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Differentiating glaucomatous from nonglaucomatous optiic atrophy: Authors’ reply
Letters to the Editor
Differentiating Glaucomatous from Nonglaucomatous Optic Atrophy Dear Editor: In the article by Greenfield et al, “The Cupped Disc: Who Needs Neuroimaging?” (Ophthalmology 1998;105:866 – 74), the authors conclude that the most specific signs of nonglaucomatous optic atrophy were age younger than 50 years, lower levels of visual acuity (less than 20/40), vertically aligned visual field defects, and neuroretinal rim pallor (in excess of cupping). In our practice, we use these same criteria in establishing a rationale for neuroimaging in patients referred to the neuro-ophthalmology service as presumed low-tension glaucoma. In addition, we have used the following criteria as “red flags” for possible nonglaucomatous optic atrophy (with or without underlying glaucomatous optic atrophy): 1. Mismatch between the degree of optic disc cupping and the degree of visual field loss (e.g., 0.5 cup but 10-degree visual field remaining). 2. The presence of an afferent pupillary defect or visual acuity loss out of proportion to the visual field loss or optic disc cupping. 3. Rapid progression of visual loss. 4. Glaucomatous-appearing visual field loss in a patient with an anomalous or hypoplastic optic nerve in which cupping can not be easily judged. Do the authors have any additional data from their work or comment from their experience with these situations? ANDREW G. LEE, MD Houston, Texas Authors’ reply Dear Editor: Dr. Lee points out that in addition to the clinical variables established in our report,1 others may be helpful in the differentiation of glaucomatous and nonglaucomatous optic atrophy. We agree. It is important to note that as a retrospective case-controlled study, the outcome variables reviewed were directed in large part by the available information contained within the medical record. For example, the presence of dyschromatopsia could not be retrospectively recorded, yet we have found this to be a helpful adjunct in the identification of patients with nonglaucomatous optic neuropathy.2 Dr. Lee comments that a mismatch between the degree of disc cupping and visual field loss may serve as a “red flag” for a nonglaucomatous mechanism. As described in our investigation, these eyes are generally not confused with glaucoma. This is precisely why eyes with small optic cups were excluded from our study. More difficult is the decision to perform neuroimaging in eyes with moderate to advanced cupping and visual field loss.
The presence of a relative afferent pupillary defect is a nonspecific finding and has been described in glaucoma.3 It corresponds to the degree of neural damage and is not uncommon in eyes with unilateral or asymmetric disease. Dr. Lee’s observations regarding visual acuity loss are indeed confirmed by our data. The rapidity with which glaucomatous progression occurs is an important point. In a study of 199 glaucomatous subjects with a mean follow-up period of 7 years, Smith and colleagues4 reported that the rate of visual loss across the entire visual field (mean deviation) had a mean slope of ⫺1.25 decibels per year using linear regression. In fact, fewer than one in three subjects progressed by any one of several criteria for progression. Clearly, the period of time necessary to detect progression depends on several factors, including the definition of progression, the technique used to establish progression, the underlying rate of disease progression, the degree of fluctuation of the parameters used to establish progression, and the frequency of examination. We agree with Dr. Lee and wish to emphasize that although exceptions exist, glaucomatous progression is a slow phenomenon. Dr. Lee correctly points out that it may be difficult to correlate an anomalous optic disc with what appears to be a glaucomatous visual field defect. This is frequently encountered in highly myopic eyes with tilted optic disc insertions. In such cases we recommend observation. Stability would be expected in a congenital optic disc anomaly and would thus obviate the need for neuroimaging to exclude an occult compressive lesion. As discussed by Mills,5 consideration to all available clinical information is essential in establishing a rationale for neuroimaging. It is our hope that by elucidating these clinical variables, cost-effective and high-quality healthcare may be provided to patients with optic disc cupping and normal intraocular pressure. DAVID S. GREENFIELD, MD R. MICHAEL SIATKOWSKI, MD JOEL S. GLASER, MD NORMAN J. SCHATZ, MD RICHARD K. PARRISH, II, MD Miami, Florida References 1. Greenfield DS, Siatkowski RM, Glaser JS, et al. The cupped disc. Who needs neuroimaging? Ophthalmology 1998;105: 1866 –74. 2. Kitizawa Y. Unilateral normal-tension glaucoma. J Glaucoma 1997;6:50 –5. 3. Kaback MB, Burde RM, Becker B. Relative afferent pupillary defect in glaucoma. Am J Ophthalmol 1976;81:462– 8. 4. Smith SD, Katz J, Quigley HA. Analysis of progressive change in automated visual fields in glaucoma. Invest Ophthalmol Vis Sci 1996;37:1419 –28. 5. Mills RP. Discussion. Ophthalmology 1998;105:1874. Comment on: Ophthalmology 1998;105:1866 –74.
