B L E P H A R O P H I M O S I S 475

3. Fuchs, E.: Textbook of Ophthalmology. Philadelphia, Lippincott, 1917, ed. 5, p. 684. 4. Parsons, J. H. : Diseases of the Eye. New York, Macmillan, 1934, ed. 7, p. 607. 5. Axenfeld, T . : Lehrbuch der Augenheilkunde. Jena, Verlag von G.. Fischer, 1910, p. 246. 6. Fox, L. W,: Diseases of the Eye. New York, Appleton, 1904. 7. Grimsdale, H., and Brewerton, E.: A Text-Book of Ophthalmic Operations. Chicago, Keener, 1907. 8. Spaeth, E. B. : Further considerations on the surgical correction of blepharophimosis (epicanthus).

Am. J. Ophth, 41:61 (Jan.) 1956. 9. Duke-Elder, S.: Textbook of Ophthalmology. St. Louis, Mosby, 1952, p. 4640. 10. von Ammon, F. A.: American Encyclopedia of Ophthalmology. Chicago, Cleveland Press 1913

v. 2, p. 1046. 11. Hughes, W. L. : Surgical treatment of congenital palpebrai phimosis. AMA Arch. Ophth., 54:586

1955. 12. Johnson, C. C : Epicanthus and blepharophimosis. Am. J. Ophth., 41:71 (Jan.) 1956. 13. Fox, S. A. : Some methods of lid repair and reconstruction: V. Displacement of the canthi. Am. J.

Ophth., 31:317 (Mar.) 1948. 14. Elschnig, A.: Zur Kenntnis der Anomalien der Lidspaltenform. Klin. Monatsbl. Augenh., 1:7,

335, 1912. 15. Dimmer, F . : Quoted by Duke-Elder, S.: Textbook of Ophthalmology. St. Louis, Mosby, 1952,

p. 5195. 16. Ball, J. M.: Modern Ophthalmology. Philadelphia, Davis, 1913, p. 188.

N E U R O H I S T O L O G Y O F L A T T I C E D Y S T R O P H Y O F T H E C O R N E A *

J . R E I M E R W O L T E R , M . D . , A N D J O H N W O O D W O R T H H E N D E R S O N , M . D .

Ann Arbor, Michigan

T h e basic p a t h o l o g y of lat t ice d y s t r o p h y of the c o r n e a h a s l ong been the sub jec t of d i s a g r e e m e n t i n t h e l i t e r a tu r e . E a r l i e r a u ­t h o r s sugges t ed tha t t he l inear opac i t ies m i g h t be d u e to d e g e n e r a t i o n of t he cornea l n e r v e s . U s i n g m a t e r i a l ob t a ined b y k e r a t o -plas ty f r o m t w o cha rac te r i s t i c cases it h a s been poss ib le t o d e m o n s t r a t e by s i lver s ta in­i n g a n d flat sec t ions t h a t t he l ines in the s t r o m a r e p r e s e n t d e g e n e r a t e d a n d hya l in ized cornea l n e r v e s . I n add i t ion , a s imi la r c h a n g e in superf icial s t r o m a cells w a s found in the cases s tud ied .

C A S E H I S T O R I E S

CASE 1

This 37-year-old white man was referred for consultation by Dr. James H. Cooper of Toledo, Ohio, on September 2, 1960. The patient gave a his­tory of ocular difficulty beginning in childhood and gradually increasing over the years. The family his-

* From the Department of Ophthalmology, Uni­versity of Michigan. This study was supported by grant No. B-2873 of the U.S. Department of Public Health, Education, and Welfare. Presented at the 98th annual meeting of the American Oph-thalmological Society in Hot Springs, Virginia, May, 1962.

tory described similar symptoms in the patient's fa­ther, one sister and in his own son, one of three children. Occasional attacks of acute pain and in­creased visual blur had punctuated the progessive visual loss.

