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Show cD 1992 Raven Press, Ltd., New York Jour/ lal of Climeal Nt'uro- ophtlllJlmology 12( 4): 230- 235, 1992. Compression of the Intracranial Optic Nerve Mimicking Unilateral Normal- Pressure Glaucoma Jeffrey W. Kalenak, M. D., Gregory S. Kosmorsky, D. O., and Samuel J. Hassenbusch, M. D. A 66- year- old man developed progressive visual field loss in the inferior arcuate region of the right eye with normal central visual acuity. Intraocular pressures were normal on all but one occasion. The right optic disk showed extensive glaucomalike cupping; the left optic disk was normal. Magnetic resonance imaging revealed a tumor of the right medial sphenoid wing impinging upon the intracranial portion of the right optic nerve. It was resected via a frontotemporal craniotomy. Histopathologic examination revealed a meningothelial meningioma. The visual field and optic disk cupping remained unchanged postoperatively. To our knowledge, this is the first report in which both glaucomalike cupping and visual field loss occurred as the result of a compressive lesion of the anterior visual pathway. Key Words: Optic nerve compression- MeningiomaCupping- Normal pressure glaucoma. From the Departments of Ophthalmology ( J. W. K., G. S. K.), Neurology ( G. S. K.), and Neurological Surgery ( S. J. H.), The Cleveland Clinic Foundation, Cleveland, Ohio, U. S. A. Address correspondence and reprint requests to Dr. Jeffrey W. Kalenak, Department of Ophthalmology/ A31, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195- 5024, U. S. A. The authors have no affiliation with or financial involvement in any organization or entity with a direct financial interest in the subject matter or material discussed in this article. Normal- pressure glaucoma is a disease of uncertain etiology. Cases of normal- pressure glaucoma likely fall into several pathophysiologic categories, including those with substantial systemic vascular disease, pigmentary glaucoma in remission, steroid- induced glaucoma in remission, and others. A unilateral normal- pressure glaucoma evokes an additional list of possibilities, including posttraumatic glaucoma in remission, uveitic glaucoma, glaucomatocyclitic crises, heterochromic iridocyclitis, myopic disk abnormalities, anterior ischemic optic neuropathy, congenital optic nerve anomalies, and compression of the optic nerve ( 1). Glaucomalike cupping of the optic disk has occurred in some patients with compressive lesions of the anterior visual pathway ( 2,3). However, these patients did not have typical glaucomatous visual field loss. Conversely, patients with welldocumented glaucomalike visual field defects have had compressive lesions without simultaneous cupping of the optic disk ( 4-- 7). We describe a man who demonstrated unilateral glaucomalike cupping of the optic disk and progressive glaucomalike visual field defects, caused by a tumor compressing the intracranial optic nerve. CASE REPORT A 66- year- old man sought evaluation for floaters and occasional photopsias of the left eye of 1 year's duration. His past ocular history included moderate myopia. In addition, for 15 years he noted blurred vision upon awakening that would clear within 15 to 20 min and remain clear for the rest of the day. His past medical history included osteoarthritis, a benign tongue lesion, previous chole- 230 MENINGIOMA MIMICKING GLAUCOMA 231 cystectomy, previous removal of an epiglottic lesion, resection of the prostate for benign prostatic hypertrophy, and allergy to radiologic contrast dye. He had no history of severe blood loss or shock. He had previously used a steroid cream for 5 years to treat a dermatitis behind the right ear. At evaluation, he was taking no topical or systemic medicines. He had no family history of glaucoma. Ophthalmic examination revealed a best corrected visual acuity of 20/ 20 in each eye. Manifest refraction in the right eye was - 5.00 + 1.00 axis 90, and in the left eye - 3.00 + 1.00 axis 55. The pupils were normal and equally reactive to light. There was no afferent pupillary defect. External and slit lamp examinations were normal. Applanation pressures were 16 mmHg in each eye. Goldmann visual field examination of the right eye revealed an inferonasal step ( Fig. 1). Goldmann visual field examination of the left eye was normal. Fundus examination revealed a large, deep cup of the right optic disk, with thinning of the neural rim superotemporally and inferotemporally ( Fig. 2). The left optic disk was normal, with a healthy neural rim ( Fig. 3). The vitreous revealed no detachment in either eye; there were no peripheral retinal breaks or traction. Several hours after initial dilation of the pupils, applanation pressures were right eye 24.5 mmHg, and left eye 20.5 mmHg. Two days after the initial examination, applanation pressures were 16 mmHg in each eye. Gonioscopy revealed open angles