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 neuroprotective in patient with acute optic neuritis.

3 for patients with previous unilateral optic neuritis.

4 a better visual outcome than AQP4-IgG optic neuritis.

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

6 uroaxonal loss and myelin repair after optic neuritis.

7 ity-dependent visual outcomes of acute optic neuritis.

8 comes in affected eyes following acute optic neuritis.

9 ements were the incidence and cause of optic neuritis.

10 ents with MS with and without previous optic neuritis.

11 syndrome, additional triceps band and ulnar neuritis.

12 novel strategy in peripheral nervous system neuritis.

13 normal visual acuity and no history of optic neuritis.

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

15 O in eyes previously affected by acute optic neuritis.

16 e optic nerve in isolated experimental optic neuritis.

17 ability in patients with NMO following optic neuritis.

18 yes previously affected by symptomatic optic neuritis.

19 ying therapies and steroids, and prior optic neuritis.

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

21 hropoietin might be neuroprotective in optic neuritis.

22 n-reactive B lymphocyte-dependent autoimmune neuritis.

23 the preclinical phase, before onset of optic neuritis.

24 nts presenting with a first episode of optic neuritis.

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

26 ntial markers of axonal loss following optic neuritis.

27 ell-tolerizing drugs for patients with optic neuritis.

28 ept trials of acute neuroprotection in optic neuritis.

29 -8.65, n=3154, p<0.0001) in MS without optic neuritis.

30 evoked potential latency) during acute optic neuritis.

31 e can prevent RGC loss in experimental optic neuritis.

32 le sclerosis without a past history of optic neuritis.

33 y for suppressing neurodegeneration in optic neuritis.

34 hese mice develop spontaneous isolated optic neuritis.

35 ive experienced a relapse or developed optic neuritis.

36 e visual cortex following an attack of optic neuritis.

37 relapse of myelitis or development of optic neuritis.

38 duced neurological deficits, including optic neuritis.

39 greater than 20/25, and no history of optic neuritis.

40 defined as history of acute unilateral optic neuritis.

41 nism of neuronal death in experimental optic neuritis.

42 ated with the primary damage caused by optic neuritis.

43 cell (RGC) and axonal loss during EAE optic neuritis.

44 6-125-induced murine experimental autoimmune neuritis.

45 icularly those with a history of acute optic neuritis.

46 hway, was studied in experimental autoimmune neuritis.

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

48 , and use of corticosteroids for acute optic neuritis.

49 al color Doppler signals suggestive of acute neuritis.

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

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

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

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

54 ns included macular degeneration (35), optic neuritis (18), retinitis pigmentosa (17), and diabetic r

55 anomalous optic discs (44%), isolated optic neuritis (19%), and optic atrophy (12%).

56 cephalitis other than ADEM (22 [19%]), optic neuritis (20 [17%]), myelitis (13 [11%]), neuromyelitis

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

58 In experimental optic neuritis, 4-AP potentiated the effects of immunomodulato

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

60 4.6 months after a clinically isolated optic neuritis (49 females, mean age 33.5 years) and were foll

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

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

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

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

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

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

67 uced neurodegeneration in experimental optic neuritis, an inflammatory demyelinating optic nerve cond

68 AQP4-IgG and MOG-IgG account for 9% of optic neuritis and are associated with recurrent attacks, but

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

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

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

72 icant autoimmune disease manifested by optic neuritis and death.

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

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

75 usting for age, sex, disease duration, optic neuritis and genetic ancestry and using a combination of

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

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

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

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

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

81 1C6 CD8(+) T cells alone can induce optic neuritis and mild EAE with delayed onset; however, 1C6 C

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

83 tential novel treatment strategies for optic neuritis and MS, and possibly other optic neuropathies a

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

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

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

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

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

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

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

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

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

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

94 ss of vision with signs of retrobulbar optic neuritis and no other neurological signs.

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

96 on with 4-AP in models of experimental optic neuritis and optic nerve crush.

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

98 immunomodulation may prevent recurrent optic neuritis and RGC damage.

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

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

101 rome characterized by attacks of acute optic neuritis and transverse myelitis.

