REVIEW ARTICLe
Updates and Controversies in the Management
of Acute Optic Neuritis
Ethan Meltzer, MD,*† and Sashank Prasad, MD*
Abstract: Optic neuritis remains a common diagnosis with controver-
sial management. Although typical optic neuritis is often associated with
“good” recovery of visual acuity, patients are often left with persistent
impairments of contrast sensitivity, color vision, and visual field. These
permanent visual deficits correlate with structural injury to the anterior
visual pathway and are closely linked to visual quality of life. High dose
corticosteroids are commonly used for patients with acute optic neuri-
tis. However, even several decades after the initial clinical trials, there
remains significant controversy regarding the efficacy and utility of this
treatment. There is a need for more effective treatments, and many new
immunomodulatory and neuroprotective agents have been investigated
recently. Atypical optic neuritis, such as that seen with neuromyelitis op-
tica spectrum disorder, often requires more aggressive initial treatment.
Thus, it is important for clinicians to have a framework for rapid diag-
nosis and triage of patients who present with typical or atypical optic
neuritis. Lastly, optic neuritis is associated with an elevated long-term
risk of developing multiple sclerosis. Some patients may benefit from
initiation of medications targeting multiple sclerosis at the time of initial
presentation of optic neuritis. Appropriate identification and treatment of
patients at highest risk of developing multiple sclerosis may help impact
their disease course, while limiting exposure to potential adverse effects
in patients who are at lower risk and do not require disease-modifying
treatment.
Key Words: optic neuritis, neuromyelitis optica spectrum disorders,
myelin oligodendrocyte glycoprotein, multiple sclerosis
(Asia-Pac J Ophthalmol 2018;7:00)
A cute optic neuritis is a common clinical dilemma and there
remain many controversial aspects to the appropriate man-
agement and treatment of this condition. It has been almost 2 de-
cades since the initial results from the Optic Neuritis Treatment
Trial (ONTT) were published, and since then the findings from
this landmark trial have been cited over 1000 times.1–7 In this re-
view on management dilemmas in the treatment of acute optic
neuritis, our goal is not only to revisit controversies stemming
from the ONTT but also to focus on several newer topics of inter-
est surrounding 1) the initial treatment of typical optic neuritis,
2) possible new emerging treatments for typical optic neuritis,
From the *Department of Neurology, Brigham and Women’s Hospital; and
†Department of Neurology, Massachusetts General Hospital, Harvard Medical
School, Boston, MA.
Received for publication March 30, 2018; accepted April 11, 2018.
The authors have no funding or conflicts of interest to declare.
Reprints: Sashank Prasad, MD, Brigham and Women’s Hospital, 75 Francis Street,
Boston, MA 02115. E‑mail: Sprasad2@bwh.harvard.edu.
Copyright © 2018 by Asia Pacific Academy of Ophthalmology
ISSN: 2162-0989
DOI: 10.22608/APO.2018108
Asia-Pacific Journal of Ophthalmology • Volume 0, Number 0, Month 2018
Copyright © 2018 Asia-Pacific Academy of Ophthalmology. Unauthorized reproduction of this article is prohibited.
3) diagnostic evaluation in atypical optic neuritis, and 4) the
determination of which patients may benefit from institution of
long-term immunosuppressive therapy after typical acute optic
neuritis.
Steroids in Typical Optic Neuritis—Treating
the Patient or the Physician?
