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Progressive Myopia with Glaucoma*
PROGRESSIVE MYOPIA W I T H GLAUCOMA* E. HOWARD B I DROSSIAN, M.D.
Drexel Hill, Pennsylvania
The purpose of this presentation is to emphasize the fact that glaucoma is not as rare in myopes as many of us are inclined to believe and, secondly, to suggest that increased intraocular pressure may explain the cause of progressive myopia in certain cases. Myopia may be classified simply into pathologic and nonpathologic types. The pathologic type is any myopia in which there is associated some eye disease, such as vitreous changes, uveitis, choroidal or ret inal changes, retinal detachment, posterior staphyloma, or any other abnormality. The nonpathologic type is a physiologic variation of the normal refraction, and is characterized by making its appearance in the prepuberty and adolescent years, rarely occurring under the age of five years. Usually minus-six diopters is accepted as a top limit for this normal variation. It is of interest to mention here, that Morrison12 found that advancing nonpathol ogic myopia in the first two decades of lite is often associated with hypothyroidism and that, in a small group of myopes with a low basal metabolism rate, the myopia decreased on thyroid therapy. Bothman2 also reported 30 cases of myopia with hypothyroidism, Weiner 20 reported that SO percent of 112 cases of myopia showed hypothyroidism, and Green12 reported that 42 percent of a series of myopes showed hypothroidism. Jackson9 has further classified myopia into anterior and posterior types. The anterior type of myopia is caused by distention of the globe at the anterior pole from such condi* From the service of Dr. Edmund B. Spaeth, chief of the Department of Ophthalmology, Gradu ate Hospital of the University of Pennsylvania, Philadelphia. Read at a meeting of the Philadelphia County Medical Society, Section on Ophthal mology, December, 19S0.
tions as conical cornea and slight lens dis locations or deformities. The posterior type is due to an increased length of the anteroposterior axis and the pathologic changes are found at the temporal side of the optic nerve. This type of myopia is also often called progressive and malignant myopia. Stacker15 examined microscopically a great number of myopic eyes and found the fol lowing anatomic changes: (1) Thinning of the sclera at the posterior pole, (2) temporal conus or crescent, (3) temporal nerve fibers loop (that is, in cases of crescent in which the retina overlaps the choroid toward the optic disc, the nerve fibers corresponding to the most temporal part of the optic nerve happen to turn around the edge of the end of the retina, following a direct retrograde direction beneath the retina to a certain point where they turn back in a sharp angle in order to reach the optic nerve), (4) supertraction of the retina over the nasal part of the disc, (5) atrophy of the choroid, (6) retinal changes, especially cystic degen eration at the ora, (7) lacunar atrophy of the optic nerve. It was Stacker's feeling that, if the stretching process of the sclera was on a purely mechanical basis, one would expect the stretching effect on the choroid and ret ina to appear when the enlargement of the globe occurred. Since choroidal and retinal atrophy begin much later, when the size of the globe becomes more stable, he felt that the mechanism was a biologic push of the retina on the sclera rather than a mechanical situation. Many theories to explain these anatomic changes have been proposed by various authors and, as is the case in any poorly understood disease, many varied treatments have been suggested. These include full correction, base-in prisms, adduction ex-
486
E. HOWARD BEDROSSIAN
ercises, restricted use of eyes for near work, atropinization, adrenalin, eserine, dionin, tenotomy of the internal recti, tenotomy of the obliques, paracentesis, iridectomy, exci sion of a scleral ring, lens extraction, ocular hygiene, calcium therapy, vitamin therapy, and endocrine therapy. A few of these theories I believe are interesting enough to mention. Jackson9 stated that excessive convergence without accommodation made the myopia worse. He felt that, since the anterior sclera is supported by the tendon insertions of the recti muscles, the ciliary ring, and the doubled capsule of Tenon, while the tem poral part of the posterior sclera is sup ported by the oblique muscle insertions, the scleral softening is narrowed down to the temporal side of the nervehead. Thus, on excess convergence, the optic nerve offers resistance to the pull and the temporal side of the nervehead stretches, while the nasal side is crammed in. This situation would therefore be corrected by wearing full minus lenses or base-in prisms. Turner offered the theory that the produc tion of acids, proteolytic ferments, or other reagents which increase the hydration capac ity of the hydrophilic colloids of the posterior segment cause a chronic water logging of the sclera, and this chemical imbalance lies be hind certain forms of congestive glaucoma as well as progressive axial myopia. He feels that diseased tonsils and pathologic condi tions of the ear, nose, or throat may cause a homolateral myopia and that undue physi cal exertion would cause further myopia by liberation of sarcolactic acid. It was Burton's 3 opinion that increased intraocular pressure was responsible for an increased anteroposterior axis of the globe. He showed that in rabbits, by experimentally increasing the intraocular pressure, the anteroposterior diameter of the globe was lengthened and this lengthening was con sistently greater in young rabbits with an elastic sclera than in adult rabbits. Lengthen
