ライフサイエンスコーパス: neuritis

1 ast 3 months after onset in studies of optic neuritis).

2 novel strategy in peripheral nervous system neuritis.

3 f 29 eyes (24%) previously affected by optic neuritis.

4 O in eyes previously affected by acute optic neuritis.

5 e optic nerve in isolated experimental optic neuritis.

6 ability in patients with NMO following optic neuritis.

7 yes previously affected by symptomatic optic neuritis.

8 and NAION (P = 0.97), and reduced for optic neuritis.

9 hropoietin might be neuroprotective in optic neuritis.

10 independent of a patient's history of optic neuritis.

11 the preclinical phase, before onset of optic neuritis.

12 nts presenting with a first episode of optic neuritis.

13 ard, in contrast to eyes with NAION or optic neuritis.

14 ntial markers of axonal loss following optic neuritis.

15 ell-tolerizing drugs for patients with optic neuritis.

16 ept trials of acute neuroprotection in optic neuritis.

17 -8.65, n=3154, p<0.0001) in MS without optic neuritis.

18 evoked potential latency) during acute optic neuritis.

19 6-125-induced murine experimental autoimmune neuritis.

20 e can prevent RGC loss in experimental optic neuritis.

21 le sclerosis without a past history of optic neuritis.

22 y for suppressing neurodegeneration in optic neuritis.

23 hese mice develop spontaneous isolated optic neuritis.

24 ive experienced a relapse or developed optic neuritis.

25 e visual cortex following an attack of optic neuritis.

26 relapse of myelitis or development of optic neuritis.

27 duced neurological deficits, including optic neuritis.

28 , and use of corticosteroids for acute optic neuritis.

29 n patients with multiple sclerosis and optic neuritis.

30 e RNFL and macula, respectively, after optic neuritis.

31 rosis who have established weakness or optic neuritis.

32 patients first presents clinically as optic neuritis.

33 re involved in the genesis of isolated optic neuritis.

34 one of these patients later developed optic neuritis.

35 nts with a first bout of demyelinating optic neuritis.

36 ditions such as orbital cellulitis and optic neuritis.

37 al color Doppler signals suggestive of acute neuritis.

38 icularly those with a history of acute optic neuritis.

39 neuroprotective in patient with acute optic neuritis.

40 for patients with previous unilateral optic neuritis.

41 ty can occur even without a history of optic neuritis.

42 uroaxonal loss and myelin repair after optic neuritis.

43 ity-dependent visual outcomes of acute optic neuritis.

44 comes in affected eyes following acute optic neuritis.

45 ents with MS with and without previous optic neuritis.

46 hway, was studied in experimental autoimmune neuritis.

47 syndrome, additional triceps band and ulnar neuritis.

48 es with a history of acute symptomatic optic neuritis (100% of eyes with microcystic changes had expe

49 nonglaucomatous optic atrophy (30%) (5 optic neuritis, 11 anterior visual pathway tumors, 2 papillede

50 One of eight optic neuritis (12%) eyes and 1 of 12 NAION (8%) eyes had posi

51 vely study eyes with papilledema (24), optic neuritis (14), nonarteritic anterior ischemic optic neur

52 n cell layer of eyes affected by acute optic neuritis 3 and 6 months after onset (P < 0.001).

53 pediatric patients with first-episode optic neuritis, 46 had at least 3 months of follow-up and 36 h

54 4.6 months after a clinically isolated optic neuritis (49 females, mean age 33.5 years) and were foll

55 optic neuritis than eyes without prior optic neuritis (50 versus 27%) and was associated with lower v

56 Acute demyelinating optic neuritis, a common feature of multiple sclerosis, can da

57 romyelitis optica without a history of optic neuritis, a disease in which subclinical disease activit

58 erious and unexpected: one patient had optic neuritis after the first bevacizumab infusion, a second

59 Patients with acute optic neuritis aged 18-60 years, presenting within 2 weeks of

60 Among 16 patients with CRMP-5-IgG and optic neuritis (aged 52-74 years; all smokers, 9 women), we do

61 ciation with demyelinating disease and optic neuritis, although evidence for this has relied solely o

62 neuropathy hard to differentiate from optic neuritis and arteritic ischemic optic neuropathy.

