Effects of Jogging Exercise onPatients with the PigmentaryDispersion Syndrome andPigmentary Glaucoma

William L. Haynes, MD, A. Tim Johnson, MD, PhD,Wallace L. M. Alward, MD

Background: Exercise-induced anterior chamber pigment dispersion with intraocularpressure (lOP) elevation has been reported in patients with the pigmentary dispersionsyndrome. Marked pigment dispersion with or without elevation of lOP could predisposethese patients to visual field loss. The authors designed this study to evaluate theeffects of jogging exercise on anterior chamber pigment and lOP in a group of patientswith the pigmentary dispersion syndrome or pigmentary glaucoma.

Methods: Fourteen subjects with the pigmentary dispersion syndrome, 10 subjectswith pigmentary glaucoma, and 10 control subjects underwent a 45-minute protocol ofjogging exercise. Anterior chamber pigment was graded and lOP was measured beforeand up to 3 hours after completion of the exercise protocol.

Results: Eyes of experimental subjects were significantly more likely to developexercise-induced pigment dispersion than were eyes of control subjects. In experimentalsubjects, eyes treated with pilocarpine at the time of the study were significantly lesslikely to develop exercise-induced pigment dispersion than eyes not treated with pilo­carpine. In two experimental subjects, pre-exercise treatment with pilocarpine appearedto inhibit exercise-induced pigment dispersion.

Conclusions: The authors do not believe that all patients with the pigmentary dis­persion syndrome or pigmentary glaucoma need to avoid exercise. However, for patientswith these disorders who regularly engage in jogging or more strenuous or more jarringtypes of exercise, they suggest an evaluation before and after the type of exercise inquestion. If marked exercise-induced pigment dispersion occurs, pilocarpine therapymay be an alternative to avoidance of the exercise. Ophthalmology 1992;99:1096-1103

Originally received: November 22, 1991.Revision accepted: January 23, 1992.

From the Department of Ophthalmology, University of Iowa Hospitalsand Clinics, Iowa City.

Supported in part by an unrestricted grant from Research to PreventBlindness, New York, New York.

Presented in part as a poster at the American Academy of OphthalmologyAnnual Meeting, Anaheim , October 1991.

The authors have no proprietary interest in the marketing of pilocarpinein any form.

Reprint requests to Wallace L. M. Alward, MD, Department of Oph­thalmology , University of Iowa Hospitals and Clinics, Iowa City, IA52242. .

1096

Pigmentary glaucoma was first described as a clinical en­tity by Sugar and Barbour' in 1949. They reported twoyoung myopic males with pigment granule deposition inthe anterior chamber and glaucoma. They suggestedthatthe elevated intraocular pressure (lOP) in these patientsresulted from mechanical obstruction of the trabecularspaces by pigment granules. Subsequently, many similarcases have been described with or without open-angleglaucoma.i" If glaucoma is not present in a patient withthe typical anterior segment findings, the patient is saidto have the pigmentary dispersion syndrome. The mosttypical anterior segment findings are deposition of pig­ment in the trabecular meshwork, deposition of pigment

Haynes et al . Exercise and Pigmentary Dispersion Syndrome

Table 1. Modified Mitsui Scale for GradingAnterior Chamber Pigment

* Average number of pigment particles in the anterior chamber in a beamapproximately 0.5 mm X 1 rom at 16x power using the Haag-Streit 900slit lamp.

this group were being treated with topical adrenergic ag­onists and 10with pilocarpine. Two subjects in this groupwere taking oral carbonic anhydrase inhibitors at the timeof the study. Subjects were instructed to take their med­ications as usual before performing the exercise protocol.

