ライフサイエンスコーパス: subarachnoid

1 of the model showed severe brain injury with subarachnoid and hemorrhage together with glial cell act

2 as associated with poor clinical grade, more subarachnoid and intraventricular blood seen on admissio

3 The importance of convective flow in the subarachnoid and paravascular spaces has long been recog

4 Previous analyses of the International Subarachnoid Aneurysm Trial (ISAT) cohort have reported

5 ng of the applicability of the International Subarachnoid Aneurysm Trial data and the roles of surgic

6 uptured Aneurysm Trial and the International Subarachnoid Aneurysm Trial II, are aimed at improving u

7 hemorrhage developed from the International Subarachnoid Aneurysm Trial in a retrospective unselecte

8 an observed probabilities, the International Subarachnoid Aneurysm Trial prediction model needs to be

9 hemoglobin-driven neurological damage after subarachnoid bleeding.

10 Our results demonstrate that subarachnoid blood causes a delayed increase in the ampl

11 Subarachnoid hemorrhage, defined as (1) subarachnoid blood on computed tomography scan; (2) xant

12 We report that subarachnoid blood profoundly impacts communication with

13 These results suggest that subarachnoid clots in sulci/fissures are sufficient to i

14 nd the associated inflammatory milieu in the subarachnoid compartment plays a role in the pathogenesi

15 d exits through paravenous spaces again into subarachnoid compartments.

16 ne in the efficiency of exchange between the subarachnoid CSF and the brain parenchyma.

17 king transforming growth factor-beta-induced subarachnoid fibrosis and protected against hydrocephali

18 nal fluid flow and drainage is obstructed by subarachnoid fibrosis in which the potent fibrogenic cyt

19 minal aortic aneurysm (0.46 [0.35-0.59]) and subarachnoid haemorrhage (0.48 [0.26-0.89]), and not ass

20 ominal aortic aneurysm (0.46, 0.35-0.59) and subarachnoid haemorrhage (0.48, 0.26-0.89).

21 hage (hazard ratio 1.44 [95% CI 1.32-1.58]), subarachnoid haemorrhage (1.43 [1.25-1.63]), and stable

22 egree relative affected (FDRA) by aneurysmal subarachnoid haemorrhage (aSAH) are at a higher lifetime

23 After aneurysmal subarachnoid haemorrhage (aSAH), extracellular haemoglob

24 erebral vasospasm (cVSP) in human aneurysmal subarachnoid haemorrhage (aSAH).

25 INTRODUCTION: Acute non-traumatic convexity subarachnoid haemorrhage (cSAH) is increasingly recognis

26 survivors in the Genetics and Observational Subarachnoid Haemorrhage (GOSH) Study, a retrospective m

27 asymptomatic UIA and the risk of subsequent subarachnoid haemorrhage (SAH) by follow-up on intensive

28 anned admission the woman was diagnosed with subarachnoid haemorrhage (SAH) in the region of the prev

29 Clinical and radiological intensity of subarachnoid haemorrhage (SAH) was evaluated by using th

30 aemic), transient ischaemic attack (TIA) and subarachnoid haemorrhage (SAH).

31 rial hypertension (HTN) is a risk factor for subarachnoid haemorrhage (SAH).

32 ogical deterioration occurs frequently after subarachnoid haemorrhage (SAH).

33 -16], intracerebral haemorrhage 28% [26-29], subarachnoid haemorrhage 16% [12-20], unspecified stroke

34 -42], intracerebral haemorrhage 44% [42-46], subarachnoid haemorrhage 22% [18-27], unspecified stroke

35 hort have reported on the risks of recurrent subarachnoid haemorrhage and death or dependency for a m

36 with confirmatory evidence of an aneurysmal subarachnoid haemorrhage and presenting less than 96 h f

37 of global as opposed to focal deficits after subarachnoid haemorrhage and traumatic brain injury in h

38 pants in six prospective cohort studies with subarachnoid haemorrhage as outcome.

39 y (ALI) occurs in up to 30% of patients with subarachnoid haemorrhage but the incidence of ALI after

40 d was diagnosed with a Hunt and Hess grade 3 subarachnoid haemorrhage from a ruptured aneurysm.