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Differentiating Glaucomatous from Nonglaucomatous Optic Atrophy Dear Editor: In the article by Greenfield et al, “The Cupped Disc: Who Needs Neuroimaging?” (Ophthalmology 1998;105:866 – 74), the authors conclude that the most specific signs of nonglaucomatous optic atrophy were age younger than 50 years, lower levels of visual acuity (less than 20/40), vertically aligned visual field defects, and neuroretinal rim pallor (in excess of cupping). In our practice, we use these same criteria in establishing a rationale for neuroimaging in patients referred to the neuro-ophthalmology service as presumed low-tension glaucoma. In addition, we have used the following criteria as “red flags” for possible nonglaucomatous optic atrophy (with or without underlying glaucomatous optic atrophy): 1. Mismatch between the degree of optic disc cupping and the degree of visual field loss (e.g., 0.5 cup but 10-degree visual field remaining). 2. The presence of an afferent pupillary defect or visual acuity loss out of proportion to the visual field loss or optic disc cupping. 3. Rapid progression of visual loss. 4. Glaucomatous-appearing visual field loss in a patient with an anomalous or hypoplastic optic nerve in which cupping can not be easily judged. Do the authors have any additional data from their work or comment from their experience with these situations? ANDREW G. LEE, MD Houston, Texas Authors’ reply Dear Editor: Dr. Lee points out that in addition to the clinical variables established in our report,1 others may be helpful in the differentiation of glaucomatous and nonglaucomatous optic atrophy. We agree. It is important to note that as a retrospective case-controlled study, the outcome variables reviewed were directed in large part by the available information contained within the medical record. For example, the presence of dyschromatopsia could not be retrospectively recorded, yet we have found this to be a helpful adjunct in the identification of patients with nonglaucomatous optic neuropathy.2 Dr. Lee comments that a mismatch between the degree of disc cupping and visual field loss may serve as a “red flag” for a nonglaucomatous mechanism. As described in our investigation, these eyes are generally not confused with glaucoma. This is precisely why eyes with small optic cups were excluded from our study. More difficult is the decision to perform neuroimaging in eyes with moderate to advanced cupping and visual field loss.
The presence of a relative afferent pupillary defect is a nonspecific finding and has been described in glaucoma.3 It corresponds to the degree of neural damage and is not uncommon in eyes with unilateral or asymmetric disease. Dr. Lee’s observations regarding visual acuity loss are indeed confirmed by our data. The rapidity with which glaucomatous progression occurs is an important point. In a study of 199 glaucomatous subjects with a mean follow-up period of 7 years, Smith and colleagues4 reported that the rate of visual loss across the entire visual field (mean deviation) had a mean slope of ⫺1.25 decibels per year using linear regression. In fact, fewer than one in three subjects progressed by any one of several criteria for progression. Clearly, the period of time necessary to detect progression depends on several factors, including the definition of progression, the technique used to establish progression, the underlying rate of disease progression, the degree of fluctuation of the parameters used to establish progression, and the frequency of examination. We agree with Dr. Lee and wish to emphasize that although exceptions exist, glaucomatous progression is a slow phenomenon. Dr. Lee correctly points out that it may be difficult to correlate an anomalous optic disc with what appears to be a glaucomatous visual field defect. This is frequently encountered in highly myopic eyes with tilted optic disc insertions. In such cases we recommend observation. Stability would be expected in a congenital optic disc anomaly and would thus obviate the need for neuroimaging to exclude an occult compressive lesion. As discussed by Mills,5 consideration to all available clinical information is essential in establishing a rationale for neuroimaging. It is our hope that by elucidating these clinical variables, cost-effective and high-quality healthcare may be provided to patients with optic disc cupping and normal intraocular pressure. DAVID S. GREENFIELD, MD R. MICHAEL SIATKOWSKI, MD JOEL S. GLASER, MD NORMAN J. SCHATZ, MD RICHARD K. PARRISH, II, MD Miami, Florida References 1. Greenfield DS, Siatkowski RM, Glaser JS, et al. The cupped disc. Who needs neuroimaging? Ophthalmology 1998;105: 1866 –74. 2. Kitizawa Y. Unilateral normal-tension glaucoma. J Glaucoma 1997;6:50 –5. 3. Kaback MB, Burde RM, Becker B. Relative afferent pupillary defect in glaucoma. Am J Ophthalmol 1976;81:462– 8. 4. Smith SD, Katz J, Quigley HA. Analysis of progressive change in automated visual fields in glaucoma. Invest Ophthalmol Vis Sci 1996;37:1419 –28. 5. Mills RP. Discussion. Ophthalmology 1998;105:1874. Comment on: Ophthalmology 1998;105:1866 –74.
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