-8).

139 nt ischemic attack. with reversible ischemic neurologic deficit, however, hyperintensity on DW images

140 without additional cranial bone fracture and neurologic deficit in the literature.

141 sruption and pathology and protected against neurologic deficit in the MS model system.

142 ns included developmental delay in 12 (63%), neurologic deficits in 10 (53%), and endocrine dysfuncti

143 f MeCP2 expression in a mouse model reverses neurologic deficits in adult animals, reactivation of th

144 ells in the development of demyelination and neurologic deficits in diseases of the central nervous s

145 Our results provide evidence that neurologic deficits in FD alter the structure and functi

146 ssociated with increased severity of chronic neurologic deficits in high-exposure boxers.

147 e been associated with protection from acute neurologic deficits in Kenyan children with cerebral mal

148 ctive COX-2 inhibitor, on infarct volume and neurologic deficits in mice with experimentally-induced

149 uding metformin, have the potential to limit neurologic deficits in multiple sclerosis and related ne

150 e blood pressure augmentation may ameliorate neurologic deficits in patients who undergo thoracoabdom

151 s degrees of neuroinflammation and long-term neurologic deficits in surgically treated patients, prov

152 a proxy of preserved function without major neurologic deficits in survivors.

153 that migraine is an important contributor to neurologic deficits in the general population.

154 The etiology of neurologic deficits in this population appears to be mul

155 Initial management of a focal neurologic deficit includes evaluation by a multidiscipl

156 Deficiency can cause neurologic deficits including loss of coordination and c

157 ome type 1 (GS1) is characterized by several neurologic deficits including quadraparesis, mental reta

158 ntal understanding of brain function and how neurologic deficits influence goal-directed, coordinated

159 barachnoid hemorrhage (SAH) leads to chronic neurologic deficits is unclear.

160 requently (46% vs. 32%, p = 0.002) and focal neurologic deficits less frequently (18% vs. 26%, p = 0.

161 have not clearly established a cause for the neurologic deficits linked with GS1, a few reports sugge

162 95% CI, 1.9-12.8), seizures accompanying the neurologic deficit (LR, 4.7; 95% CI, 1.6-14), diastolic

163 gression after brief improvement of residual neurologic deficits (<=3 weeks).

164 ficiency with the development of concomitant neurologic deficits manifested as peripheral neuropathie

165 n after intracerebral hemorrhage, but severe neurologic deficits may confound its assessment and lead

166 strains with deletions of CD4 showed severe neurologic deficits, mice with deletions of CD8 showed m

167 se mortality after 1 year, as well as severe neurologic deficit, myocardial infarction, and rehospita

168 surviving until 1 year, the rates of severe neurologic deficit, myocardial infarction, and rehospita

169 schemic attack (n=3), or reversible ischemic neurologic deficit (n=1).

170 (n = 2) or at relapse (n = 1) and permanent neurologic deficits (n = 4).

171 , 1 of 47 (2%) patients suffered a permanent neurologic deficit, none had wound infection.

172 ry: no midline cervical tenderness, no focal neurologic deficit, normal alertness, no intoxication, a

173 The composite of death or severe neurologic deficit occurred more frequently in the immed

174 Transient neurologic deficits occurred in 20 patients (0.9%) in th

175 were identified in seven other patients with neurologic deficits of unknown etiology, 6% of healthy c

176 In patients without neurologic deficits, only the presence of seizures was a

177 lts deemed eligible for evaluation who had a neurologic deficit or CS pain.

178 Study low-risk criteria because of either a neurologic deficit or pain, the optimal imaging modality

179 The presence of either neurologic deficit or seizures best predicted a positive

180 Among MICU patients, the presence of either neurologic deficit or seizures is associated with the pr

181 ck pain only if they have severe progressive neurologic deficits or signs or symptoms that suggest a

182 sient worsening of residual poststroke focal neurologic deficits or transient recurrence of prior str

183 se (OR = 11.6, 95% CI: 5.4, 25.0), and focal neurologic deficit (OR = 58, 95% CI: 12, 283).

184 equently had altered cognition, a persistent neurologic deficit, or stroke at presentation, less freq

185 eveloped a neurologic deficit, and in 9% the neurologic deficit persisted at discharge.

186 Brain injury-induced neurologic deficits persisted up to 20 wks after injury

187 reatment are crucial to stabilize or reverse neurologic deficits, prevent further nervous system inju

188 nt improvement in neuropathy assessed by the neurologic deficits, QST, electrophysiology, and IENFD.