The exercise protocol consisted of a supervised periodof jogging lasting 45 minutes. Subjects were allowed tochoose to jog indoors on a track or outdoors along a pre­determined route. A physician was present at all timesduring the protocol for each patient. This physician re­corded the amount of time each patient spent joggingduring the protocol time period. Subjects were instructedto jog at their own pace and were allowed to decrease theirpace to rapid walking if they became fatigued during theexercise. Most subjects were able to jog for the entire timeperiod. Subjects were excluded if they were able to jog forless than half of the allotted time. Anterior chamber pig­ment was graded on a modified Mitsui scale'? (Table I)using the Haag-Streit (Bern, Switzerland) 900 slit lamp at16X power with a beam approximately 0.5 X I mm . In­traocular pressure was measured by applanation tonom­etry. Grading of anterior chamber pigment and measure­ment of lOP were routinely performed 10 minutes beforethe onset of exercise and 10, 25, 40, 55, and 70 minutesafter the exercisewas completed. These times were chosenbecause, in a previous study, we had been able to docu­ment marked anterior chamber pigment dispersion andelevation of lOP in a patient with the pigmentary disper­sion syndrome within the first hour after completion ofexercise (basketball).12

To detect any delayed pressure rise, all patients with3+ or 4+ anterior chamber pigment grade in either eyeafter exercise were asked to return for repeat measure­ments at 3 hours after completion of exercise. Ten othersubjects with smaller amounts of anterior chamber pig­ment after exercise also agreed to return for evaluation 3hours after exercise.

Two patients who developed 4+ pigment dispersionin I eye after exerciseon initial testing agreed to be retestedat a later date after institution of pilocarpine therapy. Thesame exercise and measurement protocols were used inrepeat testing.

on the corneal endothelium (Krukenberg spindle), and"spoke-like" midperipheral iris transillumination defects.Histopathologic and ultrastructural studies suggest thatrubbing between the midperipheral iris and anteriorpackets of lens zonules results in the release of pigmentgranules from the posterior iris. This results in the iristransillumination defects as well as the deposition of pig­ment on anterior chamber structures." Pigment depositionin the trabecular meshwork is believed to contribute tothe development of ocular hypertension and glaucoma inthese patients, although other factors such as congenitalangle anomalies may playa role."

Several cases of exercise-induced anterior chamberpigment dispersion with elevation of lOP have been re­ported in patients with the pigmentary dispersion syn­drome. 1O- 12 If such a response to exercise is common inthese patients, it might be wise to discourage them fromexercising. We designed this study to evaluate the effectsof jogging exercise on anterior chamber pigment and lOPin patients with the pigmentary dispersion syndrome andpigmentary glaucoma. We chose jogging exercise becauseseveral of our patients regularly engage in such exerciseand it is representative of the type of exercise in whichmany patients might participate.

Patients and Methods

The experimental protocol of this study was approved bythe University of Iowa Human Subjects Research Com­mittee . Fourteen subjects (9 males, 5 females) with thepigmentary dispersion syndrome and 10subjects (9 males,I female) with pigmentary glaucoma volunteered for theexercise protocol. Ten individuals (seven males, three fe­males) with no evidence of the pigmentary dispersionsyndrome and lOP levelswithin normal limits volunteeredto serve as control subjects. We defined the pigmentarydispersion syndrome as the presence of a Krukenbergspindle and/or midperipheral iris transillumination defectsin association with typical pigmentation of the trabecularmeshwork. Subjects in the pigmentary dispersion syn­drome group could have a history of elevated lOP butwere excluded from that group if they had a visual fielddefect in either eye. We defined pigmentary glaucoma aspigmentary dispersion syndrome with a typical glauco­matous visual field defect in at least one eye. Subjectswere excluded if they had any history of cardiac or respi­ratory problems or symptoms. Subjects also wereexcludedif they had any history of intraocular surgery (other thanargon laser trabeculoplasty, which had been performedin one eye of each of three pigmentary glaucoma patientsat the time of their participation in the study).

Thirteen of the 28 eyes of patients in the pigmentarydispersion syndrome group were being treated with topicalbeta-adrenergic antagonists at the time of the study. Nonewere being treated with adrenergic agonists, cholinergicmedications, or oral carbonic anhydrase inhibitors. Nine­teen of the 20 eyes of patients in the pigmentary glaucomagroup were being treated with topical beta-adrenergic an­tagonists at the time of the study. Ten eyes of patients in

Grade

o1+2+3+4+

Number of Particlesper Beam"

<11-56-20

21-50>50

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Ophthalmology Volume 99, Number 7, July 1992

Statistical comparisons between groups of eyes wereperformed using Fisher's exact test.