63 hospital, patients with first-episode optic neuritis and at least 3 months of follow-up over a 10-ye

64 n 6 months of presenting with isolated optic neuritis and compared the findings with those seen in 50

65 mm differed significantly between the optic neuritis and control groups [+0.059 percentage units/mm

66 icant autoimmune disease manifested by optic neuritis and death.

67 is in the cervical spinal cord; radiculitis; neuritis and demyelination in the spinal roots; and infl

68 -eight consecutive patients with acute optic neuritis and eight healthy controls were assessed visual

69 patients with unilateral or bilateral optic neuritis and in 18 age-matched controls with normal visi

70 l loss in the retina in both recovered optic neuritis and in multiple sclerosis without a past histor

71 stigation in larger clinical trials in optic neuritis and in relapsing multiple sclerosis is warrante

72 t of well recognised syndromes such as optic neuritis and internuclear ophthalmoplegia, respectively.

73 is a sensitive (94%) finding in acute optic neuritis and is absent in unaffected or previously affec

74 mprehensive understanding of pediatric optic neuritis and its management remains elusive.

75 Clinical data (episodes of optic neuritis and longitudinally extensive transverse myeliti

76 1C6 CD8(+) T cells alone can induce optic neuritis and mild EAE with delayed onset; however, 1C6 C

77 to permanent neurologic disability in optic neuritis and MS patients.

78 neurologic disability in patients with optic neuritis and multiple sclerosis (MS).

79 e to the persistence of visual loss in optic neuritis and multiple sclerosis (MS).

80 the retinal nerve fibre layer in both optic neuritis and multiple sclerosis.

81 advances relevant to the management of optic neuritis and multiple sclerosis.

82 ent visual disability in patients with optic neuritis and multiple sclerosis.

83 ration and persistent visual loss from optic neuritis and multiple sclerosis.

84 ssion of costimulatory molecules and induces neuritis and myelin autoreactivity after transplantation

85 presented with simultaneous/sequential optic neuritis and myelitis (44% vs 0%; P = .005).

86 characterized by disabling relapses of optic neuritis and myelitis and the presence of aquaporin 4 an

87 f the CNS, characterized by attacks of optic neuritis and myelitis.

88 to pretangle pathology including dystrophic neuritis and neurofibrillary tangles in Alzheimer's dise

89 yes with optic disc swelling caused by optic neuritis and nonarteritic anterior ischemic optic neurop

90 Corticosteroids can suppress optic neuritis and prevent RGC loss if treatment is initiated

91 ic ophthalmological entity of combined optic neuritis and retinitis with vitreous inflammatory cells.

92 immunomodulation may prevent recurrent optic neuritis and RGC damage.

93 d showed a trend toward suppression of optic neuritis and RGC loss on day 14 that was lost by day 18.

94 in one patient; colitis in two patients, and neuritis and skin ulcer in one patient.

95 sensitivity of this modality in acute optic neuritis and whether the abnormal enhancement correlates

96 bserved for individuals with exclusive optic neuritis and/or spinal cord involvement as first and sec

97 participants during the acute phase of optic neuritis, and again 3 and 6 months later.

98 levels of immunosuppression, may mimic optic neuritis, and are a potentially reversible cause of visi

99 ve axons following the acute insult in optic neuritis, and chronically in primary and secondary progr

100 in 1 eye with papilledema, 1 eye with optic neuritis, and in 13 eyes with NAION.

101 urred in the fields of autoimmunity in optic neuritis, and in imaging the retinal nerve fibre layer i

102 slightly increased for papilledema and optic neuritis, and reduced for NAION (P = 0.02) eyes.

103 glial infiltrates in experimental autoimmune neuritis, and the inflamed pancreas of prediabetic BB ra

104 uronal layer pathology following acute optic neuritis, and to systematically characterize such change

105 ility, presence of previous unilateral optic neuritis, and use of disease-modifying therapies as cova

106 rons, tangle-bearing neurons, and dystrophic neuritis; and interference with GAB2 gene expression inc

107 of therapy for the treatment of acute optic neuritis (AON) and acute demyelination in multiple scler

108 Among patients with an acute optic neuritis (AON) history, AAs had greater loss of HCVA tha

109 r patients with multiple sclerosis and optic neuritis are needed to ensure uniformity among clinical

