Posterior
Subcapsular Cataracts
To the Editor.\p=m-\Thearticle on "Posterior Subcapsular Cataracts: Histopathologic Study of Steroid-Associated Cataracts" by Greiner and
Chylack (Archives 97:135-144, 1979)
raises an interesting question. The authors assume that all of the posterior subcapsular cataracts occurring in their patients who were not receiving steroids were "senile" posterior subcapsular cataracts. But the ages of these "senile" patients were 42, 47, 53, 55, and 63 years. It seems to me that the term "senile" is being used to describe cataracts not otherwise accounted for. We all do this. On the other hand, posterior subcapsular cataracts are often associated with other metabolic disturbances. I assume that such metabolic problems were looked for in these other five patients and not found. Statistically, however, one or more of these patients should be found on careful investigation to be an alcoholic.1,2 This history is not always easily obtained, especially if
specifically requested. Looking for differences
not
between
steroid-induced and other posterior subcapsular cataracts, some of which may also be metabolic in origin, is an obviously difficult task, as illustrated by this article. Robert C. Drews, MD Clayton, Mo 1. Drews RC: Ethanol cataract, in XXI Concilium Ophthalmologicum Mexico, 1970, Acta, Amsterdam, Excerpta Medica, 1971, pp 753-758. 2. Sabiston DW: Cataracts, Dupuytren's contracture and alcohol addiction. Am J Ophthalmol 76:1005-1007, 1973.
Pseudopapilledema To the Editor.\p=m-\TheJanuary issue of
the Archives (97:65-75, 1979) contains two articles concerning pseudopapil-
ledema. Both articles refer to a case of optic nerve drusen with associated visual loss reported by Kamin et al in the Archives (89:359-362, 1973). Dr Rosenberg and his colleagues question the visible hyaline bodies as the cause for vision loss in the case of Kamin etal.
The patient described in 1973 has been followed up to his present age of 25 years. His vision has declined steadily to a current level of counting fingers in either eye in association with increasing prominence of the hyaline bodies and increasing generalized optic atrophy. Nothing in the course of the patient's condition nor in extensive investigations supports a diagnosis of multiple sclerosis or any process other than that of the hyaline bodies to account for the vision loss. The reiteration of caution in too readily attributing vision loss to drusen of the optic nerve head, as emphasized by Dr Rosenberg and his asso¬ ciates, is well taken. However, there are patients whose drusen alone appear to generate progressive vision loss. To deny this possibility is to ignore the experiences of practicing ophthalmologists, and to subject at least a few patients to continued, and unrewarding, unpleasant searches for additional disease that isn't there. Robert S. Hepler, MD In
Los Angeles Reply.\p=m-\Weagree with Dr
Hepler
that on extremely rare occasions "there are patients whose drusen alone appear to generate progressive vision loss." There are also patients who lose vision from acquired optic nerve diseases who happen to have drusen in the nerve head. That the patient described by Kamin et al now has a counting fingers level of vision and that the hyaline bodies are more prominent does not categorically infer cause and effect. With both demyelinative optic neuritis and Leber's hereditary optic atrophy, vision may improve,
fluctuate,
or worsen.
Fortunately, with the advent of modern neuroradiologic techniques, including polytomography of bones and computerized axial tomography
of bones and soft tissues, the clinical dilemma of whether nerve head drusen are the cause of central visual loss may usually be resolved. Given the nearly inviolate rule that optic nerve drusen do not cause loss of acuity (without macular hemorrhage), we would not hesitate to subject those
Downloaded From: http://archopht.jamanetwork.com/ by a University of Manitoba User on 06/16/2015
"few patients" to radiologic procedures that may potentially save vision or life. It is only through a diligent search for potentially treatable mass lesions that we may distinguish acuity loss directly related to disc drusen. I am sure Dr Hepler would agree, and we are delighted to again have the opportunity to restate this admonition. Michael Rosenberg, MD
Chicago Peter
Savino, MD
Philadelphia
Joel Glaser, MD Miami Monofixational Intermittent