Results

Table 2 shows anterior chamber pigment grade and lOPbefore and after exercise in 28 eyes from the 14 subjectswith the pigmentary dispersion syndrome . Twelve of the28 eyes (43%) had a measurable increase in anteriorchamber pigment after exercise. The increases were typ­ically small. No subject developed an elevation of lOP of5 mmHg or greater in either eye by 70 minutes after ex­ercise. One subject who developed 4+ anterior chamberpigment in I eye after exercise had a 6 mmHg rise in lOPin that eye 3 hours after exercise. Table 3 shows anterior

chamber pigment grade and lOP before and after exercisein 20 eyes of the 10 subjects with pigmentary glaucoma.Six of the 20 eyes (30%) had a measurable increase inanterior chamber pigment after exercise. Again, the in­creases were typically small. No eyes of subjects in thisgroup had a rise in lOP of 5 mmHg or greater at any timeduring the study protocol, although I subject did develop4+ anterior chamber pigment in I eye after exercise. Table4 shows anterior chamber pigment grade and lOP beforeand after exercise in 20 eyes of the 10 control subjects.Only I of20 eyes (5%)had any increase in anterior cham­ber pigment after exercise, and no subject developed arise in lOP of 5 mmHg or greater in either eye at any timepoint.

Figure 1 summarizes the data on exercise-induced in­creases in anterior chamber pigment. This figure shows

Table 2. Anterior Chamber Pigment Grade and Intraocular Pressure beforeand after Exercise in Subjects with the Pigmentary Dispersion Syndrome

lOP (mmHg) lOP (mmHg)Pigment Grade Pigment Grade before after

Subject Eye before Exercise after Exercise" Exercise Exercise"

OD 2+ 2+ 22 20OS 0 1+ 18 16

2t OD 0 0 19 17OS 0 1+ 22 19

3 OD 0 0 16 14OS 0 0 16 13

4 OD 0 1+ 21 19OS 0 1+ 24 22

5t OD 1+ 1+ 16 16OS 1+ 1+ 18 16

6 OD 2+ 2+ 30 28OS 2+ 2+ 20 20

7 OD 2+ 2+ 20 18OS 0 2+ 20 18

8 OD 1+ 2+ 18 22OS 0 1+ 23 22

9 OD 1+ 1+ 17 17OS 1+ 2+ 17 16

lOt OD 2+ 4+ 18 24OS 1+ 2+ 16 18

llt OD 1+ 2+ 16 17OS 1+ 1+ 16 15

12t OD 1+ 1+ 13 12OS 0 0 14 13

13 OD 1+ 1+ 19 19OS 0 0 18 17

14t OD 0 3+ 16 16OS 0 0 16 16

lOP = intraocular pressure; OD = right eye; OS = left eye.

• Refers to the maximum pigment grade or lOP after exercise.

t Indicates patients who returned for measurements 3 hours after exercise.

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Haynes et al . Exercise and Pigmentary Dispersion Syndrome

Table 3. Anterior Chamber Pigment Grade and Intraocular Pressure beforeand after Exercise in Subjects with Pigmentary Glaucoma

lOP (mmHg) lOP (mmHg)Pigment Grade Pigment Grade before after

Subject Eye before Exercise after Exercise" Exercise Exercise"

1 ODt 0 0 15 16OSt 0 0 16 18

2t ODt 0 0 14 13OSt 0 0 10 10

3 OD 0 1+ 14 14OS 0 0 14 14

4t ,'"' OD 1+ 1+ 15 17OS 1+ 1+ 14 16

5t ODt 0 0 17 17OSt 1+ 1+ 17 18

6 ODt 0 1+ 16 12OSt 0 0 16 12

7t OD 1+ 1+ 18 19OS 0 0 16 18

8t OD 0 1+ 14 18OSt 1+ 1+ 13 14

9t OD 1+ 2+ 29 30OS 2+ 4+ 35 34

lot OD 0 1+ 16 16OSt 0 0 19 ZO

lOP = intraocular pressure; 00 = right eye; OS = left eye.

