ライフサイエンスコーパス: optic neuritis

1 (at least 3 months after onset in studies of optic neuritis).

2 measurements were the incidence and cause of optic neuritis.

3 ntegrity can occur even without a history of optic neuritis.

4 of neuroaxonal loss and myelin repair after optic neuritis.

5 ethnicity-dependent visual outcomes of acute optic neuritis.

6 ty outcomes in affected eyes following acute optic neuritis.

7 with normal visual acuity and no history of optic neuritis.

8 g patients with MS with and without previous optic neuritis.

9 -modifying therapies and steroids, and prior optic neuritis.

10 ng 7 of 29 eyes (24%) previously affected by optic neuritis.

11 ith NMO in eyes previously affected by acute optic neuritis.

12 of the optic nerve in isolated experimental optic neuritis.

13 al disability in patients with NMO following optic neuritis.

14 y in eyes previously affected by symptomatic optic neuritis.

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

16 t erythropoietin might be neuroprotective in optic neuritis.

17 uring the preclinical phase, before onset of optic neuritis.

18 patients presenting with a first episode of optic neuritis.

19 ed inward, in contrast to eyes with NAION or optic neuritis.

20 s potential markers of axonal loss following optic neuritis.

21 of T-cell-tolerizing drugs for patients with optic neuritis.

22 f-concept trials of acute neuroprotection in optic neuritis.

23 (5.52-8.65, n=3154, p<0.0001) in MS without optic neuritis.

24 isual evoked potential latency) during acute optic neuritis.

25 course can prevent RGC loss in experimental optic neuritis.

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

27 multiple sclerosis without a past history of optic neuritis.

28 trategy for suppressing neurodegeneration in optic neuritis.

29 n of these mice develop spontaneous isolated optic neuritis.

30 onegative experienced a relapse or developed optic neuritis.

31 in the visual cortex following an attack of optic neuritis.

32 edicts relapse of myelitis or development of optic neuritis.

33 and induced neurological deficits, including optic neuritis.

34 dies in patients with multiple sclerosis and optic neuritis.

35 in the RNFL and macula, respectively, after optic neuritis.

36 y was defined as history of acute unilateral optic neuritis.

37 e sclerosis who have established weakness or optic neuritis.

38 n many patients first presents clinically as optic neuritis.

39 nses are involved in the genesis of isolated optic neuritis.

40 s, and one of these patients later developed optic neuritis.

41 mechanism of neuronal death in experimental optic neuritis.

42 associated with the primary damage caused by optic neuritis.

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

44 , particularly those with a history of acute optic neuritis.

45 .03), independent of a patient's history of optic neuritis.

46 atment, and use of corticosteroids for acute optic neuritis.

47 is has a better visual outcome than AQP4-IgG optic neuritis.

48 oin is neuroprotective in patient with acute optic neuritis.

49 is eye for patients with previous unilateral optic neuritis.

50 in eyes with a history of acute symptomatic optic neuritis (100% of eyes with microcystic changes ha

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

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

53 spectively study eyes with papilledema (24), optic neuritis (14), nonarteritic anterior ischemic opti

54 nditions included macular degeneration (35), optic neuritis (18), retinitis pigmentosa (17), and diab

55 (47%), anomalous optic discs (44%), isolated optic neuritis (19%), and optic atrophy (12%).

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

57 anglion 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 immunomo

59 the 59 pediatric patients with first-episode optic neuritis, 46 had at least 3 months of follow-up an

60 an of 4.6 months after a clinically isolated optic neuritis (49 females, mean age 33.5 years) and wer

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

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

63 th neuromyelitis optica without a history of optic neuritis, a disease in which subclinical disease a

64 both serious and unexpected: one patient had optic neuritis after the first bevacizumab infusion, a s

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

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

67 n association with demyelinating disease and optic neuritis, although evidence for this has relied so

68 ss-induced neurodegeneration in experimental optic neuritis, an inflammatory demyelinating optic nerv

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

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

71 iatric hospital, patients with first-episode optic neuritis and at least 3 months of follow-up over a

72 within 6 months of presenting with isolated optic neuritis and compared the findings with those seen

73 er 1-5 mm differed significantly between the optic neuritis and control groups [+0.059 percentage uni

74 significant autoimmune disease manifested by optic neuritis and death.