Exotropia To the Editor.\p=m-\Weread with interest the report on "Monofixational Intermittent Exotropia" in the January Archives (97:93-95, 1979) by Baker and Davies and can confirm their observations. We, too, have cared for a number of patients with intermittent exotropia who had, in fact, an ultra\x=req-\ small-angle monofixational exotropia when their eyes were "straight," and who maintained the same level of sensory binocular cooperation after surgical correction of the exotropia. We question, however, the prevalence of monofixation syndrome that Baker and Davies found in one third of their patients. They noted this frequency to be higher than expected according to Parks.1 Diagnosing monofixation syndrome in children solely on the basis of Titmus stereo test stereoacuity is difficult, since performance on this test is age related and variable.2 Using this test, a stereoacuity of 60 s of arc is found in only 50% of normal children at the age 4\m=1/2\years, and not until 7 years old may one expect all normal children to obtain 60 s of arc. Therefore, the Titmus stereo test cannot be used all by itself, as these authors have used it, to define the presence of monofixation syndrome below the age of 7 years. It would be of interest to know, if the authors' data on stereoacuity were corrected for this age factor, whether the prevalence of monofixation syn-
drome would be as high as it appears to be in their group of patients. Their supporting source1 for a high inci¬ dence of monofixation syndrome in exotropia similarly defined the monofixation syndrome solely by the Titmus stereo test without correction for patient age. Paul E. Romano, MD Judith A. Romano, CO James E. Puklin, MD
Chicago
1. Parks MM: The monofixation syndrome. Trans Am Ophthalmol Soc 67:609-657, 1969. 2. Romano PE, Romano JA, Puklin JE: Stereoacuity development in children with normal binocular single vision. Am J Ophthalmol 79:966\x=req-\ 971, 1975. 3. Boyd TAS, Budd GE: Monofixation exotropia and asthenopia, in Moore S (ed): Orthoptics: Past, Present, Future. New York, Stratton Intercontinental Medical Book Corp, 1976, pp 173\x=req-\ 177.
In
Reply.\p=m-\Iappreciated reading
the comments of Dr Paul E. Romano et al regarding our article. Some of their thoughts were similarly raised by us during the course of our study. Monofixation occurring in one third of patients with intermittent exotropia seemed at first a surprisingly high incidence to us also. We subsequently reviewed retrospectively all patients with intermittent exotropia operated on during the three years of the study from our private practice. Those with anisometropia and amblyopia greater than one Snellen chart line were eliminated. Twenty-seven individuals were too young at the conclusion of the study to give accurate reproducible stereopsis test results and were also dropped. This left 99 patients operated on during the three years of the study with reproducible stereopsis test results obtainable at the end of the study period. These patients were not included in the published study groups since their preoperative stereopsis testing was unreliable. Of this larger group, 28, or 28%, had monofixation stereopsis test results. The approximately 30% incidence of monofixation in this larger group of patients with intermittent exotropia we believe helps support the similar findings seen in the smaller study group reported. The age at which stereopsis devel¬ ops and is testable has been of interest to many investigators, including Dr Romano.1"4 Test results vary depen¬ dent on several factors, not the least of which is the socioeconomic, cultural, and educational environment of the population tested. In my private prac¬ tice, a large percentage of the children are from homes providing good educa¬ tional stimuli and many have had
preschool experience
at the ages of 3 4 years. In this nonclinical popula¬ tion, there are several children with reproducible Titmus stereopsis of 40 to 50 s of arc measured before the age of 4 years. By 5 years, 80% measure better than 60 s and this number increases to 95% at 6 years. At the conclusion of our study, no children were under the age of 5 years and most were 6 years of age or older. Therefore, with 90% to 95% of this group expected to have good stereop¬ sis in the absence of amblyopia, anisometropia, and other conditions, adjustment was made for their stereo or
testing.
I thank Dr Romano and his asso¬ ciates for their comments and hope that the above explanations will be of interest. John D. Baker, MD Detroit 1. Scott WE, Marsh J: Stereoacuity in normal individuals. Ann Ophthalmol 6:99-101, 1974. 2. Jani SN: The age factor in stereopsis screening. Am J Optom 43:653-657, 1966. 3. Amigo G: Pre-school vision study. Br J Ophthalmol 57:125-132, 1973. 4. Tatsumi S, Tahira K: Study on the stereotest (Titmus). Folia Ophthalmol Jpn 23:620, 1972.
Takata Interferometric Device To the Editor.\p=m-\Notlong ago, my colleagues and I published a brief article in the Archives describing the use of the Takata Interferometric Acuity Meter in early detection of possible demyelinating disease. The article
described the use of a Takata Interferometric Device for this purpose
(Archives 97:76-78, 1979).
