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1 (at least 3 months after onset in studies of optic neuritis).
2 ith NMO in eyes previously affected by acute optic neuritis.
3  of the optic nerve in isolated experimental optic neuritis.
4 al disability in patients with NMO following optic neuritis.
5 y in eyes previously affected by symptomatic optic neuritis.
6  .03), independent of a patient's history of optic neuritis.
7 ledema and NAION (P = 0.97), and reduced for optic neuritis.
8 t erythropoietin might be neuroprotective in optic neuritis.
9 uring the preclinical phase, before onset of optic neuritis.
10  patients presenting with a first episode of optic neuritis.
11 ed inward, in contrast to eyes with NAION or optic neuritis.
12 s potential markers of axonal loss following optic neuritis.
13 of T-cell-tolerizing drugs for patients with optic neuritis.
14 f-concept trials of acute neuroprotection in optic neuritis.
15  (5.52-8.65, n=3154, p<0.0001) in MS without optic neuritis.
16 isual evoked potential latency) during acute optic neuritis.
17  course can prevent RGC loss in experimental optic neuritis.
18 multiple sclerosis without a past history of optic neuritis.
19 , particularly those with a history of acute optic neuritis.
20 trategy for suppressing neurodegeneration in optic neuritis.
21 n of these mice develop spontaneous isolated optic neuritis.
22 onegative experienced a relapse or developed optic neuritis.
23  in the visual cortex following an attack of optic neuritis.
24 edicts relapse of myelitis or development of optic neuritis.
25 and induced neurological deficits, including optic neuritis.
26 atment, and use of corticosteroids for acute optic neuritis.
27 dies in patients with multiple sclerosis and optic neuritis.
28  in the RNFL and macula, respectively, after optic neuritis.
29 e sclerosis who have established weakness or optic neuritis.
30 n many patients first presents clinically as optic neuritis.
31 nses are involved in the genesis of isolated optic neuritis.
32 s, and one of these patients later developed optic neuritis.
33  patients with a first bout of demyelinating optic neuritis.
34 on conditions such as orbital cellulitis and optic neuritis.
35 als for the second year, after an episode of optic neuritis.
36 mic optic neuropathy, and one had unilateral optic neuritis.
37 ze the area of inflammation in patients with optic neuritis.
38 d/or translational levels) in a rat model of optic neuritis.
39 lomyelitis (EAE), an animal model for MS and optic neuritis.
40 cannot be used for differential diagnosis of optic neuritis.
41 esence of visual disease such as "recovered" optic neuritis.
42  neurologic symptoms prior to the episode of optic neuritis.
43 oin is neuroprotective in patient with acute optic neuritis.
44 is eye for patients with previous unilateral optic neuritis.
45 ntegrity can occur even without a history of optic neuritis.
46  of neuroaxonal loss and myelin repair after optic neuritis.
47 ethnicity-dependent visual outcomes of acute optic neuritis.
48 ty outcomes in affected eyes following acute optic neuritis.
49 g patients with MS with and without previous optic neuritis.
50 ng 7 of 29 eyes (24%) previously affected by optic neuritis.
51  in eyes with a history of acute symptomatic optic neuritis (100% of eyes with microcystic changes ha
52  with nonglaucomatous optic atrophy (30%) (5 optic neuritis, 11 anterior visual pathway tumors, 2 pap
53                                 One of eight optic neuritis (12%) eyes and 1 of 12 NAION (8%) eyes ha
54 spectively study eyes with papilledema (24), optic neuritis (14), nonarteritic anterior ischemic opti
55 y (69 versus 15%, P: < 0.002); and bilateral optic neuritis (23 versus 8%, not significant).
56 anglion cell layer of eyes affected by acute optic neuritis 3 and 6 months after onset (P < 0.001).