75 Twenty-eight consecutive patients with acute optic neuritis and eight healthy controls were assessed

76 ls adjusting for age, sex, disease duration, optic neuritis and genetic ancestry and using a combinat

77 in 11 patients with unilateral or bilateral optic neuritis and in 18 age-matched controls with norma

78 axonal loss in the retina in both recovered optic neuritis and in multiple sclerosis without a past

79 r investigation in larger clinical trials in optic neuritis and in relapsing multiple sclerosis is wa

80 lopment of well recognised syndromes such as optic neuritis and internuclear ophthalmoplegia, respect

81 A comprehensive understanding of pediatric optic neuritis and its management remains elusive.

82 Clinical data (episodes of optic neuritis and longitudinally extensive transverse m

83 1C6 CD8(+) T cells alone can induce optic neuritis and mild EAE with delayed onset; however,

84 leads to permanent neurologic disability in optic neuritis and MS patients.

85 are potential novel treatment strategies for optic neuritis and MS, and possibly other optic neuropat

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

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

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

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

90 permanent visual disability in patients with optic neuritis and multiple sclerosis.

91 degeneration and persistent visual loss from optic neuritis and multiple sclerosis.

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

93 O) is characterized by disabling relapses of optic neuritis and myelitis and the presence of aquapori

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

95 s in eyes with optic disc swelling caused by optic neuritis and nonarteritic anterior ischemic optic

96 neration 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 init

98 oplastic ophthalmological entity of combined optic neuritis and retinitis with vitreous inflammatory

99 ronic immunomodulation may prevent recurrent optic neuritis and RGC damage.

100 ion and showed a trend toward suppression of optic neuritis and RGC loss on day 14 that was lost by d

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

102 was observed for individuals with exclusive optic neuritis and/or spinal cord involvement as first a

103 in 20 participants during the acute phase of optic neuritis, and again 3 and 6 months later.

104 tive patients, 4 of 6 patients had recurrent optic neuritis, and all 6 had a final visual acuity of 2

105 y low levels of immunosuppression, may mimic optic neuritis, and are a potentially reversible cause o

106 ic nerve axons following the acute insult in optic neuritis, and chronically in primary and secondary

107 ncluding ischemic optic neuropathy, previous optic neuritis, and compressive and inherited optic neur

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

109 ve occurred in the fields of autoimmunity in optic neuritis, and in imaging the retinal nerve fibre l

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

111 nal neuronal layer pathology following acute optic neuritis, and to systematically characterize such

112 disability, presence of previous unilateral optic neuritis, and use of disease-modifying therapies a

113 nstays of therapy for the treatment of acute optic neuritis (AON) and acute demyelination in multiple

114 Among patients with an acute optic neuritis (AON) history, AAs had greater loss of HC

115 er characterization of the cause of atypical optic neuritis: AQP4-IgG and MOG-IgG.

116 ses for patients with multiple sclerosis and optic neuritis are needed to ensure uniformity among cli

117 signal on MRI of the optic nerve affected by optic neuritis are said to correlate with the severity o

118 nd macular volume in eyes with no history of optic neuritis as a biomarker of disability worsening in

119 We used optic neuritis as a model of multiple sclerosis relapse

120 l marker and may help to distinguish between optic neuritis associated with multiple sclerosis and op

121 ection with phenytoin in patients with acute optic neuritis at concentrations at which it blocks volt

122 Patients with optic neuritis at onset were more likely to develop blin

123 set NMO, the median time from onset to first optic neuritis attack (54 months) was similar to the med

124 ents with rLETM (range, 2-22), and the first optic neuritis attack for those with rLETM-onset NMO fol

125 tients positive for AQP4-IgG had more than 1 optic neuritis attack, 2 with residual no light percepti

126 vision loss that was initially thought to be optic neuritis attacks.

127 e sclerosis who had at least one eye without optic neuritis available.