110 on MRI of the optic nerve affected by optic neuritis are said to correlate with the severity of init

111 ular volume in eyes with no history of optic neuritis as a biomarker of disability worsening in a coh

112 We used optic neuritis as a model of multiple sclerosis relapse to qua

113 Acute demyelinating optic neuritis associated with multiple sclerosis (MS) is the

114 er and may help to distinguish between optic neuritis associated with multiple sclerosis and optic ne

115 with phenytoin in patients with acute optic neuritis at concentrations at which it blocks voltage-ga

116 O, the median time from onset to first optic neuritis attack (54 months) was similar to the median di

117 ith rLETM (range, 2-22), and the first optic neuritis attack for those with rLETM-onset NMO followed

118 loss that was initially thought to be optic neuritis attacks.

119 rosis who had at least one eye without optic neuritis available.

120 Optic neuritis began 9 days after immunization.

121 e (scleritis, conjunctivitis, and peri-optic neuritis), brain (choriomeningoencephalitis), stomach, p

122 ally isolated syndromes (CIS), such as optic neuritis, brainstem or spinal cord syndromes are frequen

123 The beneficial effect is present for optic neuritis, brainstem-cerebellar syndromes, and spinal cor

124 lly definite multiple sclerosis in the optic neuritis, brainstem-cerebellar, and spinal cord syndrome

125 rrhages, iritis, keratic precipitates, optic neuritis, branch retinal artery occlusions, and choriore

126 day 14, mice rapidly developed EAE and optic neuritis by day 18, but RGC loss was still reduced.

127 d potential neuroprotective effects in optic neuritis by SRT647 and SRT501, two structurally and mech

128 and by SLP (14/16 eyes) in contrast to optic neuritis (by OCT, 0/12, P = 0.006; and by SLP, 1/12, P =

129 Atypical forms of optic neuritis can occur, either in association with other inf

130 ome of both optic nerve and brain post-optic neuritis changes.

131 e report that, before manifestation of optic neuritis, characterized by inflammatory infiltration and

132 models for MS and in a phase II acute optic neuritis clinical trial (RENEW).

133 thy ("CAR"-IgG [23kDa, recoverin]) and optic neuritis collapsin response-mediated protein 5 (CRMP-5-I

134 rocystic changes had experienced prior optic neuritis compared with 71% of NMO eyes without microcyst

135 euronal layer thinning following acute optic neuritis, corroborating the hypothesis that axonal injur

136 O), and chronic relapsing inflammatory optic neuritis (CRION).

137 Optic neuritis developed in two thirds of eyes with significan

138 Acute optic neuritis due to an inflammatory demyelinating lesion of

139 g enlargement of nerves in leprosy and acute neuritis due to lepra reactions, guides the duration of

140 nd its animal model, experimental autoimmune neuritis (EAN), are typically acute monophasic diseases

141 6-125-induced murine experimental autoimmune neuritis (EAN).

142 5 years) with a first unilateral acute optic neuritis episode within 28 days from study baseline.

143 cinumab given soon after a first acute optic neuritis episode.

144 s, disease duration, treatments, prior optic neuritis episodes, and quality of life (QOL; based on th

145 retinal problem could be confused with optic neuritis, especially in a patient with a normal appearin

146 neuromyelitis optica and a history of optic neuritis exhibited the greatest reduction in ganglion ce

147 optic neuritis or the value of the non-optic neuritis eye for patients with previous unilateral optic

148 o levels similar to those of untreated optic neuritis eyes.

149 patients were recruited who had acute optic neuritis for a median of 13 days (range 7-24 days) since

150 as the mean value of both eyes without optic neuritis for patients without a history of optic neuriti

151 their first attack of acute unilateral optic neuritis for up to 18 months.

152 anese cohort, commonly presenting with optic neuritis, had a high risk of visual disability while old

153 The treatment of optic neuritis has been investigated in several trials, the re

154 The current approach to patients with optic neuritis has been modified by the results of the Control

155 that most patients with demyelinating optic neuritis have an excellent prognosis for recovery of cen

156 Particularly myelitis and bilateral optic neuritis have poor remission rates.

157 th multiple sclerosis without previous optic neuritis have thinner retinal layers than healthy contro

158 the more pronounced thinning caused by optic neuritis if present.