57 the 59 pediatric patients with first-episode optic neuritis, 46 had at least 3 months of follow-up an
58 an of 4.6 months after a clinically isolated optic neuritis (49 females, mean age 33.5 years) and wer
59 prior optic neuritis than eyes without prior optic neuritis (50 versus 27%) and was associated with l
60                          Acute demyelinating optic neuritis, a common feature of multiple sclerosis,
61 th neuromyelitis optica without a history of optic neuritis, a disease in which subclinical disease a
62 both serious and unexpected: one patient had optic neuritis after the first bevacizumab infusion, a s
63                          Patients with acute optic neuritis aged 18-60 years, presenting within 2 wee
64        Among 16 patients with CRMP-5-IgG and optic neuritis (aged 52-74 years; all smokers, 9 women),
65 n association with demyelinating disease and optic neuritis, although evidence for this has relied so
66  optic neuropathy hard to differentiate from optic neuritis and arteritic ischemic optic neuropathy.
67 iatric hospital, patients with first-episode optic neuritis and at least 3 months of follow-up over a
68  within 6 months of presenting with isolated optic neuritis and compared the findings with those seen
69 er 1-5 mm differed significantly between the optic neuritis and control groups [+0.059 percentage uni
70 significant autoimmune disease manifested by optic neuritis and death.
71 Twenty-eight consecutive patients with acute optic neuritis and eight healthy controls were assessed
72  in 11 patients with unilateral or bilateral optic neuritis and in 18 age-matched controls with norma
73  axonal loss in the retina in both recovered optic neuritis and in multiple sclerosis without a past
74 r investigation in larger clinical trials in optic neuritis and in relapsing multiple sclerosis is wa
75 lopment of well recognised syndromes such as optic neuritis and internuclear ophthalmoplegia, respect
76  nerve is a sensitive (94%) finding in acute optic neuritis and is absent in unaffected or previously
77   A comprehensive understanding of pediatric optic neuritis and its management remains elusive.
78                   Clinical data (episodes of optic neuritis and longitudinally extensive transverse m
79          1C6 CD8(+) T cells alone can induce optic neuritis and mild EAE with delayed onset; however,
80  leads to permanent neurologic disability in optic neuritis and MS patients.
81                                              Optic neuritis and multiple sclerosis (MS) are common ca
82 s and neurologic disability in patients with optic neuritis and multiple sclerosis (MS).
83 tribute to the persistence of visual loss in optic neuritis and multiple sclerosis (MS).
84 maging the retinal nerve fibre layer in both optic neuritis and multiple sclerosis.
85 almic advances relevant to the management of optic neuritis and multiple sclerosis.
86 permanent visual disability in patients with optic neuritis and multiple sclerosis.
87 degeneration and persistent visual loss from optic neuritis and multiple sclerosis.
88 ently presented with simultaneous/sequential optic neuritis and myelitis (44% vs 0%; P = .005).
89 O) is characterized by disabling relapses of optic neuritis and myelitis and the presence of aquapori
90 ease of the CNS, characterized by attacks of optic neuritis and myelitis.
91 s in eyes with optic disc swelling caused by optic neuritis and nonarteritic anterior ischemic optic
92                 Corticosteroids can suppress optic neuritis and prevent RGC loss if treatment is init
93 oplastic ophthalmological entity of combined optic neuritis and retinitis with vitreous inflammatory
94 ronic immunomodulation may prevent recurrent optic neuritis and RGC damage.
95 ion and showed a trend toward suppression of optic neuritis and RGC loss on day 14 that was lost by d
96 ne the sensitivity of this modality in acute optic neuritis and whether the abnormal enhancement corr
97  was observed for individuals with exclusive optic neuritis and/or spinal cord involvement as first a
98 in 20 participants during the acute phase of optic neuritis, and again 3 and 6 months later.
99 y low levels of immunosuppression, may mimic optic neuritis, and are a potentially reversible cause o
100 ic nerve axons following the acute insult in optic neuritis, and chronically in primary and secondary
101 adrant in 1 eye with papilledema, 1 eye with optic neuritis, and in 13 eyes with NAION.