ing was also greater the longer the increased intraocular pressure was maintained. Burton then measured the lid pull in hu mans and found that of the upper lid to be 50 to 70 gm.; that of the lower lid, 40 to 50 gm. Finally, he measured the effect exerted on intraocular pressure by the orbicularis in anesthetized rabbits. The average normal pressure of 20 mm. Hg was found to be in creased to 40 mm. Hg or more when the lids were tightened and the palpebral fissure narrowed by placing the thumb on each canthus and stretching the lids. From these experiments, it was concluded that, when under-corrected myopes squeeze to obtain better vision, they increase the in traocular pressure and stretch the sclera, thus increasing the myopia. Carpenter4 felt that glaucoma was caused by the same process that caused myopia; that is, increased intraocular fluids, and Dransart 4 said that myopia may assume the course of glaucoma. Weichselbaum4 con cluded that an increase in intraocular pres sure and absorption of increased fluids softens the sclera, especially so if inflam matory changes coexist. The sclera then stretches, lengthening the anteroposterior axis and producing myopia more easily in the young patient. On the other hand, if the sclera is sclerosed it does not stretch. The intraocular pressure goes up and optic cupping results, producing glaucoma in the older patient. Rolandi4 noted that, in myopes with glau coma, some had staphylomas with no disc changes, and Priestly-Smith 4 noted that both can be present or a staphyloma alone may be found. It is interesting to mention here that von Hippel4 found an increased, but stabilized, intraocular pressure in all cases of myopia over 20D. Thus, the routine prescribing of miotics for progressive myopia, as has been done in some clinics, may not be a bad idea after all.
PROGRESSIVE MYOPIA WITH GLAUCOMA In summarizing these theories, then, it may be said that some cases of glaucoma may be secondary to myopic changes (such as lowgrade uveitis causing obstruction to the angle and outflow of fluids); in other cases the myopia is secondary to glaucoma; and, finally, the two conditions may coexist with out cause and effect. That the two conditions do coexist more frequently than we are led to believe may be borne out by the report of Lange and Gil bert4 that myopia is present in 30 percent of simple glaucoma cases and in 10 percent of inflammatory glaucoma cases. Knapp 4 described 32 cases of glaucoma with myopia, the myopia varying up to — 10.0D. These patients had deep chambers, low tension, and cupping. De Cori4 reported 34 cases of primary glaucoma in myopia; both the myopia and increased tensions were controlled by glaucoma surgery. Thomas 16 reported 39 patients with nor mal tensions, fields, and fundi (aged 54 to 83 years), all of whom accepted minus lenses of 0.5D. to 2.5D. in addition to their correc tions; 31 of these responded to miotics with return of normal vision (with their old glasses) in three weeks to three months, and remained so for six months to seven years under continuous treatment. Of the remain ing eight patients, five developed frank glau coma ; in two the myopia progressed without glaucoma; one showed retinal hemorrhages. Because of these findings, he felt that in creased myopia was an early sign of impend ing glaucoma. As Duke-Elder 5 states: "A rapidly increas ing presbyopia is an early warning of im pending glaucoma," so, also, must we sus pect impending glaucoma in a case of in creasing myopia. The case of increasing myopia may be more difficult to diagnose, especially when the tonometer readings are within normal. In this instance, scleral rigidity must be con sidered in the tension readings for apparent lower pressure readings in myopes may be
487
due to decreased scleral rigidity and the in traocular pressure may actually be higher than recorded. Other diagnostic tests such as visual fields, gonioscopic examinations, tension curves, and provocative tests should be performed routinely in all cases of progressive myopia. Otherwise, the presence of glaucoma may be overlooked and the patient may become blind from glaucoma when his condition is being treated as myopic choroiditis. Cer tainly, this would be a tragic situation when better results may be obtained in treating glaucoma than progressive malignant myopia. The first case report exemplifies this situa tion. CASE REPORTS CASE 1
History. Mr. A. V., aged 22 years, first visited the Graduate Hospital eye clinic on April 4, 1950, with the complaint of progres sive loss in vision more marked in the past six months. He first began to wear glasses at the age of five years, when he was told he was nearsighted. At that time, he was seen at Wills Hospital and his atropine refrac tion was: O.D., - 2 2 D . sph.; O.S., - 2 0 D . sph. Examination showed the oval discs and stretched fundi of high myopia. At the age of 14 years, he was seen by an optometrist who found his refraction to be: O.D., - 3 2 D . sph. =20/100; O.S., - 3 4 D . sph. = counting fingers at nine feet. Since then he has been having his glasses changed frequently, until at present he is wearing a — 38D. myodisc over the right eye and —30.D. over the left eye. He has a pair of contact lenses which he does not wear because they are a nuisance and do not improve his vision over the myodiscs. Vision was: O.D., 1/60, correctible to 6/30; O.S., light perception and with cor rection, light perception, no projection or color perception. Refraction showed that no improvement in visual acuity over present correction could be obtained.
