Primary Angle-Closure Glaucoma: Postoperative tonography tests

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HUMAN EXTRAOCULAR MUSCLE

muscle fibers of the frog. J. Cell Biol. 13:177, 1962. 4. Kuffler, S. W., and Vaughan Williams, E. M.: Properties of the slow skeletal muscle fibers of the frog. J. Physiol. 121:318, 1953. 5. Hess, A.: The structure of extrafusal mus­ cle fibers in the frog and their innervation studied by the cholinesterase technique. Am. J. Anat. 107:129, 1960. 6. : Two kinds of extrafusal muscle fibers and their nerve endings in the garter snake. Am. J. Anat. 113:347, 1963. 7. : Structural differences of fast and slow extrafusal muscle fibers and their nerve end­ ings in chickens. J. Physiol. 157:221, 1961. 8. Kern, R.: A comparative pharmacologic-histologic study of slow and twitch fibers in the su­ perior rectus muscle of the rabbit. Invest. Ophth. 4:901, 1965. 9. Hess, A.: The structure of slow and fast extrafusal muscle fibers in the extraocular mus­ cles and their nerve endings in guinea pigs. J. Cell. Comp. Physiol. 58:63, 1961. 10. : Slow fibers in the extraocular mus­ cles of the cat. J. Physiol. 169 :780, 1963. 11. Cheng, K., and Breinin, G. M.: Fine struc-

487

ture of nerve endings in extraocular muscle. Arch. Ophth. 74:822, 1965. 12. Dietert, S. E.: The demonstration of different types of muscle fibers in human extraoc­ ular muscle by electron microscopy and cholines­ terase staining. Invest. Ophth. 4:51, 1965. 13. Kupfer, C.: Motor innervation of extraocu­ lar muscle. J. Physiol. 153:522, 1960. 14. Cheng, K.: Cholinesterase activity in human extraocular muscles. Jap. J. Ophth. 7:174, 1963. 15. Zenker, W., and Anzenbacher, H.: On the different forms of myoneural junction in two types of muscle fiber from the external ocular muscles of the rhesus monkey. J. Cell. E. Comp. Physiol. 63 :273, 1964. 16. Wolter, J. R., and O'Keefe, N. T.: Localiza­ tion of nerve endings in relation to cholinesterase deposits in normal human eye muscles. Invest. Ophth. 2 :558, 1963. 17. Porter, K. R.: The sarcoplasmic reticulum: Its recent history and present status. J. Biophys. Biochem. Cytology, 10:219 (Suppl) 1961. 18. Muscatello, U., et al: The sarcotubular sys­ tem of frog skeletal muscle. J. Biophys. Biochem. Cytology, 10:201, (Suppl) 1961.

PRIMARY ANGLE-CLOSURE GLAUCOMA POSTOPERATIVE TONOGRAPHY TESTS RONALD F.

LOWE,

F.R.A.C.S.

Melbourne, Australia A previous paper 1 showed that some per­ sons who have been treated for recurrent or acute angle-closure glaucoma and have open peripheral iridectomies may show high rises of pressure postoperatively when their pu­ pils are dilated with homatropine or they are subjected to dark-room tests. Many of these patients describe continuing discom­ fort of their eyes with such activities as reading, sewing or television and their longterm prognosis still needs to be determined. From a large number of primary angleclosure glaucoma patients who have been closely followed over the last several years one has been selected for repeat tonography with various provocative tests. This patient was chosen because her right eye always gave normal tests yet her left eye gave con­ sistently large rises of pressure every time her left pupil was dilated with tropine eyedrops and every time she was submitted to a

simple dark-room test. Like most other pa­ tients she very much disliked being placed in the dark with her eyes bandaged but she co-operated very well despite the inconve­ niences requested of her, and h e r tonog­ raphy tests were reliable and consistent. C A S E REPORT

Mrs. V. H., Case 6, attended the casualty depart­ ment of The Royal Victorian Eye and Ear Hospital May 2, 1958, when she was aged 57 years. She stated that her left eye had been very painful for a week and that she was unable to sleep owing to the pain. She was a sewing machinist and with con­ centration on the sewing her left eye ached and the vision blurred. Casualty examination showed no urgent abnormality, her ocular tensions were 18 mm Hg both eyes, so she was referred to the out-patient clinic. She attended the clinic May 8, 1958, and because she said her vision blurred with sewing she was ordered homatropine and cocaine 2% eyedrops for refraction. The refraction was: R.E., +2.5D cyl ax 60°, % 2 ; L.E., +1.0D sph C +0.5D cyl ax 90°, %. The optic discs and fundi were described as nor-