• Refers to the maximum pigment grade or lOP after exercise.

t Indicates eyes on pilocarp ine at th e time of the exercise protocol.

t Indicates pat ient s who returned for measurements 3 hours after exercise.

that among eyes of patients with either pigmentary dis­persion syndrome or pigmentary glaucoma, 18 of48 eyes(38%) developed a measurable increase in anterior cham­ber pigment after exercise. Exercise-induced increases inanterior chamber pigment were typically small, although4 of 48 eyes (8%) had an increase in pigment of2 or moregrades (i.e., from 0 to 2+,2+ to 4+, etc.). Only I of 20eyes (5%) of control patients had any measurable exercise­induced increase in anterior chamber pigment. Eyes ofsubjects with pigmentary dispersion syndrome or pig­mentary glaucoma were significantly more likely to de­velop an exercise-induced increase in anterior chamberpigment when compared with eyes of control subjects(P < 0.0 I, Fisher's exact test).

Figure 2 shows the lOP response to exercise in the eyesof each group of patients (pigmentary dispersion syn­drome, pigmentary glaucoma, and control) by plottingmean lOP versus time for each group. All three groupsshowed a tendency toward a fall in lOP soon after com­pletion of the exercise protocol with a subsequent risetoward baseline over time. Onl y one patient (subject 10from the pigmentary dispersion syndrome group) had anincrease in lOP of 5 mmHg or greater in either eye at anytime point after exercise.

Two subjects who developed 4+ anterior chamber pig­ment dispersion in I eye in response to initial exercisetesting agreed to be retested at a later date after institutionof pilocarpine therapy. The first subject (subject 9 fromthe pigmentary glaucoma group) underwent the same ex­ercise protocol several weeks after treatment with pilo­carpine Ocuserts (Alza, Palo Alto, CA) (P40) was begunin both eyes for routine treatment of his glaucoma withelevated lOP. Table 5 shows the results of testing beforeand after institution of pilocarpine therapy. No measur­able increase in anterior chamber pigment was noted ineither eye after exercise in the postpilocarpine trial. In­terestingl y, the baseline anterior chamber pigment gradebefore exercise also was less in both eyes after pilocarpinetherapy was introduced. In each trial , the lOP was similarbefore and after exercise. In the postpilocarpine trial forthe second subject (subject 10 from the pigmentary dis­persion syndrome group), I drop of 0.5% pilocarpine wasgiven only in the right eye (the eye that previously devel­oped 4+ anterior chamber pigment after exercise) 30minutes before the exercise protocol. There was no mea­surable increase in anterior chamber pigment in that eyein the postpilocarpine trial. The fellow (untreated) eyehad a similar small increase in anterior chamber pigment

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Ophthalmology V olume 99, Number 7, July 1992

Table 4. Anterior Chamber Pigment Grade and Intraocular Pressure before andafter Exercise in Control Subjects

lOP (mmHg) lOP (mmHg)Pigment Grade Pigment Grade before after

Subject Eye before Exercise after Exercise" Exercise Exercise"

1 aD a a 13 13as a a 12 13

2 aD a a 12 12as a a 10 12

3 OD a 1+ 15 13as a a 16 13

4 aD a a 13 13as a a 13 12

5 aD a a 16 16as a a 18 18

6 OD a a 15 14as a a 14 14

7 aD a a 11 12as a a 12 12

8 aD a a 13 15as a a 14 14

9 aD a a 15 13as a a 15 13

10 aD a a 18 14as a a 18 16

rop = intraocular pressure; 00 = right eye; OS = left eye.

• Refer s to the maximum pigment grade or ropafter exercise.