Ocular examination demonstrated vision of 20/60—3 and J4 in the right eye, less than 20/200 and Til in the left. The ocular motility was normal, the corneas were hazy and gross fundus details normal. Under the biomicroscope an exten­sive lattice dystrophy was present in both eyes together with central corneal scarring, more marked in the left eye (fig. 1). Keratoplasty was advised.

On February 14, 1961, a seven-mm. circular par­tial penetrating keratoplasty was carried out on the left eye. The postoperative course was uncompli­cated and the sutures were removed on March 9, 1961. Since that time the graft has remained clear, with gradual leveling off of one area of elevated border. No dystrophy has entered the transplant.

His most recent examination on January 24, 1962, showed visual acuity in the left eye of 20/25— 2 and JO with a correction of —6.0D. sph. C —4.5D. cyl. ax. 52°. The dystrophy in the right eye had become worse, with vision now recorded as 20/200+2 and J l l .

CASE 2

This 42-year-old housewife was seen in the Ophthalmology Clinic on February 10, 1961, on referral from Dr. M. D. Bentley of Cadillac, Michigan. She gave a history of "corneal ulcers" since the age of four years, requiring treatment on many occasions. Her vision had been much worse for over a year. A strong family history was in-

476 J. REIMER WOLTER AND JOHN WOODWORTH HENDERSON

Fig. 1 (Wolter and Henderson). Artist's con­ception of the slitlamp view of the right cornea with lattice dystrophy, Case 1.

dicated and the Department of Medical Genetics analyzed her pedigree, stating that "it agrees well with a dominant autosomal type of inheritance of corneal dystrophy which typically, for this pedigree, begins at a very early age (two to three years) and is associated with periodic acute attacks in­volving ulcération of the cornea as well as con­tinual decrease in visual acuity." Eleven individuals were said to be involved over four generations. Three of the patient's four children also are af­fected.

Ocular examination demonstrated visual acuity of counting fingers only in each eye. The motility was normal and no external inflammation evident. The fundi were blurred but grossly normal. Ex­tensive lattice dystrophy, as well as dense central corneal scarring, was seen with the biomicroscope in both eyes.

On February 14, 1961, a seven-mm. circular partial penetrating keratoplasty was performed on the right eye. The postoperative course was un­eventful and the sutures were removed on March 8, 1961. A transient elevation in intraocular pressure was discovered during the first three months after surgery. This was treated by oral Diamox, then by local pilocarpine and, recently, the tension has been normal without medication on both Schi ftz and applanation tonometry.

Her most recent examination of March 15, 1962, showed visual acuity correctible to 20/50 and JO in the right eye with a lens of —5.5D. cyl. ax. 52°. She preferred not to attempt the use of a con­tact lens. Vision in the left eye remained at a level of counting fingers and the dystrophy had not pro­gressed.

HlSTOLOGIC METHODS

The corneal buttons were fixed in brom-

formalin (ammonium bromide formalin, known as Cajal solution) immediately after their removal. Flat sections were cut of the buttons on the freezing microtome. The pan-optic silver carbonate technique of del Rio Hortega1 was used to stain these sections.

HLSTOPATHOLOGIC FINDINGS

CASE 1

The microscopic examination reveals the corneal epithelium to be continuous. How­ever, it appears very irregular in its thick­ness and cellular architecture. Bowman's membrane shows many irregular defects which are filled with scar tissue. The remain­ing areas of Bowman's membrane appear thickened. An interlacing network of star-shaped hyaline depositions is found in and underneath Bowman's membrane as well as in the scars replacing the defects of Bow­man's membrane. The star-shaped hyaline depositions stain black with silver carbon­ate.

Figure 2 shows this network in a flat sec-

Fig. 2 (Wolter and Henderson). Network of star-shaped hyaline depositions as seen in a flat section through the corneal stroma directly under­neath Bowman's membrane in the cornea of the first case. (Frozen section, Hortega stain, photo­micrograph.)

LATTICE DYSTROPHY OF CORNEA 477

tion through the corneal stroma directly un­derneath Bowman's membrane in the cor­nea of the first case. Islands of normal-stain­ing stroma are seen between the star-shaped formations. Figure 3 shows similar hyaline formations in a section just a little deeper through the superficial stroma.

