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Adult Optic Neuritis Clinical Presentation

  • Author: Erhan Ergene, MD; Chief Editor: Edsel Ing, MD, FRCSC  more...
Updated: May 26, 2016


A history of preceding viral illness may be present. Typically, patients with first time acute optic neuritis (ON) are otherwise healthy young adults. Patients with optic neuritis experience rapidly developing impairment of vision in 1 eye or, less commonly, both eyes during an acute attack.[3]

Dyschromatopsia (change in color perception) in the affected eye occasionally may be more prominent than the decreased vision.[4] In nearly all cases, the visual changes are associated with a retro-orbital or ocular pain, usually exacerbated by eye movement. The pain may precede the visual loss.

Patients may complain of vision loss exacerbated by heat or exercise (Uhthoff phenomenon). Objects moving in a straight line may appear to have a curved trajectory (Pulfrich phenomenon), presumably due to asymmetrical conduction between the optic nerves.

Patients with MS may have recurrent attacks of optic neuritis.[5] Therefore, a history of previous episodes of decreased vision in the same or the fellow eye may be elicited. A previous history of neurologic problems, such as transient episodes of extremity/facial numbness or weakness, suggests a diagnosis of MS. A family history of MS may exist.

NMO is characterized by optic neuritis and myelitis in a close temporal relationship.[6, 7, 8, 9] However, optic neuritis can occasionally precede the myelopathy. Some patients with NMO develop relapses limited to the optic nerves and spinal cord.

In patients, especially males with bilateral, sequential optic neuropathy with little recovery of vision, exclude Leber hereditary optic neuropathy (LHON). Patients with LHON may have a history of vision loss in maternal uncles.


Physical Examination

In a typical first-time, acute case of optic neuritis, the general physical examination is normal. Pupillary light reaction is decreased in the affected eye and a relative afferent pupillary defect (RAPD) or Marcus Gunn pupil commonly is found. In bilateral cases, the RAPD may not be apparent.

Measurement of visual acuity reveals varying degrees of reduction in vision, from a mildly decreased visual acuity to complete visual loss. However, visual acuity may be normal, with only a limited, mild visual-field defect. Almost all patients with decreased visual acuity also have abnormal contrast sensitivity and color vision, as revealed by examination using a Pelli-Robson chart and Ishihara color plates, respectively.

Classic dictum states that a central scotoma most commonly is seen in optic neuritis. However, the Optic Neuritis Treatment Trial (ONTT) suggested that altitudinal field defects, arcuate defects, and nasal steps were more common than central scotomas and cecocentral scotomas. Visual field examination typically shows a central scotoma. Peripheral extension of the scotoma in any direction, and even a generalized depression of the entire visual field, may be encountered.

In acute optic neuritis, the fundus appears normal because two thirds of cases of optic neuritis are retrobulbar. With time, the optic nerve may become pale.

One third of patients with optic neuritis have a swollen disc (papillitis). The disc edema of optic neuritis often is diffuse. The presence of segmental changes, altitudinal swelling, pallor, arterial attenuation, and splinter hemorrhages suggest other diagnoses (eg, AION).[39]

If a dilated fundus examination is not performed, retinal problems, such as central serous retinopathy and retinal detachment, may be mistaken for optic neuritis.[40]

Patients with NMO often develop a severe, bilateral form of optic neuritis and myelitis. Bitemporal or junctional visual-field defects, indicating chiasm involvement, may be present. Myelitis may be associated with localized back or radicular pain and Lhermitte's sign (spine or limbs paresthesias elicited by neck flexion) early in the course of the disease. Severe degrees of neurologic deficits, including paraplegia, are usual. Symptoms such as respiratory failure or hiccups may occur when the cervical spinal cord lesions extend into the medulla.

Contributor Information and Disclosures

Erhan Ergene, MD Clinical Assistant Professor, Department of Neurology, University of Illinois College of Medicine at Peoria; Medical Director, Comprehensive Epilepsy Program and Clinical Neurophysiology, Illinois Neurological Institute at OSF Saint Francis Medical Center

Erhan Ergene, MD is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.


Nancy A Machens, APN, CNP Professor of Nursing, Bradley University; Advanced Practice Nurse, Nurse Practitioner, Department of Neurology, Illinois Neurological Institute at OSF Saint Francis Medical Center

Disclosure: Nothing to disclose.

Chief Editor

Edsel Ing, MD, FRCSC Associate Professor, Department of Ophthalmology and Vision Sciences, University of Toronto Faculty of Medicine; Consulting Staff, Hospital for Sick Children and Sunnybrook Hospital

Edsel Ing, MD, FRCSC is a member of the following medical societies: American Academy of Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, American Society of Ophthalmic Plastic and Reconstructive Surgery, Royal College of Physicians and Surgeons of Canada, Canadian Ophthalmological Society, North American Neuro-Ophthalmology Society, Canadian Society of Oculoplastic Surgery, European Society of Ophthalmic Plastic and Reconstructive Surgery, Canadian Medical Association, Ontario Medical Association, Statistical Society of Canada, Chinese Canadian Medical Society

Disclosure: Nothing to disclose.


Edsel Ing, MD, FRCSC Associate Professor, Department of Ophthalmology and Vision Sciences, University of Toronto Faculty of Medicine; Consulting Staff, Toronto East General Hospital, Canada

Edsel Ing, MD, FRCSC is a member of the following medical societies: American Academy of Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, American Society of Ophthalmic Plastic and Reconstructive Surgery, Canadian Ophthalmological Society, North American Neuro-Ophthalmology Society, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD Associate Professor of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Brian R Younge, MD Professor of Ophthalmology, Mayo Clinic School of Medicine

Brian R Younge, MD is a member of the following medical societies: American Medical Association, American Ophthalmological Society, and North American Neuro-Ophthalmology Society

Disclosure: Nothing to disclose.


The authors and editors of Medscape Reference gratefully acknowledge the assistance of Ryan I Huffman, MD, with the literature review and referencing for this article.

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A case of acute optic neuritis. A. 1.5 Tesla, contrast-enhanced spin echo T1-weighted, fat-suppressed coronal MRI through the orbits shows enlargement and contrast enhancement of the left optic nerve in the retrobulbar portion (arrow). B. Coronal spin echo T1-weighted, fat-suppressed MRI of the same patient shows enlargement and contrast enhancement of the nerve in a parasagittal oblique section (arrow).
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