Figure 1. Exercise-induced incr eases in anterior chamber pigment com­paring eyes of control patients with those of patient s with pigmentarydispersion syndrome (POS) or pigmentary glaucoma (PO). Each bar rep ­resents th e percentage of eyes in a particular group that had an incre asein anterior chamber pigment of the amount shown on the X-axis.

in both trials. In the prepilocarpine trial, this patient hada 6 mmHg rise in lOP in the right eye by 3 hours afterexercise. In the postpilocarpine trial, the lOP remainedlower than the baseline value in that eye up to 3 hoursafter exercise.

Figure 3 shows the effect of pilocarpine therapy on ex­ercise-induced pigment dispersion in patients with pig­mentary dispersion syndrome or pigmentary glaucoma.Of the eyes of these patients not receiving pilocarpinetherapy at the time of the exercise testing, 17 of 38 (45%)

• Controls

Pigmentary glaucoma can cause significant visual loss inyoung, otherwise healthy patients. Pigmentary dispersionsyndrome appears to be a precursor of pigmentary glau­coma." The exact pathogenesis of pigmentary glaucomais not known. Ultrastructural studies by Richardson andassociates" of eyes with pigmentary glaucoma showed

Discussion

had a measurable increase in anterior chamber pigmentafter exercise. Of the eyes receiving pilocarpine therapyat the time of exercise testing, only 1 of 10 (10%) had ameasurable increase in anterior chamber pigment afterexercise. Eyes of pigmentary dispersion syndrome andpigmentary glaucoma patients not receiving pilocarpinetherapy were significantly more likely to have exercise­induced pigment dispersion than eyes receiving pilocar­pine therapy (P = 0.04, Fisher's exact test). In comparison,in the same group of patients , 7 of 18 eyes (39%) notreceiving beta-adrenergic antagonist therapy at the timeof the exercise protocol had a measurable increase in an­terior chamber pigment after exercise as compared with12 of 30 eyes (40%) of patients receiving beta-adrenergicagonist therapy at the time of the exercise protocol(P = 0.59, Fisher's exact test).

4

l1li PDS & PG Patients

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Incre••o In Pigment (numbor 01 grad e. )

o

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1100

Haynes et al . Exercise and Pigmentary Dispersion Syndrome

20...---------------, Intraocular pressure usually falls after exercise in nor­mal patients and patients with primary open-angle glau­coma. IS

-20 However, previous reports have documented

pigment dispersion and lOP elevation after exercise insome patients with the pigmentary dispersion syn­drome. 1O

-12 This may be due to mechanical obstruction

of trabecular outflow spaces by pigment." It is possiblethat patients with pigmentary dispersion syndrome andpigmentary glaucoma have intermittent episodes of pig­ment dispersion and lOP elevation in response to exercise(and/or in other situations) which, over time, could resultin glaucomatous optic nerve damage.

Should marked dispersion of pigment with or withoutacute elevation of lOP occur in patients with the pig­mentary dispersion syndrome or pigmentary glaucomain response to exercise, it might be wise to instruct thesepatients to avoid exercise. Alternatively, one could try toinhibit the adverse response to exercise with pharmaco­logic intervention.

Many of our patients with the pigmentary dispersionsyndrome and pigmentary glaucoma regularly engage insome form of moderate exercise. It is important to knowthe effects of such exercise on the eyes of these patients.Smith and associates'! reported on 10 patients with pig­mentary glaucoma who underwent several 1-to 2-minuteperiods of exercise over 25 minutes. Some pigment dis­persion was noted in 16 of 19 eyes of these patients, al­though the amount of pigment dispersion was not reportedfor each eye. Only 2 eyes had a 5 mm or greater rise inlOP (6 mmHg in 1 eye and 7 mmHg in another), andthese pressure elevations were transient. Our study looksat the effects of a more continuous exercise protocol per­formed over a longer period of time. We also have in­cluded a group of subjects with the pigmentary dispersionsyndrome without glaucoma in addition to the pigmentaryglaucoma and control groups. We chose to evaluate the

