Optic Neuritis



About half of MS patients present with optic neuritis (ON) as a clinically isolated syndrome (CIS). It is still difficult to predict which CIS patients will go on to develop clinically definite multiple sclerosis (CDMS) and which will have a benign course.

More advanced methods of detecting and quantifying ON in multiple sclerosis (MS) have been developed in the past 15 years, especially on recent developments in optical coherence tomography measurement of the retinal nerve fiber layer (RNFL) and its role in monitoring axonal loss in the course of the disease. New clinical trial methods of measuring visual acuity include high-contrast visual acuity testing with the Early Treatment Diabetic Retinopathy Study charts, low-contrast letter acuity, and contrast sensitivity testing. More advanced neuroimaging techniques include magnetization transfer imaging and diffusion tensor imaging to quantify visual pathway lesions. Other tests of visual function, such as multifocal visual evoked potentials (mVEP) and functional MRI, have been shown to be more sensitive than conventional VEP or MRI in detecting early, subtle visual impairment in ON and early recovery of visual function related to cortical plasticity. In addition to the beta-interferons for CIS, newer agents are currently being investigated in ongoing clinical trials. In the future, CIS patients may be stratified according to their risk of development of CDMS and therefore, receive the appropriate treatment.

Another disorder that mimics MS is neuromyelitis optica (NMO), which is typically characterized as ON and transverse myelitis. Either can present months to years apart or simultaneously. Unlike ON in MS where the maculopapillar bundles are selectively injured, NMO is a vascular-mediated optic neuropathy that can cause injury to the arcuate fibers of the RNFL. At least 60 % of NMO patients accumulate nonspecific white matter lesions over time and up to 10 % meet the radiological criteria for the diagnosis of MS. Brain MRI lesions do not exclude the diagnosis of NMO. The course of NMO involves stepwise accumulation of disability because of poor recovery with each relapse. Treatment includes corticosteroids and steroid-sparing agents, such as azathioprine and mycophenolate mofetil. For treatment-resistant NMO, rituximab has been shown to be effective.

Other etiologies of ON include paraneoplastic optic neuropathy, polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes syndrome and autoimmune-related retinopathy and optic neuropathy syndrome.


Multiple Sclerosis Optical Coherence Tomography Expand Disability Status Scale Retinal Nerve Fiber Layer Optic Neuritis 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


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© Springer Science+Business Media New York 2014

Authors and Affiliations

  1. 1.Department of Neurology, Neuro-OphthalmologyUniversity of Nevada School of MedicineRenoUSA

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