Figure 4 represents single star-shaped hy­aline formations taken from flat sections through this corneal button. Figure 4-A shows a hyaline star from directly under­neath Bowman's membrane. Figure 4-B, C and D show such formations from progres­sively deeper layers of the corneal stroma of this case. This figure demonstrates that all the star-shaped hyaline bodies represent stroma cells in different stages of hyaliniza-tion. This hyalinization has progressed more in the superficial layers of the corneal stroma.

In the deeper parts of the superficial lay­ers the cellular structures (nuclei, cytoplasm and processes) can still be recognized (fig. 4-B and C). In the intermediate stromal lay­ers the stroma cells are virtually normal and contain only a little hyaline (fig. 4-D). The stroma cells of the deep stroma appear nor­mal.

Many thin lines of filaments of hyaline are found in the flat sections of intermedi­ate and deep corneal stroma of this case of lattice dystrophy in addition to the superfi­cial hyalinized stroma cells. Most of these lines are of radial arrangement and they show angular dichotomous branching to­wards the center of the corneal button. These lines or filaments run a straight course (fig. 5) . They have no relations to the hy­alinized stroma cells (fig. 5). In some areas they appear double contoured—somewhat like a delicate glass rod—and show inter­ruptions (fig. 6-A). In other areas the black stained hyalinized filaments are surrounded by brownish hyaline granules (fig. 6-B). The dichotomous branchings can be well ob­served and all of them are directed towards the center of the button (fig. 7). After studying these filaments, one has the definite impression that all filaments represent de-

Fig. 3 (Wolter and Henderson). Similar hyaline formations in the superficial stroma of the cornea of the first case in a somewhat deeper flat section. (Frozen section, Hortega stain, photomicrograph.)

generated and hyalinized corneal nerves. Descemet's membrane and the corneal en-

dothelium are perfectly normal. Figure 8 shows these two layers in a transitional sec­tion through the posterior stroma (a) , Descemet's membrane (b), and the endo-thelium (c) .

CASE 2

The histologie findings in the second case of lattice dystrophy are very similar to those of the first. Again networks of star-shaped hyalinized stroma cells are found in the su­perficial stroma and Bowman's membrane. Figure 9 shows these star-shaped hyaline for­mations in a transitional section through epithelium (a) , Bowman's membrane (b), and superficial stroma (e) .

Figure 10 represents the same black-stain­ing hyaline network in Bowman's membrane in a flat section. The normal substance of Bowman's membrane is seen in the inter­spaces. The deep stroma again exhibits nor­mal stroma cells and progressive hyaliniza­tion is observed as one studies the flat sec­tions going from the deep to the superficial

478 J. R E I M E R W O L T E R A N D J O H N W O O D W O R T H H E N D E R S O N

Fig. 4 (Wolter and Henderson). Star-shaped hyaline formations in flat sections of the cornea of the first case. (A) shows a hyaline star from directly underneath Bowman's membrane. (B, C and D) show similar formations from progressively deeper layers of the superficial stroma of this case. In the deeper layers it is obvious that the hyaline formations represent degenerated corneal stroma cells. (Frozen sec­tions, Hortega stain, photomicrographs.)

LATTICE DYSTROPHY OF CORNEA 479

Fig. S (Wolter and Henderson). Hyaline fila­ment from the deeper corneal stroma of the first case. Part of a hyalinized stroma cell is seen in the left lower corner of the photograph. (Frozen section, Hortega stain, photomicrograph.)

stroma. Descemet's membrane and the endo-thelium are normal.

Again hyaline filaments representing de­generated corneal nerves in their normal pat­tern are observed all through the stroma of the button. Figure 11-A and B show exam­ples of these hyalinized nerves as they are seen in the second case under medium mag­nification.