189 effects of Xueshuan Xinmai tablets (XXMT) on neurologic deficits, quality of life and brain functiona

190 ation (SPK) underwent detailed assessment of neurologic deficits, quantitative sensory testing (QST),

191 Susceptibilities were higher with increasing neurologic deficits (r = 0.34, P < .01) and lower with n

192 erienced temporary improvement from baseline neurologic deficits (range, 2 to >12 months), and seven

193 Surgery resulted in anticipated neurologic deficits related to the region of brain resec

194 In all 15 patients, the neurologic deficits resolved within two weeks.

195 produced favorable results; approximately 1 neurologic deficit saved for every 20 uses of adjunct ov

196 unctional evaluation was performed using the Neurologic Deficit Score (NDS).

197 functional recovery as indicated by improved neurologic deficit score and spontaneous locomotor activ

198 IQ values correlated strongly with 72-hr Neurologic Deficit Score as early as 30 mins post-cardia

199 ction was assessed using a well-standardized neurologic deficit score assigned at 6, 12, and 24 hrs a

200 Neurologic deficit score at 72 hrs after asphyxial cardi

201 after cardiopulmonary resuscitation using a neurologic deficit score before the brains were harveste

202 ion predicted good neurologic outcome (72-hr Neurologic Deficit Score of > or = 60), with a specifici

203 Performance Category (1, normal; 5, death), Neurologic Deficit Score, Histologic Damage Score, and b

204 Outcome was assessed by a neurologic deficit score, the Morris water maze, and CA1

205 Neurologic recovery was evaluated using the Neurologic Deficit Score.

206 y; 3, severe disability; 4, coma; 5, death), neurologic deficit scores (NDS 0-10%, normal; 100%, brai

207 p was associated with significantly improved neurologic deficit scores and survival time when compare

208 n showed strokes of smaller volume and lower neurologic deficit scores in parallel with increased bra

209 reated animals showed significantly improved neurologic deficit scores over time (day 1 = 59.0 6 27.0

210 Overall performance categories and neurologic deficit scores were assessed from 24 to 96 hr

211 asured hourly for 4 hrs after resuscitation; neurologic deficit scores were measured daily for 7 days

212 -segment elevation, better postresuscitation neurologic deficit scores, and longer duration of surviv

213 Survival, neurologic deficit scores, overall performance category,

214 Neurologic deficit scores, overall performance category,

215 abnormal myelination, which could cause the neurologic deficits seen with GS1.

216 ia and leukopenia with or without associated neurologic deficits should have copper and ceruloplasmin

217 discusses applications of such knowledge to neurologic deficits, specifically, steering in the prese

218 ons in multiple brain regions and results in neurologic deficits such as seizures.

219 e striatum, and the mice demonstrated severe neurologic deficits that appeared within 60 min and rema

220 e clues into the pathogenic mechanism of the neurologic deficits that are associated with gluten sens

221 The neurologic deficits that characterize multiple sclerosis

222 delirium assessment tools do not account for neurologic deficits that often interfere with convention

223 toms, although it may take up to 3 years for neurologic deficits to be ameliorated.

224 Immediate neurologic deficit was 18 (2.4%) of 741 with adjunct and

225 The neurologic deficit was reduced by 35% and 90%, respectiv

226 ntibiotic therapy followed by rapid onset of neurologic deficits was the most common clinical present

227 of 0 to 2, signifying an absence of or minor neurologic deficit, was 35.1% in the thrombectomy group

228 No differences in neurologic deficit were detectable between males and fem

229 of observing an SSEP change among those with neurologic deficits were 14 times higher than in individ

230 New postoperative neurologic deficits were categorized on the basis of tim

231 The blood-brain barrier permeability and neurologic deficits were investigated at 24 and 72 hours

232 farct volume was significantly increased and neurologic deficits were more severe in GCV- compared to

233 duction of infarct volume and improvement of neurologic deficits were noted more than 24 h after the

234 Late severe neurologic deficits were observed in 3.4% (95% CI, 2.3%

235 Neurologic deficits were observed with all tested chemot

236 90 days in 3 patients (18.8%), and residual neurologic deficits were seen in 8 survivors (72.7%).

237 Most patients have neurologic deficits when the injury is diagnosed.

238 ats with MPABP 70-90 mm Hg recovered without neurologic deficits, whereas those that underwent aortic

239 e of the affected AQP2-V168M individuals had neurologic deficits, which also suggested a milder form

240 otype resulted in frequent deaths and severe neurologic deficits within 16 days of infection compared

241 otype resulted in frequent deaths and severe neurologic deficits within 2 weeks of infection as compa

242 ly smaller brain infarctions and less severe neurologic deficits without an increase in infarct-assoc

243 hether there is differential breakdown under neurologic deficit - would provide even stronger support