Patients with typical optic neuritis can usually expect to
have a rapid, significant recovery of visual acuity in the weeks
to months after their initial symptoms.5,7,8 Overall, approximately
95% of all patients enrolled in the ONTT at 1-year follow-up had
a visual acuity better than 20/40, and over 70% had a visual acuity
of 20/20 or better.9 Over the 15-year follow-up period, only a few
patients that remained in the study had recurrent optic neuritis or
worsening visual deficits, and 90% of patients still had a visual
acuity better than 20/40.5 The patient population studied in this
trial was representative of typical optic neuritis. Recent serum
testing of available stored samples from the trial (40% of the total
study population) showed that no patients harbored the aquapo-
rin-4 (AQP4) antibody and only 3 patients tested positive for the
myelin oligodendrocyte glycoprotein (MOG) antibody.10
Even though visual acuity improves substantially for the
vast majority of patients with typical acute optic neuritis, many
patients have permanent deficits demonstrated by more sensitive
measures of visual outcome, including low-contrast visual acuity,
contrast sensitivity, color vision, and visual fields. In fact, up to
59% of patients with typical courses of optic neuritis report visual
impairment at 1 year.11 The more sensitive indicators of long-term
visual loss are closely linked to quality of life, despite good im-
provement of high-contrast visual acuity.12–14 Patients with more
severe vision loss at onset of symptoms are more likely to have
lasting visual impairment.7 In addition, patients who were later
diagnosed with clinically definite multiple sclerosis (MS) were
more likely to have permanent visual deficits compared with pa-
tients who did not develop MS.5,15
Because even the seemingly “benign” course of optic neu-
ritis often leads to persistent disability, it remains an important
question whether patients may benefit from treatment at the time
of diagnosis that improves the long-term visual prognosis. The
best data addressing this question remains that from the ONTT,
which showed improvement in color vision and contrast sensitiv-
ity at 6 months in patients who received high dose intravenous
(IV) steroids compared with patients who received lower dose
oral prednisone or oral placebo.7 However, the study showed no
differences in any functional outcomes between these treatment
groups at 1 year.9 The authors reported that high dose intravenous
steroids hastened visual recovery at 15 days, although this differ-
ence in rate of improvement was not a prespecified endpoint of
the trial.7 Subsequent analyses suggested that the group treated
with oral prednisone had a higher rate of recurrent optic neuritis
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Meltzer and Prasad
at 24-month follow-up (although this finding also was not a pre-
specified primary outcome, and the result has not been replicated
in any other trial since). In addition, the study suggested that high
dose IV steroids reduce the risk of developing clinically definite
MS over the subsequent 2 years, but no effect was seen at 5-year
follow-up. Some have criticized this finding, suggesting that ob-
servation can be attributed to post-hoc recoding of baseline MS
diagnoses in the original cohort.16–18 In addition to the limitations
in the reported data, other criticisms of the methodology of the
ONTT include the lack of an IV placebo group, particularly as
most of the results pertain to the efficacy of IV steroids.
A 2015 updated Cochrane review that looked at data from
the ONTT and 5 additional clinical trials analyzing steroid treat-
ment for acute optic neuritis (conducted in Denmark, Germany,
India, Japan, and the United Kingdom) concluded that there was
no available evidence demonstrating beneficial effect from treat-
ment of typical optic neuritis with oral or intravenous steroids
with respect to the outcome of visual acuity.19 Although group
analyses of clinical trial data for typical optic neuritis does not
show a long-term benefit of treatment with IV or oral steroids, it
remains unclear whether there are particular subsets of patients
that might benefit or how those subgroups could be predicted. In
contrast, certain atypical cases of optic neuritis may substantially
benefit from steroid and other immunosuppressive treatment (this
situation is discussed later).
Because the findings of the ONTT remain challenging to in-
terpret, a range of justifiable treatment approaches are common
in practice. Practicing neurologists and ophthalmologists often
either prescribe IV steroids or withhold treatment completely.
In our experience in a high volume clinical center in the United
States, neurologists are much more likely than ophthalmologists
to prescribe high dose intravenous steroids. This is in part due
to neurologists being more comfortable prescribing intravenous
steroids and weighing the benefit of faster visual recovery as ade-
quate justification for treatment. On the other hand, ophthalmolo-
gists more commonly do not prescribe intravenous steroids, partly
in recognition of the known (and sometimes severe) complica-
tions of high dose steroid therapy. Our experience is borne out by
international survey data. The Optic Neuritis Survey Group has
published several papers detailing this lack of consensus within
the international community of ophthalmologists and neurolo-
gists.20–23 A survey of neurologists and ophthalmologists in the
United States, Canada, Australia/New Zealand, Denmark, France,
and Thailand showed that neurologists were more likely than
ophthalmologists to treat acute optic neuritis with high dose in-
travenous steroids (at the far ends of the spectrum, approximately
97% of neurologists in France prescribe IV steroids whereas 65%
of ophthalmologists in Denmark do not treat with any steroids).20
In addition to illuminating the range of current practices
among physicians, the Optic Neuritis Survey Group has also
highlighted some persistent misinterpretation of the literature.
