84 Lynn Investigative OphthalmologyFebruary 1969

the visual field. We cannot rule out glau-coma by testing a predetermined or spe-cific area in the visual field. A completeexamination of the visual field is best per-formed by using both static and kineticperimetry together. This seems to con-stitute the best means of modern quanti-tative perimetry. Scatter of test points canbe controlled only by careful attention tonumerous details involving physical, phar-macological, physiological, and psycholog-ical factors, the "chaff" which must bedifferentiatied from the "wheat"—the pa-thological patterns to be delineated intesting the visual field. The factors causingscatter also influence the reproducibilityof a given visual field from one date toanother, as do the refractive media, pupilsize, mental status, and choice of datapoints.

REFERENCES1. Aulhorn, E., and Harms, H.: Fruhe gesitchts-

feldausfalle beim Glaukom, Tr. Internat.

Congr. Ophth. Munich, 1966, GlaucomaTutzing Symposium, Basel, 1967, S. KargerAG.

2. Drance, S., Wheeler, C , and Fattullo, M.:The use of static perimetry in the early de-tection of glaucoma, Canad. J. Ophth. 2: 249,1967.

3. Garner, Hake, and Eriksen: Operationismand the concept of perception, Psychol. Rev.149, 1956.

4. Goldmann, H.: Grundlagen exakter Peri-metrie, Ophthalmologica 109: 5, 1945.

5. Lynn, J. R.: Current trends in quantitativeperimetry, Internat. Ophth. Clin. 2: 49, 1962.

6. Ourgaud, A. G., and Etienne, R.: L'explora-tion fonctionnelle de l'oeil glaucomateux,Paris, 1961, Masson & Cie., Vol. II.

7. Schmidt, T.: Perimetrie relativer Scotome,Ophthalmologica 129: 303, 1955.

8. Sloan, L. L.: Area and luminance of test ob-ject as variables in examination of the visualfield by projection perimetry, Vision Res. 1:121, 1961.

9. Swets, J. A., Tanner, W. P., Jr., and Birdsall,T. G.: Decision processes in perception, Psy-chol. Rev. 68:301, 1961.

10. Teichner, W. A.: Recent studies of simplereaction time, Psychol. Bull. 51:128, 1954.

The early field defects in glaucoma

Stephen M. Drance

The origins of the depression of central isopter known as "baring of the blind spot" as anearly sign of glaucoma were traced. Changes in isopter occurring with aging were reported.Baring of the blind spot could be produced in everybody with threshold targets and wastherefore not a pathognomonic sign of the disease. A more rapid depression of the isopterwith ocular hypertension has not yet been demonstrated but remains a possibility. The earliestchanges in eyes with open angle glaucoma that could be discovered with the use of staticperimetry were paracentral scotomas in the Bjerrum area separated from the blind spot,coalescing into an arcuate scotoma joining the blind spot.

From the Department of Ophthalmology, Uni-versity of British Columbia, the Department ofOphthalmology, Shaughnessy DVA Hospital,and the Glaucoma Clinic of the VancouverCeneral Hospital, Vancouver, B. C, Canada.

This study was supported in part by MRC GrantMA1578 and in part by DVA Grant 10/63.

A knowledge of the earliest stages ofdamage in a chronic disease process, pref-erably at a stage when it is still reversible,seems fundamental to an understandingand rational management of the disease.In chronic simple glaucoma, which many

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Symposium on effect of glaucoma on visual function 85

ophthalmologists will diagnose only whendamage to visual function has occurred,it is essential to know the earliest repro-ducible disturbances and their mode ofprogression in order to ensure that recog-nition is not unnecessarily delayed and yettreatment should not be commenced un-necessarily early in all ocular hypertensionwithout an understanding of those factorswhich will predict damage to the eye. Itis not certain that reversible changes oc-cur, though we suspect they do. It is pos-sible that the production of small nervefiber bundle defects may be sudden,precipitous, and irreversible. Progressionwould then be due to the fallout of morenerve fiber bundles rather than to a moresevere disturbance of those already dam-aged. It must be remembered that thenerve fiber bundle defect can occur inconditions other than glaucoma. Suchchanges as a contraction of the isopterand the consequent baring of the blindspot are quite nonspecific. They may wellbe accentuated and occur earlier in eyeswith elevated intraocular pressure andmight be reversible.