in each eye, with moderate pigmentation of the trabecular meshwork. Five months later, he returned with no visual complaints. Visual acuity was unchanged. Goldmann FIG. 1. Initial Goldmann visual field shows an inferonasal step, right eye. X indicates inconsistent response. visual field examination of the right eye revealed a slightly more prominent inferonasal step. Applanation pressures were right eye 19 mmHg, and left eye 18 mmHg. Magnetic resonance imaging of the optic nerves was recommended, but the patient declined. Nine months later he returned, complaining of a slight decrease in vision of the right eye and a noticeable constriction of the peripheral vision of the right eye. He also complained of infrequent headaches above his right brow. His visual acuity corrected in the right eye to 20/ 25, and left eye 20/ 20. There was a detectable right afferent pupillary defect. Isochromatic color plate testing revealed no deficiencies in either eye. Goldmann visual field examination of the right eye revealed further progression of the inferonasal step ( Fig. 4). Exophthalmometry showed no proptosis. The optic disks were unchanged. Magnetic resonance imaging revealed a mass lesion of the right lesser sphenoid wing that was compressing the intracranial portion of the right optic nerve ( Fig. 5). 14 months after his initial examination, the patient underwent a right frontotemporal craniotomy and resection of a right medial sphenoid wing tumor that was attached by a pedicle to the anterior clinoid and was easily removed. One month postoperatively, the patient complained of trouble focusing with his right eye. His visual acuity corrected to right eye 20/ 30, and left eye 20/ 20. The Goldmann visual field of the right eye was not substantially changed. The right optic disk appeared unchanged. The visual field and op- Oats. " · 29 · 89 7 mm D1ame18r Pupil 1eli" Neuro- ophthalmol. Vol. 12. No. 4. 1992 232 FIG. 2. Right optic disk shows a deep cup with thinning of the neural rim superotemporally and inferotemporally. J. W. KALENAK ET AL. tic disk of the left eye remained normal. After removal of the tumor, his blurring of vision upon awakening ceased. PATHOLOGIC FINDINGS The specimen was fixed in 10% buffered formaldehyde solution. Gross examination showed a spherical mass measuring 1.5 cm in diameter. The tissue was processed for light microscopy. Sections from paraffin- embedded tissue were stained with hematoxylin and eosin. Histologically, the specimen contained meningothelial cells with typical whorls ( Fig. 6). The tumor cells were uniform, with regular nuclei and frequent nucleoli. The pathologic diagnosis was meningothelial meningioma. DISCUSSION Compressive lesions of the optic nerve have been documented to produce glaucomalike cupping or visual field changes mimicking glaucoma. However, to our knowledge there has been no previous case report documenting the simultaneous presence of typical glaucomalike cupping and glaucomatous visual field changes associated with a mass lesion, and with preservation of normal central visual acuity. The compressive lesion need not be a neoplasm. I Cl", Nellro- op" t" almol, Vol. 12. No. 4, 1992 FIG. 3. Left optic disk is normal. MENINGIOMA MIMICKING GLAUCOMA FIG. 4. Subsequent Goldmann visual field shows progression of the inferonasal step and a new superior paracentral scotoma. right eye. X indicates inconsistent response. 233 Date ' · 291 4 mm Daameter Pupil Isaac Gutman and coworkers ( unpublished data, presented at the International Glaucoma Symposium, Jerusalem, 1991) reported a series of 56 patients with apparently classical signs of normalpressure glaucoma whose computed tomograms demonstrated optic nerve compression by the carotid arteries adjacent to the intracranial opening of the optic canal. A subset of these patients had visual field changes that appeared to respect the vertical midline. Trobe et al. ( 2) reported on 29 eyes of 22 patients who were diagnosed with optic nerve cupping from various lesions. Ten eyes were misdiagnosed as having glaucomatous cupping, when, in fact, FIG. 5. Coronal magnetic resonance image shows a mass lesion of the right lesser sphenoid wing compressing the intracranial portion of the right optic nerve. compressive lesions were responsible for the cupping. They observed that the only significant observer error in their study was the overdiagnosis of glaucoma in eyes with normotensive optic atrophy. Kupersmith and Krohn ( 3) demonstrated pathologic cupping in 16 patients with lesions compressing the anterior visual pathway. All of these patients had intraocular pressures no greater than 22 mmHg. Visual fields demonstrated bitemporal defects in most patients, and none had visual fields typical of glaucoma. The typical visual field defect caused by a compressive lesion is a central or cecocentral scotoma ( 8- 10). However, many types of visual field defects, with and