806020 40

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Time from End of Exercise (minutes)Figure 2. Change in intraocular pressure with exercise. The mean intra­ocular pressure of all eyes of patients in a particular group is plottedversus time from the end of the exercise period. PDS = pigmentarydispersion syndrome; PO = pigmentary glaucoma.

large amounts of melanin pigment within endothelial cellsof the trabecular meshwork as well as scarring and struc­tural damage to the trabecular beams. They suggested thatthe trabecular endothelial cells are damaged over timedue to the accumulation of pigment and that these cellsthen migrate away from the trabecular beams, resultingin poor endothelial coverage and scarring. This wouldlead to decreased outflow facility and elevation of lOP,predisposing to glaucomatous optic nerve damage.

Table 5. Inhibition of Exercise-induced Pigment Dispersion by Pilocarpine

lOPlOP (mmHg) (mmHg)

Pigment Grade Pigment Grade before afterPatient Eye before Exercise after Exercise" Exercise Exercise"

1 (before pilocarpine) aD 1+ 2+ 29 30as 2+ 4+ 35 34

1 (after pilocarpine) aD 0 0 20 20as 0 0 20 20

2 (before pilocarpine) aD 2+ 4+ 18 24as 1+ 2+ 16 18

2 (after pilocarpine) aD 2+ 2+ 22 17on only as 1+ 2+ 18 17

lOP = intraocular pressure; OD = right eye; OS = left eye.

Patient 1 was started on pilocarpine in both eyes as part of routine management of his glaucoma and was retested afterward with the same exerciseprotocol.

Patient 2 agreed to be retested with the same exercise protocol after having 0.5% pilocarpine placed in the right eye only 30 minutes before exercise.

• Refers to the maximum pigment grade or lOP measured up to 3 hours after exercise.

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Ophthalmology Volume 99, Number 7, July 1992

Figure 3. Effect of pilocarpine on exercise-induced increases in anteriorchamber pigment comparing eyes of PDS and PO patients that werereceiving pilocarpine therapy at the time of the exercise protocol withthose eyes not receiving pilocarpine therapy at the time of the exerciseprotocol. Each bar represents the percentage of eyes in a particular groupthat had any measurable increase in anterior chamber pigment after ex­ercise.

effects ofjogging because it is an exercise in which severalof our patients participate and because it is a popularform of exercise in the United States.

In our study, the eyes of subjects with the pigmentarydispersion syndrome or pigmentary glaucoma were sig­nificantly more likely to have a measurable increase inanterior chamber pigment than were the eyes of controlsubjects in response to our exercise protocol. Of the eyesof patients with the pigmentary dispersion syndrome orpigmentary glaucoma, 38% had a measurable increase inanterior chamber pigment after exercise. The increases inpigment were typically small, although a few eyes dem­onstrated more marked pigment dispersion. Only onesubject had an increase in lOP of 5 mmHg or greater ineither eye by 3 hours after exercise.

Previous case reports, including one from our insti­tution, have documented marked anterior chamber pig­ment dispersion and elevation ofIOP after very strenuousexercise (such as prolonged periods of playing basketball)in patients with the pigmentary dispersion syndrome.l'':'?It could be that more ofour patients would have developedmarked anterior chamber pigment dispersion with orwithout lOP elevation with more strenuous or more jar­ring exercise such as basketball. This idea is supported bythe fact that the subject of our previous report who re­peatedly developed severe anterior chamber pigment dis­persion and lOP elevation after 2 hours of playing bas­ketball had only a small amount of pigment dispersionin I eye and no lOP elevation in either eye up to 3 hoursafter being subjected to the exercise protocol ofthis study.

A lower percentage of eyes of our subjects developedmeasurable pigment dispersion in response to exercisewhen compared with the study ofSmith and associates.PThis may be due to the difference in the exercise protocols.It should be noted that both our study and that of Smithand associates'? could suffer from observer bias. The ob­server making measurements ofanterior chamber pigmentand lOP was not masked to whether a given subject had

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the pigmentary dispersion syndrome or pigmentary glau­coma or was a control subject. Similarly, in our study,the observer could not be masked to whether a given eyewas being treated with pilocarpine. Although our mea­surements were made carefully to minimize any observerbias, the possibility that observer bias had some effect onour results still exists.