To study early changes in visual func-tion, a prospective study of people withall levels of ocular pressures must becarried out over the years and manyparameters, including the field, must berecorded. Such studies are in progress butno concrete results are yet available. Evenfor such studies it is crucial to know ex-actly what the early stages and sequencesof change of the visual field are so thatthe field techniques may be set up to givethe answers sought after. Such prospectivestudies may be most rewarding in familiesof patients with chronic simple glaucomabecause this raises the incidence of ocularhypertension and might yield a higher in-cidence of damage of the visual field.Another way of getting at early changesis to study those patients who have ad-vanced damage produced by open angleglaucoma in one eye and in whom theother eye does not yet show a visual fielddefect but may or may not show rises inintraocular pressure.

Almost 100 years ago, Von Graefe1 de-scribed the paracentral scotoma in thecentral field in cases of glaucoma. Theadvent of the perimeter then shifted theemphasis from the paracentral area to theperiphery of the visual field until Bjerrunrand his disciple Ronne3 reverted to test-ing of the visual field with the use ofsmall stimuli and a 2 meter screen. Theydescribed the classical sequence of theglaucomatous visual field, including thearcuate scotoma with nasal step, breakingthrough to the periphery and joining theblind spot. Traquair,'~G whose painstakingquantitative perimetry remains a classic,introduced the concept of depression ofthe central isopter known as "baring of theblind spot" as the earliest change ofchronic simple glaucoma. This was fol-lowed by paracentral scotomas with theirdense nuclei separated from the blindspot. Traquair's concepts from which"baring of the blind spot" were developedand their relationship to the early

li 1500-

10 15 20 25 30 35 40 45 50 55 60 65 70 75 80

AGE IN YEARS

Fig. 1. Linear regression of visual field area onage in 134 eyes. The broken line shows the 95per cent confidence interval for the means of anyage while the confidence interval of the individualreadings is shown by the faint solid line.

86 Drance Investigative OphthalmologyFebruary 1969

Nomen: S.F. Age 67

Datum: May 11/1965

Diagnosis: normal

2 c - 63%transmisj.

Fig. 2.63 per

Visual field in a 67-year-old normal man. The I2 Goldmann target was used with acent transmission filter, baring of the blind spot occurred.

L EYE

30° 30° 10° 20° 30°

Fig. 3. Right: static profiles along 3 meridians showing 2 absolute paracentral scotomas. Thereis a relative scotoma 2° from fixation in the 45° meridian. Left: kinetic plot shows the sco-toma and nasal step. The small superior and relative scotoma could not be plotted kinetically.

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Symposium on effect of glaucoma on visual function 87

•ft. '

Fig. 4. Upper: static profiles showing dense para-central scotoma. Lower: shows that the densescotoma is surrounded by extensive areas of rela-tive depression. On nasal side scotoma comes towithin 3° from fixation.

sis of chronic simple glaucoma should beanalyzed. In order to set the scene, Iwould like to quote from his very exactwritings: (1) "The forms of glaucoma re-ferred to as subacute, acute congestive, orinflammatory are to be regarded as ex-acerbations in simple glaucoma fromwhich they differ only in violence but notin essential nature."5 (2) "The most usualsymptom of which the patient complainsis the presence of recurrent dimness ofvision in one eye. This may last for a fewhours or a day but disappears spontane-ously. These symptoms indicate exacerba-tions of pressure and may be present formany years before a subacute or acuteattack of glaucoma occurs or before cup-ping of the disc or change in the field of

vision develop."5 These two statementsindicate that, as angle closure and chronicsimple glaucoma were not differentiated,the bulk of his patients had angle closureglaucoma and that the proof of an eyehaving early glaucoma was the subsequentoccurrence of an acute attack.

He then stated that "since glaucoma isa bilateral disease, we search for the earlystages in the apparently healthy eye of apatient who has undoubted glaucoma inone eye,"1 and divided the eyes in whichno obvious visual field defects were pres-ent into 5 groups: (1) "the suspectedeye," which was in every way normal andhealthy but was suspect because of defi-nite glaucoma in the other eye; (2) eyeswith no field defects in whom a history ofhalos and ocular discomforts and othersuggestive features were present but witha normal optic nervehead and normal in-traocular pressure; (3) eyes with cuppingor pallor of the optic nerve found duringroutine examination; (4) increased pres-sure alone on routine examination; and(5) various combinations of the above.This group of people was then investi-gated with the smallest visual angles andthe depression of the central field or bar-ing of the blind spot was elucidated. Hestated, "it (baring of the blind spot) isthe earliest field change I have found incases of suspected glaucoma. It is interest-ing to note that, although baring of theblind spot is undoubtedly the precursor ofthe arcuate scotoma, the arcuate scotomadoes not appear to go out of the baringbut seems to arise independently as asmall curved scotoma on or about the 15°circle, a little distance from the blindspot. The baring of the blind spot may bepresent in the upper part of the field withan early arcuate scotoma in the lowerpart."5 Traquair therefore examined mostlysecond eyes of patients who had estab-lished angle closure glaucoma in the firsteye or who had prodromal symptoms ofangle closure glaucoma in an eye whichhad not yet been damaged. One of themain pieces of evidence for baring of the