DISCUSSION

In his Textbook, Duke-Elder2 writes:

The reticular or lattice-like type (Biber, Haab, Dimmer) is characterized by the presence of lines. Sometimes the lines are fine and delicate and can be seen to be made up of minute spots linearly ar­ranged. Sometimes they are independent, at other

tit» r

Fig. 7 (Wolter and Henderson). Dichotomous branching of a hyaline filament in the corneal stroma of the first case. The type of branching is typical for corneal nerve fibers. (Frozen flat sec­tion, Hortega stain, photomicrograph.)

Fig. 6 (Wolter and Henderson). Views of hya­line filaments from the corneal stroma of the first case at high power show double contouration and interruptions (A) and in some areas accumulation of hyaline granules (B). (Frozen sections, Hortega stain, photomicrograph.)

480 J. REIMER WOLTER AND JOHN WOODWORTH HENDERSON

Fig. 8 (Wolter and Henderson). A transitional section through the inner layers of the central cornea of the first case shows the inner stroma, Descemet's membrane, and the corneal endothelium (arrow) to be entirely normal. (Frozen section, Hortega stain, photomicrograph.)

times they criss-cross, forming angular patterns. The linear types may form an unmixed pattern, or they may be mixed with nodular formations.

I t is of interest to note that the first cases of this dominantly inherited type of familial corneal dystrophy described in the literature (Biber,3 Haab,4 Dimmer5) were of the mixed form mentioned by Duke-Elder. The two cases presented in this paper also exhib­it linear deeper opacities mixed with star-shaped superficial nodular formations.

The clinical appearance of our cases was very much like a case of advanced lattice dys­trophy contained in Donaldson's Atlas of Corneal Dystrophies of the Howe Labora­tory of Ophthalmology.6 Cases of mixed lat­tice dystrophy must be differentiated from somewhat similar cases of Groenouw's mac­ular dystrophy which may exhibit threadlike extensions of superficial macular opacities (Berl iner7) .

Jones and Zimmerman8 have discovered that hyalinization is found in the opacities of lattice dystrophy, while the depositions in Groenouw's macular dystrophy are mainly mucoid in character. Thus, there can be no doubt that the mixed type of lattice dystro­phy and macular dystrophy with threadlike extensions are different entities.

The clinical diagnosis of lattice dystrophy depends on careful biomicroscopic observa­tion. Typically, the branching linear opaci­ties extend from the center to the periphery and have a somewhat radial arrangement. Usually the lines do not extend to the lim-bus (Busacca9) . They may be seen rather deep in the stroma. The lines may be double contoured (Berliner7) or appear to be filled with fine granules (Duke-Elder 2 ) . Haab 4

was the first to suggest that the branching

J /""

Fig. 9 (Wolter and Henderson). Transitional section through the outer layers of the cornea of the second case shows star-shaped hyaline forma­tions within and underneath Bowman's membrane. The corneal epithelium can be recognized in the upper part of the picture. (Frozen section, Hortega stain, photomicrograph.)

LATTICE DYSTROPHY OF CORNEA 481

Fig. 10 (Wolter and Hender­son). Network of coarse hyaline depositions in a flat section directly underneath Bowman's membrane in the cornea of the second case. (Frozen section, Hortega stain, photomicrograph. )

linear opacities of lattice dystrophy resemble the pattern of the corneal nerve branches as they may normally be seen in medullation of the corneal nerves or after méthylène blue vital stain. Superficial nodular opacities are seen centrally in most cases of advanced lattice dystrophy. In our cases they appeared star-shaped when examined with the slit-lamp at high magnification. Their develop­ment is accompanied by partial destruction of Bowman's membrane and resulting irreg­ularities of the epithelial surface (irregular astigmatism). A decrease of corneal sensi­tivity has been observed by many in lattice dystrophy.

Several theories have been suggested to explain the development and nature of lat­tice corneal dystrophy. All authors agree that hyalinization of corneal structures causes the opacities. This is supported by the recent studies of Jones and Zimmerman.8·10

Haab4 was the first to suggest that the linear opacities may be the result of some patho­logic alteration of the corneal nerves. Dim­mer5 suggested that folding of the anterior stroma could cause lines similar to linear opacities caused by folds of the posterior stroma in corneal edema.