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AMERICAN JOURNAL OF OPHTHALMOLOGY

mal and eserine eyedrops were instilled. After a week, she came again for postmydriatic tests and a new presbyopic correction was ordered. (Fortun­ ately she had no untoward results from the unin­ tentional homatropine provocative test.) She returned three months later (August 12, 1958) and reported persistent eye pains that fre­ quently interrupted sleep. Her ocular tensions were R.E., 34: L.E., 40 (mm H g 1955 scale), her optic discs were normal and the 2/2,000 Bjerrum screen fields were slightly constricted but no abnormal scotomas were present. Gonioscopy showed very narrow angles with ballooned irises so that the depths of the angles could not be seen. Bilateral peripheral iridectomies were arranged and she was asked to use 1% pilocarpine drops in both eyes, three times daily while awaiting surgery. She was admitted to hospital August 8, 1958, and the following more detailed history was obtained. For two years she had attacks of pain, blurred vision and haloes around lights affecting only her left eye. These occurred at night especially in the presence of bright lights, if she were upset or excited. If she were out, she would come home and go to bed and by next morning the attack would cease. She had stopped going to the movies because the pain would invariably occur. She had received no treatment until she attended this hospital. Recently the pain had become worse and she had not been free of it for some weeks. Since using the pilo­ carpine, she continued to see haloes but they were paler. The pain persisted intermittently and felt sharp and boring. On August 19, 1958, a sealed left peripheral iridectomy was performed followed by a sealed right peripheral iridectomy on August 26, 1958. The operations were conducted under local anesthesia using Chandler's 2 technique. The anterior chambers quickly reformed, postoperative pupil dilatation was achieved by 10% phenylephrine eyedrops, no poste­ rior synechiae formed and convalescence was un­ eventful. She was reviewed at three-month intervals. Vi­ sion remained unchanged, no defects were found in her visual fields and ocular tensions and tonography were normal. Gonioscopv showed relaxed irises, open peripheral iridectomies, angles still rather nar­ row but open and free of peripheral anterior synechiae. The iris root was a little closer to the angle wall in the left eye when compared with the right. The patient should have been completely cured but she continued to report uncomfortable symptoms associated with her left eye—sight sometimes blurred, the eye ached with sewing and frequently felt uncomfortable, but the colored haloes had dis­ appeared. POSTOPERATIVE

TONOGRAPHY

I n 1962, a s e r i e s of t o n o g r a p h i c i n v e s t i g a ­ tions w e r e begun, and were continued for t h r e e y e a r s . T h e r e s u l t s a r e s h o w n in T a b l e 1. C o n d i t i o n s w e r e k e p t a s s t a n d a r d a s p o s ­

S E P T E M B E R , 1966

sible. All tonographic tests were performed by Dr. Magda Horvat, beginning at 2:00 P.M. Wednesday afternoons. Following tonog­ raphy (using a Mueller or Schwarzer to­ nometer with recorder) a half-hour rest was allowed, then the provocative agent was ap­ plied and tonography was repeated after a further two hours. With all tests, the right eye of the patient herein reported gave uniformly normal re­ sults ; there were no rises of tension, no im­ pairments of outflow and no angle closure. Somewhat similarly, the left eye always gave normal tonographic results unless pro­ voked. However, in contrast with the right eye, astounding rises of tension and altered tonography could be produced in the left eye by provocative testing. Although these tests appeared strikingly different at times, they were consistent in their differences. When similar tests were found to occur in other people new propositions became necessary to explain the unexpected results. P U P I L DILATATION TESTS

When the pupils were dilated with eyedrops of cyclopentolate 1% (Cyclogyl), homatropine and cocaine 2%, bistropamide 0.5% (Mydriacil) and euphthalmine 4% (Ucatropine), the angle of the left eye closed firmly with the iris folded over the trabeculae, tensions rose and outflow fell but, when equal or greater pupil dilatation was achieved with 1-epinephrine base 1% (Eppy) or phenylephrine 10% (Neosynephrine), the left angle remained open and outflow was increased. The peripheral iri­ dectomies were at no time closed by pupil dilatation. These results have been ex­ plained by the pharmacologic differences in action of these two groups of drugs, 3 the tropine group by weakening the iris sphinc­ ter and the epinephrine group by stimu­ lating the dilator without sphincter paraly­ sis. DARK-ROOM TESTS

After both eyes were patched and the pa­ tient was placed in the dark for two hours,

TABLE 1 SUMMARY OF POSTOPERATIVE REPEAT TONOGRAPHY TESTS

(Upper number is tonography, lower number shows repeat tonography two and one-half hours later which was two hours after any provocative agent) Date

Test

Po.R.