159 NMOSD in 10 patients (40%) preceded by optic neuritis in 13 patients (52%) and preceded by a nausea a

160 protect retinal ganglion cells during optic neuritis in a mouse model of multiple sclerosis.

161 ollowed serial changes in MTR in acute optic neuritis in combination with clinical and electrophysiol

162 BRI3 colocalizes with APP along neuritis in differentiated N2a cells; endogenous BRI3-AP

163 ted disparate outcomes following acute optic neuritis in individuals of African descent compared with

164 I 17.91-22.86, n=2063, p<0.0001) after optic neuritis in MS, and of 7.08 microm (5.52-8.65, n=3154, p

165 evelopment of neurodegeneration during optic neuritis in myelin-specific T cell receptor transgenic m

166 associated with multiple sclerosis and optic neuritis in neuromyelitis optica.

167 aphy study in patients presenting with optic neuritis in order to define the temporal evolution of re

168 ith multiple sclerosis with or without optic neuritis in PubMed, Web of Science, and Google Scholar b

169 emographic and presenting features for optic neuritis in the pediatric population.

170 he ganglion cell layer following acute optic neuritis, in the absence of evidence of baseline swellin

171 (days 0-14) suppressed EAE and reduced optic neuritis incidence through day 14.

172 ial clinical episode of demyelination (optic neuritis, incomplete transverse myelitis, or brain-stem/

173 on with this recombinant virus induces optic neuritis independent of virus dose, major histocompatibi

174 pheral nerve myelin (experimental autoimmune neuritis), indicating they function by bystander suppres

175 in the setting of neuritis, likely relieving neuritis-induced pain by this mechanism.

176 ating optic nerve inflammation, termed optic neuritis, induces permanent visual dysfunction due to re

177 In the few eyes that developed optic neuritis, inflammation was mild, and RGC loss was attenu

178 usly develop a chronic autoimmune peripheral neuritis instead of diabetes.

179 multifocal or isolated spinal cord or optic neuritis involvement at onset in comparison to those wit

180 Acute optic neuritis is a cardinal manifestation of neuromyelitis op

181 Optic neuritis is a common condition that causes reversible lo

182 Acute optic neuritis is a common, often presenting manifestation, bu

183 Pediatric optic neuritis is an uncommon disorder with significant distin

184 predilection of these mice to develop optic neuritis is associated with higher expression of MOG in

185 Optic neuritis is frequently associated with MS and often prec

186 Optic neuritis is rare among those who initiate anti-TNF thera

187 Acute optic neuritis is the most common optic neuropathy affecting y

188 Optic neuritis is the most widely studied visual disturbance i

189 thy in diabetes (also referred to as insulin neuritis) is considered a rare iatrogenic small fibre ne

190 e we review the diagnostic features of optic neuritis, its differential diagnosis, and give practical

191 anti-inflammatory profile in the setting of neuritis, likely relieving neuritis-induced pain by this

192 males, lower incidence of simultaneous optic neuritis, lower frequency of conus involvement, and high

193 rneal microdeposits (>90%), optic neuropathy/neuritis (< or =1%-2%), blue-gray skin discoloration (4%

194 do not develop multiple sclerosis; the optic neuritis may be monophasic illness or recurrent.

195 isual pathways in patients with MS and optic neuritis may be used as a model.

196 al swelling during the acute stages of optic neuritis may confound baseline measurements.

197 s that early steroid treatment in vestibular neuritis may improve long term outcome.

198 ing that retrograde degeneration after optic neuritis may not extend into the deeper retinal layers.

199 ultiple sclerosis without a history of optic neuritis (MS non-ON).

200 , multiple sclerosis with a history of optic neuritis (MS-ON), and multiple sclerosis without a histo

201 (MSON), and multiple sclerosis without optic neuritis (MSNON).

202 ontrols, multiple-sclerosis-associated optic neuritis (MSON), and multiple sclerosis without optic ne

203 one episode of transverse myelitis or optic neuritis, multiple sclerosis (MS), anti-aquaporin-4 (AQP

204 yer has been detected in patients with optic neuritis, multiple sclerosis, neuromyelitis optica, Alzh

205 ng anterior ischemic optic neuropathy, optic neuritis/multiple sclerosis, neuromyelitis optica, pseud

206 n response-mediator protein-5-IgG with optic neuritis (n = 3).