41 how that axonal injury also occurs following subarachnoid haemorrhage in an animal model.

42 Here we studied acute sequelae of subarachnoid haemorrhage in the gyrencephalic brain of p

43 of statins in patients with acute aneurysmal subarachnoid haemorrhage is unclear.

44 33 patients had a recurrent subarachnoid haemorrhage more than 1 year after their in

45 ety concerns, we conclude that patients with subarachnoid haemorrhage should not be treated routinely

46 Prognosis seems worse in patients with subarachnoid haemorrhage than in those without.

47 Most patients with subarachnoid haemorrhage undergo surgical or endovascula

48 ated ipsilateral basal ganglia bleeding with subarachnoid haemorrhage with no aetiology is uncommon.

49 agnosed ischaemic or haemorrhagic (excluding subarachnoid haemorrhage) stroke 5-42 days before random

50 tudy (cardiac arrest, pneumonia, sepsis, and subarachnoid haemorrhage), none were deemed treatment re

51 Subarachnoid haemorrhage, a particularly deadly form of

52 ere intracerebral haemorrhage, 702 (2%) were subarachnoid haemorrhage, and 1002 (2%) were an unspecif

53 52% for rural areas and 32% for urban areas) subarachnoid haemorrhage, and 24% (22-27) for unspecifie

54 ars or older with hypertension, a history of subarachnoid haemorrhage, and a giant-sized (>20 mm) pos

55 schaemia (DCI) which occurs after aneurysmal subarachnoid haemorrhage, and often leads to cerebral in

56 ischaemic stroke, intracerebral haemorrhage, subarachnoid haemorrhage, and unspecified type).

57 redictors were age, hypertension, history of subarachnoid haemorrhage, aneurysm size, aneurysm locati

58 cal clipping or endovascular coiling after a subarachnoid haemorrhage, assuming treatment equipoise,

59 nts with ischaemic and haemorrhagic strokes, subarachnoid haemorrhage, cerebrovascular malformations,

60 atment (one retroperitoneal haemorrhage, one subarachnoid haemorrhage, one respiratory distress, and

61 can present with headache, ischaemic stroke, subarachnoid haemorrhage, or symptoms associated with ma

62 s also a functionally significant feature of subarachnoid haemorrhage, raising the prospect of common

63 is also a prominent feature of experimental subarachnoid haemorrhage.

64 ort-term outcome in patients with aneurysmal subarachnoid haemorrhage.

65 mmon in poor-grade patients after aneurysmal subarachnoid haemorrhage.

66 antiplatelet therapy or in the setting of a subarachnoid haemorrhage.

67 rebral vasospasm in patients with aneurysmal subarachnoid haemorrhage; (4) the use in the biomechanic

68 was lower in patients with thick versus thin subarachnoid hemorrhage (1.92 vs 1.99 mg/dL; p = 0.022).

69 n-Hispanic black patients aged 45 to 54 with subarachnoid hemorrhage (13.2/10000 to 10.3/10000 hospit

70 Subarachnoid hemorrhage (20%) was the most common type o

71 c stroke (19%), 936 ventilated patients with subarachnoid hemorrhage (32%), and 1,404 ventilated pati

72 Of 383 patients enrolled, there were 128 subarachnoid hemorrhage (33.4%), 134 subdural hematoma (

73 Patients with coma attributable to subarachnoid hemorrhage (4/80; 5%) or global hypoxic-isc

74 and 131 met CT criteria for PM nonaneurysmal subarachnoid hemorrhage (53 women; mean age, 53 years [r

75 and unstable angina, and inverse (0.69) for subarachnoid hemorrhage (all P<0.001).

76 VSP) is a common phenomenon after aneurysmal subarachnoid hemorrhage (aSAH) and contributes to neuroc

77 nosis of patients with high-grade aneurysmal subarachnoid hemorrhage (aSAH) is only insufficiently di

78 ed the prognosis differed between aneurysmal subarachnoid hemorrhage (aSAH) patients with surgical cl

79 In aneurysmal subarachnoid hemorrhage (aSAH), accurate diagnosis of an

80 adverse outcomes in patients with aneurysmal subarachnoid hemorrhage (aSAH), defining an unmet need f

81 asospasm is a dreaded sequelae of aneurysmal subarachnoid hemorrhage (aSAH), requiring timely interve

82 ribute to poor outcomes following aneurysmal subarachnoid hemorrhage (aSAH).