There is no question about the validof our findings; rather, we have discovered that the particular Takata instrument available to us was improperly wired and literally put out a far more intense beam than the instrument is rated to provide. Since then, that instrument has failed and in making repairs we have discovered the fault. At issue was the fact that it had been wired for a voltage system different than that in use in the United States. As this was the first unit delivered to this country, this is a reasonable error. At any rate, the issue is that our success in revealing the early changes in possible demyelinating diseases and/or optic neuritis and others in part revolved about the use of a very intense stimuli. The instrument at that time emitted up to about 100,000 trolands of red light. Standard models are rated to provide much less light. It is my guess that if
ity
someone
specifically purchased
this
Downloaded From: http://archopht.jamanetwork.com/ by a University of Manitoba User on 06/16/2015
instrument for this particular purpose our findings could not be replicated, because clearly the instrument ob¬ tained would not be identical. Howev¬ er, some effects would be recorded. Those effects clearly would be lesser than those we described. One of us, Emilio C. Campos, MD, writes that his instrument (same model) does provide somewhat comparable data. We are modifying our available instrument to provide enhanced light. I have also suggested to Mr Takata that he make an enhanced light source a purchase option of his instrument. Jay M. Enoch, PhD Gainesville, Fla Ocular
Injuries From Exploding Beverage Bottles To the Editor.\p=m-\Ipublished, with
some
associates, an article in Harefuah (95:69, 1978) describing 24 patients
were hospitalized during the years 1975 through 1977 because of ocular injuries from exploding beverage bottles as described by Mondino et al in the November issue of the Archives (96:2040-2041, 1978). The cork of the bottle produced 80% of the injuries and glass fragments caused the other 20%. Nearly 25% of the injured eyes became blind and another 13% lost a considerable amount of vision. We found that the main cause of the explosion is the high pressure within the bottle (we measured in a 1-L bottle a pressure of 8 atm). This pressure increases when the bottles are in hot outside temperatures and with agitation and transportation of the bottles. Because of our findings, the factories in Israel changed the bottle cap to a soft ring. Hanna Savir, MD Petah Tiqvah, Israel
who
Ocular Hypertensive Response to
Therapy
To the Editor.\p=m-\Ihave recently observed an ocular hypertensive response to topically administered dexamethasone that was greater in magnitude and more abrupt in onset than any previously reported in the literature. I thought I might share this with the readership of the Archives. A highly myopic 45-year-old man was first seen in December 1974 with a retinal detachment in his right eye. This detachment was successfully repaired, with restoration of normal vision. Several months after the surgery, the patient was seen again, this time for a change of glasses. Results of his entire examination at
Subcapsular Cataracts
To the Editor.\p=m-\Thearticle on "Posterior Subcapsular Cataracts: Histopathologic Study of Steroid-Associated Cataracts" by Greiner and
Chylack (Archives 97:135-144, 1979)
raises an interesting question. The authors assume that all of the posterior subcapsular cataracts occurring in their patients who were not receiving steroids were "senile" posterior subcapsular cataracts. But the ages of these "senile" patients were 42, 47, 53, 55, and 63 years. It seems to me that the term "senile" is being used to describe cataracts not otherwise accounted for. We all do this. On the other hand, posterior subcapsular cataracts are often associated with other metabolic disturbances. I assume that such metabolic problems were looked for in these other five patients and not found. Statistically, however, one or more of these patients should be found on careful investigation to be an alcoholic.1,2 This history is not always easily obtained, especially if
specifically requested. Looking for differences
not
between
steroid-induced and other posterior subcapsular cataracts, some of which may also be metabolic in origin, is an obviously difficult task, as illustrated by this article. Robert C. Drews, MD Clayton, Mo 1. Drews RC: Ethanol cataract, in XXI Concilium Ophthalmologicum Mexico, 1970, Acta, Amsterdam, Excerpta Medica, 1971, pp 753-758. 2. Sabiston DW: Cataracts, Dupuytren's contracture and alcohol addiction. Am J Ophthalmol 76:1005-1007, 1973.
Pseudopapilledema To the Editor.\p=m-\TheJanuary issue of
the Archives (97:65-75, 1979) contains two articles concerning pseudopapil-
ledema. Both articles refer to a case of optic nerve drusen with associated visual loss reported by Kamin et al in the Archives (89:359-362, 1973). Dr Rosenberg and his colleagues question the visible hyaline bodies as the cause for vision loss in the case of Kamin etal.