For example, although the majority of neurologists surveyed in
the southeastern United States indicated that they were familiar
with the ONTT, 72% reported believing that intravenous steroids
were shown to improve long-term visual outcome.20
Although the ONTT was a landmark study that shed some
light on the effects of corticosteroid treatment of acute optic neu-
ritis, we still clearly have a need for more definitive data sup-
porting treatments for optic neuritis that improve its long-term
prognosis.
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Asia-Pacific Journal of Ophthalmology • Volume 0, Number 0, Month 2018
Acute Optic Neuritis Treatment—Are
Neuroprotective Drugs and Alternative
Immunotherapies Ready for Prime Time?
Multiple trials have assessed a variety of treatments other than
corticosteroids to improve visual outcome after acute optic neuri-
tis. An important point to note is that most of these recent trials are
relatively small studies probing possible efficacy. For this reason,
the studies are not powered to detect an effect on visual function
directly, and the primary outcomes of these trials generally are
structural measures [ie, measurement of retinal nerve fiber layer
(RNFL) by optical coherence tomography (OCT)] or functional
surrogate measures [ie, P100 latency on visual evoked potentials
(VEP)]. Some of these studies show promising candidates, and
future studies will hopefully define their therapeutic role.
Studies in animal models have shown that neurodegenera-
tion in the form of permanent axonal loss after an attack of acute
inflammatory demyelination may in part be mediated by dysregu-
lation of small molecules called neurotrophins, which normally
promote axonal growth and plasticity via receptor tyrosine kinas-
es.24,25 Because erythropoietin is known to exhibit neurotrophin-
like properties, it was evaluated in patients with acute optic neuri-
tis in a randomized, placebo-controlled trial. The trial did show a
decrease in RNFL thinning in patients treated with erythropoietin,
meeting its primary outcome, but the treatment effect is difficult
to interpret because it was a small study with significant variance
among the baseline characteristics of the placebo and treatment
arms.24 Further work is needed to draw definitive conclusions
about the utility of erythropoietin in treating acute optic neuritis.
Neuronal energy failure is another important proposed mech-
anism that may contribute to long-term axonal damage after acute
relapses. Animal models have shown that phenytoin, a sodium
channel inhibitor, may have neuroprotective effects by limiting
intracellular accumulation of sodium ions.26 A randomized, pla-
cebo-controlled trial showed that administration of phenytoin led
to reduction in RNFL thinning 6 months after acute optic neuri-
tis.26 Further studies are needed to determine whether phenytoin
or other treatments targeting ion channels effectively improve
long-term functional visual outcomes.
Intravenous immunoglobulin (IVIg) has been studied as an
alternative immunotherapy to corticosteroids in the treatment of
acute optic neuritis but has not shown significant efficacy. One
double-blind, randomized, placebo-controlled trial evaluating
IVIg found no difference in visual acuity, color vision, contrast
sensitivity, or VEP measures 6 months after acute optic neuri-
tis.27 A separate trial comparing IVIg with placebo in patients with
chronic visual deficits after prior optic neuritis also did not show
any benefit.28
More recent studies have focused on novel mechanisms po-
tentially supporting remyelination. One potential therapeutic tar-
get is the leucine-rich repeat and immunoglobulin domain-con-
taining neurite outgrowth inhibitor receptor-interacting protein-1
(LINGO-1), which is an inhibitor of oligodendrocyte differentia-
tion and remyelination.29 Animal models have shown that block-
ing LINGO-1 may improve remyelination and have additional
neuroprotective effects. The first randomized, double-blind,
placebo-controlled phase 2 trial in humans administering a hu-
man monoclonal antibody at the time of acute optic neuritis did
not meet its primary endpoint, (assessment of P100 latency on
full-field VEP) in an intention-to-treat analysis, although a per-
protocol analysis did show a statistically significant difference.29
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Asia-Pacific Journal of Ophthalmology • Volume 0, Number 0, Month 2018
This trial was limited by a delayed enrollment (average 24 days)
after initial symptoms. Although the primary endpoint was nega-
tive, there were positive signals that LINGO-1 blockade might be
beneficial.
An additional double-blind, randomized, placebo-controlled,
crossover trial evaluated clemastine fumarate for the treatment of
chronic optic neuropathy.30 Clemastine is a molecule that has been
shown to stimulate differentiation of oligodendrocyte precursor
cells in animal models and in vitro human cell culture. The results
of this trial showed an improvement in optic nerve conduction as-
sessed by the VEP P100 latency. However, patients with a history
of optic neuritis within the past 6 months were excluded, and the
average time elapsed until trial enrollment for patients with a his-
tory of optic neuritis was 4.3 years.30 Future studies are necessary
to further assess efficacy in patients with acute optic neuritis.