83 al hemorrhage (HR, 1.9; 95% CI, 1.5-2.4) and subarachnoid hemorrhage (HR, 2.4; 95% CI, 1.7-3.5) than

84 95% CI, 0.14-0.77; p = 0.011) and with thick subarachnoid hemorrhage (odds ratio 0.29 per 1 mg/dL inc

85 rhages, whereas SCARA5 decreased the risk of subarachnoid hemorrhage (OR=0.61; 95% CI, 0.47-0.81; P=5

86 hemorrhage (RR: 0.96; 95% CI: 0.84, 1.10) or subarachnoid hemorrhage (RR: 1.01; 95% CI: 0.90, 1.14).

87 ce of intracranial aneurysms (IA) and suffer subarachnoid hemorrhage (SAH) at younger ages than the g

88 Subarachnoid hemorrhage (SAH) carries a 50% mortality ra

89 mic neurological damage following aneurysmal subarachnoid hemorrhage (SAH) have remained elusive.

90 Aneurysmal subarachnoid hemorrhage (SAH) is a potentially devastati

91 soconstriction in brain slices obtained from subarachnoid hemorrhage (SAH) model rats.

92 rospective observational study of aneurysmal subarachnoid hemorrhage (SAH) patients, we explored the

93 Subarachnoid hemorrhage (SAH) results in significant ner

94 ness (LOC) is a common presenting symptom of subarachnoid hemorrhage (SAH) that is presumed to result

95 Subarachnoid hemorrhage (SAH) usually results from ruptu

96 stoperative ICU management of patients after subarachnoid hemorrhage (SAH), especially with regards t

97 Significance statement: Aneurysmal subarachnoid hemorrhage (SAH)--strokes involving cerebra

98 ere and pervasive consequences of aneurysmal subarachnoid hemorrhage (SAH).

99 re accounts for the majority of nontraumatic subarachnoid hemorrhage (SAH).

100 us, especially in the early period following subarachnoid hemorrhage (SAH).

101 More than 30% of patients with RCVS develop subarachnoid hemorrhage (SAH).

102 critically contribute to the pathogenesis of subarachnoid hemorrhage (SAH).

103 t and unfavorable prognosis in patients with subarachnoid hemorrhage (SAH).

104 ation plays a key role in the progression of subarachnoid hemorrhage (SAH).

105 merous neuropathological processes including subarachnoid hemorrhage (SAH).

106 The aggregate traumatic subarachnoid hemorrhage (tSAH) component of the Stockhol

107 patients: adjusted odds ratios (95% CI) for subarachnoid hemorrhage 0.17 (0.06-0.45) and intracerebr

108 % vs. 32%), and more intracranial pathology (subarachnoid hemorrhage 62% vs. 44%; intraparenchymal le

109 Retrospective analysis of all subarachnoid hemorrhage admissions.

110 ology of types of stroke, such as aneurysmal subarachnoid hemorrhage and cerebral vein thrombosis, th

111 gh intracranial pressure peaked 3 days after subarachnoid hemorrhage and declined after day 7.

112 protective against early brain injury after subarachnoid hemorrhage and determined whether this effe

113 seizure like activity found to have diffuse subarachnoid hemorrhage and extensive dural venous sinus

114 Conclusion In patients with PM nonaneurysmal subarachnoid hemorrhage and initial DSA negative for ane

115 Hemorrhagic stroke (HS), ie, subarachnoid hemorrhage and intracerebral hemorrhage, is

116 O administered for 8h improved recovery from subarachnoid hemorrhage and reduced the inflammatory res

117 ocity were improved between acute aneurysmal subarachnoid hemorrhage and stable state (p </= .005); c

118 lactate and glucose levels after aneurysmal subarachnoid hemorrhage are associated with delayed cere

119 chemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage as defined by validated diagnosi

120 2000 to 2013, 252 consecutive patients with subarachnoid hemorrhage at computed tomography (CT) and