Collins,11 in an outstanding discussion of "Hereditary ocular degenerations" called lattice dystrophy "abiotrophy of the corneal

nerves." He re-emphasized what Haab4 had already said and considered degeneration and hyalinization of the corneal nerves the primary pathology of lattice dystrophy. He emphasized that corneal sensitivity is usu­ally impaired in this disease. Collins finally

Fig. 11 (Wolter and Henderson). Two hya-linized corneal nerves (hyaline filaments) as seen in the stroma of the second case. (Frozen flat section, Hortega stain, photomicrograph.)

482 J. REIMER WOLTER AND JOHN WOODWORTH HENDERSON

wrote: For any final decision as to the primary seat of

this disease, further research is necessary. I would suggest that the employment of Dogiel's method of methylene-blue staining to a fragment of affected cornea might be of considerable assistance in clearing up the problem.

It must be emphasized at this point that the methylene-blue nerve fiber stains are not very useful for the demonstration of patho­logic corneal nerves. Silver stain is far su­perior for such a study. Thus, it seems that in the present paper we are finally doing what Collins suggested 40 years ago.

The value of silver stain for the demon­stration of the pathologic changes in the corneal degenerations has been demonstrated in earlier studies of Fuchs' primary corneal dystrophy,12"14 syphilitic secondary cornea guttata,14"16 and granular corneal dystrophy.17

Degeneration of endothelial cells and forma­tion of hyaline excrescences on the posterior surface of Descemet's membrane were seen in primary and secondary cornea guttata. Granular corneal dystrophy exhibited de­generation of stroma cells with "epithelioid" swelling and hyalinization beginning in the superficial stroma and progressing posterior­ly. This was seen to result in extensive hyaline deposition and ultimate destruction of Bowman's membrane. The corneal nerves appeared not to be involved in the process of hyalinization in granular dystrophy.

Pillât,18 in 1922, also published clinical studies of lattice dystrophy. He came to the conclusion that lattice dystrophy must repre­sent nerve pathology. Kraupa, in 1923,19

also agreed with Haab4 and Collins11 and coined the name "familial neurotic corneal degeneration" (familaere neurotische Horn­hautdegeneration) for the disease. He again suggested that someone should stain for nerve pathology in the corneas with lattice dystrophy.

Stanka20 did vital staining for corneal nerves in lattice dystrophy with méthylène blue. We are not surprised that he was unable to stain the hyalinized nerve trunks,

since a satisfactory vital stain is extremely difficult to obtain even with normal corneal nerves.

In 1929, Loewenstein21 published an ex­cellent clinical study on lattice corneal dys­trophy and again tended to accept the "neurotrophic" theory for the development of this hereditary disease. Loewenstein ob­served direct continuation of corneal nerves in the periphery into the linear opacities with the slitlamp.

Buecklers,22 however, disagreed with the neurotrophic theory and stated that there is no connection or relationship between the lattice fibers and the corneal nerves. Thomas23 in his recent extensive book on the cornea does not take a stand in this dis­cussion.

Recently, Vrabec24 was able to examine the whole cornea of a case of lattice dystro­phy in flat sections with silver stain. In this study, Vrabec found the hyaline lines of lat­tice dystrophy in the stroma to be degener­ated corneal nerves. Some of his illustrations are very similar to the ones of the present paper. In addition, Vrabec24 found hyaliniza­tion of sensory nerve endings at the limbus and in the peripheral corneal epithelium of his case. The following sentence is trans­lated from this paper:

Well in agreement with most authors who sup­pose that pathological modifications of the corneal nerves are the base for the changes found with the slitlamp, we have seen in our neurohistological study a dystrophy of the corneal nerve trunks, that we believe to be always first localized in the sheath of Schwann.

Vrabec also observed hyalinization of superficial stroma cells in addition to the nerve pathology in the cornea of his case.

