CT findings in acute optic neuritis

Radio/. Vol. 8, No. 2, pp. 91-94, 1984 Printed in the U.S.A. All rights reserved

Computerized

CT FINDINGS MICHAEL Department

of Neurology

and Psychiatry

Copyright

0730-4862184 S3.00 + 0.00 ‘j‘ 1984 Pergamon Press Ltd

IN ACUTE OPTIC NEURITIS WALL

and LEON A. WEISBERG

of the Tulane Medical LA 70112, U.S.A.

Center,

1430 Tulane Avenue,

New Orleans.

(Received 26 May 1983; received,for puhlicution 8 November 1983)

Abstract-A patient with unilateral in nerve size with treatment Optic neuritis

optic neuritis is reported.

Optic nerve sheath

with CT evidence of optic nerve enlargement

Visual loss

and reduction

Corticosteroids

INTRODUCTION The diagnosis of optic neuritis of the idiopathic variety or that due to multiple sclerosis is established by characteristic clinical findings and course. These include the following; (1) age of onset between 20 and 50, (2) retroorbital pain which is most severe with eye movement, (3) progressive monocular reduction in visual acuity over about 1 week followed by significant improvement over several months. (4) visual field defect especially involving the central region (central scotoma), (5) impaired direct pupillary light reaction on the involved side, (6) defects in color vision testing [l-4]. Funduscopic examination in optic neuritis in the acute phase is dependent upon whether the inflammatory process involves the anterior portion of the optic nerve i.e. papillitis in which case the optic disc appears swollen and elevated. If the nerve is involved posterior to the globe. funduscopic examination is initially normal. Although there is histopathological evidence of edema and inflammatory cell infiltration of the optic nerve, there is no clinical evidence to support the value of treatment of optic neuritis with corticosteroids in altering the final visual outcome [5]. However, corticosteroids may speed recovery and reduce retroorbital pain. Since tumors simulating optic neuritis may also respond to corticosteroids, diagnostic errors are made if response to steroids is used as a criteria for diagnosis of optic neuritis [Ml. Due to the optic nerve edema, CT may show enlargement of the involved optic nerve. This nerve enlargement may return to normal size with treatment. This case report describes a patient with acute unilateral optic nerve enlargement demonstrated by CT which normalized following treatment with corticosteroids.

CASE

REPORT

A 3 1-yr-old woman developed frontal headaches and right sided orbital pain which was made worse by eye movement. One day later while she was putting on her makeup she noticed that she could not see well in the superior visual field of her right eye. Initial neuro-ophthalmological examination showed that the left eye was normal; however, in the right eye her visual acuity was finger counting at 2 ft and there was a superior altitudinal visual field defect with a central scotoma. There was impaired direct pupillary response to light on the involved side and funduscopic evidence of disc edema. The remainder of the neurological examination was normal. Over the next 6 days, without treatment, there was spontaneous improvement in visual acuity to 20/25, resolution of the superior altitudinal visual field defect, and some resolution of the disc edema. Six days later, (2 weeks after the initial onset) right temporal pain recurred and visual acuity worsened in the right eye to 20/200. Funduscopic examination showed increased disc edema and the superior altitudinal-central scotoma pattern reappeared on visual field testing. The following neurodiagnostic studies were normal-skull radiogram, optic canal polytomography, sinus series, CSF examination including gamma globulin, myelin basic protein, oligoclonal bands, brain stem and somatosensory evoked potentials. These laboratory studies were negative-fasting blood glucose, erythrocyte sedimentation rate, serological tests for syphilis, complete blood count. 91

MI(.HAEI.

92

WAI.I

and lxau

A. WHSREKC,

Fig. 1. Right (readers left) optic nerve shows uniform enlargement throughout its course. The density and ehancement is identical to the left optic nerve. There is no proptosis. The parasellar region and paranasal sinus regions are normal.

Computed tomography of the brain and orbit was performed with 2mm sections through the orbit and parasellar region. The right optic nerve appeared enlarged compared to left; however there was no difference in density or enhancement characteristics. The enlargement was uniform throughout the course of the nerve from the posterior portion of the globe to the optic canal (Fig. 1). Over the subsequent 72 hr, visual acuity worsened to l/200 and further visual field loss occurred. Because of the deterioration in visual function, the patient was treated with prednisone 80 mg daily. Within 48 hr there was improvement in visual acuity, decrease in visual field defect and decreased disc edema. Within 2 weeks, visual acuity had markedly improved; and optic disc examination and visual fields were almost completely normal. The prednisone dosage was rapidly tapered over 2 weeks. A repeat orbital CT after completion of the corticosteroid therapy showed definite reduction in the size of the right optic nerve with no change in density or enhancement characteristics (Fig. 2). Seven months later, visual function has shown no subsequent deterioration and is almost completely normal.