488
E. HOWARD 15KDROSSIAN Perimeter Record
15 mm. Hg; O.S., 40 mm. Hg. He was con tinued on pilocarpine and 0.035 percent DFP was added at bedtime for the left eye in which the tension remained at 40 mm. Hg in spite of increasing the strength of the DFP until about one week later when 0.075 percent D F P was used. Two hours after in stillation of DFP (0.075 percent), the pa tient suffered severe ciliary spasm which lasted about three hours, but the following morning his tension had come down to 11 mm. Hg and he stated that the left eye no longer felt swollen. The patient's tension has remained between 13 and 19 mm. Hg in both eyes on miotic therapy up to the present time. CASE 2
5/8/50
5/11/50
Fig. 1 (Bedrossian). Visual field study in Case 1.
Just recently we examined a boy, aged 20 months, who was found to have a compound myopic astigmatism of: O.D., — 10.5D. sph. C +3.0D. cyl. ax. 90°; O.S., -15.5D. sph. C +3.0D. cyl. ax. 80°. The anterior segment and fundus exami nations of both eyes were normal, but his tension was: O.D., 20 mm. Hg, and O.S., 35 mm. Hg (Schio'tz). Further evaluation of this case will be necessary, but it is in teresting to note the higher tension in the more myopic eye.
Cornea. The cornea was normal. Keratometer reading: O.D., 43.50 and 42.50 (verti cal) ; O.S., 43.37 and 42.25 (vertical). Fundus. The right eye was seen through the patient's correcting lenses and showed a high degree of myopic choroiditis with a pos terior staphyloma. The disc itself did not show any definite cupping as seen in glau coma. In the left eye, the macular region was seen with a —24D. lens placed over the SUMMARY AND CONCLUSIONS patient's correcting lenses, thus making the degree of myopia — 54D. There was a very 1. A case of progressive axial myopia of high degree of myopic choroiditis and the O.D., - 3 8 D . and O.S., - 5 4 D . associated disc could not be visualized clearly. Only with ocular hypertension is reported. the location of the central retinal vessels 2. It is concluded that increased intra could be made out. ocular pressure may be one cause for the Tension was: O.D., 40 mm. Hg lengthening of the anteroposterior axis of (Schi^tz); O.S., 48 mm. Hg. Gonioscopy the globe. Therefore, all cases of progressive showed normal wide or open angles in both axial myopia should have careful studies to eyes. Field studies of the right eye revealed rule out the presence of glaucoma. The find a glaucomatous defect (fig. 1). ing of a normal tension alone would not Diagnosis. A diagnosis of progressive rule out glaucoma since the increased intra myopia with glaucoma was established and ocular pressure could be temporarily ab the patient was placed on one-percent pilo- sorbed by a pathologic stretching of the carpine, three times daily, O.U. sclera. Course. The next day tension was: O.D., 4501 State Road.