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

103 atients, 4 of 6 patients had recurrent optic neuritis, and all 6 had a final visual acuity of 20/30 o

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

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

106 ng ischemic optic neuropathy, previous optic neuritis, and compressive and inherited optic neuropathi

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

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

109 ons of neuroborreliosis (meningitis, cranial neuritis, and radiculoneuritis), as these have withstood

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

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

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

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

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

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

116 racterization of the cause of atypical optic neuritis: AQP4-IgG and MOG-IgG.

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

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

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

120 Patients with optic neuritis at onset were more likely to develop blindness

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

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

123 positive for AQP4-IgG had more than 1 optic neuritis attack, 2 with residual no light perception vis

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

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

126 Optic neuritis began 9 days after immunization.

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

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

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

130 al injection of this strain can induce optic neuritis by retrograde axonal transport from the brain t

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

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

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

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

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

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

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

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

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

140 Optic neuritis developed in two thirds of eyes with significan

141 Acute optic neuritis due to an inflammatory demyelinating lesion of

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

143 6-125-induced murine experimental autoimmune neuritis (EAN).

144 5 years) with a first unilateral acute optic neuritis episode within 28 days from study baseline.

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

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

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

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

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

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

151 ses meningoencephalitis, myelitis, and optic neuritis followed by axonal loss and demyelination.

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

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

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

155 ed with recurrent attacks, but MOG-IgG optic neuritis has a better visual outcome than AQP4-IgG optic

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 In a model of chronic autoimmune neuritis, homeostatic myeloid cells were outnumbered by

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

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

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

162 e case of CAR with chorioretinitis and optic neuritis in a patient with occult SCLC.

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

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

165 al evoked potential (VEP) latencies in optic neuritis in MS may identify demyelination and remyelinat

166 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

167 of therapeutic strategies tailored for optic neuritis in MS.

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

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

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

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

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

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

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

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

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

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

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

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

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

181 Acute optic neuritis is a cardinal manifestation of neuromyelitis op

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

183 Pediatric optic neuritis is an uncommon disorder with significant distin

184 Optic neuritis is common in MS and leads to visual disability.

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 characterized by recurrent episodes of optic neuritis, longitudinally extensive transverse myelitis,

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

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

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

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

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

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

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

198 an be followed by symptoms such as carditis, neuritis, meningitis, or arthritis if not treated.

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 isorder (NMOSD) and related syndromes (optic neuritis, myelitis and brainstem encephalitis), but rare

207 old of 4mum for identifying unilateral optic neuritis (n = 477).

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

209 atus), multiple sclerosis (MS) (n=69), optic neuritis (n=5) and non-neurological controls (n=37).

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

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

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

213 sex were similar between cohorts, with optic neuritis occurring most frequently at onset (Japanese: 6

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

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

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

217 7%) and Spectralis (61.7%) in both the optic neuritis (ON) and non-ON group and by Stratus (58.8%) in

218 teral geniculate nucleus (LGN), due to optic neuritis (ON) and the ventral posterior nucleus (VPN), d

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

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

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

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

223 In optic neuritis (ON) eyes, the NMOSD patients had more severe G

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

242 Optic neuritis or transverse myelitis developed after vomiting

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

244 owing them to survive long enough to develop neuritis outside of the transfer setting.

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

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

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

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

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

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

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

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

253 Optic neuritis produced large sensitivity losses mediated by t

254 age of onset were more likely to have optic neuritis relapses (P < 0.001).

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

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

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

258 Ab depletion studies showed neuritis still developed in the absence of NOD-PerIg CD8

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

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

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

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

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

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

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

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

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

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

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

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

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

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

276 In most patients with optic neuritis, visual recovery is rapid.

277 as been associated with paraneoplastic optic neuritis, vitritis, retinitis, or a combination thereof,

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

279 Optic neuritis was detected by inflammatory cell infiltration

280 Optic neuritis was diagnosed in 110 patients, providing an ann

281 This neuritis was predominantly composed of CD4(+) and CD8(+)

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

283 Isolated optic neuritis was the most frequent clinical presentation in

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

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

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

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

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

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

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

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

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

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

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

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

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

297 se development, can also elicit a peripheral neuritis (with secondary myositis).

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

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

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