207 is (n=4), idiopathic AQP4-IgG-negative optic neuritis (n=4), other demyelinating syndromes (n=3) and

208 area of the affected optic nerve after optic neuritis nor the damage in optic radiations was associat

209 decreased with distance from them; in optic neuritis, normal-appearing white matter magnetization tr

210 A proportion of cases of optic neuritis occur in patients who do not develop multiple s

211 produced, as anticipated, long and extensive neuritis on nerve growth factor induction.

212 ients with MS in 28 eyes with the last optic neuritis (ON) >or=6 months prior (ON group) and 33 eyes

213 We evaluated the risk of optic neuritis (ON) after vaccines, using a case-centered anal

214 To determine the relationship between optic neuritis (ON) and EAE, we examined the incidence of ON i

215 7%) and Spectralis (61.7%) in both the optic neuritis (ON) and non-ON group and by Stratus (58.8%) in

216 dynamics of retinal injury after acute optic neuritis (ON) and their association with clinical visual

217 positive for AQP4-Abs and present with optic neuritis (ON) and transverse myelitis (TM) are diagnosed

218 ase clinically characterised by severe optic neuritis (ON) and transverse myelitis (TM).

219 sis (MS) in 357 children with isolated optic neuritis (ON) as a first demyelinating event who had a m

220 ple sclerosis (MS), demyelination, and optic neuritis (ON) associated with anti-tumor necrosis factor

221 ng for age, sex, disease duration, and optic neuritis (ON) history.

222 ressive MS, 14 had clinical history of optic neuritis (ON) in a single eye; the remaining patients ha

223 Optic neuritis (ON) is a condition involving primary inflammat

224 ual Evoked Potentials (VEPs) following optic neuritis (ON) remain chronically prolonged, although sta

225 rom four patients with monosymptomatic optic neuritis (ON) were analyzed by single-cell reverse trans

226 Optic neuritis (ON), an inflammatory demyelinating optic nerve

227 Optic neuritis (ON), inflammation of the optic nerve, is stron

228 cell loss relates to history of acute optic neuritis (ON), retinal nerve fiber layer (RNFL) thinning

229 In patients with isolated optic neuritis (ON), the presence of antibodies to aquaporin 4

230 h and without a prior history of acute optic neuritis (ON).

231 ently of other confounders, especially optic neuritis (ON).

232 tis optica (NMO) and one with isolated optic neuritis (ON).

233 que after long-term latency changes in optic neuritis (ON)/multiple sclerosis (MS), mfVEPs were recor

234 entation, 40% NMO cases had unilateral optic neuritis (ON); 20% bilateral ON; 15% transverse myelitis

235 Ab-mediated ICAM-1 blockade triggers neuritis only in young NOD mice.

236 ticosteroid treatment initiated before optic neuritis onset (days 0-14) suppressed EAE and reduced op

237 Corticosteroid treatment after optic neuritis onset (days 10-14) slowed EAE progression and s

238 ommonly women, had concurrent or prior optic neuritis or intractable vomiting episodes more frequentl

239 less likely in patients with a CIS of optic neuritis or sensory symptoms only, few or no MRI lesions

240 itis for patients without a history of optic neuritis or the value of the non-optic neuritis eye for

241 Optic neuritis or transverse myelitis developed after vomiting

242 imic peripheral disorders such as vestibular neuritis, or when there is hearing involvement may be mi

243 nuclear layers) of eyes with previous optic neuritis (P < 0.05).

244 se myelitis and 1 of 9 (11%) developed optic neuritis (p = 0.004).

245 ), and for unilateral versus bilateral optic neuritis (p = 0.020).

246 er the past decade in understanding of optic neuritis pathophysiology, and these developments have be

247 and whole brain analysis comparing all optic neuritis patients and controls revealed a selective decr

248 le vaccinees in the USA, 86.3 cases of optic neuritis per 10 million population would be expected wit

249 affected optic nerves at 3 months post-optic neuritis predicted lower fractional anisotropy and highe

250 In its typical form, optic neuritis presents as an inflammatory demyelinating disor

251 Optic neuritis produced large sensitivity losses mediated by t

252 etinal neuronal layers following acute optic neuritis remains largely unexplored.

