| OCR Text |
Show Journal of Neuro- Ophlhalmology 19( 4): 235- 237, 1999. © 1999 Lippincott Williams & Wilkins, Inc., Philadelphia Optic Nerve Enhancement on Magnetic Resonance Imaging in Arteritic Ischemic Optic Neuropathy Andrew G. Lee, M. D., Eric R. Eggenberger, D. O., David I. Kaufman, D. O., and Carlos Manrique, M. D. Although optic nerve enhancement may be seen in magnetic resonance imaging of radiation- induced ischemic optic neuropathy, similar enhancement in ischemic optic neuropathy has not been previously reported in the English- language neuro-ophthalmologic literature. We report three cases of optic nerve enhancement in biopsy- proven arteritic ischemic optic neuropathy. Clinicians should consider giant cell arteritis in the differential diagnosis of an optic neuropathy with optic nerve enhancement on magnetic resonance imaging. Key Words: Ischemic optic neuropathy- Optic nerve enhancement. Optic nerve enhancement after the administration of gadolinium contrast material on magnetic resonance imaging is a nonspecific but pathologic finding. Although such enhancement of the optic nerve has been reported previously in neoplastic, inflammatory, radiation-induced, infiltrative, and infectious optic neuropathies, to our knowledge this finding has not been described in non- radiation- induced ischemic optic neuropathy ( 1). We describe three cases of optic nerve enhancement in ischemic optic neuropathy ( ION) caused by biopsy proven giant- cell arteritis ( GCA). CASE REPORTS Case 1 An 82- year- old woman developed acute, bilateral visual loss on awakening on June 1, 1994. She had had a 2- month history of anorexia, scalp tenderness, and jaw claudication. Past medical history was significant for coronary artery disease, myocardial infarction, and diabetes mellitus. Neuro- opthalmic examination on June 8, Manuscript received April 12, 1999; accepted August 24, 1999. From the Departments of Ophthalmology, Neurology, and Neurosurgery, Baylor College of Medicine and the Department of Neurosurgery, The M. D. Anderson Cancer Center, The University of Texas, Houston, Texas, U. S. A. ( A. G. L.); the Michigan State University Center for Clinical Neuroscience and Ophthalmology, East Lansing, Michigan, U. S. A. ( CM., E. R. E., D. I. K.); and the Department of Surgery, Division of Ophthalmology, Texas A & M College of Medicine and the Scott & White Clinic ( CM.), Temple, Texas, U. S. A. Address correspondence to Andrew G. Lee, 6565 Fannin Street, NC- 205, Houston, TX 77030. 1994 revealed a visual acuity of 20/ 400 in the right eye ( OD) and no light perception in the left eye ( OS). Gold-mann kinetic perimetry revealed a residual superotem-poral island to the V4e stimulus OD. Ophthalmoscopy revealed bilateral pallid optic disc edema. Westergren erythrocyte sedimentation rate ( ESR) was elevated at 113 mm/ h. Magnetic resonance ( MR) scan of the head revealed bilateral optic nerve enhancement after the administration of gadolinium- DTPA ( Fig. 1). A temporal artery biopsy demonstrated findings consistent with GCA. The patient was treated with intravenous methyl-prednisolone ( 1,000 mg/ d) followed by oral prednisone tapered slowly. Visual function remained unchanged. Case 2 An 86- year- old woman developed acute, bilateral visual loss on July 24, 1994. Past medical history was significant for diabetes mellitus, coronary artery disease, FIG. 1. Coronal, postgadolinium, T1- weighted fat- suppressed orbital magnetic resonance ( MR) scan ( case 1) reveals enhancement around the optic nerve of the left eye in this image. Right optic nerve enhancement was observed in an adjacent coronal section T1- weighted postcontrast magnetic resonance image ( not shown). 235 236 A. G. LEE ET AL. hypothyroidism, and ischemic cardiomyopathy. She had a 6- week history of fatigue, scalp tenderness, anorexia, and jaw claudication. Neuro- ophthalmologic examination on August 2, 1994 revealed a visual acuity of counting fingers at 1 m OD and no light perception OS. Gold-mann kinetic perimetry revealed a small temporal island to the V4e stimulus OD. Ophthalmoscopy revealed diffuse optic nerve pallor OD and pallid optic disc edema with peripapillary hemorrhage OS. MR scan of the orbit with fat suppression revealed bilateral enhancement of the optic nerves after gadolinium- DTPA. Westergren ESR was 85 mm/ h. A temporal artery biopsy was positive for GCA. The patient was treated with oral steroids and the visual function stabilized. Case 3 An 80- year- old man developed new- onset headaches, scalp tenderness, weight loss, and fatigue during a 3- month period. In January 1999, he developed loss of vision OS and was diagnosed with a nonembolic branch retinal artery occlusion. ESR was 20 mm/ h. A carotid Doppler study showed normal results. In April 1999, 3 months after the visual loss OS, he developed acute painless loss of vision OD. Examination revealed a visual acuity of counting fingers OD and 20/ 20 OS. There was a right relative afferent pupillary defect. Ophthalmoscopy of the OD revealed a normal retina and optic