121 All patients with a diagnosis of subarachnoid hemorrhage between 2009 and 2014.

122 redict 60-day case fatality after aneurysmal subarachnoid hemorrhage developed from the International

123 rted on a case of a 16-year-old patient with subarachnoid hemorrhage diagnosed due to a ruptured cere

124 dministration of sodium nitrite after severe subarachnoid hemorrhage differentially influences quanti

125 ees of freedom = 1; p < 0.001), higher daily Subarachnoid hemorrhage Early Brain Edema Score (adjuste

126 logical scores (modified Fisher Scale (mFS), Subarachnoid Hemorrhage Early Brain Edema Score) (P < 0.

127 four percent of participants with aneurysmal subarachnoid hemorrhage experienced augmented renal clea

128 nterventions for intracerebral hemorrhage or subarachnoid hemorrhage generally hinge on whether they

129 Patients with aneurysmal subarachnoid hemorrhage had a higher mean measured creat

130 nt ameliorating early brain injury following subarachnoid hemorrhage has been nonexistent.

131 common complication in the first week after subarachnoid hemorrhage in severe cases admitted to ICU.

132 One hour after subarachnoid hemorrhage induction via endovascular perfo

133 Astaxanthin mitigates subarachnoid hemorrhage injury primarily by increasing s

134 imal timing of tracheostomy in patients with subarachnoid hemorrhage is controversially debated.

135 Thus, subarachnoid hemorrhage may constitute an important exce

136 Argon application after experimental subarachnoid hemorrhage met the primary endpoint of redu

137 ssociated with inferior outcomes, to compare subarachnoid hemorrhage mortality with other neurologica

138 tion with isoflurane in patients with severe subarachnoid hemorrhage not having intracranial hyperten

139 Aneurysmal subarachnoid hemorrhage often leads to death and poor cl

140 ubstantial group of patients with aneurysmal subarachnoid hemorrhage or intracerebral hemorrhage expe

141 als were euthanized 6, 24, or 72 hours after subarachnoid hemorrhage or sham surgery.

142 Subarachnoid hemorrhage patients admitted to ICU in Aust

143 Pregnant subarachnoid hemorrhage patients also had a higher likel

144 Fifty aneurysmal subarachnoid hemorrhage patients and 30 intracerebral he

145 ly and particularly to vulnerable regions in subarachnoid hemorrhage patients at risk for delayed cer

146 omparison with other neurological diagnoses, subarachnoid hemorrhage patients had significantly great

147 udy was to describe in-hospital mortality in subarachnoid hemorrhage patients requiring ICU admission

148 lity physiological recordings in 48 comatose subarachnoid hemorrhage patients to better characterize

149 A total of 11,327 subarachnoid hemorrhage patients were identified in the

150 Pregnant versus nonpregnant subarachnoid hemorrhage patients were less impaired at a

151 Nevertheless, subarachnoid hemorrhage patients who are at risk for vas

152 rial in a retrospective unselected cohort of subarachnoid hemorrhage patients.

153 complications and poor functional outcome in subarachnoid hemorrhage patients.

154 ence of acute kidney injury in patients with subarachnoid hemorrhage patients.

155 time points: on admission (acute aneurysmal subarachnoid hemorrhage phase) and at least 21 days late

156 determinant of outcome with intracranial or subarachnoid hemorrhage predicting a extremely high mort

157 ation rates for intracerebral hemorrhage and subarachnoid hemorrhage remained stable, with the except

158 e polycystic kidney disease, presenting with subarachnoid hemorrhage secondary to a ruptured intracra

159 ons between serum magnesium and radiographic subarachnoid hemorrhage severity.

160 ment behavioral assessments of patients with subarachnoid hemorrhage shortly after the injury.

161 Critically ill patients with subarachnoid hemorrhage show a strong association betwee

162 ncreased due to sympathetic activation after subarachnoid hemorrhage similar to critically ill patien

163 diagnoses, and to explore the variability in subarachnoid hemorrhage standardized mortality ratios.

164 nd at least 21 days later (stable aneurysmal subarachnoid hemorrhage state).