128 Optic neuritis began 9 days after immunization.

129 eft eye (scleritis, conjunctivitis, and peri-optic neuritis), brain (choriomeningoencephalitis), stom

130 Clinically isolated syndromes (CIS), such as optic neuritis, brainstem or spinal cord syndromes are f

131 l hemorrhages, iritis, keratic precipitates, optic neuritis, branch retinal artery occlusions, and ch

132 ed on day 14, mice rapidly developed EAE and optic neuritis by day 18, but RGC loss was still reduced

133 acranial injection of this strain can induce optic neuritis by retrograde axonal transport from the b

134 xamined potential neuroprotective effects in optic neuritis by SRT647 and SRT501, two structurally an

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

136 Atypical forms of optic neuritis can occur, either in association with oth

137 l outcome of both optic nerve and brain post-optic neuritis changes.

138 We report that, before manifestation of optic neuritis, characterized by inflammatory infiltrati

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

140 tinopathy ("CAR"-IgG [23kDa, recoverin]) and optic neuritis collapsin response-mediated protein 5 (CR

141 th microcystic changes had experienced prior optic neuritis compared with 71% of NMO eyes without mic

142 inal neuronal layer thinning following acute optic neuritis, corroborating the hypothesis that axonal

143 ca (NMO), and chronic relapsing inflammatory optic neuritis (CRION).

144 Optic neuritis developed in two thirds of eyes with sign

145 Acute optic neuritis due to an inflammatory demyelinating lesi

146 d 18-55 years) with a first unilateral acute optic neuritis episode within 28 days from study baselin

147 of opicinumab given soon after a first acute optic neuritis episode.

148 scores, disease duration, treatments, prior optic neuritis episodes, and quality of life (QOL; based

149 ys, a retinal problem could be confused with optic neuritis, especially in a patient with a normal ap

150 e with neuromyelitis optica and a history of optic neuritis exhibited the greatest reduction in gangl

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

152 ased to levels similar to those of untreated optic neuritis eyes.

153 s) causes meningoencephalitis, myelitis, and optic neuritis followed by axonal loss and demyelination

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

155 lated as the mean value of both eyes without optic neuritis for patients without a history of optic n

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

157 he Japanese cohort, commonly presenting with optic neuritis, had a high risk of visual disability whi

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

159 The treatment of optic neuritis has been investigated in several trials,

160 The current approach to patients with optic neuritis has been modified by the results of the C

161 a show that most patients with demyelinating optic neuritis have an excellent prognosis for recovery

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

163 nts with multiple sclerosis without previous optic neuritis have thinner retinal layers than healthy

164 on to the more pronounced thinning caused by optic neuritis if present.

165 on of NMOSD in 10 patients (40%) preceded by optic neuritis in 13 patients (52%) and preceded by a na

166 ble to protect retinal ganglion cells during optic neuritis in a mouse model of multiple sclerosis.

167 a rare case of CAR with chorioretinitis and optic neuritis in a patient with occult SCLC.

168 tudy followed serial changes in MTR in acute optic neuritis in combination with clinical and electrop

169 onstrated disparate outcomes following acute optic neuritis in individuals of African descent compare

170 f visual evoked potential (VEP) latencies in optic neuritis in MS may identify demyelination and remy

171 (95% CI 17.91-22.86, n=2063, p<0.0001) after optic neuritis in MS, and of 7.08 microm (5.52-8.65, n=3

172 pment of therapeutic strategies tailored for optic neuritis in MS.

173 the development of neurodegeneration during optic neuritis in myelin-specific T cell receptor transg

174 ritis associated with multiple sclerosis and optic neuritis in neuromyelitis optica.

175 tomography study in patients presenting with optic neuritis in order to define the temporal evolution

176 ople with multiple sclerosis with or without optic neuritis in PubMed, Web of Science, and Google Sch

177 g of demographic and presenting features for optic neuritis in the pediatric population.

