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The optic nerve comprises axons that emerge from the retina of the eye and carry visual information to the primary visual nuclei, most of which is relayed to the occipital cortex of the brain to be processed into vision. Inflammation of the optic nerve causes loss of vision usually because of the swelling and destruction of the myelin sheath covering the optic nerve. Direct axonal damage may also play a role in nerve destruction in many cases.
The most common etiology is multiple sclerosis. Up to 50% of patients with MS will develop an episode of optic neuritis, and 20-30% of the time optic neuritis is the presenting sign of MS. The presence of demyelinating white matter lesions on brain MRI at the time of presentation of optic neuritis is the strongest predictor for developing clinically definite MS. Almost half of the patients with optic neuritis have white matter lesions consistent with multiple sclerosis. At five years follow-up, the overall risk of developing MS is 30%, with or without MRI lesions. Patients with a normal MRI still develop MS (16%), but at a lower rate compared to those patients with three or more MRI lesions (51%). From the other perspective, however, almost half (44%) of patients with any demyelinating lesions on MRI at presentation will not have developed MS ten years later.
Some other causes include viral-bacterial infections (e.g. herpes zoster), autoimmune disorders (e.g. lupus), chloramphenicol and the inflammation of vessels (vasculitis) nourishing the optic nerve. Ethambutol, an antitubercular drug, can also cause optic neuritis.
Major symptoms are sudden loss of vision (partial or complete), or sudden blurred or "foggy" vision, and pain on movement of the affected eye. Many patients with optic neuritis may lose some of their color vision in the affected eye, with colors appearing subtly washed out compared to the other eye. A study found that 92.2% of patients experienced pain, which actually preceded the visual loss in 39.5% of cases.
On medical examination the head of the optic nerve can easily be visualised by an ophthalmoscope; however frequently there is no abnormal appearance of the nerve head in optic neuritis, though it may be swollen in some patients. In many cases, only one eye is affected and patients may not be aware of the loss of color vision until the doctor asks them to close or cover the healthy eye.
Optic neuritis typically affects young adults ranging from 18–45 years of age, with a mean age of 30–35 years. There is a strong female predominance. The annual incidence is approximately 5/100,000, with a prevalence estimated to be 115/100,000.
In most cases, visual functions return to near normal within eight to ten weeks, but they may also advance to a complete and permanent state of visual loss. Therefore, systemic intravenous treatment with corticosteroids, which may quicken the healing of the optic nerve, is often recommended, but it does not have a significant effect on the visual acuity at one year, when compared against placebo. Intravenous corticosteroids have also been found to reduce the risk of developing MS in the following two years in those patients who have MRI lesions; but this effect disappears by the third year of follow up.
Paradoxically it has been demonstrated that oral administration of corticosteroids in this situation may lead to more recurrent attacks than in non-treated patients (though oral steroids are generally prescribed after the intravenous course, to wean the patient off the medication). This effect of corticosteroids seems to be limited to optic neuritis and has not been observed in other diseases treated with corticosteroids.
Very occasionally, if there is concomitant increased intracranial pressure the sheath around the optic nerve may be cut to decrease the pressure.
When optic neuritis is associated with MRI lesions suggestive of multiple sclerosis (MS) then general immunosuppressive therapy for MS is most often prescribed (IV methylprednisolone may shorten attacks; initial only oral prednisone may increase relapse rate).