Fig. 2. Repeat

scan shows reduction

in size of the right optic nerve

CT findings in acute optic neuritis

93

DISCUSSION In patients with neuro-ophthalmological findings consistent with acute optic neuritis, neurodiagnostic studies should be performed to rule out mass lesions that can mimic optic neuritis which quickly deteriorate e.g. sphenoid sinus mucocele [9], pituitary tumors with pituitary apoplexy [lo]. Temporal arteritis may simulate acute unilateral visual loss of optic neuritis; however funduscopic findings, temporal artery tenderness and laboratory findings e.g. elevated erythrocytesedimentation rate, should permit differentiation. The patient may be followed closely to the clinical course of optic neuritis. This course is monocular central visual loss, color vision defects and diminished direct pupillary response to light which worsens over about 1 week and then gradually recovers over months. In patients with insidious progressive unilateral optic nerve dysfunction, neurodiagnostic studies to exclude causes of incipient prechiasmal optic nerve compression are definitively indicated. In these cases with slow deterioration in vision the term “chronic optic neuritis” is sometimes used but should be avoided because this type of visual loss is usually caused by an expanding structural lesion [l 11. In acute optic neuritis, there is rapid and sudden impairment in optic nerve function due to edema and inflammatory cell infiltration; therefore the optic nerve is swollen and enlarged. Prior to CT, there was no diagnostic technique which could image optic nerve enlargement in acute optic neuritis. There have been prior reports of enlargement of the optic nerve with increased densities in the entire course of the optic nerve and the densities of the nerve usually appear homogeneous. There is no tapering of the enlarged optic nerve as may be seen in optic nerve gliomas and meningiomas. In optic neuritis there is no abnormal orbital enhancement. There should be reduction in optic nerve during spontaneous remission or following treatment with corticosteroids. It is imperative to document the reduction in size of the enlarged optic nerve with follow-up CT studies. This is because there may be clinical improvement in visual function following treatment with corticosteroids in some patients with optic nerve neoplasms; however it would be unlikely that the neoplastic enlargement of the optic nerve would also be permanently reduced following discontinuation of corticosteroid medication. In our present case, the reduction in optic nerve size was most consistent with optic neuritis despite the atypical biphasic course. In assessing the presence of unilateral optic nerve enlargement, it is imperative that CT scanning technique be meticulous. Even minor degrees of head tilt of asymmetric eye position (horizontal or vertical) may cause scanning through nonhomologous portions of the optic nerve. This may create the false impression of unilateral optic nerve enlargement. Since the optic nerve is approximately 4 min in size, tissue sections which are thicker than 4 mm may not detect small degrees of optic nerve enlargement. We are able to demonstrate optimally the size of the optic nerve with 2 mm axial sections. and this should be supplemented with coronal images of the optic nerve.

REFERENCES I. W. G. Bradley and C. W. M. Whitty, Acute optic neuritis: its clinical features and their relation to prognosis for recovery of vision, J. Neural. Neurosurg. Psychiat. 30, 531-538 (1967). 2. F. B. Walsh and W. F. Hoyt Clinical Neuro-ophthalmology, 3rd edn. Williams & Wilkins, Baltimore, MD (1969). 3. R. M. Burde, Retrobulbar optic neuritis, in Neuro-ophthalmology. Svmposium of the Universitv of Miami and the Bascom Palmer Eye Institute. J. S. baser and J. L. Smith, ids, Vol. I% Mosby, St. Louis, MO (1976). 4. E. Nikoskelainen and P. Riekkinen, Retrospective study of 117 patients with optic neuritis, Acta ophthal., suppl (Kbh) 123, 202-208 (1974). 5. A. N. Bowden, P. M. A. Bowden, A. I. Friedman et al., A trial of corticotrophin gelatin injection in acute optic neuritis, J. Neurol. Neurosurg. Psychiat. 37, 869-873 (1974). 6. R. C. Senehck and H. J. L. Van Dyk, Chromophobe adenoma masquerading as corticosteroid-responsive optic neuritis Am. J. Ophthal. 78, 485-488 (1974). 7. J. S. Kennerdall, P. J. Janetta and B. L. Johnson, A steroid-sensitive solitary intracranial plamacytoma. Archs Ophrhal. 92, 393-398 (1974). 8. H. Mohan and D. K. Sen, Br. J. Ophthal. 54, 206-207 (1970). 9. W. J. McCarthy Jr, M. Fronkel M. and B. J. Busse, Am. J. Ophthal. 74, 1134 (1972). 10. N. J. David, F. P. Gargano and J. S. Glaser, In Neuro-ophthalmology, Miami Symposium J. S. Glaser and J. L. Smith, Eds, pp. 14C-164. Mosby, St. Louis, MO (1975). II. C. L. Knight, W. F. Hoyt and C. B. Wilson, Syndrome of incipient prechiasmal optic nerve compression. Archs Ophrhal. 87, l-10 (1972). 12. U. Salvolini, E. A. Cabanis, A. Rodalec et al.. Computed tomography of the optic nerve: Part 1. Normal results, J. Compur. assist. Tomogr. 2, 241.-249 (1978).

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LEON A. WFXEKG

13. E. A. Cabanis, U. Salvolmt. A. Rodalec c/ (I/., Computed tomography of the optic nerve. Part II. SIX and shape modifications in papilledema. J. Conrpu/. (~J.\~,sI.Tomogr. 2, 250-255 (1978). 14. C. W. Howard, R. H. Osher and R. C. Tomasak. Computed tomographic features in optic neurttis. Anr. ./. Ophrhal. 89, 699.-702 (1980). WALL, M.D. is an Assistant Professor of Neurology in the Department of Neurology and Psychiatry of Tulane School of Medicine. He is a graduate of Tulane School of Medicine and completed his neurology residency at the Washington University School of Medicine, St. Louis. Missouri.

About the Author-h&HAEL

the Author-LEON A. WEISBERG, M.D. graudated from Columbia Medical Center in 1968 and completed his neurology residency at the Neurological Institute of the Columbia-Presbyterian Medical Center in New York. He is the Director of Neurology at the Charity Hospital of New Orleans and the Tulane Medical Center and Professor of Neurology. He has authored Clinical Computed Tomography: A Text Atlas and Computerized Tomography of the Orbit and Sellu Turcica. About