Severe and/or Atypical
Optic Neuritis—Does Something More
Sinister Lurk Underneath?
In contrast to patients who present with mild optic neuritis
who had high rates of visual recovery, a significant percentage
of patients presenting with severe vision loss (counting fingers or
light perception only) often have poor visual recovery. Within this
subset of patients in the ONTT, 15% had poor long-term visual
outcomes with high-contrast visual acuity worse than 20/100, and
10% of patients had visual acuity worse than 20/400.5
Several studies have reliably shown that patients with a se-
vere demyelinating syndrome, including optic neuritis, who do
not respond to high dose steroids are likely to benefit from more
potent immunotherapy such as plasma exchange.31–34 These stud-
ies include many patients with non-MS phenotypes (such as re-
current or bilateral optic neuritis related to neuromyelitis optica),
but for the majority the severe optic neuritis is still idiopathic or a
manifestation of MS. Knowing that there is a subset of patients in
whom the long-term recovery can be quite limited, it is critical to
ask whether there is an atypical optic neuritis phenotype that the
clinician must recognize at onset and treat more aggressively to
avoid a poor outcome.
Further investigation since the era of the ONTT has identified
neuromyelitis optica spectrum disorder (NMOSD) as an AQP4
antibody‒associated disorder with distinct pathophysiology, out-
comes, and optimal treatment protocols from MS. In contrast to
patients with idiopathic or MS-related optic neuritis, patients with
NMOSD often have severe, permanent vision loss. Eighty percent
of patients with NMOSD present with severe vision loss (visual
acuity worse than 20/200) and many have poor recovery with se-
vere, permanent deficits. These patients typically show a pattern
of contrast enhancement on magnetic resonance imaging (MRI)
that is greater than half the length of the optic nerve or involves
the optic chiasm. In addition, they lack MRI findings typical for
MS, can have a neutrophilic pleocytosis in the cerebrospinal fluid
(CSF), and do not have oligoclonal bands in the CSF.35 As will
be discussed below, screening for and identifying these patients
early is critical because steroid treatment may not be adequate;
these patients often require more potent immunotherapy such as
plasma exchange and ongoing immunosuppression to achieve op-
timal outcomes.
Screening for atypical or alternative causes of optic neuri-
tis is particularly important in populations with relatively low
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Acute Optic Neuritis Update
prevalence of multiple sclerosis. Although rates of MS have in-
creased in recent years (particularly in Japan), East Asia has the
lowest rates of MS prevalence in the world.36–39 Additionally,
NMOSD seems to have important ethnic variations in its preva-
lence.40 The combination of lower rates of MS and higher rates
of NMOSD leads to a much higher proportion of NMOSD in pa-
tients presenting with demyelinating syndromes including optic
neuritis. For example, NMOSD comprises 39.5% of acquired de-
myelinating disease in Thailand compared with only 1‒2% in the
United States.41
We routinely screen for AQP4 antibodies in patients with
severe vision loss, chiasmal or bilateral involvement, markedly
inflammatory CSF profile, ethnicities in which there is a greater
prevalence of NMOSD, or if there are other clinical features sug-
gestive of NMOSD such as longitudinally extensive transverse
myelitis. In these cases, we often start treatment with high dose
corticosteroids, but if there is high enough pretest probability
for NMOSD in patients with the above features, we commonly
treat with adjuvant plasma exchange at initial presentation before
receiving confirmatory AQP4 antibody laboratory results. A re-
cent retrospective review showed that early, rapid escalation of
therapy from high dose steroids to plasma exchange resulted in
increased rates of recovery for patients with optic neuritis sec-
ondary to NMOSD.42 It is important to identify this population
early both because these patients can be refractory to corticoste-
roid monotherapy and require additional, more aggressive acute
treatment but also because NMOSD can be exacerbated by ad-
ministering particular MS medications such as beta interferons
and natalizumab.35
Many patients with a suspected NMOSD phenotype will
have negative testing for the AQP4 antibody. Recent studies have
shown that up to 20% of these patients will test positive for the
MOG antibody.43 These antibodies are readily identified on cell-
based assay with high sensitivity and specificity.44 The features
of anti-MOG–related optic neuritis are still being characterized,
and there has been some discrepancy in the literature regarding
the clinical phenotype. Initial smaller studies found that these
patients had slightly different characteristics than the overall
NMOSD population, suggesting that they were more likely to be
men, present with bilateral optic neuritis, and have a monophasic
illness with better prognosis.45,46 However, several other studies
have shown that patients with MOG antibodies do not necessar-
ily have a more benign course. Two cohorts out of Germany and
Spain of approximately 50 adult patients with MOG antibodies
and acute demyelinating syndromes demonstrated that adults with
MOG antibodies were likely to have optic neuritis with a recurrent
disease course (71% and 80%) and high rates of NMOSD (25%
and 32%).47,48 It remains unclear whether patients with anti-MOG
antibodies can have a neurological syndrome that resembles MS;
one study found that 25% had lesions on MRI suggestive of MS
whereas another study found these changes in just 2%.47,48 Over-
all, anti-MOG antibody‒related optic neuritis seems to present
with more severe visual loss than either idiopathic or MS-related
optic neuritis. These patients are also possibly at higher risk of re-
lapse.49 The severity of MOG-related optic neuritis can resemble
NMOSD, but the long-term clinical outcome seems to be more
favorable.