Po.L.

C.R.

C.L.

F.R.

F.L.

Po/C R.

Po/C L.

Angle

12/12/60

Tonography

13

13

0.27

0.22

1.1

0.9

51

64

Open R & L

5/23/62

Tonography

13

13

0.23

0.18

0.9

0.7

61

77

Open R & L

9/26/62

Tonography

12

13

0.28

0.23

0.8

0.9

46

61

Open R & L

Cyclogyl 1 %

15 15

15 53

0.25 0.20

0.25 0.03

1.2 1.0

1.2 1.3

60 60

60 2550

2 hr dark

12 15

14 37

0.32 0.37

0.28 0.19

0.6 1.8

1.1 5.1

37 40

50 195

Eppy 1 %

13 14

13 13

0.28 0.34

0.25 0.33

0.8 1.4

0.8 1.0

46 41

52 39

2 hr dark

16 12

13 37

0.45 0.27

0.20 0.21

2.7 0.8

0.6 5.7

35 48

65 176

14

14

0.25

0.23

1.0

0.9

56

61

15

15

0.49

0.46

2.5

0.9

30

21

Open

15

15

0.25

0.21

1.2

1.0

70

71

17

29

0.33

0.17

2.3

3.2

51

170

AC depth R 1.90, L 1.95. Open

10% Phenyleph

16 17

15 15

0.32 0.36

0.23 0.34

1.9 2.5

1.2 1.7

50 47

65 44

Well open

Water drink 1 hr

16 16

16 16

0.21 0.21

0.21 0.20

1.3 1.3

1.3 1.3

76 76

76 76

Goldmann fields N.A.D.