nerve. There was mild superior retinal artery narrowing OS and mild optic atrophy OS. ESR was 95 mm/ hr. MR scan of the head and orbit revealed mild bilateral optic nerve enhancement after gadolinium- DTPA ( Fig. 2). The patient was treated with intravenous methylprednisolone 1,000 mg/ d for 3 days followed by an oral prednisone FIG. 2. Axial, postgadolinium, T1- weighted, fat- suppressed, orbital magnetic resonance scan of case 3 reveals mild enhancement of the optic nerve seen best on the left ( arrow). taper. A right temporal artery biopsy was positive for active GCA. DISCUSSION Ischemic optic neuropathy ( ION) is the most common acute optic neuropathy of older adults. The anterior form of ION ( AION) is characterized by optic disc edema, whereas the posterior or retrobulbar form shows no optic disc edema ( PION). AION may be caused by GCA ( ar-teritic AION) or more commonly, may occur without arteritis ( nonarteritic AION, or NA- AION). Although MR imaging of the head is usually not required in typical AION, imaging should be considered in atypical cases. Atypical features might include bilateral and simultaneous onset optic neuropathy ( case 1), optic atrophy and contralateral optic disc edema ( pseudo- Foster- Kennedy syndrome) ( case 2), or retrobulbar ( PION) optic neuropathy ( case 3). In all three of our cases, MR imaging was performed to exclude other etiologies of a bilateral acute optic neuropathy ( e. g., infiltrative inflammatory, neoplastic etiologies). In all of our cases, MR scan revealed optic nerve enhancement after the administration of gadolinium- DTPA. However, enhancement of the optic nerve on MR scan is not specific. This finding may occur in any process that disrupts the blood- brain barrier, including the following: 1) infiltrative or inflammatory ( e. g., sarcoid, Wegener granulomatosis); 2) demyelinating ( optic neuritis); 3) infectious ( e. g., syphilis); and 4) neoplastic ( e. g., optic nerve meningiomas, gliomas, metastatic lesions, carcinomatous meningitis) optic neuropathies ( 1). Typically, enlargement as well as enhancement occurs in patients with optic nerve tumors. There was no evidence of optic nerve enlargement or optic nerve tumor in any of our cases. Although ischemia caused by radiation necrosis of the optic nerve may show enhancement on MR, we are unaware of any reports in the English- language literature of ION and enhancement of the optic nerve. An MR scan is not generally indicated in typical NA- AION, but a few papers have reported the MR findings in this condition. Arnold et al. ( 2) described MR imaging of the brain in 13 patients with NA- AION and reported an increased number of central nervous system white matter lesions. Although not the primary goal of their article, optic nerve enhancement was not seen in these patients ( personal communication, Anthony Arnold, M. D.). Jay and Williamson performed MR scans on nine patients with NA- AION and reported only white matter ischemic lesions, and no comment was made on optic nerve enhancement ( 3). Jay and Williamson believed that AION might involve microvascular changes that are undetectable with an MR scan ( 3). Although we do not recommend MR imaging for NA- AION, many patients are referred for neuro- ophthalmic evaluation after having already completed an MR scan. We have never encountered a case of optic nerve enhancement in NA-AION. Unfortunately, our work does not answer the question regarding optic nerve enhancement on MR scan J Neuro- Ophthalmol, Vol. 19, No. 4, 1999 OPTIC NERVE ENHANCEMENT ON MRI 237 in NA- AION. To our knowledge, this is the first report of MR imaging enhancement of the optic nerve in arteritic ION. We suspect that the pathophysiology of arteritic ION in our cases is different from NA- AION. The presumed pathophysiology of NA- AION is microvascular ischemia of small posterior ciliary vessels of the anterior optic nerve. The ischemia in arteritic ION in either the anterior or posterior form is presumably caused by a more widespread inflammatory vasculitis involving the posterior optic nerve and choroidal circulation and thus may be more likely to demonstrate enhancement because of blood- brain barrier disruption. Clinicians should be aware that arteritic ION might cause optic nerve enhancement on MR and that NA- AION is less likely in this setting. Acknowledgment: This work was supported in part by an unrestricted grant from Research to Prevent Blindness, Inc., New York, NY and the Baylor Neuro- ophthalmology Academic Fund. REFERENCES 1. Guy J, Mancuso A, Quisling RG, et al. Gadolinium- DTPA enhanced magnetic resonance imaging in optic neuropathies. Ophthalmology 1990; 97: 592- 9. 2. Arnold AC, Hepler RS, Hamilton DR, Lufkin RB. Magnetic resonance imaging of the brain in nonarteritic ischemic optic neuropathy. J Neuroophthalmol I995; 158- 60. 3. Jay WM, Williamson MR. Incidence of subcortical lesions not increased in nonarteritic ischemic optic neuropathy on magnetic resonance imaging. Am J Ophthalmol 1987; 104: 398- 400. J Neuro- Ophthalmol, Vol. 19. No. 4, 1999 |