102 ve occurred in the fields of autoimmunity in optic neuritis, and in imaging the retinal nerve fibre l
103 P was slightly increased for papilledema and optic neuritis, and reduced for NAION (P = 0.02) eyes.
104 ns and for studying patients with amblyopia, optic neuritis, and residual vision in homonymous hemian
105 pilepsies, polymyositis, multiple sclerosis, optic neuritis, and the stiff-man syndrome.
106 nal neuronal layer pathology following acute optic neuritis, and to systematically characterize such
107  disability, presence of previous unilateral optic neuritis, and use of disease-modifying therapies a
108 nstays of therapy for the treatment of acute optic neuritis (AON) and acute demyelination in multiple
109                 Among patients with an acute optic neuritis (AON) history, AAs had greater loss of HC
110 ses for patients with multiple sclerosis and optic neuritis are needed to ensure uniformity among cli
111 signal on MRI of the optic nerve affected by optic neuritis are said to correlate with the severity o
112 nd macular volume in eyes with no history of optic neuritis as a biomarker of disability worsening in
113                                      We used optic neuritis as a model of multiple sclerosis relapse
114 ears after treatment for an episode of acute optic neuritis as part of the Optic Neuritis Treatment T
115                          Acute demyelinating optic neuritis associated with multiple sclerosis (MS) i
116 l marker and may help to distinguish between optic neuritis associated with multiple sclerosis and op
117 ection with phenytoin in patients with acute optic neuritis at concentrations at which it blocks volt
118 set NMO, the median time from onset to first optic neuritis attack (54 months) was similar to the med
119 ents with rLETM (range, 2-22), and the first optic neuritis attack for those with rLETM-onset NMO fol
120 vision loss that was initially thought to be optic neuritis attacks.
121 e sclerosis who had at least one eye without optic neuritis available.
122                                              Optic neuritis began 9 days after immunization.
123 eft eye (scleritis, conjunctivitis, and peri-optic neuritis), brain (choriomeningoencephalitis), stom
124 Clinically isolated syndromes (CIS), such as optic neuritis, brainstem or spinal cord syndromes are f
125         The beneficial effect is present for optic neuritis, brainstem-cerebellar syndromes, and spin
126 linically definite multiple sclerosis in the optic neuritis, brainstem-cerebellar, and spinal cord sy
127 l hemorrhages, iritis, keratic precipitates, optic neuritis, branch retinal artery occlusions, and ch
128 steroids remain the mainstay of treatment of optic neuritis, but alternate dosages and routes of admi
129 ed on day 14, mice rapidly developed EAE and optic neuritis by day 18, but RGC loss was still reduced
130 xamined potential neuroprotective effects in optic neuritis by SRT647 and SRT501, two structurally an
131 eyes) and by SLP (14/16 eyes) in contrast to optic neuritis (by OCT, 0/12, P = 0.006; and by SLP, 1/1
132                            Atypical forms of optic neuritis can occur, either in association with oth
133 logical syndrome, characterized by recurrent optic neuritis, cervical myelopathy from syringomyelia,
134 l outcome of both optic nerve and brain post-optic neuritis changes.
135      We report that, before manifestation of optic neuritis, characterized by inflammatory infiltrati
136 animal models for MS and in a phase II acute optic neuritis clinical trial (RENEW).
137 tinopathy ("CAR"-IgG [23kDa, recoverin]) and optic neuritis collapsin response-mediated protein 5 (CR
138 th microcystic changes had experienced prior optic neuritis compared with 71% of NMO eyes without mic
139  Our understanding of the natural history of optic neuritis continues to expand.
140 inal neuronal layer thinning following acute optic neuritis, corroborating the hypothesis that axonal
141 ca (NMO), and chronic relapsing inflammatory optic neuritis (CRION).