without central scotomas, have been described in association with compressive lesions, such as generalized depression ( 10- 12), altitudinal defects (~ 6), arcuate defects ( 7), temporal defects ( 13,14), nasal scotomas ( 11), and any combination of visual field defects ( 15,16). Glaucoma typically spares central vision, while compressive lesions frequently cause depression of central visual acuity. Our patient's initial visual acuity was 20/ 20 in each eye. At follow- up 9 months later, his vision had diminished slightly to 20/ 25 in the right eye, while maintaining 20/ 20 in the left eye. Rather than having progressive central visual field damage, our patient manifested progressive nasal visual loss, which is characteristic of glaucoma. We initially thought our patient had unilateral normal- pressure glaucoma. The definition of normal- pressure glaucoma includes: ( a) acquired glaucomalike visual field defects in one or both eyes, ( b) acquired glaucomalike disk changes in one or Jeli.. Neuro- ophthalmol, Vol. 12, No. 4, 1992 234 FIG. 6. Histologic section consists of meningothelial cells with whorls typical of meningothelial meningioma. ( Original magnification x200). J. W. KALENAK ET AL. both eyes, ( c) clustering of spontaneous untreated pressures within the statistical normal range in both eyes, and ( d) open angles in both eyes ( 1). In order to diagnose normal- pressure glaucoma, one must exclude entities such as " burned- out" primary open- angle glaucoma, pigmentary glaucoma, steroid- induced glaucoma, posttraumatic glaucoma, quiescent uveitic glaucoma, glaucomatocyclitic crises, myopic disk abnormalities, blood loss or shock, anterior ischemic optic neuropathy, and congenital optic nerve anomalies. The differential diagnosis also includes highpressure glaucoma that is " masked" by certain systemic medications, including beta- blockers ( 17), nitrendipine ( 18) ( a calcium- channel blocking agent), Parlodel ( 19), and others ( 0. Geyer, A. Lowenstein, and M. Lazar, unpublished data, presented as a poster at the International Glaucoma Symposium, Jerusalem, 1991). Our patient demonstrated none of these predisposing conditions. Classically, normal- pressure glaucoma is bilateral. Steroid- induced glaucoma, secondary to our patient's previous use of steroid cream, was considered unlikely because his cupping and visual field loss were unilateral. Furthermore, the visual field loss progressed during a period when he was not using steroid cream. Because of these unusual features, particularly the unilaterality, we felt it was appropriate to exclude a compressive lesion. Although it is remotely possible that two lesions ( meningioma and glaucoma) accounted for the changes in the right eye, we also considered this unlikely because of the lack of matching glaucomatous damage in the left eye. Our approach to the patient with suspected nor- , Clin Ncuro- ophthalmol. Vol. 12. No. 4. 1992 mal- pressure glaucoma is, first, to perform a complete ophthalmic examination, including gonioscopy and visual field testing, in an attempt to exclude evidence of past glaucoma, including pigment dispersion syndrome, uveitis, acute- angle closure, and angle recession. We also obtain a focused history in the form of a questionnaire to identify risk factors thought to be associated with normal- pressure glaucoma ( anemia, severe blood loss, systemic hypotension, steroid use, systemic vascular disease, and a family history of glaucoma). If no evidence of past glaucoma is discovered in this evaluation, then the patient is brought back for a 1- day, hourly applanation pressure measurement ( 8 a. m. to 3 p. m.). A patient taking antiglaucoma medical therapy is asked to discontinue such therapy, and return for hourly pressure testing after an appropriate washout period. The patient in this report could not arrange diurnal pressure testing. If elevated intraocular pressure or another explanation for the findings is not identified, then we suggest that multiplanar, high- resolution imaging of the anterior visual pathway to exclude the presence of a compressive lesion should be considered in a patient presenting an apparent unilateral normal- pressure glaucoma. We do not perform imaging prior to the complete office workup. The use of such imaging in typically bilateral cases of normalpressure glaucoma is not generally indicated in the absence of clinical features suggestive of optic nerve compression. We feel the workup is justified in unilateral cases because the likelihood of compression is greater and because the treatment of glaucoma and compressive lesions is quite differ- MENINGIOMA MIMICKING GLAUCOMA 235 ent. To have treated our patient with medications or surgery to lower his intraocular pressure would have been inappropriate and likely would have allowed the compressive visual loss to progress. REFERENCES 1. 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