The present study of two typical cases indicates to us that Haab, Collins, Pillât, Kraupa, Loewenstein and Vrabec-—a number of great names in ophthalmology—were right with their theory of a "neurotrophic" development of lattice dystrophy. Our his­tologie slides show that the lines found in the stroma actually represent degenerated and hyalinized corneal nerves. In some areas

LATTICE DYSTROPHY OF CORNEA 483

these nerves can still be well recognized. In other areas they are surrounded by granular depositions of hyaline. Some of the nerves represent tubelike structures of hyaline with an optically empty lumen (after staining). All these histologie observations coincide with what had been seen with the slitlamp by earlier observers and the findings in our two cases are in good agreement with the one case of Vrabec.24 Our slides, of course, give no indication as to the nature of the cause of the hyalinization of the corneal nerves in this disease. For the time being we have to call this "primary" pathology.

In addition to the hyalinized nerves of lattice dystrophy there is pathology of the superficial stroma cells. The corneal stroma cells normally represent flat cells with long interconnected processes (Wolter, 19S825). These superficial cells along with the nerve fibers are found to be degenerated and hya­linized in our cases. Destruction of areas of Bowman's membrane and epithelial irregu­larity are found along with this degeneration of the stroma cells.

In closing we would like to express our admiration for the earlier authors we have mentioned, who were able to understand the corneal changes in lattice dystrophy after slitlamp examination many years ago exactly as they were found in this histologie study.

SUMMARY

Using material obtained by keratoplasty from two characteristic cases of lattice dys­trophy of the cornea is has been possible to demonstrate by flat sections and silver stain that the typical lines in the stroma represent degenerated and hyalinized corneal nerves. In addition a similar change in superficial stroma cells was found in both cases.

The study confirms the histologie observa­tions of Vrabec and indicates that a number of famous ophthalmologists—Haab, Collins, Pillât, Kraupa and Loewenstein—were right in their theory of "neurotrophic" develop­ment of lattice dystrophy.

University Medical Center.

REFERENCES

1. Scharenberg, K., and Zeman, W.: Zur Leistungsfaehigkeit und zur Technik der Hortega'schen Silberkarbonatmethoden. Arch. f. Psychiat, 188:430-439, 1952.

2. Duke-Elder, W. S.: Textbook of Ophthalmology. St. Louis, Mosby, 1938, p. 201S. 3. Biber, H.: Cited from Haab.4

4. Haab, O.: Die gittrige Keratitis. Ztschr. f. Augenh., 2:235-246, 1899. 5. Dimmer, F.: Ueber oberflaechliche gittrige Hornhauttruebung. Ztschr. f. Augenh., 2:354-361, 1899. 6. Donaldson, D. D.: Atlas of corneal dystrophies of Howe Laboratory of Ophthalmology, Harvard

Univ. Med. School, Massachusetts Eye and Ear Infirmary. 1959, ed. 3. 7. Berliner, M. L.: Biomicroscopy of the Eye. New York, Hoeber, 1949, pp. 332-339. 8. Jones, S. T., and Zimmerman, L. E. : Macular dystrophy of cornea. Am. J. Ophth., 47:1-16, 1959. 9. Busacca, A.: Biomikroskopie und Histopathologie des Auges. Zurich, Schweizer Druck-und Ver­

laghaus, 1945, v. 1, p. 421. 10. Jones, S. T., and Zimmerman, L. E.: Histopathologie differentiation of granular, macular and

lattice dystrophies of the cornea. Am. J. Ophth., 51:394-410, 1961. 11. Collins, E. T.: Hereditary ocular degenerations. Tr. Internat. Cong. Ophth., Washington, 1922,

v. 1, pp. 103-143. 12. Wolter, J. R., Henderson, J. W., and Gates, K.: Endothelial and epithelial dystrophy of the cornea.