253 axoplasmic transport proximal to a localized neuritis significantly reduced inflammation-induced AMS

254 in patients assigned ozanimod 0.5 mg: optic neuritis, somatoform autonomic dysfunction, and cervical

255 n properties of optic radiations after optic neuritis suggesting trans-synaptic degeneration; (ii) th

256 r or outer nuclear layers of eyes with optic neuritis, suggesting that retrograde degeneration after

257 urred more commonly in eyes with prior optic neuritis than eyes without prior optic neuritis (50 vers

258 this cohort of pediatric patients with optic neuritis, the majority of patients regained normal visua

259 Optic neuritis, the most common ocular manifestation of multip

260 For 31 patients with ulnar neuritis, the sensitivity, specificity, and accuracy inc

261 eficient mice induced colitis and peripheral neuritis, the severity of which was aggravated if the IL

262 r longitudinal study shows that, after optic neuritis, there is progressive damage to the optic radia

263 Following an episode of optic neuritis, thinning of the retinal nerve fibre layer, whi

264 y with visual outcomes following acute optic neuritis through application of longitudinal data analys

265 th a first episode of acute unilateral optic neuritis to assess the effects of a single acute inflamm

266 ort of black race/ethnicity with acute optic neuritis to be studied and represents the first evidence

267 The relationship of optic neuritis to MS is not well understood.

268 factors for progression from isolated optic neuritis to systemic demyelinating processes, such as mu

269 ent study used a model of acute inflammatory neuritis to test the efficacy and mechanisms of action o

270 a 51-year-old woman who had relapsing optic neuritis, transverse myelitis, AQP4-IgG seropositivity,

271 ients with monofocal syndromes such as optic neuritis, transverse myelitis, or isolated brainstem syn

272 nalyses of the prospectively collected Optic Neuritis Treatment Trial (ONTT) data identified no assoc

273 The Optic Neuritis Treatment Trial (ONTT) has provided important c

274 Acute vision loss from optic neuritis typically resolves; however, recovery is often

275 transgenic mice that develop isolated optic neuritis usually without any other characteristic lesion

276 mission rates were higher for isolated optic neuritis versus isolated myelitis (p < 0.001), and for u

277 d VP function in 25 patients with vestibular neuritis (VN) acutely (2 days after onset) and after com

278 Optic neuritis was detected by inflammatory cell infiltration

279 Perineural involvement without frank neuritis was present in advanced rejection.

280 Perineural involvement without frank neuritis was present in advanced rejection.

281 ess, also in eyes without a history of optic neuritis, was associated with fluid-attenuated inversion

282 t model of MS that frequently leads to optic neuritis, we have investigated the interconnection betwe

283 patients with MS without a history of optic neuritis were associated with cortical gray matter (P=.0

284 ed parameters from the eye affected by optic neuritis were compared with those from the normal eye us

285 h acute clinically isolated unilateral optic neuritis were recruited to undergo optical coherence tom

286 optica, with and without a history of optic neuritis, when compared with healthy controls (P < 0.001

287 ased (P = 0.002) over 1 year following optic neuritis, whereas optic radiation measures were unchange

288 P) subtype resembles experimental autoimmune neuritis, which is predominantly caused by T cells direc

289 te (n = 388) race/ethnicity with acute optic neuritis who enrolled in the ONTT within 8 days of sympt

290 f this axonal protein in patients with optic neuritis who had a poor visual outcome are likely also d

291 s who had a previous single episode of optic neuritis with a recruitment bias to those with incomplet

292 elbow results in a tractional and frictional neuritis with classical symptoms of peripheral neuralgia

293 of optic neuropathy were studied: (1) optic neuritis with multiple sclerosis (MS), (2) idiopathic in

294 Treatment of experimental autoimmune neuritis with rIL-5 markedly reduced clinical paralysis,

295 lar volume at baseline in eyes without optic neuritis with the risk of subsequent disability worsenin

296 uring a 15-year period following acute optic neuritis, with black race/ethnicity being associated wit

297 nal ganglion cell loss in experimental optic neuritis, with reduced inflammation and demyelination.

298 ic mice spontaneously develop isolated optic neuritis without any clinical nor histological evidence

299 Optic neuritis without EAE could also be induced in these mice

300 es of recurrent non-multiple sclerosis optic neuritis without myelitis will be shown to be associated