142  and nonarteritic ischemic optic neuropathy, optic neuritis, Cuban epidemic optic neuropathy, toxic a
143 creased from days 3 to 14, and retinitis and optic neuritis decreased from days 3 to 9.
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 y-nine patients were recruited who had acute optic neuritis for a median of 13 days (range 7-24 days)
154 lated as the mean value of both eyes without optic neuritis for patients without a history of optic n
155 after their first attack of acute unilateral optic neuritis for up to 18 months.
156 he Japanese cohort, commonly presenting with optic neuritis, had a high risk of visual disability whi
157  multiple sclerosis (MS) after an episode of optic neuritis has been confirmed with longitudinal stud
158                             The treatment of optic neuritis has been investigated in several trials,
159        The current approach to patients with optic neuritis has been modified by the results of the C
160 a show that most patients with demyelinating optic neuritis have an excellent prognosis for recovery
161          Particularly myelitis and bilateral optic neuritis have poor remission rates.
162 nts with multiple sclerosis without previous optic neuritis have thinner retinal layers than healthy
163 on to the more pronounced thinning caused by optic neuritis if present.
164 on of NMOSD in 10 patients (40%) preceded by optic neuritis in 13 patients (52%) and preceded by a na
165 ble to protect retinal ganglion cells during optic neuritis in a mouse model of multiple sclerosis.
166 tudy followed serial changes in MTR in acute optic neuritis in combination with clinical and electrop
167 onstrated disparate outcomes following acute optic neuritis in individuals of African descent compare
168 (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
169  the development of neurodegeneration during optic neuritis in myelin-specific T cell receptor transg
170 ritis associated with multiple sclerosis and optic neuritis in neuromyelitis optica.
171 tomography study in patients presenting with optic neuritis in order to define the temporal evolution
172 ople with multiple sclerosis with or without optic neuritis in PubMed, Web of Science, and Google Sch
173 g of demographic and presenting features for optic neuritis in the pediatric population.
174 g of the ganglion cell layer following acute optic neuritis, in the absence of evidence of baseline s
175 onset (days 0-14) suppressed EAE and reduced optic neuritis incidence through day 14.
176 n initial clinical episode of demyelination (optic neuritis, incomplete transverse myelitis, or brain
177  a first acute clinical demyelinating event (optic neuritis, incomplete transverse myelitis, or brain
178 7, retinitis increased from days 3 to 9, and optic neuritis increased from days 3 to 14.
179 nfection with this recombinant virus induces optic neuritis independent of virus dose, major histocom
180 myelinating optic nerve inflammation, termed optic neuritis, induces permanent visual dysfunction due
181               In the few eyes that developed optic neuritis, inflammation was mild, and RGC loss was
182 s with multifocal or isolated spinal cord or optic neuritis involvement at onset in comparison to tho
183                                        Acute optic neuritis is a cardinal manifestation of neuromyeli
184                                              Optic neuritis is a common condition that causes reversi
185                                        Acute optic neuritis is a common, often presenting manifestati
186                                          CSD optic neuritis is also described.
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 frequently associated with MS and ofte
190          Contrary to common clinical wisdom, optic neuritis is not characterized by selective RG defe
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  of females, lower incidence of simultaneous optic neuritis, lower frequency of conus involvement, an
196 s who do not develop multiple sclerosis; the optic neuritis may be monophasic illness or recurrent.
197 ole for calpain in myelin destruction during optic neuritis may be relevant to the pathogenesis of th
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 llapsin response-mediator protein-5-IgG with optic neuritis (n = 3).