The patient described in 1973 has been followed up to his present age of 25 years. His vision has declined steadily to a current level of counting fingers in either eye in association with increasing prominence of the hyaline bodies and increasing generalized optic atrophy. Nothing in the course of the patient's condition nor in extensive investigations supports a diagnosis of multiple sclerosis or any process other than that of the hyaline bodies to account for the vision loss. The reiteration of caution in too readily attributing vision loss to drusen of the optic nerve head, as emphasized by Dr Rosenberg and his asso¬ ciates, is well taken. However, there are patients whose drusen alone appear to generate progressive vision loss. To deny this possibility is to ignore the experiences of practicing ophthalmologists, and to subject at least a few patients to continued, and unrewarding, unpleasant searches for additional disease that isn't there. Robert S. Hepler, MD In
Los Angeles Reply.\p=m-\Weagree with Dr
Hepler
that on extremely rare occasions "there are patients whose drusen alone appear to generate progressive vision loss." There are also patients who lose vision from acquired optic nerve diseases who happen to have drusen in the nerve head. That the patient described by Kamin et al now has a counting fingers level of vision and that the hyaline bodies are more prominent does not categorically infer cause and effect. With both demyelinative optic neuritis and Leber's hereditary optic atrophy, vision may improve,
fluctuate,
or worsen.
Fortunately, with the advent of modern neuroradiologic techniques, including polytomography of bones and computerized axial tomography
of bones and soft tissues, the clinical dilemma of whether nerve head drusen are the cause of central visual loss may usually be resolved. Given the nearly inviolate rule that optic nerve drusen do not cause loss of acuity (without macular hemorrhage), we would not hesitate to subject those
Downloaded From: http://archopht.jamanetwork.com/ by a University of Manitoba User on 06/16/2015
"few patients" to radiologic procedures that may potentially save vision or life. It is only through a diligent search for potentially treatable mass lesions that we may distinguish acuity loss directly related to disc drusen. I am sure Dr Hepler would agree, and we are delighted to again have the opportunity to restate this admonition. Michael Rosenberg, MD
Chicago Peter
Savino, MD
Philadelphia
Joel Glaser, MD Miami Monofixational Intermittent
Exotropia To the Editor.\p=m-\Weread with interest the report on "Monofixational Intermittent Exotropia" in the January Archives (97:93-95, 1979) by Baker and Davies and can confirm their observations. We, too, have cared for a number of patients with intermittent exotropia who had, in fact, an ultra\x=req-\ small-angle monofixational exotropia when their eyes were "straight," and who maintained the same level of sensory binocular cooperation after surgical correction of the exotropia. We question, however, the prevalence of monofixation syndrome that Baker and Davies found in one third of their patients. They noted this frequency to be higher than expected according to Parks.1 Diagnosing monofixation syndrome in children solely on the basis of Titmus stereo test stereoacuity is difficult, since performance on this test is age related and variable.2 Using this test, a stereoacuity of 60 s of arc is found in only 50% of normal children at the age 4\m=1/2\years, and not until 7 years old may one expect all normal children to obtain 60 s of arc. Therefore, the Titmus stereo test cannot be used all by itself, as these authors have used it, to define the presence of monofixation syndrome below the age of 7 years. It would be of interest to know, if the authors' data on stereoacuity were corrected for this age factor, whether the prevalence of monofixation syn-
drome would be as high as it appears to be in their group of patients. Their supporting source1 for a high inci¬ dence of monofixation syndrome in exotropia similarly defined the monofixation syndrome solely by the Titmus stereo test without correction for patient age. Paul E. Romano, MD Judith A. Romano, CO James E. Puklin, MD
Chicago
1. Parks MM: The monofixation syndrome. Trans Am Ophthalmol Soc 67:609-657, 1969. 2. Romano PE, Romano JA, Puklin JE: Stereoacuity development in children with normal binocular single vision. Am J Ophthalmol 79:966\x=req-\ 971, 1975. 3. Boyd TAS, Budd GE: Monofixation exotropia and asthenopia, in Moore S (ed): Orthoptics: Past, Present, Future. New York, Stratton Intercontinental Medical Book Corp, 1976, pp 173\x=req-\ 177.
