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Spontaneous Resolution of Optic Perineuritis

Tung, Cynthia MD; Hashemi, Nafiseh MD; Lee, Andrew G. MD

Journal of Neuro-Ophthalmology: March 2013 - Volume 33 - Issue 1 - p 93–95
doi: 10.1097/WNO.0b013e31827a3e31
Letter to the Editor

Department of Ophthalmology, The University of Texas Medical Branch, Galveston, TexasDepartment of Ophthalmology, The Methodist Hospital, Houston, Texas

Department of Ophthalmology, The Methodist Hospital, Houston, Texas

Department of Ophthalmology, The University of Texas Medical Branch, Galveston, Texas, Department of Ophthalmology, The Methodist Hospital, Houston, Texas, Baylor College of Medicine, Houston, Texas, Departments of Ophthalmology, Neurology, and Neurosurgery, Weill Cornell Medical College, New York, New York, Department of Ophthalmology, The University of Iowa Hospitals and Clinics, Iowa City, Iowa, aglee@tmhs.org

Supported in part by an unrestricted grant from Research to Prevent Blindness (RPB) to the University of Texas Medical Branch, Galveston, Texas.

The authors report no conflicts of interest.

Optic perineuritis (OPN) is a clinical entity characterized by painful visual loss and a distinctive neuroimaging sign of optic nerve sheath enhancement (1). It may be a manifestation of a systemic disease as recently reported by McClelland et al (2). OPN may be severe and recurrent and typically requires treatment with systemic corticosteroids. While steroids are thought to be essential in the management of OPN, we recently evaluated a patient with OPN, which resolved completely without treatment.

A 60-year-old African American woman reported a 2-week history of visual loss, severe pain around both eyes, and headache worsened when lying down. She denied nausea, vomiting, photophobia, sonophobia, pulsatile tinnitus, or diplopia. Medical history was significant for well-controlled hypertension and glucose intolerance. Surgical history included cholecystectomy, appendectomy, and hysterectomy. She took only multivitamins, calcium, and omega-3. She denied use of tobacco, alcohol, or recreational drugs.

Visual acuity was 20/25 in both eyes. Examination of the pupils, extraocular movements, and anterior segments was normal. Automated perimetry showed a superior arcuate defect in the right eye, while the left visual field showed generalized depression. Ophthalmoscopy revealed swelling of the right optic disc and a normal left optic disc (Fig. 1).

Orbital magnetic resonance imaging (MRI) demonstrated thin uniform concentric enhancement along the sheath of both optic nerves (Fig. 2). Serum angiotensin-converting enzyme, syphilis serology, and lysozyme measurements were within normal limits as was a chest x-ray. The patient declined a lumbar puncture and a course of systemic corticosteroids.

Six weeks later, without any treatment, her eye pain resolved. Subsequently, her visual fields became normal and she developed mild, bilateral optic disc pallor. Follow-up MRI showed near complete resolution of the bilateral peripheral optic nerve enhancement.

Evaluation of patients with OPN may lead to a specific etiology, but, at times, the cause of the optic neuropathy remains unknown. Documented causes include Wegener granulomatosis (3), sarcoidosis (4), syphilis (5,6), and inflammatory bowel disease (2). Short of comprehensive ophthalmic and systemic evaluations, there is no way to distinguish cases of OPN due to a systemic disorder from those that are idiopathic.

It has been proposed that failure to treat OPN patients with corticosteroids will result in a poor visual outcome (1). Yet, our case suggests that there is a spectrum of severity in OPN, and some patients may experience spontaneous resolution of their optic neuropathy and retain good visual acuity.

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REFERENCES

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© 2013 by North American Neuro-Ophthalmology Society