Even though there are conflicting data regarding long-term
visual prognosis in patients with optic neuritis associated with
anti-MOG antibodies, some studies have demonstrated objective
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Meltzer and Prasad
markers of more severe injury. A cohort of patients with anti-MOG
antibodies with a history of optic neuritis, with or without an MS-
like illness, showed RNFL thinning on OCT that was more severe
than both patients with a history of idiopathic optic neuritis and
those with a history of AQP4-related optic neuritis.50 These pa-
tients also had high rates of RNFL thinning in eyes without a clini-
cal history of optic neuritis along with high rates of microcystic
macular edema (24%).50 One caveat in this cohort is that patients
with anti-MOG antibodies had higher rates of optic neuritis than
their counterparts. A different study out of Japan saw conflicting
results, with retinal thinning on OCT actually being worse in the
MS and NMO cohorts compared with the anti-MOG cohort.51
We do not yet have any clinical trials evaluating treatment for
these patients. However, clinical observation suggests that these
patients are highly steroid responsive and may require a longer
steroid taper, often with “steroid-sparing” adjuvant immunother-
apy (ie, mycophenolate, azathioprine) after initial treatment.52,53
Thus, we routinely send testing for anti-MOG in patients with se-
vere vision loss or bilateral involvement, as seropositive patients
seem to benefit from a prolonged steroid course but can be spared
the toxicities associated with more potent immunotherapies.
In contrast to adult patients with optic neuritis, children are
more likely to have features that we would call atypical in the
adult population. Vision loss in pediatric optic neuritis is often
more severe; 70% of patients will have a visual acuity of worse
than 20/200 at onset.54,55 In addition, 70% of children under the
age of 10 will have bilateral involvement. However, similar to
adults, almost all patients will have significant improvement in
visual acuity, whereas more sensitive measures such as color
vision and low-contrast vision remain impaired, corresponding
to permanent structural and functional alterations of nerve fiber
thickness on OCT and VEP latency.56,57
The most recent work studying pediatric patients with MOG
antibodies was done by a large multinational cohort in Europe.58
They made several important clinical observations. The preva-
lence of MOG antibodies was quite common, seen in approxi-
mately one third in their cohort of children presenting with acute
demyelinating syndromes. In addition, there were 2 subgroups
of presentation. Younger children, median age of 4.5 years, were
more likely to present with acute disseminated encephalomyelitis
and have transient presence of antibodies. Older children, me-
dian age 8 years, were more likely to be female and have a recur-
rent demyelinating syndrome, including recurrent optic neuritis.
These patients were more likely to have persistently elevated ti-
ters of MOG antibodies.58
Further work in a prospective study showed that standard MS
disease-modifying therapy did not result in clinical improvement
for patients with an acquired demyelinating syndrome associated
with anti-MOG antibodies (including optic neuritis).59 However,
these patients did respond to a host of other immunotherapies,
including azathioprine, rituximab, and IVIg, which seemed to be
the most efficacious.59 This responsiveness to IVIg in particular
stands in contrast to the prior clinical trials showing poor efficacy
in adult optic neuritis.