178 g of the ganglion cell layer following acute optic neuritis, in the absence of evidence of baseline s

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

180 nfection with this recombinant virus induces optic neuritis independent of virus dose, major histocom

181 myelinating optic nerve inflammation, termed optic neuritis, induces permanent visual dysfunction due

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

183 s with multifocal or isolated spinal cord or optic neuritis involvement at onset in comparison to tho

184 Acute optic neuritis is a cardinal manifestation of neuromyeli

185 Optic neuritis is a common condition that causes reversi

186 Acute optic neuritis is a common, often presenting manifestati

187 Pediatric optic neuritis is an uncommon disorder with significant

188 The predilection of these mice to develop optic neuritis is associated with higher expression of M

189 Optic neuritis is common in MS and leads to visual disab

190 Optic neuritis is frequently associated with MS and ofte

191 Optic neuritis is rare among those who initiate anti-TNF

192 Acute optic neuritis is the most common optic neuropathy affec

193 Optic neuritis is the most widely studied visual disturb

194 Here we review the diagnostic features of optic neuritis, its differential diagnosis, and give pra

195 pe is characterized by recurrent episodes of optic neuritis, longitudinally extensive transverse myel

196 of females, lower incidence of simultaneous optic neuritis, lower frequency of conus involvement, an

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

198 rior visual pathways in patients with MS and optic neuritis may be used as a model.

199 otential swelling during the acute stages of optic neuritis may confound baseline measurements.

200 uggesting that retrograde degeneration after optic neuritis may not extend into the deeper retinal la

201 and multiple sclerosis without a history of optic neuritis (MS non-ON).

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

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

204 lthy controls, multiple-sclerosis-associated optic neuritis (MSON), and multiple sclerosis without op

205 ADEM), one episode of transverse myelitis or optic neuritis, multiple sclerosis (MS), anti-aquaporin-

206 bre layer has been detected in patients with optic neuritis, multiple sclerosis, neuromyelitis optica

207 ncluding anterior ischemic optic neuropathy, optic neuritis/multiple sclerosis, neuromyelitis optica,

208 trum disorder (NMOSD) and related syndromes (optic neuritis, myelitis and brainstem encephalitis), bu

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

210 threshold of 4mum for identifying unilateral optic neuritis (n = 477).

211 myelitis (n=4), idiopathic AQP4-IgG-negative optic neuritis (n=4), other demyelinating syndromes (n=3

212 serostatus), multiple sclerosis (MS) (n=69), optic neuritis (n=5) and non-neurological controls (n=37

213 ional area of the affected optic nerve after optic neuritis nor the damage in optic radiations was as

214 es and decreased with distance from them; in optic neuritis, normal-appearing white matter magnetizat

215 A proportion of cases of optic neuritis occur in patients who do not develop mult

216 e and sex were similar between cohorts, with optic neuritis occurring most frequently at onset (Japan

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

218 We evaluated the risk of optic neuritis (ON) after vaccines, using a case-centere

219 To determine the relationship between optic neuritis (ON) and EAE, we examined the incidence o

220 s (64.7%) and Spectralis (61.7%) in both the optic neuritis (ON) and non-ON group and by Stratus (58.

221 the lateral geniculate nucleus (LGN), due to optic neuritis (ON) and the ventral posterior nucleus (V

222 s the dynamics of retinal injury after acute optic neuritis (ON) and their association with clinical

223 test positive for AQP4-Abs and present with optic neuritis (ON) and transverse myelitis (TM) are dia

224 a disease clinically characterised by severe optic neuritis (ON) and transverse myelitis (TM).

225 sclerosis (MS) in 357 children with isolated optic neuritis (ON) as a first demyelinating event who h

226 multiple sclerosis (MS), demyelination, and optic neuritis (ON) associated with anti-tumor necrosis

227 In optic neuritis (ON) eyes, the NMOSD patients had more se

228 djusting for age, sex, disease duration, and optic neuritis (ON) history.

229 y progressive MS, 14 had clinical history of optic neuritis (ON) in a single eye; the remaining patie

230 Optic neuritis (ON) is a condition involving primary inf

231 Visual Evoked Potentials (VEPs) following optic neuritis (ON) remain chronically prolonged, althou

232 luid from four patients with monosymptomatic optic neuritis (ON) were analyzed by single-cell reverse

233 Optic neuritis (ON), an inflammatory demyelinating optic

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

235 nglion cell loss relates to history of acute optic neuritis (ON), retinal nerve fiber layer (RNFL) th

236 In patients with isolated optic neuritis (ON), the presence of antibodies to aquap

237 dependently of other confounders, especially optic neuritis (ON).

238 omyelitis optica (NMO) and one with isolated optic neuritis (ON).

239 es with and without a prior history of acute optic neuritis (ON).