LENS-INDUCED UVEITIS AND GLAUCOMA
489
REFERENCES
1. Borley, W. E., and Tanner, O. R.: The use of scleral resection in high myopia. Am. J. Ophth., 28: 517-520 (May) 1945. 2. Bothman, L.: Am. J. Ophth., 14:918, 1931. 3. Burton, E. W.: Progressive myopia: A possible etiologic factor. Tr. Am. Ophth. Soc, 40:340-354, 1942. 4. De Cori, R.: Glaucoma and myopia. Boll, d'ocul., 13 :875-927 (July) 1934. 5. Duke-Elder, W. S.: Textbook of Ophthalmology. St. Louis, Mosby, 1941, v. 3, p. 3379. 6. Hayden, R.: Development and prevention of myopia at the U. S. Naval Academy. Arch. Ophth., 25 :539-547 (Apr.) 1941. 7. Heinonen, O.: Ueber die Atiologie der hochgradigen einseltigen Myopie und des Astigmatismus: Acta Ophth., 13 :240-255, 1935. 8. Hildreth, H. R., Meinberg, W. H., Milder, B., Post, L. T., and Sanders, T. E.: The effect of visual training on existing myopia. Tr. Am. Acad. Ophth., 51:260-277 (Mar.-Apr.) 1947. 9. Jackson, E.: The control of myopia. Tr. Sect. Ophth., A.M.A., 1935, pp. 36-49. 10. Knapp, A. A.: Vitamin B complex in progressive myopia. Am. J. Ophth., 22:1329-1337 (Dec.) 1939. 11. Moller, H. U.: Excessive myopia and glaucoma. Acta Ophth., 26:185-193, 1948. 12. Morrison, F. M.: Myopia and hypothyroidism. Tr. Am. Ophth. Soc, 45 :527-536, 1947. 13. Schenck, C. P.: Glaucoma in myopia. Texas State J. Med., 24:36-39 (May) 1928. 14. Stansbury, F. C.: Pathogenesis of myopia. Arch. Ophth., 39:273-299 (Mar.) 1948. 15. Stacker, F. W.: Pathologic anatomy of myopic eye with regard to newer theories of etiology and pathogenesis of myopia. Arch. Ophth., 30:476-488 (Oct.) 1943. 16. Thomas, F. C.: An early warning of impending glaucoma. Kentucky M. J., 34:440-441 (Oct.) 1936. 17. Thomassen, T. L.: Tonometry in cases of excessive myopia. Acta Ophth., 26:305-311, 1948. 18. Thompson, W., Moore, and Nugent, O. B.: Progressive myopia. Illinois M. J., 75:231-234 (Mar.) 1939. 19. Turner, H. H.: The etiology and control of progressive axial myopia. Pennsylvania M. J., 47: 793-801 (May) 1944. 20. Weiner, M.: Discussion of Bothman's paper. Tr. Sect. Ophth., A.M.A., 1932, p. 261. 21. Woods, A. C.: Report from the Wilmer Institute on the results obtained in the treatment of myopia by visual training. Am. J. Ophth., 29 :28-57 (Jan.) 1946.
LENS-INDUCED UVEITIS AND PART III.
GLAUCOMA*
" P H A C O G E N E T I C G L A U C O M A " : L E N S - I N D U C E D GLAUCOMA; MATURE OR H Y P E R MATURE CATARACT; OPEN IRIDOCORNEAL ANGLE S. R O D M A N I R V I N E , M.D.,
AND A L E X A N D E R R A Y I R V I N E , J R . ,
M.D.
Beverly Hills, California III.
" P H A C O G E N E T I C GLAUCOMA"
(Cases 12 through 19) Clinically this group shows: ( 1 ) H y p e r mature cataract; ( 2 ) normal to deep an terior chamber, or if the chamber is shallow, the angle is not closed by iris adhesions; ( 3 ) glaucoma; ( 4 ) faulty light projection; ( 5 ) * From the Estelle Doheny Eye Foundation Lab oratory, Los Angeles, California. Presented before the Western Section of the Association for Re search in Ophthalmology, Portland, Oregon, 1950. Part I of this paper appeared in the February, 1952, pages 177-186, and Part II in the March, 1952, issues of the JOURNAL, pages 370-375.
