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 on which higher scores indicate more severe neurologic deficits).

3 s drive the EAE pathogenesis to irreversible neurologic deficit.

4 rithm was strongly predictive of seizure and neurologic deficit.

5 survived to hospital discharge had residual neurologic deficit.

6 operative renal failure, and lower extremity neurologic deficit.

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

8 14 times higher than in individuals without neurologic deficit.

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

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

11 nial aneurysm often results in postoperative neurologic deficits.

12 setting is essential to prevent irreversible neurologic deficits.

13 Three developed persistent neurologic deficits.

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

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

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

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

18 rrelated with the severity of the presenting neurologic deficits.

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

20 om other processes that manifest with sudden neurologic deficits.

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

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

23 poreal membrane oxygenation, and significant neurologic deficits.

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

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

26 seven of the survivors had permanent severe neurologic deficits.

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

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

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

30 e future opportunities to treat or alleviate neurologic deficits.

31 plications, including both focal and diffuse neurologic deficits.

32 None of the animals had neurologic deficits.

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

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

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

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

37 igh-dose treatment consistently improved all neurologic deficits.

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

39 severe headaches with or without associated neurologic deficits.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

54 Neurologic deficit and MR imaging were utilized at vario

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

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

57 Neurologic deficits and cerebral apoptosis were assessed

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 Permanent neurologic deficits are common in patients that survive,

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

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

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

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

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

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

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

86 Neurologic deficit at admission, MCA recanalization, sym

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

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

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

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

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

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

93 4 hrs, and she was discharged home with mild neurologic deficit (Cerebral Performance Category 2) on

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

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

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

97 The neurologic deficits do not necessarily correlate with bl

98 Three patients had transient neurologic deficits during BAE.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

120 95% CI, 1.9-12.8), seizures accompanying the neurologic deficit (LR, 4.7; 95% CI, 1.6-14), diastolic

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

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

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

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

125 , 1 of 47 (2%) patients suffered a permanent neurologic deficit, none had wound infection.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

150 Neurologic deficit score at 72 hrs after asphyxial cardi

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

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

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

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

155 Neurologic recovery was evaluated using the Neurologic Deficit Score.

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

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

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

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

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

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

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

163 Survival, neurologic deficit scores, overall performance category,

164 Neurologic deficit scores, overall performance category,

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

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

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

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

169 The neurologic deficits that characterize multiple sclerosis

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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