209 myelitis (n=4), idiopathic AQP4-IgG-negative optic neuritis (n=4), other demyelinating syndromes (n=3
210 ional area of the affected optic nerve after optic neuritis nor the damage in optic radiations was as
211 es and decreased with distance from them; in optic neuritis, normal-appearing white matter magnetizat
212                     A proportion of cases of optic neuritis occur in patients who do not develop mult
213                                   Unilateral optic neuritis occurred only in the multiple sclerosis p
214 in patients with MS in 28 eyes with the last optic neuritis (ON) >or=6 months prior (ON group) and 33
215                     We evaluated the risk of optic neuritis (ON) after vaccines, using a case-centere
216        To determine the relationship between optic neuritis (ON) and EAE, we examined the incidence o
217 s (64.7%) and Spectralis (61.7%) in both the optic neuritis (ON) and non-ON group and by Stratus (58.
218 s the dynamics of retinal injury after acute optic neuritis (ON) and their association with clinical
219  test positive for AQP4-Abs and present with optic neuritis (ON) and transverse myelitis (TM) are dia
220 a disease clinically characterised by severe optic neuritis (ON) and transverse myelitis (TM).
221 sclerosis (MS) in 357 children with isolated optic neuritis (ON) as a first demyelinating event who h
222  multiple sclerosis (MS), demyelination, and optic neuritis (ON) associated with anti-tumor necrosis
223 djusting for age, sex, disease duration, and optic neuritis (ON) history.
224 y progressive MS, 14 had clinical history of optic neuritis (ON) in a single eye; the remaining patie
225                                              Optic neuritis (ON) is a condition involving primary inf
226    Visual Evoked Potentials (VEPs) following optic neuritis (ON) remain chronically prolonged, althou
227 luid from four patients with monosymptomatic optic neuritis (ON) were analyzed by single-cell reverse
228                                              Optic neuritis (ON), an inflammatory demyelinating optic
229                                              Optic neuritis (ON), inflammation of the optic nerve, is
230 nglion cell loss relates to history of acute optic neuritis (ON), retinal nerve fiber layer (RNFL) th
231                    In patients with isolated optic neuritis (ON), the presence of antibodies to aquap
232 es with and without a prior history of acute optic neuritis (ON).
233 dependently of other confounders, especially optic neuritis (ON).
234 omyelitis optica (NMO) and one with isolated optic neuritis (ON).
235 technique after long-term latency changes in optic neuritis (ON)/multiple sclerosis (MS), mfVEPs were
236 t presentation, 40% NMO cases had unilateral optic neuritis (ON); 20% bilateral ON; 15% transverse my
237 Is that were normal initially (when they had optic neuritis only) and when repeated after they had de
238    Corticosteroid treatment initiated before optic neuritis onset (days 0-14) suppressed EAE and redu
239               Corticosteroid treatment after optic neuritis onset (days 10-14) slowed EAE progression
240 more commonly women, had concurrent or prior optic neuritis or intractable vomiting episodes more fre
241  MS is less likely in patients with a CIS of optic neuritis or sensory symptoms only, few or no MRI l
242 c neuritis for patients without a history of optic neuritis or the value of the non-optic neuritis ey
243                                              Optic neuritis or transverse myelitis developed after vo
244  inner nuclear layers) of eyes with previous optic neuritis (P < 0.05).
245 ansverse myelitis and 1 of 9 (11%) developed optic neuritis (p = 0.004).
246  0.001), and for unilateral versus bilateral optic neuritis (p = 0.020).
247 red over the past decade in understanding of optic neuritis pathophysiology, and these developments h
248 ortex and whole brain analysis comparing all optic neuritis patients and controls revealed a selectiv
249 n female vaccinees in the USA, 86.3 cases of optic neuritis per 10 million population would be expect
250 as of affected optic nerves at 3 months post-optic neuritis predicted lower fractional anisotropy and
251                         In its typical form, optic neuritis presents as an inflammatory demyelinating
252                                              Optic neuritis produced large sensitivity losses mediate
253 mon neuro-opthalmological disorders, such as optic neuritis, pseudotumour cerebri and nonarteritic an
254 t of retinal neuronal layers following acute optic neuritis remains largely unexplored.