removal of the lens brings about prompt re lief of symptoms and good vision. In our cases, glaucoma was sudden in onset, but in the literature insidious glau coma also is reported by Knapp 6 and by Gifford in the discussion of a paper by Heath. Pathologically, in this group, a hypermature lens is found and globules of lens ma terial are seen in the vitreous or in the an terior chamber, and characteristically large eosinophilic macrophages are found around the lens, usually in the posterior lentile space or in the vitreous, and particularly obstruct-
Drexel Hill, Pennsylvania
The purpose of this presentation is to emphasize the fact that glaucoma is not as rare in myopes as many of us are inclined to believe and, secondly, to suggest that increased intraocular pressure may explain the cause of progressive myopia in certain cases. Myopia may be classified simply into pathologic and nonpathologic types. The pathologic type is any myopia in which there is associated some eye disease, such as vitreous changes, uveitis, choroidal or ret inal changes, retinal detachment, posterior staphyloma, or any other abnormality. The nonpathologic type is a physiologic variation of the normal refraction, and is characterized by making its appearance in the prepuberty and adolescent years, rarely occurring under the age of five years. Usually minus-six diopters is accepted as a top limit for this normal variation. It is of interest to mention here, that Morrison12 found that advancing nonpathol ogic myopia in the first two decades of lite is often associated with hypothyroidism and that, in a small group of myopes with a low basal metabolism rate, the myopia decreased on thyroid therapy. Bothman2 also reported 30 cases of myopia with hypothyroidism, Weiner 20 reported that SO percent of 112 cases of myopia showed hypothyroidism, and Green12 reported that 42 percent of a series of myopes showed hypothroidism. Jackson9 has further classified myopia into anterior and posterior types. The anterior type of myopia is caused by distention of the globe at the anterior pole from such condi* From the service of Dr. Edmund B. Spaeth, chief of the Department of Ophthalmology, Gradu ate Hospital of the University of Pennsylvania, Philadelphia. Read at a meeting of the Philadelphia County Medical Society, Section on Ophthal mology, December, 19S0.
tions as conical cornea and slight lens dis locations or deformities. The posterior type is due to an increased length of the anteroposterior axis and the pathologic changes are found at the temporal side of the optic nerve. This type of myopia is also often called progressive and malignant myopia. Stacker15 examined microscopically a great number of myopic eyes and found the fol lowing anatomic changes: (1) Thinning of the sclera at the posterior pole, (2) temporal conus or crescent, (3) temporal nerve fibers loop (that is, in cases of crescent in which the retina overlaps the choroid toward the optic disc, the nerve fibers corresponding to the most temporal part of the optic nerve happen to turn around the edge of the end of the retina, following a direct retrograde direction beneath the retina to a certain point where they turn back in a sharp angle in order to reach the optic nerve), (4) supertraction of the retina over the nasal part of the disc, (5) atrophy of the choroid, (6) retinal changes, especially cystic degen eration at the ora, (7) lacunar atrophy of the optic nerve. It was Stacker's feeling that, if the stretching process of the sclera was on a purely mechanical basis, one would expect the stretching effect on the choroid and ret ina to appear when the enlargement of the globe occurred. Since choroidal and retinal atrophy begin much later, when the size of the globe becomes more stable, he felt that the mechanism was a biologic push of the retina on the sclera rather than a mechanical situation. Many theories to explain these anatomic changes have been proposed by various authors and, as is the case in any poorly understood disease, many varied treatments have been suggested. These include full correction, base-in prisms, adduction ex-
486
E. HOWARD BEDROSSIAN
ercises, restricted use of eyes for near work, atropinization, adrenalin, eserine, dionin, tenotomy of the internal recti, tenotomy of the obliques, paracentesis, iridectomy, exci sion of a scleral ring, lens extraction, ocular hygiene, calcium therapy, vitamin therapy, and endocrine therapy. A few of these theories I believe are interesting enough to mention. Jackson9 stated that excessive convergence without accommodation made the myopia worse. He felt that, since the anterior sclera is supported by the tendon insertions of the recti muscles, the ciliary ring, and the doubled capsule of Tenon, while the tem poral part of the posterior sclera is sup ported by the oblique muscle insertions, the scleral softening is narrowed down to the temporal side of the nervehead. Thus, on excess convergence, the optic nerve offers resistance to the pull and the temporal side of the nervehead stretches, while the nasal side is crammed in. This situation would therefore be corrected by wearing full minus lenses or base-in prisms. Turner offered the theory that the produc tion of acids, proteolytic ferments, or other reagents which increase the hydration capac ity of the hydrophilic colloids of the posterior segment cause a chronic water logging of the sclera, and this chemical imbalance lies be hind certain forms of congestive glaucoma as well as progressive axial myopia. He feels that diseased tonsils and pathologic condi tions of the ear, nose, or throat may cause a homolateral myopia and that undue physi cal exertion would cause further myopia by liberation of sarcolactic acid. It was Burton's 3 opinion that increased intraocular pressure was responsible for an increased anteroposterior axis of the globe. He showed that in rabbits, by experimentally increasing the intraocular pressure, the anteroposterior diameter of the globe was lengthened and this lengthening was con sistently greater in young rabbits with an elastic sclera than in adult rabbits. Lengthen