14

13

0.34

0.23

1.4

0.7

41

56

12

30

0.21

0.22

1.3

4.4

57

136

15

12

0.43

0.29

2.0

0.6

35

41

15

17

0.40

0.39

2.0

2.7

37

43

Mydracil 0 . 5 %

13 14

12 51

0.44 0.22

0.24 0.03

1.3 0.9

0.5 1.2

29 66

50 1700

2 h r dark

14 14

12 49

0.46 0.25

0.29 0.20

1.8 1.0

0.6 7.8

30 56

41 245

12

11

0.35

0.39

3.7

0.4

34

28

15

12

0.49

0.41

2.5

0.8

30

30

Dark-room test

13 12

11 36

0.36 0.24

0.29 0.20

1.1 0.5

0.3 5.2

36 50

37 118

Eucatrop. 4 %

13 12

11 43

0.36 0.22

0.29 0.03

1.1 0.4

1.0

38 54

38 1430

15

12

0.46

0.32

2.3

0.6

32

37

10

27

0.39

0.26

4.4

25

103

34

38

11/14/62 3/13/63 4 / 3/63 7/17/63 10/ 9/63

12/ 4 / 6 3

1/22/64 3 / 4/64 5 / 6/64

9/23/64

10/21/64

11/25/64 1/ 6/65

2/10/65 4/14/65

5 / 5/65

11/10/65

12/ 8/65

2 Diamox+eppy l % + 2 hrdark 2 Codein Co tabs + 2 hr dark

Largact 100 rag + 2 hr dark Pilo. 2 % 3 d.u. 5 days + 2 hr dark

Pilo 2 % 3 d.u. 5 days Left o n l y + 2 hr dark

Diamox 500 mg + 2 hr dark 10% Phenyleph + 2 hr dark

15

11

0.43

0.29

2.1

16

15

0.54

0.37

3.2

1.8

30

40

2 hr dark

13 13

13 51

0.27 0.20

0.28 0.05

0.8 0.6

0.8 0.20

48 65

46 1020

Open T R, all L closed Open Well open Open

Open R crowded L well open R crowded L tightly closed Open L

L open

R crowded L tightly closed

L well open 2/2,000 N.A.D. R & L L open slit L'nicely'open

490

AMERICAN JOURNAL OF OPHTHALMOLOGY

her left eye always showed a high rise in pressure. Until the last test (some two years after the first), no fall in outflow was dem­ onstrated by repeat tonography despite these tests being performed in the dimmest red light necessary to see the instruments. Whenever gonioscopy was performed either with the Koeppe lens or the Goldmann mir­ ror lens, the angle aways appeared open de­ spite whether the gonioscopy was performed before or after the tonography. A closed angle was expected but on no occasion could it be found. With straight dark-room tonographies all the flow ( F ) figures for the left eye indi­ cated marked hypersecretion. The extent of the hypersecretion appeared too great to be reasonably expected. Becker4 advised that the hypersecretion figures were spurious be­ cause the measurements were taken when the eye was not in a steady-state. The high pressure would be built by angle closure in the dark and the tonographic manipula­ tions (even in the presence of an open iridectomy) would open the angle, so that the high pressure acting with now unobstructed outflow would give excessive flow which was not caused by hypersecretion. Insuperable difficulties were that there was no other way of measuring secretion under the dark-room conditions, and gonios­ copy could not be performed without light capable of constricting the pupil and so pos­ sibly opening a closed angle. Pupil dilatation in the dark might be pre­ vented by fixing the pupil in miosis, and this was achieved by ordering pilocarpine eyedrops three times daily for five days prior to dark-room tonography. The test was repeated on two separate days. On each occasion no high rises of pressure occurred, although these were regularly produced with previous and subsequent plain dark-room tests. The first pilocarpine-dark-room test suggested a moderate change in secretion in the left eye but with the second test no change was indicated. There was then strong presumption that

SEPTEMBER, 1966

pupil dilatation, angle closure and pressure rise occurred with darkness, followed by angle opening just prior to or with tonog­ raphy, leading to spurious secretion re­ sults. If the dark-room test caused high pres­ sures by pupil dilatation and angle closure, the mechanism appeared to be similar to that after the application of tropine eyedrops, namely by the sphincter muscle weakening and the iris moving slightly lat­ erally, with pupil dilatation and iris folding into the angle. It appeared unlikely that angle closure occurred by dilator muscle stimulation through darkness similar to that following application of epinephrine type eyedrops because these drugs did not close any angles in this type of patient.3 How­ ever, if a dark-room test were performed after the application of phenylephrine eyedrops, dilator stimulation and sphincter weakness might act synergistically and cause a firm angle closure that could be observed gonioscopically. Surprisingly, the phenylephrine-darkroom test gave results completely unlike those produced by the tropine drugs, but very similar to the second pilocarpine-darkroom test. Thus it appeared that phenyl­ ephrine and darkness were not synergistic and that the phenylephrine (in the presence of an open peripheral iridectomy) probably fixed the angle in an open condition and prevented the darkness from closing it. Two years previously 500 mg of acetazolamide (Diamox) were given orally before the dark-room test but a drop of Eppy 1% was instilled as well in error. The acetazolamide appeared to prevent a rise of pres­ sure in the dark but, in retrospect, this was probably prevented by the Eppy acting similarly to phenylephrine and fixing the angle open.6 A later dark-room test after 500 mg of oral acetazolamide showed a significant rise of pressure in the left eye. On other occasions a dark-room test was performed after 100 mg chlorpromazine (Largactil, Thorazine) given orally in syrup

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PRIMARY ANGLE-CLOSURE GLAUCOMA

as a sedative, and two aspirin and codein tablets as an analgesic but these did not pre­ vent dark-room pressure rises. OTHER EYE EXAMINATIONS

In spite of two years of intermittent at­ tacks of angle-closure glaucoma, and the ap­ parent persisting instability of the left eye for the seven years since the peripheral iridectomies, the optic discs have remained normal, the visual fields have been normal when charted with 2/2,000 white targets and on the Goldmann perimeter, tonographic outflow has shown no indication of reduc­ tion and ocular tensions have been normal except under provocation with tropine mydriasis or dark-room tests. The anterior chambers were measured repeatedly with the Jaeger apparatus of the Zeiss and HaagStreit slitlamps and they remained practical­ ly constant and of the shallow type. The axial depth of the right anterior chamber has been 1.90 mm and that of the left eye has measured 1.95 mm. Despite the lack of any organic change in the patient's eyes, she has continued to de­ scribe persistent headaches, uncomfortable eyes and the inability to read, sew or watch television more than a short time. The an­ noying symptoms were not relieved by pilocarpine eyedrops or by acetazolamide tablets but were considerably eased by amylobarbitone. Such postoperative symptoms are not uncommon after angle-closure glaucoma op­ erations but in the absence of damaged eyes they are most likely to be psychosomatic, the glaucoma perhaps acting as a localizing or precipitating factor. CONCLUSIONS