Drance Inoestigatioe OphthalmologyFebruary 1969

Fig. 5. Upper right and left: Absolute scotoma in Bjerrum area surrounded by relative scotoma.Lower left: shows kinetic plot of the area. Lower right: circular static plot 14° from fixationshows that the absolute nucleus is separated from blind spot by a relative scotoma.

blind spot being a precursor of the classi-cal field defects of chronic simple glau-coma was the fact that many of Traquair'spatients developed acute or subacute at-tacks of glaucoma within two or threeyears. Traquair himself stated that classi-cal arcuate scotoma often occurred in theopposite part of the field from that whichbared the blind spot.

The aging process, with changes inpupil size, changes in the clarity of media,narrowing of the palpebral aperture, andpossibly some changes in the neuroretinalmechanism, leads to a diminution of theentire visual field with advancing years.7

In addition, the slope of the field aroundthe blind spot is flattest.8 Small visualangles become threshold stimuli for manyolder normal individuals and it is charac-teristic of examinations with thresholdtargets that classical baring of the blindspot, more often above than below, de-velops as part of the change in the isopter(Figs. 1 and 2). We were able to establishbaring of the blind spot in almost every-body, young or old, by choosing threshold

targets. Standard targets, such as the1/1,000 or 1/2,000 or the 2/1,000 or2/2,000 or Goldmann targets Ii or I2, willbe threshold for some individuals withaging and must be expected in them tobare the blind spot at that time. This typeof visual field defect can therefore not beconsidered as an entity indicating earlydamage from chronic simple glaucoma.The fact that in chronic simple glaucomaor in ocular hypertension there may be amore rapid change in the isopter andretinal sensitivity could be true, but hasnot as yet been established.

Taking our cue from Traquair we car-ried out a study, choosing a group ofpeople in whom one eye showed the ad-vanced changes of open angle glaucoma,with an atrophic nervehead and a veryadvanced classical glaucomatous visualfield defect in the presence of a normalangle, in whom the other eye was appar-ently not damaged to a 1 mm. or 2/1,000white target.9 Static and kinetic perimetrywas performed with the use of the Tubin-gen perimeter to plot the photopic visual

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Symposium on effect of glaucoma on visual function 89

Fig. 6. Sequential fields showing the occurrence of fresh paracentral scotomas in an area ofrelative disturbance below and in an undisturbed area above. The relative scotomas becomeconfluent and form an absolute arcuate scotoma still separated from the blind spot.

thresholds at 1° intervals along theoblique meridians. The entire centralfields were searched diligently for evi-dence of other scotomas and the kineticisopters were plotted at the end. In thosepatients in whom the badly damaged eyehad elevated intraocular pressures, onecould assume that any changes found by

the more sophisticated techniques whicheluded preliminary discovery with thetangent screen are likely to be early mani-festations of chronic simple glaucoma. Theclassical changes in the second10 eye werefound to be small absolute paracentralscotomas with their long axis usually di-rected in the line of the arcuate nerve

90 Drance Investigative OphthalmologyFebruary 1969

Fig. 7. Visual fields carried out 4 months apart showing change of relative scotoma into anabsolute paracentral scotomas (5° above fixation).

fibers surrounded by a zone of relativescotoma and separated from the blindspot either by a completely normal field ora very much less disturbed area of visualfunctions (Figs. 3, 4, and 5). These para-central scotomas often come to within 2to 3° fixation on the nasal side and wereusually further away from fixation on thetemporal side. They occurred in the classi-cal Bjerrum area although they did notform a complete scotoma at this stage.Some patients had a similar type of defectin the same locations but the defect wasonly relative. These relative defects weremore difficult to interpret and their sig-nificance and progress are being evalu-ated at this time. Such scotomas can occurin people who do not have any evidenceof glaucoma in either eye; we have notedthem to correspond to cotton wool exu-dates seen after severe gastrointestinalhemorrhage and systemic hypertension.We have not found the classical Seidelscotoma, which is a scotoma arising fromthe blind spot, following a slightly curved

course and being widest at the blind spotand then tapering out in a pointed wayaway from the blind spot. Traquair stated,"I have never been able to establish thepresence of defects of this kind, even byserial testing."