Optic Neuritis as a Clinically
Isolated Syndrome—When to Start MS
Disease-Modifying Treatment?
Optic neuritis can be idiopathic but is often associated with
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Asia-Pacific Journal of Ophthalmology • Volume 0, Number 0, Month 2018
MS. Worldwide, the incidence of MS is approximately 1‒6 per-
sons per 100,000 per year, and optic neuritis is the presenting fea-
ture in approximately 25% of cases.60–64 The risk of subsequently
converting to clinically definite MS varies for different ethnic
and geographic populations. In Western Europe and the United
States, over half of patients who present with optic neuritis will
have lesions identified on MRI suggestive of MS (borne out in
the ONTT where ultimately 75% of patients were diagnosed with
clinically definite MS within 15 years if they had an abnormal
MRI at presentation). In contrast, in Japan only 14% of patients
with optic neuritis are found to have lesions on MRI suspicious
for MS.5,65 Appropriate initiation of long-term disease-modifying
therapy must account for this ethnic and geographic variation in
trying to calculate risk of developing MS in an individual patient.
The following discussion will focus mostly on the available data
from studies of European and North American populations.
Given that many patients presenting with optic neuritis will
have no future neurological relapses, there is an imperative need
for robust clinical biomarkers at first clinical presentation to help
guide the decision to initiate long-term immunomodulatory treat-
ment. The most robust predictor of possible progression to clini-
cally definite MS remains MRI of the brain and spinal cord. Other
ancillary tests such as the presence of oligoclonal bands in the
CSF have modest predictive value and VEP or OCT may reveal
underlying asymptomatic optic neuropathy, which could also hint
at prior episodes of demyelination.42
To date, there have been 6 randomized controlled trials that
investigated the impact of MS medications on the risk of con-
version from high-risk clinically isolated syndrome (an acute
demyelinating event with lesions on brain MRI typical of MS)
to clinically definite MS. These studies, which used interferons,
glatiramer acetate, and teriflunomide as treatment after an initial
demyelinating event, showed a reduction in developing MS of
28‒45% over the subsequent 2‒3-year follow-up period, reduc-
tion in accrual of lesions detected on brain MRI, and decrease
in brain atrophy.66–72 However, these studies did not demonstrate
any improvement in long-term disability. Nevertheless, starting
treatment early and decreasing the number of early relapses theo-
retically may decrease the severity of the natural history of MS,
and population studies have shown prolongation of disability-free
survival.73,74 Along these lines, several studies have shown that
decreasing lesion burden on MRI delays or prevents secondary
progressive MS and that 75% of patients with an elevated lesion
volume on MRI early in the disease course will advance to an
Expanded Disability Status Scale worse than 6 within 5 years.75,76
Although the lack of clinical trial data definitively showing im-
provement in long-term disability is disheartening, the MS medi-
cations that are considered more potent (ie, natalizumab) have not
been studied at the time of initial presentation with a clinically
isolated syndrome. These treatments could arguably have more
robust results but conversely can have more deleterious adverse
effects.
It is our routine practice to discuss starting an MS medica-
tion with patients presenting with optic neuritis that have an MRI
showing lesions suggesting a high risk of conversion to clini-
cally definite MS; however, this practice is not uniform across
the world. The Optic Neuritis Survey Group demonstrated how
varied practice is among different communities—99% of neu-
rologists in the United States would recommend starting an MS
medication to patients with an abnormal MRI and optic neuritis,
© 2018 Asia-Pacific Academy of Ophthalmology
Asia-Pacific Journal of Ophthalmology • Volume 0, Number 0, Month 2018
whereas only 53% of neurologists would recommend the same
in Thailand. This discrepancy reflects the overall prevalence of
MS in these populations. In addition, some providers recommend
disease-modifying agents for MS in patients with isolated optic
neuritis and a normal brain MRI, although current evidence does
not support this practice.20
Conclusions
To a large degree, the approach to the treatment of optic
neuritis and the decision to use corticosteroids still relies heavily
on results from the ONTT. However, with several new exciting
therapies currently in phase 2 and phase 3 trials, we are hopeful
that we will soon see a more targeted approach to the treatment of
optic neuritis and further improvement in patient outcomes. We
anticipate that treatment options for optic neuritis will continue to
evolve, encompassing immunosuppressive, neuroprotective, and
possibly remyelinative strategies.
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