The patient presented had attacks of in­ termittent (subacute) angle-closure glauco­ ma for two years, affecting her left eye much more than her right. Peripheral iridectomies appear clinically to have cured her glaucoma and made her eyes safe, al­ though distressing symptoms persist. Her left eye remains unstable to provocative

491

tests by pupil dilatation with tropine drugs, apparently because even though her left an­ terior chamber is slightly deeper than her right, the left iris inserts slightly closer to the angle wall. When her pupils are dilated with tropine drugs, the right angle can be seen to be crowded by iris which has folded and moved laterally at the periphery, but the right angle remains just wide enough to pre­ vent angle closure. The left angle is, however, just a little narrower than the right so that the iris fold­ ing and movement of the peripheral iris can close the angle and cause greatly reduced outflow, resulting in high tensions. During dark-room tests, high tensions apparently occur in the left eye by similar pupil dilata­ tion, iris shift and angle closure. These propositions suggest that tropine drugs and darkness act in the same way in causing pupil dilatation, namely by iris sphincter paresis. The sphincter paresis causes the iris to shift a little laterally and when angles are sufficiently narrow they will close. Tests on numerous patients show that the effect is quantitative depending upon the degree of sphincter muscle paresis. Just as fewer angles close with weak tropine drugs, such as euphthalmine 4% and bistropamide 0.5% in comparison with cyclopentolate 1% or homatropine 4%, so postoperative dark­ room tests are much less frequently positive than when homatropine 4% or cyclopento­ late 1% is used as the provocative agent. Despite the relatively frequent finding that postoperative pupil dilatation can close angles and raise pressures, the patients ap­ pear to be cured of the destructive features of the angle-closure glaucoma. This again em­ phasizes the importance of the pupil-block mechanism which is abolished by iridectomy. ANGLE-CLOSURE PROVOCATIVE TESTS

It now appears that the most popular pro­ vocative tests for preoperative assessment of angle-closure glaucoma (euphthalmine, dark-room) are inappropriate because they

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AMERICAN JOURNAL OF OPHTHALMOLOGY

depend more upon pupil dilatation than in­ creasing pupil block which is the significant cause of this type of glaucoma. Drugs that more definitely increase the pupil block with pupil dilatation (phenylephrine) would give more appropriate provocative tests, but their actions can so readily lead to severe acute angle-closure glaucoma that their use is not usually recommended, especially unless the patient can be quickly admitted to hospital.6 The whole subject of provocative tests for angle-closure glaucoma needs re-examina­ tion. P U P I L DILATATION WITH DARKNESS

The mechanisms of human pupil dilata­ tion in darkness need consideration. In the second edition of his textbook, Physiology of the Eye, Adler7 reviewed the literature at some length. In later editions he greatly re­ duced this chapter to give only a truncated version of the propositions of Gullberg, Olmsted and Wagman. 8 Working with rab­ bits they found that, in dark adaption, pupil dilatation begins with simultaneous relaxa­ tion of the sphincter and contraction of the dilator assisted by iris elasticity. When dila­ tation is about two thirds complete, relaxa­ tion of the sphincter ceases but contraction of the dilator continues.8 The sphincter maintains some tone and pupil dilation is only maximal when dilator action continues after the sphincter has been paralyzed by third nerve section or with atropine.9 Lowenstein and Loewenf eld10 also consid­ ered that the darkness reflex is caused by relaxation of the sphincter pupillae plus sympathetic activity. Many workers, however, deny any active role of the sympathetic system in causing reflex pupil dilatation11 and maintain that the reaction is controlled by variations in the activity of the oculomotor nerve.12 Prac­ tically all these studies were performed on animals, especially cats, in which pupil reflexes may be somewhat different from those in humans. Present gonioscopic examinations have

SEPTEMBER, 1966

not shown closed angles with postoperative dark-room tests so this feature of the tropine-pupil-dilatation tests is missing, but angle closure appears to be the best explana­ tion for the high pressure rises produced by darkness. Two hours of darkness, in the ab­ sence of sleep, appears to affect these types of human eyes similarly to weak tropine eyedrops and maintain pupil dilatation by weakening the sphincter pupillae. There is no suggestion that prolonged darkness causes dilator muscle stimulation compara­ ble with that achieved by epinephrine or phenylephrine eyedrops, nor enhanced dila­ tor stimulation acting synergistically with sphincter paresis. SUMMARY