ing was also greater the longer the increased intraocular pressure was maintained. Burton then measured the lid pull in hu mans and found that of the upper lid to be 50 to 70 gm.; that of the lower lid, 40 to 50 gm. Finally, he measured the effect exerted on intraocular pressure by the orbicularis in anesthetized rabbits. The average normal pressure of 20 mm. Hg was found to be in creased to 40 mm. Hg or more when the lids were tightened and the palpebral fissure narrowed by placing the thumb on each canthus and stretching the lids. From these experiments, it was concluded that, when under-corrected myopes squeeze to obtain better vision, they increase the in traocular pressure and stretch the sclera, thus increasing the myopia. Carpenter4 felt that glaucoma was caused by the same process that caused myopia; that is, increased intraocular fluids, and Dransart 4 said that myopia may assume the course of glaucoma. Weichselbaum4 con cluded that an increase in intraocular pres sure and absorption of increased fluids softens the sclera, especially so if inflam matory changes coexist. The sclera then stretches, lengthening the anteroposterior axis and producing myopia more easily in the young patient. On the other hand, if the sclera is sclerosed it does not stretch. The intraocular pressure goes up and optic cupping results, producing glaucoma in the older patient. Rolandi4 noted that, in myopes with glau coma, some had staphylomas with no disc changes, and Priestly-Smith 4 noted that both can be present or a staphyloma alone may be found. It is interesting to mention here that von Hippel4 found an increased, but stabilized, intraocular pressure in all cases of myopia over 20D. Thus, the routine prescribing of miotics for progressive myopia, as has been done in some clinics, may not be a bad idea after all.
PROGRESSIVE MYOPIA WITH GLAUCOMA In summarizing these theories, then, it may be said that some cases of glaucoma may be secondary to myopic changes (such as lowgrade uveitis causing obstruction to the angle and outflow of fluids); in other cases the myopia is secondary to glaucoma; and, finally, the two conditions may coexist with out cause and effect. That the two conditions do coexist more frequently than we are led to believe may be borne out by the report of Lange and Gil bert4 that myopia is present in 30 percent of simple glaucoma cases and in 10 percent of inflammatory glaucoma cases. Knapp 4 described 32 cases of glaucoma with myopia, the myopia varying up to — 10.0D. These patients had deep chambers, low tension, and cupping. De Cori4 reported 34 cases of primary glaucoma in myopia; both the myopia and increased tensions were controlled by glaucoma surgery. Thomas 16 reported 39 patients with nor mal tensions, fields, and fundi (aged 54 to 83 years), all of whom accepted minus lenses of 0.5D. to 2.5D. in addition to their correc tions; 31 of these responded to miotics with return of normal vision (with their old glasses) in three weeks to three months, and remained so for six months to seven years under continuous treatment. Of the remain ing eight patients, five developed frank glau coma ; in two the myopia progressed without glaucoma; one showed retinal hemorrhages. Because of these findings, he felt that in creased myopia was an early sign of impend ing glaucoma. As Duke-Elder 5 states: "A rapidly increas ing presbyopia is an early warning of im pending glaucoma," so, also, must we sus pect impending glaucoma in a case of in creasing myopia. The case of increasing myopia may be more difficult to diagnose, especially when the tonometer readings are within normal. In this instance, scleral rigidity must be con sidered in the tension readings for apparent lower pressure readings in myopes may be
487
due to decreased scleral rigidity and the in traocular pressure may actually be higher than recorded. Other diagnostic tests such as visual fields, gonioscopic examinations, tension curves, and provocative tests should be performed routinely in all cases of progressive myopia. Otherwise, the presence of glaucoma may be overlooked and the patient may become blind from glaucoma when his condition is being treated as myopic choroiditis. Cer tainly, this would be a tragic situation when better results may be obtained in treating glaucoma than progressive malignant myopia. The first case report exemplifies this situa tion. CASE REPORTS CASE 1
History. Mr. A. V., aged 22 years, first visited the Graduate Hospital eye clinic on April 4, 1950, with the complaint of progres sive loss in vision more marked in the past six months. He first began to wear glasses at the age of five years, when he was told he was nearsighted. At that time, he was seen at Wills Hospital and his atropine refrac tion was: O.D., - 2 2 D . sph.; O.S., - 2 0 D . sph. Examination showed the oval discs and stretched fundi of high myopia. At the age of 14 years, he was seen by an optometrist who found his refraction to be: O.D., - 3 2 D . sph. =20/100; O.S., - 3 4 D . sph. = counting fingers at nine feet. Since then he has been having his glasses changed frequently, until at present he is wearing a — 38D. myodisc over the right eye and —30.D. over the left eye. He has a pair of contact lenses which he does not wear because they are a nuisance and do not improve his vision over the myodiscs. Vision was: O.D., 1/60, correctible to 6/30; O.S., light perception and with cor rection, light perception, no projection or color perception. Refraction showed that no improvement in visual acuity over present correction could be obtained.