In
Reply.\p=m-\Iappreciated reading
the comments of Dr Paul E. Romano et al regarding our article. Some of their thoughts were similarly raised by us during the course of our study. Monofixation occurring in one third of patients with intermittent exotropia seemed at first a surprisingly high incidence to us also. We subsequently reviewed retrospectively all patients with intermittent exotropia operated on during the three years of the study from our private practice. Those with anisometropia and amblyopia greater than one Snellen chart line were eliminated. Twenty-seven individuals were too young at the conclusion of the study to give accurate reproducible stereopsis test results and were also dropped. This left 99 patients operated on during the three years of the study with reproducible stereopsis test results obtainable at the end of the study period. These patients were not included in the published study groups since their preoperative stereopsis testing was unreliable. Of this larger group, 28, or 28%, had monofixation stereopsis test results. The approximately 30% incidence of monofixation in this larger group of patients with intermittent exotropia we believe helps support the similar findings seen in the smaller study group reported. The age at which stereopsis devel¬ ops and is testable has been of interest to many investigators, including Dr Romano.1"4 Test results vary depen¬ dent on several factors, not the least of which is the socioeconomic, cultural, and educational environment of the population tested. In my private prac¬ tice, a large percentage of the children are from homes providing good educa¬ tional stimuli and many have had
preschool experience
at the ages of 3 4 years. In this nonclinical popula¬ tion, there are several children with reproducible Titmus stereopsis of 40 to 50 s of arc measured before the age of 4 years. By 5 years, 80% measure better than 60 s and this number increases to 95% at 6 years. At the conclusion of our study, no children were under the age of 5 years and most were 6 years of age or older. Therefore, with 90% to 95% of this group expected to have good stereop¬ sis in the absence of amblyopia, anisometropia, and other conditions, adjustment was made for their stereo or
testing.
I thank Dr Romano and his asso¬ ciates for their comments and hope that the above explanations will be of interest. John D. Baker, MD Detroit 1. Scott WE, Marsh J: Stereoacuity in normal individuals. Ann Ophthalmol 6:99-101, 1974. 2. Jani SN: The age factor in stereopsis screening. Am J Optom 43:653-657, 1966. 3. Amigo G: Pre-school vision study. Br J Ophthalmol 57:125-132, 1973. 4. Tatsumi S, Tahira K: Study on the stereotest (Titmus). Folia Ophthalmol Jpn 23:620, 1972.
Takata Interferometric Device To the Editor.\p=m-\Notlong ago, my colleagues and I published a brief article in the Archives describing the use of the Takata Interferometric Acuity Meter in early detection of possible demyelinating disease. The article
described the use of a Takata Interferometric Device for this purpose
(Archives 97:76-78, 1979).
There is no question about the validof our findings; rather, we have discovered that the particular Takata instrument available to us was improperly wired and literally put out a far more intense beam than the instrument is rated to provide. Since then, that instrument has failed and in making repairs we have discovered the fault. At issue was the fact that it had been wired for a voltage system different than that in use in the United States. As this was the first unit delivered to this country, this is a reasonable error. At any rate, the issue is that our success in revealing the early changes in possible demyelinating diseases and/or optic neuritis and others in part revolved about the use of a very intense stimuli. The instrument at that time emitted up to about 100,000 trolands of red light. Standard models are rated to provide much less light. It is my guess that if
ity
someone
specifically purchased
this
Downloaded From: http://archopht.jamanetwork.com/ by a University of Manitoba User on 06/16/2015
instrument for this particular purpose our findings could not be replicated, because clearly the instrument ob¬ tained would not be identical. Howev¬ er, some effects would be recorded. Those effects clearly would be lesser than those we described. One of us, Emilio C. Campos, MD, writes that his instrument (same model) does provide somewhat comparable data. We are modifying our available instrument to provide enhanced light. I have also suggested to Mr Takata that he make an enhanced light source a purchase option of his instrument. Jay M. Enoch, PhD Gainesville, Fla Ocular
Injuries From Exploding Beverage Bottles To the Editor.\p=m-\Ipublished, with
some
associates, an article in Harefuah (95:69, 1978) describing 24 patients
were hospitalized during the years 1975 through 1977 because of ocular injuries from exploding beverage bottles as described by Mondino et al in the November issue of the Archives (96:2040-2041, 1978). The cork of the bottle produced 80% of the injuries and glass fragments caused the other 20%. Nearly 25% of the injured eyes became blind and another 13% lost a considerable amount of vision. We found that the main cause of the explosion is the high pressure within the bottle (we measured in a 1-L bottle a pressure of 8 atm). This pressure increases when the bottles are in hot outside temperatures and with agitation and transportation of the bottles. Because of our findings, the factories in Israel changed the bottle cap to a soft ring. Hanna Savir, MD Petah Tiqvah, Israel
who
Ocular Hypertensive Response to
Therapy
To the Editor.\p=m-\Ihave recently observed an ocular hypertensive response to topically administered dexamethasone that was greater in magnitude and more abrupt in onset than any previously reported in the literature. I thought I might share this with the readership of the Archives. A highly myopic 45-year-old man was first seen in December 1974 with a retinal detachment in his right eye. This detachment was successfully repaired, with restoration of normal vision. Several months after the surgery, the patient was seen again, this time for a change of glasses. Results of his entire examination at