Traquair believed that the true arcuatescotoma arose quite quickly and was oftenquite a large defect when first noticed."It seems extremely difficult to detect itsfirst appearance and to trace its early de-velopment, though I have observed manycases of glaucoma and never been able tofollow its growth step by step and for thisparticular reason, I believe it developsrapidly." It is our impression at this timethat most of the paracentral absolutescotomas in the Bjerrum region do in factdevelop quickly as one would expect fromthe fact that they are vascular in origin(Fig. 6).

We have, however, many recordedsequential fields in which relative nucleibecame gradually denser and ultimatelyabsolute side by side with the occurrence

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Symposium on effect of glaucoma on visual function 91

of fresh defects (Fig. 7). If the occur-rence of maximal defects were the onlysequence occurring in glaucoma then thechances of finding reversible and predic-tive signs in the visual field would besmall and unlikely, but the early incom-plete evidence, such as we have at thistime, suggests that established defects doundergo change; this gives us hope thatby employing more sophisticated physio-logical parameters of visual function suchas spatial, temporal summation, size ofreceptive field, and their change withstates of adaptation may lead to a reliablepredictor during a reversible stage. This isbeing investigated at this time in ourlaboratories and clinics.

REFERENCES1. Von Graefe, A.: Beitrage zur Pathologie und

Therapie des Glaukoms, Arch. J. Ophth. 15:108, 1869.

2. Bjerrum, J.: t)ber eine Zufugung zur gewo-hnlichen Gesichtsmessung und iiber das Ge-

sichtsfeld beim Glaukom, 10th Internat. M.Kongr. Berlin, p. 66, 1890.

3. Ronne, H.: Uber das Gesichtsfeld beim Glau-kom, Klin. Monatsbl. Augenh. 47: 12, 1909.

4. Traquair, H. M.: Perimetry in the study ofglaucoma, Tr. Ophth. Soc. United Kingdom51: 585, 1948.

5. Traquair, H. M.: Glaucoma with special ref-erence to medical aspects and early diagno-sis, Brit. M. J. No. 3906, 922, 1935.

6. Traquair, H. M.: Clinical detection of earlychanges in the visual field, Am. Arch. Ophth.22: 947, 1939.

7. Drance, S. M., Berry, V., and Hughes, A.:The effects of age on the central isopter ofthe normal visual field, Canad. J. Ophth. 2:79, 1967.

8. Aulhorn, E., and Harms, H.: Early visualfield defects in glaucoma, in Glaucoma, Basel,1966, S. Karger, Ltd., p. 151.

9. Drance, S. M., Wheeler, C , and Pattullo,M.: Uniocular open angle glaucoma, Am. J.Ophth. 65: 891, 1968.

10. Drance, S. M., Wheeler, C, and Pattullo,M.: The use of static perimetry in the earlydetection of glaucoma, Canad. J. Ophth. 2:249, 1967.

The Bjerrum area in ocular hypertension

R. M. H. Pinkerton

Circular static perimetry was carried out on preselected points in the Bjerrum area on normaleyes and eyes with ocular hypertension. It was found that in the normal subject there was adecline in sensitivity with age, most particularly marked in the upper field. Eyes with ocularhypertension showed more reduction in sensitivity than normal eyes in the same age group. Itis postulated that in ocular hypertension there is premature aging of the field in the Bjerrum

W,e have yet to establish a definition ofthe glaucomatous state and lacking thiswe are even less able to define the condi-tions variously called ocular hypertension,preglaucoma, or glaucoma suspect. For the

From Queens University, Kingston, Ont, Canada.Supported in part by Ontario Provincial Public

Health Grant 605/9/258 (glaucoma clinic).

purposes of this study, ocular hypertensionwas defined as follows: tension: 21 to 25mm. Hg, with a 4 to 5 mm. rise on waterdrinking; tonography: C values 0.12 to0.20 before or after water drinking, andPo/C values 100 to 150; optic disc: noophthalmoscopically visible abnormality;visual fields: no abnormality detected onkinetic Goldmann perimetry; family his-tory: no known family history of glaucoma.