488
E. HOWARD 15KDROSSIAN Perimeter Record
15 mm. Hg; O.S., 40 mm. Hg. He was con tinued on pilocarpine and 0.035 percent DFP was added at bedtime for the left eye in which the tension remained at 40 mm. Hg in spite of increasing the strength of the DFP until about one week later when 0.075 percent D F P was used. Two hours after in stillation of DFP (0.075 percent), the pa tient suffered severe ciliary spasm which lasted about three hours, but the following morning his tension had come down to 11 mm. Hg and he stated that the left eye no longer felt swollen. The patient's tension has remained between 13 and 19 mm. Hg in both eyes on miotic therapy up to the present time. CASE 2
5/8/50
5/11/50
Fig. 1 (Bedrossian). Visual field study in Case 1.
Just recently we examined a boy, aged 20 months, who was found to have a compound myopic astigmatism of: O.D., — 10.5D. sph. C +3.0D. cyl. ax. 90°; O.S., -15.5D. sph. C +3.0D. cyl. ax. 80°. The anterior segment and fundus exami nations of both eyes were normal, but his tension was: O.D., 20 mm. Hg, and O.S., 35 mm. Hg (Schio'tz). Further evaluation of this case will be necessary, but it is in teresting to note the higher tension in the more myopic eye.
Cornea. The cornea was normal. Keratometer reading: O.D., 43.50 and 42.50 (verti cal) ; O.S., 43.37 and 42.25 (vertical). Fundus. The right eye was seen through the patient's correcting lenses and showed a high degree of myopic choroiditis with a pos terior staphyloma. The disc itself did not show any definite cupping as seen in glau coma. In the left eye, the macular region was seen with a —24D. lens placed over the SUMMARY AND CONCLUSIONS patient's correcting lenses, thus making the degree of myopia — 54D. There was a very 1. A case of progressive axial myopia of high degree of myopic choroiditis and the O.D., - 3 8 D . and O.S., - 5 4 D . associated disc could not be visualized clearly. Only with ocular hypertension is reported. the location of the central retinal vessels 2. It is concluded that increased intra could be made out. ocular pressure may be one cause for the Tension was: O.D., 40 mm. Hg lengthening of the anteroposterior axis of (Schi^tz); O.S., 48 mm. Hg. Gonioscopy the globe. Therefore, all cases of progressive showed normal wide or open angles in both axial myopia should have careful studies to eyes. Field studies of the right eye revealed rule out the presence of glaucoma. The find a glaucomatous defect (fig. 1). ing of a normal tension alone would not Diagnosis. A diagnosis of progressive rule out glaucoma since the increased intra myopia with glaucoma was established and ocular pressure could be temporarily ab the patient was placed on one-percent pilo- sorbed by a pathologic stretching of the carpine, three times daily, O.U. sclera. Course. The next day tension was: O.D., 4501 State Road.