165 Consecutive patients with aneurysmal subarachnoid hemorrhage treated with clipping or coiling

166 At baseline, the severity of aneurysmal subarachnoid hemorrhage was assessed clinically (Hunt an

167 CT evidence of subarachnoid hemorrhage was associated with a multivaria

168 ng manual PVI (1%), an SCL with asymptomatic subarachnoid hemorrhage was detected; the bleeding compl

169 Subarachnoid hemorrhage was induced in mice by endovascu

170 In 18 patients (30%), subarachnoid hemorrhage was present.

171 spital between 2006 and 2011 with poor-grade subarachnoid hemorrhage were prospectively entered into

172 omatose patients with high-grade spontaneous subarachnoid hemorrhage who underwent continuous surface

173 r delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage with hemoglobin 7-13 g/dL.

174 al aneurysm (CA) rupture is a major cause of subarachnoid hemorrhage with high morbidity and mortalit

175 m in depth] subarachnoid hemorrhage; 2, thin subarachnoid hemorrhage with intraventricular hemorrhage

176 [>= 1 mm] subarachnoid hemorrhage; 4, thick subarachnoid hemorrhage with intraventricular hemorrhage

177 ctive properties of argon after experimental subarachnoid hemorrhage with mortality as the primary en

178 isher scale) and dichotomized (thick vs thin subarachnoid hemorrhage) univariate and adjusted logisti

179 tients (25 traumatic brain injured and seven subarachnoid hemorrhage) were included.

180 es/L after excluding patients diagnosed with subarachnoid hemorrhage).

181 SH score (Functional Recovery Expected after Subarachnoid Hemorrhage).

182 erated, subarachnoid hemorrhage-vehicle, and subarachnoid hemorrhage+2% isoflurane.

183 with traumatic brain injury, 10% to 14% with subarachnoid hemorrhage, 1% to 21% with intracerebral he

184 ing and 2) an open-field test 24 hours after subarachnoid hemorrhage, 3) protein analysis of hippocam

185 Rupture of an intracranial aneurysm leads to subarachnoid hemorrhage, a severe type of stroke.

186 ange of disorders including ischemic stroke, subarachnoid hemorrhage, and brain trauma, and suggest a

187 ies in patients with traumatic brain injury, subarachnoid hemorrhage, and intracranial hemorrhage hav

188 ute ischemic stroke, traumatic brain injury, subarachnoid hemorrhage, and postcardiac arrest anoxic e

189 f cerebral ischemia, traumatic brain injury, subarachnoid hemorrhage, and spinal cord injury.

190 idase outside the subventricular zone (SVZ), subarachnoid hemorrhage, and ventriculomegaly.

191 For patients with subarachnoid hemorrhage, autoregulation reactivity index

192 For patients with subarachnoid hemorrhage, autoregulation reactivity index

193 (brain infarction, intracerebral hemorrhage, subarachnoid hemorrhage, coronary heart disease and deat

194 Subarachnoid hemorrhage, defined as (1) subarachnoid blo

195 In stroke, traumatic brain injury or subarachnoid hemorrhage, endothelin-1 (ET-1) is induced

196 luding migraine, ischemic stroke, aneurysmal subarachnoid hemorrhage, intracerebral hematoma, and tra

197 Patients were included when subarachnoid hemorrhage, intracranial hemorrhage, ischem

198 hereas gabapentin/pregabalin were favored in subarachnoid hemorrhage, intracranial hemorrhage, spine,

199 ular outcomes, including ischemic stroke and subarachnoid hemorrhage, leading to long-term physical a

200 tal cardiac arrest, 86 were included (mainly subarachnoid hemorrhage, n = 73).

201 orrhage severity in patients with aneurysmal subarachnoid hemorrhage, potentially through a hemostati

202 ated with poor outcome, but after aneurysmal subarachnoid hemorrhage, this has not been investigated.

203 Urgent surgery patients and patients with a subarachnoid hemorrhage, trauma, acute renal failure, or

204 ointensive care," "neurological," "stroke," "subarachnoid hemorrhage," "intracerebral hemorrhage," or

205 als were randomly assigned to sham-operated, subarachnoid hemorrhage-vehicle, and subarachnoid hemorr

206 from patients with traumatic brain injury or subarachnoid hemorrhage.

