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Optic neuritis

Optic neuritis is an inflammation of the optic nerve. As optic neuritis affects the ability to see, it is most frequently called an ophthalmology problem. Indeed, when an optic nerve is involved, it is almost always a symptom of the systemic disease. Optic neuritis can be most often seen as a complication of a multiple sclerosis. An eye doctor needs to get involved to manage the vision and inflammation of the optic disc. A neuro-ophthalmologist is a specialist who treats optic neuritis. The main symptom is sudden vision loss and pain in one eye that is worse with eye movement.

In this article:


What is the treatment for optic neuritis?

The main purpose of treatment is to rapidly reduce inflammation, which will preserve vision. Administration of high doses of corticosteroids is the standard treatment for acute optic neuritis. Studies in patients with relapsing MS or optic neuritis have demonstrated that doses of corticosteroid equivalent to 1gm methylprednisolone, administered intravenously or orally, provides an equivalent therapeutic effect of accelerated recovery. 

Adrenocorticotropic hormone (ACTH) is also approved for the treatment of acute optic neuritis and provides an alternative option for enhancing corticosteroid signaling. 

Lower doses of oral prednisone (1 mg/kg/d or less) should be avoided in cases of idiopathic optic neuritis as an increased risk of relapse exists. Chronic treatment with low-dose oral prednisone, however, is important for the treatment of sarcoid optic neuritis and recurrent optic neuritis due to chronic relapsing inflammatory optic neuropathy. 

If infection is prominent in the differential diagnosis of a patient with optic neuritis, it is appropriate to begin appropriate antibiotic therapy as soon as possible. Symptomatic therapy with corticosteroids may be started. Antibiotic or antiviral therapies may be tailored or discontinued based on diagnostic imaging, serology, cultures, or CSF analysis. For optic neuritis associated with Bartonella infection, the utility of antibiotic therapy remains unclear; however, significant vision loss, systemic infection, and immunocompromised status should bolster consideration for antibiotics. 

Immunomodulatory agents such as interferon β-1a (Avonex (Biogen Idec, Research Triangle Park, NC, USA), Rebif (EMD Serono, Inc., Rockland, MA, USA)), interferon β-1b (Betaseron, Bayer, Emeryville, CA, USA) and glatirimer acetate (Copaxone, Teva, Petach Tikva, Israel) have been referred to as ‘disease-modifying agents’ because of their role in increasing the time to onset of the second episode, and the frequency of subsequent MS relapses and demyelinating lesions, whether clinical or radiologically defined.

No controlled trials have yet addressed the question what to do next if visual acuity fails to improve. The treatment options in such cases are documented by nothing more than individual case studies and small case series. In most cases of persistently poor visual acuity, the treatment that was given initially is given a second time, sometimes in a double dose and/or for a longer duration. The last option for acute treatment is plasmapheresis, which is sometimes very effective 

No current treatment can restore the function of a damaged optic nerve. In a phase 2 trial, an antibody against LINGO (leucine-rich repeat and Ig domain containing 1, a protein inhibitor of axonal growth) was found to shorten the latency of visual evoked potentials; this may reflect optic nerve regeneration. The results of another phase 2 trial of anti-LINGO-1 are expected in 2016 (the SYNERGY trial, NCT 01864148). Pilot trials have shown benefit from erythropoietin and simvastatin. A prospective controlled trial of erythropoietin is in progress (NCT01962571www.tone-studie.de).


Complications

After ON resolves the disc often develops optic atrophy most commonly in the temporal aspect. Additional clinical findings of residual decreased subjective relative light intensity; contrast loss and dyschromatopsia; exercise- or heat-induced exacerbation of visual symptoms (Uhthoff phenomenon) can be seen.

Permanent vision loss can follow untreated or missed optic neuritis.


What is the prognosis for optic neuritis?

In most cases, visual recovery will occur spontaneously. But intravenous steroids can speed the rate of recovery. There is an association of optic neuritis with multiple sclerosis (MS), when optic neuritis can be actually the first sign of the disease. MRI imaging provides important prognostic information for MS. 


References

The Diagnosis and Treatment of OpticNeuritis. Wilhelm H, Schabet M.Dtsch Arztebl Int. 2015 Sep 11;112(37):616-25; quiz 626. doi: 10.3238/arztebl.2015.0616.PMID: 26396053 Free PMC article. Review.

Optic Neuritis. Bennett JL.Continuum (Minneap Minn). 2019 Oct;25(5):1236-1264. doi: 10.1212/CON.0000000000000768.PMID: 31584536 Free PMC article. Review.

Beck RW, Cleary PA, Anderson MM, et al. A randomized, controlled trial of corticosteroids in the treatment of acute optic neuritis. The Optic Neuritis Study Group. N Engl J Med 1992;326(9): 581–588. doi:10.1056/NEJM199202273260901. [PubMed] [CrossRef] [Google Scholar]

2. Jarius S, Paul F, Aktas O, et al. MOG encephalomyelitis: international recommendations on diagnosis and antibody testing. J Neuroinflammation 2018;15(1):134. doi:10.1186/s12974-018-1144-2. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

3. Jurynczyk M, Messina S, Woodhall MR, et al. Clinical presentation and prognosis in MOG-antibody disease: a UK study. Brain 2017;140(12): 3128–3138. doi:10.1093/brain/awx276. [PubMed] [CrossRef] [Google Scholar]

4. Ramanathan S, Prelog K, Barnes EH, et al. Radiological differentiation of optic neuritis with myelin oligodendrocyte glycoprotein antibodies, aquaporin-4 antibodies, and multiple sclerosis. Mult Scler 2016;22(4):470–482. doi:10.1177/1352458515593406. [PubMed] [CrossRef] [Google Scholar]

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