LENS-INDUCED UVEITIS AND GLAUCOMA
489
REFERENCES
1. Borley, W. E., and Tanner, O. R.: The use of scleral resection in high myopia. Am. J. Ophth., 28: 517-520 (May) 1945. 2. Bothman, L.: Am. J. Ophth., 14:918, 1931. 3. Burton, E. W.: Progressive myopia: A possible etiologic factor. Tr. Am. Ophth. Soc, 40:340-354, 1942. 4. De Cori, R.: Glaucoma and myopia. Boll, d'ocul., 13 :875-927 (July) 1934. 5. Duke-Elder, W. S.: Textbook of Ophthalmology. St. Louis, Mosby, 1941, v. 3, p. 3379. 6. Hayden, R.: Development and prevention of myopia at the U. S. Naval Academy. Arch. Ophth., 25 :539-547 (Apr.) 1941. 7. Heinonen, O.: Ueber die Atiologie der hochgradigen einseltigen Myopie und des Astigmatismus: Acta Ophth., 13 :240-255, 1935. 8. Hildreth, H. R., Meinberg, W. H., Milder, B., Post, L. T., and Sanders, T. E.: The effect of visual training on existing myopia. Tr. Am. Acad. Ophth., 51:260-277 (Mar.-Apr.) 1947. 9. Jackson, E.: The control of myopia. Tr. Sect. Ophth., A.M.A., 1935, pp. 36-49. 10. Knapp, A. A.: Vitamin B complex in progressive myopia. Am. J. Ophth., 22:1329-1337 (Dec.) 1939. 11. Moller, H. U.: Excessive myopia and glaucoma. Acta Ophth., 26:185-193, 1948. 12. Morrison, F. M.: Myopia and hypothyroidism. Tr. Am. Ophth. Soc, 45 :527-536, 1947. 13. Schenck, C. P.: Glaucoma in myopia. Texas State J. Med., 24:36-39 (May) 1928. 14. Stansbury, F. C.: Pathogenesis of myopia. Arch. Ophth., 39:273-299 (Mar.) 1948. 15. Stacker, F. W.: Pathologic anatomy of myopic eye with regard to newer theories of etiology and pathogenesis of myopia. Arch. Ophth., 30:476-488 (Oct.) 1943. 16. Thomas, F. C.: An early warning of impending glaucoma. Kentucky M. J., 34:440-441 (Oct.) 1936. 17. Thomassen, T. L.: Tonometry in cases of excessive myopia. Acta Ophth., 26:305-311, 1948. 18. Thompson, W., Moore, and Nugent, O. B.: Progressive myopia. Illinois M. J., 75:231-234 (Mar.) 1939. 19. Turner, H. H.: The etiology and control of progressive axial myopia. Pennsylvania M. J., 47: 793-801 (May) 1944. 20. Weiner, M.: Discussion of Bothman's paper. Tr. Sect. Ophth., A.M.A., 1932, p. 261. 21. Woods, A. C.: Report from the Wilmer Institute on the results obtained in the treatment of myopia by visual training. Am. J. Ophth., 29 :28-57 (Jan.) 1946.
LENS-INDUCED UVEITIS AND PART III.
GLAUCOMA*
" P H A C O G E N E T I C G L A U C O M A " : L E N S - I N D U C E D GLAUCOMA; MATURE OR H Y P E R MATURE CATARACT; OPEN IRIDOCORNEAL ANGLE S. R O D M A N I R V I N E , M.D.,
AND A L E X A N D E R R A Y I R V I N E , J R . ,
M.D.
Beverly Hills, California III.
" P H A C O G E N E T I C GLAUCOMA"
(Cases 12 through 19) Clinically this group shows: ( 1 ) H y p e r mature cataract; ( 2 ) normal to deep an terior chamber, or if the chamber is shallow, the angle is not closed by iris adhesions; ( 3 ) glaucoma; ( 4 ) faulty light projection; ( 5 ) * From the Estelle Doheny Eye Foundation Lab oratory, Los Angeles, California. Presented before the Western Section of the Association for Re search in Ophthalmology, Portland, Oregon, 1950. Part I of this paper appeared in the February, 1952, pages 177-186, and Part II in the March, 1952, issues of the JOURNAL, pages 370-375.
removal of the lens brings about prompt re lief of symptoms and good vision. In our cases, glaucoma was sudden in onset, but in the literature insidious glau coma also is reported by Knapp 6 and by Gifford in the discussion of a paper by Heath. Pathologically, in this group, a hypermature lens is found and globules of lens ma terial are seen in the vitreous or in the an terior chamber, and characteristically large eosinophilic macrophages are found around the lens, usually in the posterior lentile space or in the vitreous, and particularly obstruct-