Am. J. Ophth., 44:191-200, 1957. 13. Wolter, J. R., and Henderson, J. W.: Cornea guttata. Klin. Monatsbl. Augenh., 131:725-737, 1957. 14. Wolter, J. R., and Larsen, B. F.: Pathology of cornea guttata. Am. J. Ophth., 48:161-169, 1959. 15. Wolter, J. R.: Secondary cornea guttata. Am. J. Ophth., 50:17-25, 1960. 16. Chi, H. H., Teng, C. C, and Katzin, H. M.: Histopathology of the corneal endothelium. Scientific

Exhibit, Ann. meet. AMA, New York, June, 1961. 17. Wolter, J. R., and Cutler, W. H.: Granular dystrophy of the cornea. Am. J. Ophth., 45:1-11, 1958. 18. Pillât, A.: Ueber gittrige und andere Formen degenerativer Hornhauterkrankungen. Klin. Monatsbl.

Augenh., 69:681-682, 1922. 19. Kraupa, E. : Die familiaeren degenerativen Hornhautveraenderungen (neurotische Dystrophy und

484 J. REIMER WOLTER AND JOHN WOODWORTH HENDERSON

Ichtyosis corneae) im System der sogenannten Dystrophien der Hornhaut. Klin. Monatsbl. Augenh., 70: 396, 1923.

20. Stanka, R.: Ueber familaere gittrige Hornhautdegeneration. Klin. Monatsbl. Augenh., 74:357-360, 1925.

21. Loewenstein, A.: Zur Klinik, Histologie und Therapie der gitterfoermigen Hornhautdegeneration. Klin. Monatsbl. Augenh, 82:752-762, 1929.

22. Buecklers, M. : Die erblichen Hornhautdystrophien. Buecherei des Augenarztes. Stuttgart, Ferdinand Enke, 1938.

23. Thomas, C. I.: The Cornea. Springfield, 111, Charles C Thomas, 1955, p. 281. 24. Vrabec, Fr. : Etude neurohistologique d'un cas de dystrophie grillagée de la cornée. Ophthalmologica,

133:160, 1957. 25. Wolter, J. R.: Reactions of the cellular elements of the corneal stroma. Arch. Ophth, 59:873, 1958.

T H E MADDOX ROD TEST: A TEN-YEAR FOLLOW-UP*

DANIEL SNYDACKER, M.D. Chicago, Illinois

The value of the Maddox rod as an in­strument for measuring muscle imbalance has been amply demonstrated by widespread clinical use. A number of careful statistical studies attesting to its value have been re­ported, of which those by Cridland1 and Scobee and Green2'3 are of particular value.

It is generally assumed that measurements with this instrument show an increase in exophoria with advancing age, particularly at the near-point. The explanation is offered that advancing age brings a decrease in ac­commodation and an associated decrease in converging power.4

To test this assumption, 100 consecutive private patients were studied who had meas­urements with a Maddox rod made on ini­tial examination and again at an interval of 10 years or more.

TECHNIQUE OF EXAMINATION

A multiple red Maddox rod combined with a Risley rotary prism was used to measure the phoria (fig. 1). As shown, the Maddox rod was positioned in front of the prism with a specially constructed clip. The prism was hand-held and, when possible, measurements were made with the patient wearing his own glasses.

* Presented in part at the 98th annual meeting of the American Ophthalmological Society, Hot Springs, Virginia, May, 1962.

The instrument was invariably held be­fore the patient's right eye, no attention being paid to ocular dominance.

Patients were asked to sit erect and the prism was held so that base horizontal prism could be produced. Patients were found to be extremely critical in judging any devia­tion of the observed streak of light from the true vertical, so it was not difficult to judge whether the zero point of the prism was at 180 degrees. Measurements were made without screening, as described by Scobee.2

Measurements were made in a 7.5 meter refracting lane. The distance fixation point was a small muscle light. The near fixation point was a small ophthalmoscope bulb held in the reading position about 25 degrees below the horizontal plane. Diffuse, dim over-all illumination provided by an indirect overhead light was the same for each meas­urement.

Only those patients were included in this

Fig. 1 (Snydacker). Risley prism with Maddox rod held in front of it by specially constructed clip.