207 the patient died after an acute large-volume subarachnoid hemorrhage.

208 ts with perimesencephalic (PM) nonaneurysmal subarachnoid hemorrhage.

209 he argon group was discovered 24 hours after subarachnoid hemorrhage.

210 assessment of consciousness in patients with subarachnoid hemorrhage.

211 ncluding stroke, traumatic brain injury, and subarachnoid hemorrhage.

212 beneficial effect of argon application after subarachnoid hemorrhage.

213 The primary objective was mortality after subarachnoid hemorrhage.

214 rmed of 83 consecutively treated adults with subarachnoid hemorrhage.

215 ool for risk stratification after aneurysmal subarachnoid hemorrhage.

216 ot in control patients with intracerebral or subarachnoid hemorrhage.

217 Federation of Neurosurgical Societies, 3-5) subarachnoid hemorrhage.

218 ical-device associated hemolysis, or after a subarachnoid hemorrhage.

219 an, and ischemic lesion within 72 hours from subarachnoid hemorrhage.

220 safe procedure for patients with poor-grade subarachnoid hemorrhage.

221 eadache requiring investigations to rule out subarachnoid hemorrhage.

222 27.5% (95% CI, 25.6%-29.5%) specificity for subarachnoid hemorrhage.

223 d with LRDA were intracranial hemorrhage and subarachnoid hemorrhage.

224 f the 2131 enrolled patients, 132 (6.2%) had subarachnoid hemorrhage.

225 AH Rule was highly sensitive for identifying subarachnoid hemorrhage.

226 n the CA group, 1 patient died at 1 month of subarachnoid hemorrhage.

227 s occur during the early phase of aneurysmal subarachnoid hemorrhage.

228 efficacy of RIPC in protecting brain against subarachnoid hemorrhage.

229 d brain edema at 24 hrs but not 72 hrs after subarachnoid hemorrhage.

230 prevent cerebral vasospasm after aneurysmal subarachnoid hemorrhage.

231 nt of hemorrhage in patients with aneurysmal subarachnoid hemorrhage.

232 patients with acute brain injury, including subarachnoid hemorrhage.

233 tal detection of UIA and no prior history of subarachnoid hemorrhage.

234 lmark of delayed cerebral ischemia following subarachnoid hemorrhage.

235 raphic hemorrhage; 1, thin [< 1 mm in depth] subarachnoid hemorrhage; 2, thin subarachnoid hemorrhage

236 raventricular hemorrhage; 3, thick [>= 1 mm] subarachnoid hemorrhage; 4, thick subarachnoid hemorrhag

237 ial bleeding, specifically intracerebral and subarachnoid hemorrhages.

238 % vs 28.2%, p<0.001), with larger amounts of subarachnoid (Hijdra Sum Score 17 vs 14, p<0.001) and in

239 Subarachnoid infusion of 1-2 ml of fresh blood at 200 mi

240 annotations of the five hemorrhage subtypes (subarachnoid, intraventricular, subdural, epidural, and

241 Treatment of subarachnoid neurocysticercosis (NCC) is complicated, an

242 The clinical sensitivity in detecting active subarachnoid or ventricular disease in symptomatic patie

243 fluid (CSF) samples taken from patients with subarachnoid or ventricular disease using quantitative p

244 TNFSF12 also increased the risk of subarachnoid (OR=1.53; 95% CI, 1.31-1.78; P=3.32x10(-8))

245 Patients with intracerebral, subarachnoid, or subdural hemorrhages who had at least 1

246 l hemorrhage not extending to cortex/insula, subarachnoid, or subdural spaces.

247 d increased cerebrospinal fluid (CSF) in the subarachnoid space (i.e., extra-axial CSF) from 6 to 24

248 llowing spinal delivery into the lumbosacral subarachnoid space (intrathecal; i.t.).

249 erebral ventricles and circulates within the subarachnoid space (SAS) of the brain and spinal cord, w

250 nsular cistern width - 0.020-0.074; index of subarachnoid space - 0.017-0.081.