240 technique after long-term latency changes in optic neuritis (ON)/multiple sclerosis (MS), mfVEPs were

241 t presentation, 40% NMO cases had unilateral optic neuritis (ON); 20% bilateral ON; 15% transverse my

242 Corticosteroid treatment initiated before optic neuritis onset (days 0-14) suppressed EAE and redu

243 Corticosteroid treatment after optic neuritis onset (days 10-14) slowed EAE progression

244 more commonly women, had concurrent or prior optic neuritis or intractable vomiting episodes more fre

245 MS is less likely in patients with a CIS of optic neuritis or sensory symptoms only, few or no MRI l

246 c neuritis for patients without a history of optic neuritis or the value of the non-optic neuritis ey

247 Optic neuritis or transverse myelitis developed after vo

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

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

250 0.001), and for unilateral versus bilateral optic neuritis (p = 0.020).

251 red over the past decade in understanding of optic neuritis pathophysiology, and these developments h

252 ortex and whole brain analysis comparing all optic neuritis patients and controls revealed a selectiv

253 n female vaccinees in the USA, 86.3 cases of optic neuritis per 10 million population would be expect

254 as of affected optic nerves at 3 months post-optic neuritis predicted lower fractional anisotropy and

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

256 Optic neuritis produced large sensitivity losses mediate

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

258 t of retinal neuronal layers following acute optic neuritis remains largely unexplored.

259 ported in patients assigned ozanimod 0.5 mg: optic neuritis, somatoform autonomic dysfunction, and ce

260 ffusion properties of optic radiations after optic neuritis suggesting trans-synaptic degeneration; (

261 e inner or outer nuclear layers of eyes with optic neuritis, suggesting that retrograde degeneration

262 ma occurred more commonly in eyes with prior optic neuritis than eyes without prior optic neuritis (5

263 In this cohort of pediatric patients with optic neuritis, the majority of patients regained normal

264 Optic neuritis, the most common ocular manifestation of

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

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

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

268 nts with a first episode of acute unilateral optic neuritis to assess the effects of a single acute i

269 st cohort of black race/ethnicity with acute optic neuritis to be studied and represents the first ev

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

271 risks factors for progression from isolated optic neuritis to systemic demyelinating processes, such

272 ort on a 51-year-old woman who had relapsing optic neuritis, transverse myelitis, AQP4-IgG seropositi

273 Patients with monofocal syndromes such as optic neuritis, transverse myelitis, or isolated brainst

274 shed analyses of the prospectively collected Optic Neuritis Treatment Trial (ONTT) data identified no

275 The Optic Neuritis Treatment Trial (ONTT) has provided impor

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

277 (TCR+) transgenic mice that develop isolated optic neuritis usually without any other characteristic

278 Remission rates were higher for isolated optic neuritis versus isolated myelitis (p < 0.001), and

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

280 IgG) has been associated with paraneoplastic optic neuritis, vitritis, retinitis, or a combination th

281 Optic neuritis was detected by inflammatory cell infiltr

282 Optic neuritis was diagnosed in 110 patients, providing

283 Isolated optic neuritis was the most frequent clinical presentati

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

285 g a rat model of MS that frequently leads to optic neuritis, we have investigated the interconnection

286 yes of patients with MS without a history of optic neuritis were associated with cortical gray matter

287 e fitted parameters from the eye affected by optic neuritis were compared with those from the normal

288 s) with acute clinically isolated unilateral optic neuritis were recruited to undergo optical coheren

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

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

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

292 ions of this axonal protein in patients with optic neuritis who had a poor visual outcome are likely

293 atients who had a previous single episode of optic neuritis with a recruitment bias to those with inc

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

295 r macular volume at baseline in eyes without optic neuritis with the risk of subsequent disability wo

296 001) during a 15-year period following acute optic neuritis, with black race/ethnicity being associat

297 d retinal ganglion cell loss in experimental optic neuritis, with reduced inflammation and demyelinat

298 ansgenic mice spontaneously develop isolated optic neuritis without any clinical nor histological evi

299 Optic neuritis without EAE could also be induced in thes

300 ny cases of recurrent non-multiple sclerosis optic neuritis without myelitis will be shown to be asso