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Show lou mal or Cllllleal Nellru- ol, htiwl", oloXY 12( 4): 236- 237, 1992. Editorial Comment © 1992 Raven Press, Ltd., New York Compression of the Intracranial Optic Nerve Mimicking Unilateral Normal- Pressure Glaucoma The article by Kalenak, Kosmorsky, and Hassenbusch provoked some interesting discussion by editorial board reviewers that prompted this editorial comment. The first reviewer, a " heavy hitter" neuro- ophthalmologist, commented: " The authors report a case in which a 66- year- old man developed progressive visual loss in the right eye associated with central vision that was normal and an optic disk appearance that suggested glaucoma. The patient was found to have a right sphenoid wing meningioma. The patient had no change in vision postoperatively. There are several bothersome aspects of this case. First, the authors contend that there was no afferent pupillary defect. I cannot accept that any unilateral optic neuropathy, glaucomatous or otherwise, fails to produce an afferent pupillary defect. Second, the patient never underwent measurement of diurnal curves or measurement of pressures at different times of the day to determine if, in fact, he had glaucoma, Finally, and most importantly, I do not believe that the illustration of the right optic disk ( Fig. 2) shows glaucomatous cupping. In fact, the remaining neuroretinal rim nasally appears pale and the nerve fiber layer is diminished compared with the nerve fiber layer of the left disk ( Fig. 3). Thus, by the criteria set forth by Trobe et al. ( 1980) [ authors' ref. 2] this is not glaucomatous cupping...." Because of the serious objections of this reviewer, the paper was then submitted to an eminent glaucoma expert, who also made some pertinent comments as follows: " The authors present an instructive case in which a compressive lesion thoroughly mimicked normal tension glaucoma. The patient exhibited vertical oval cupping, corresponding and progressive visual field changes, and initially no decrease in central acuity. However, the patient had the additional symptom of 236 blurred vIsion upon awakening, present for 15 years, likely due in retrospect to the compression lesion as the symptom cleared after neurosurgery. Despite the rarity of their case, the authors recommend neuroimaging for all cases of normal tension glaucoma with unilateral presentation. They had not obtained an MRI until the condition progressed, but evidently on the basis of this experience suggest earlier complete evaluation. While such a recommendation might benefit the very rare patient such as this one, it is probably / lot a sound recommendation when considered in context. Based upon epidemiologic studies such as the Baltimore Eye Study, it can be estimated that 50% of the two million cases of glaucoma in this country show initial damage in one or both eyes at tensions under 22 mm Hg, If half of these cases were discovered in a unilateral state, 500,000 unnecessary MRI scans would be performed at a cost of over $ 1,000 apiece, resulting in an expense of one- half billion dollars. On the other hand, if neuroimaging is delayed until the central acuity is affected, as in this case, no important overall functional impairment will be likely to occur ( e. g., when he sees 20/ 20 and 20/ 30 and has a minor field defect in one eye only), and the expenditure of health- care dollars will be more appropriate. Actually, in this case the report of blurred vision in the morning was also a reason to consider an MRI and helps to distinguish this case from the usual case of normal tension glaucoma." On the basis of this review, the authors were asked to submit a revision of their paper, and that revised version is now published in this issue of The Journal. I believe that the issue of differentiating normal- pressure glaucoma from neurologic lesions involving the anterior visual pathways is of sufficient frequency in practice to warrant publish- EDITORIAL COMMENT 237 ing this paper and the editorial comments. It is interesting to note that a neuro- ophthalmologist considered that the disks did not represent glaucoma in this case ( and that reviewer was subsequently proven to be correct in this particular patient) but that a glaucoma specialist stated that the disk changes " thoroughly mimicked normaltension glaucoma." A final point that I should like to add is that the patient presented with a lower nasal arcuate defect in the peripheral field of right eye. I have always found it helpful to remember the famous peripheral field defect of " Roenne's upper nasal step" in glaucoma. It helps to remember that common things are common and rare things are rare. The commonest cause of a big temporal field defect is chiasmal compression. The commonest cause of a big nasal field defect is optic nerve involvement. The commonest causes of lower nasal field defects are ischemic optic neuropathy, optic disk drusen, and neglected chronic papilledema. The commonest cause of an upper nasal field defect is glaucoma. I am not saying that one cannot get a lower nasal arcuate defect in glaucoma; however, upper nasal Roenne's steps are certainly more common in glaucoma, and when I encounter the lower nasal arcuates, I like to take a second thought and a second look. Many thanks to the authors and to the reviewers for this interesting paper and it is hoped that their comments and workup and these suggestions will help you, dear reader, when you next try to resolve this differential diagnosis. J. L. Smith, M. D. Editor Miami, Florida JClin Neuro- ophthalmol, Vol. 12, No. 4, 1992 |