The destructive effects of angle-closure glaucoma appear to be halted by the relief of pupil block by peripheral iridectomy even though annoying postoperative symptoms may persist, angles may be closed by pupil dilatation with tropine drugs and high rises of pressure may be produced by dark-room tests. Attempts are made to explain these phenomena by using as examples many re­ peat postoperative tonography tests per­ formed with different provocative agents over several years. 82 Collins Street (C.l) ACKNOWLEDGMENTS

These investigations were part of Research Project No. 14 of The Ophthalmic Research In­ stitute of Australia conducted in The Glaucoma Unit of The Royal Victorian Eye and Ear Hos­ pital. I am grateful to my patient for her sus­ tained co-operation and to Dr. Magda Horvat for technical assistance. REFERENCES

1. Lowe, R. F.: Primary angle-closure glauco­ ma. Investigations after surgery for pupil block. Am. J. Ophth. 57:931, 1964. 2. Chandler, P.: Narrow-angle glaucoma. Arch. Opth. 47:69S, 1952. 3. Lowe, R. F.: Angle-closure glaucoma, pupil dilatation and pupil block. Brit. J. Ophth in press, 1966. 4. Becker, B.: Personal communication, 1964.

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PRIMARY ANGLE-CLOSURE GLAUCOMA

5. Lowe, R. F . : Primary angle-closure glauco­ ma. Postoperative tests with 1-epinephrine base. Am. J. Ophth. 58:41S, 1965. 6. : Primary angle-closure glaucoma: Investigations using 10% phenylephrine eye-drops. Am. J. Ophth. 60:41S, 1965. 7. Adler, F. H.: Physiology of the Eye. St. Louis, Mosby, 1953 ed. 2, 1959 ed. 3, 1965 ed. 4. 8. Gullberg, J. E., Olmsted, J. M. D , and Wagman, I. H.: Reciprocal innervation of the sphinc­ ter and dilator pupillae. Am. J. Physiol. 122:160, 1938.

493

9. : Reciprocal action of the constrictor and dilator pupillae during light adaptation. Proc. Soc. Exper. Biol. & Med. 38 :616, 1938. 10. Lowenstein, G., and Loewenfeld, I. E.: The pupil. In Davson, H. (editor): The Eye. New York & London, Academic Press, v. 3. 11. Hodes, R.: The efferent pathway for reflex pupillo-motor activity. Am. J. Physiol. 131:144, 1940. 12. Seybold, W. D., and Moore, R. M.: Oculomo­ tor nerve and reflex dilatation of pupil. J. Neurophysiol. 3 :436, 1940.

PATHOGENESIS O F UNILATERAL GLAUCOMA A REVIEW OF 1 0 0 CASES D O N A L D R.

MILES,

M.D.

Phoenix, Arizona AND MILTON BONIUK,

M.D.

Houston, Texas

The treatment of unilateral glaucoma often presents the ophthalmologist with a challenging problem. Since the glaucoma is of a secondary nature, the treatment will vary depending upon its pathogenesis. Some of the underlying causes are quite obvious but occasionally an eye may be salvaged if the correct diagnosis is made clinically and if proper therapy is instituted. In other cases, enucleation of tumor-containing eyes is often unnecessarily delayed in patients who have opaque media and unilateral glau­ coma. To meet the challenge of proper treat­ ment, therefore, the ophthalmologist must utilize a systematic approach including care­ ful history, thorough ophthalmologic exami­ nation and radiologic studies of the eye and orbit. Statistics regarding the incidence of uni­ lateral glaucoma in enucleated eyes differ greatly from statistics regarding patients seen in clinical practice. Nevertheless, infor­ mation that may have clinical application may be obtained by a study of pathologic From the Department of Ophthalmology and the Department of Pathology, Baylor University College of Medicine, Houston.

material; therefore, we have reviewed 100 consecutive cases of unilateral glaucoma from the Eye Pathology Laboratory of the Baylor University College of Medicine. Ex­ cluded from the study were cases in which intraocular surgery had been performed on the involved eye prior to the onset of glau­ coma. In some cases, however, operations for glaucoma were performed prior to re­ moval of the glaucomatous eye. RESULTS OF STUDY

The cases were classified under five major headings (table 1) indicating the primary cause of the glaucoma. In 10 eyes that had sustained trauma, there were associated mechanisms including inflammation in three cases and lens changes in seven cases (table 5). In these cases trauma was felt to be the initiating factor. Trauma. Table 2 lists the pathologic findings in the 39 eyes of the traumatic group. The average age of the patients in this traumatic group was 44 years, with males comprising 76%. The most common type of injury encountered in clinical ophthalmology