251 mphatic vessels absorb CSF from the adjacent subarachnoid space and brain interstitial fluid (ISF) vi

252 o iron-positive haemosiderin deposits in the subarachnoid space and superficial cortical layers, indi

253 The subarachnoid space around the optic nerve was identified

254 (CRV), peripapillary choroid and sclera, and subarachnoid space around the optic nerve, were investig

255 omeningeal coverings of blood vessels in the subarachnoid space as potential access points allowing s

256 The mean (SD) size of the subarachnoid space before and 1 hour after IV fluid bolu

257 aphy evaluation to determine the size of the subarachnoid space before and after IV fluids.

258 e small, dense fat droplets scattered in the subarachnoid space corresponding to a dermoid cyst ruptu

259 l processes that affect ventricular outflow, subarachnoid space function, or cerebral venous complian

260 Free hemoglobin (Hb) within the subarachnoid space has been implicated in the pathogenes

261 therapeutic transgene, IL-10, to the spinal subarachnoid space have yielded promising results in ani

262 lves and capillaries located adjacent to the subarachnoid space in mice.

263 s included the difference in the size of the subarachnoid space in millimeters squared before and 1 h

264 Instead, viral spread into the subarachnoid space in rCDV(SH)-infected animals was trig

265 rospinal fluid (CSF) is transported from the subarachnoid space into brain parenchyma to exchange wit

266 brain was attenuated and transport from the subarachnoid space into dcLNs was abrogated.

267 in confined tissue compartments such as the subarachnoid space is an important driver of disease.

268 aSAH), extracellular haemoglobin (Hb) in the subarachnoid space is bound by haptoglobin, neutralising

269 ues allow us to determine if the size of the subarachnoid space is within the normal range for a give

270 ngeal cells ensheathing blood vessels in the subarachnoid space may provide unique entry sites into t

271 Interobserver consistency for the subarachnoid space measurement between attending radiolo

272 ned-rank test was used to examine changes in subarachnoid space measurements (millimeters squared).

273 Outflow of CSF tracers from the spinal subarachnoid space occurred predominantly from intravert

274 ne (90-100 mug/kg) was administered into the subarachnoid space of cats 30 h prior to EA or sham-oper

275 ecrosis factor and interferon gamma into the subarachnoid space of female Dark Agouti rats pre-immuni

276 e hypothesized that IV fluids would increase subarachnoid space size.

277 inal fluid (CSF) barriers to spread into the subarachnoid space to induce dramatic viral meningoencep

278 within both the central canal and the spinal subarachnoid space toward the caudal end of the spine.

279 CSF column extending extracranially from the subarachnoid space with or without brain/ meningeal hern

280 n lead to locally increased pressures in the subarachnoid space within the orbit, which impinges on t

281 rast distribution in the perivascular space, subarachnoid space, and space surrounding large veins dr

282 racerebral tissue (scalp, skull, dura mater, subarachnoid space, etc.) and the bottom layer (layer 2)

283 ized by excessive cerebrospinal fluid in the subarachnoid space, particularly over the frontal lobes.

284 how abnormalities in CSF dynamics within the subarachnoid space, which are pronounced even further if

285 nographic measure of the neonatal and infant subarachnoid space.

286 fluid connecting lateral ventricle with the subarachnoid space.

287 ial bones and dura, and those located in the subarachnoid space.

288 ix molecules, laminin and fibronectin in the subarachnoid space.

289 periaqueductal gray (PAG) or into the spinal subarachnoid space.

290 ocytes from meningeal blood vessels into the subarachnoid space.

291 pial arteries and cerebrospinal fluid in the subarachnoid space.

292 of large B cell clusters in the spinal cord subarachnoid space.

293 stration for delivery of nanomedicine to the subarachnoid space.

294 antly circulating through the ventricles and subarachnoid space.

295 s to the diagnosis of changes in size of the subarachnoid space.

296 es (seven of 37; 19%), prominent optic nerve subarachnoid spaces (20 of 36; 56%), and enhancement of

297 reach the outer surface of the brain in the subarachnoid spaces from where it drains into venous blo

298 mal hemorrhage as isolated deep (no insular, subarachnoid, subdural extension) or lobar.

299 ing cortical and subcortical deformation and subarachnoid/ventricular expansion to cognitive and moto

300 onset is restricted to IL-1R1(+) subpial and subarachnoid vessels.