255 ported in patients assigned ozanimod 0.5 mg: optic neuritis, somatoform autonomic dysfunction, and ce
256 ffusion properties of optic radiations after optic neuritis suggesting trans-synaptic degeneration; (
257 e inner or outer nuclear layers of eyes with optic neuritis, suggesting that retrograde degeneration
258 ma occurred more commonly in eyes with prior optic neuritis than eyes without prior optic neuritis (5
259    In this cohort of pediatric patients with optic neuritis, the majority of patients regained normal
260                                              Optic neuritis, the most common ocular manifestation of
261     Our longitudinal study shows that, after optic neuritis, there is progressive damage to the optic
262                      Following an episode of optic neuritis, thinning of the retinal nerve fibre laye
263 hnicity with visual outcomes following acute optic neuritis through application of longitudinal data
264 nts with a first episode of acute unilateral optic neuritis to assess the effects of a single acute i
265 st cohort of black race/ethnicity with acute optic neuritis to be studied and represents the first ev
266 patients (57%) with isolated monosymptomatic optic neuritis to have 1 to 20 brain lesions, by magneti
267                          The relationship of optic neuritis to MS is not well understood.
268  risks factors for progression from isolated optic neuritis to systemic demyelinating processes, such
269 ort on a 51-year-old woman who had relapsing optic neuritis, transverse myelitis, AQP4-IgG seropositi
270    Patients with monofocal syndromes such as optic neuritis, transverse myelitis, or isolated brainst
271 shed analyses of the prospectively collected Optic Neuritis Treatment Trial (ONTT) data identified no
272                                          The Optic Neuritis Treatment Trial (ONTT) has provided impor
273 st decade major clinical trials, such as the Optic Neuritis Treatment Trial and Ischemic Optic Neurop
274 l trials in neuro-ophthalmology to date, the Optic Neuritis Treatment Trial, the Controlled High-Risk
275 isode of acute optic neuritis as part of the Optic Neuritis Treatment Trial.
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                                              Optic neuritis was detected by inflammatory cell infiltr
280 he finding of an abnormal MRI at the time of optic neuritis was significantly related to the subseque
281 thickness, also in eyes without a history of optic neuritis, was associated with fluid-attenuated inv
282 g a rat model of MS that frequently leads to optic neuritis, we have investigated the interconnection
283 yes of patients with MS without a history of optic neuritis were associated with cortical gray matter
284 e fitted parameters from the eye affected by optic neuritis were compared with those from the normal
285                     Vitritis, retinitis, and optic neuritis were graded from 0(+)-4+ for 14 days to s
286 s) with acute clinically isolated unilateral optic neuritis were recruited to undergo optical coheren
287 elitis optica, with and without a history of optic neuritis, when compared with healthy controls (P <
288  increased (P = 0.002) over 1 year following optic neuritis, whereas optic radiation measures were un
289  with other vision measures in patients with optic neuritis, which shows that the SKILL card measures
290 nd white (n = 388) race/ethnicity with acute optic neuritis who enrolled in the ONTT within 8 days of
291 ions of this axonal protein in patients with optic neuritis who had a poor visual outcome are likely
292 atients who had a previous single episode of optic neuritis with a recruitment bias to those with inc
293  types of optic neuropathy were studied: (1) optic neuritis with multiple sclerosis (MS), (2) idiopat
294 r macular volume at baseline in eyes without optic neuritis with the risk of subsequent disability wo
295 001) during a 15-year period following acute optic neuritis, with black race/ethnicity being associat
296 d retinal ganglion cell loss in experimental optic neuritis, with reduced inflammation and demyelinat
297 ansgenic mice spontaneously develop isolated optic neuritis without any clinical nor histological evi
298                                              Optic neuritis without EAE could also be induced in thes
299 ny cases of recurrent non-multiple sclerosis optic neuritis without myelitis will be shown to be asso

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