Two previous case reports have suggested that exercise­induced anterior chamber pigment dispersion in patientswith the pigmentary dispersion syndrome can be phar­macologically inhibited by cholinergic medications suchas pilocarpine.l':'? This may be due to the fact that themiotic effect of these medications results in movement ofthe iris away from the lens zonules, thereby lessening thelikelihood of iris-zonule contact. Two ofour subjects un­derwent exercise testing before and after institution ofpilocarpine therapy. Each patient had marked anteriorchamber pigment dispersion in one eye on initial testing(before starting pilocarpine) but had no measurable pig­ment dispersion in the affected eye when retested afterpilocarpine therapy was instituted in that eye. We alsocompared the eyes of our subjects with the pigmentarydispersion syndrome or pigmentary glaucoma who werereceiving pilocarpine therapy at the time of the exerciseprotocol with the eyes of those subjects not receiving pi­locarpine therapy at the time of the exercise protocol interms of the likelihood of developing a measurable in­crease in anterior chamber pigment after exercise. Eyesreceiving pilocarpine therapy were significantly less likelyto develop a measurable increase in pigment than wereeyes not receiving pilocarpine therapy. In comparison,beta-adrenergic antagonist therapy appeared to have noeffect on the likelihood of exercise-induced pigment dis­persion in these patients.

Our data suggest that a significant number of subjectswith the pigmentary dispersion syndrome and pigmentaryglaucoma will have some anterior chamber pigment dis­persion after jogging exercise. In most ofour subjects, theincreases in pigment were small and were not associatedwith elevation of lOP. The significance of such smallamounts of pigment dispersion is not known. We do notbelieve that all patients with the pigmentary dispersionsyndrome or pigmentary glaucoma should be instructedto avoid exercise, especially less strenuous and jarringforms of exercise. However, a small percentage of ourpatients did develop marked anterior chamber pigmentafter our exercise protocol, and I patient had a 6 mmHgelevation ofIOP in I eye after exercise. Additionally, sev­eral case reports have documented marked anteriorchamber pigment dispersion and elevation of lOP aftermore vigorous and jarring exercise such as playing bas­ketball. IO

-12 Therefore, we believe that patients who reg­

ularly engage in jogging exercise or more vigorous exercisesuch as basketball should be evaluated to determinewhether they develop marked anterior chamber pigmentdispersion and/or lOP elevation after such exercise. Forthose patients who have marked exercise-induced pigmentdispersion, pilocarpine therapy may be an alternative toavoidance of the exercise.

1102

Haynes et al . Exercise and Pigmentary Dispersion Syndrome

References

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2. Sugar HS. Pigmentary glaucoma. A 25-year review. Am JOphthalmol 1966;62:499-507.

3. Speakman JS. Pigmentary dispersion. Br J Ophthalmol1981;65:249-51.

4. Scheie HG, Cameron JD. Pigment dispersion syndrome: aclinical study. Br J Ophthalmol 1981;65:264-9.

5. Richter CU, Richardson TM, Grant WM. Pigmentary dis­persion syndrome and pigmentary glaucoma. A prospectivestudy of the natural history. Arch Ophthalmol 1986;104:211-15.

6. Migliazzo CV, Shaffer RN, Nykin R, Magee S. Long-termanalysis of pigmentary dispersion syndrome and pigmentaryglaucoma. Ophthalmology 1986;93:1528-36.

7. Lichter PR, Shaffer RN. Diagnostic and prognostic signs inpigmentary glaucoma. Trans Am Acad Ophthalmol Oto­laryngol 1970;74:984-98.

8. Farrar SM, Shields MB, Miller KN, Stoup CM. Risk factorsfor the development and severity of glaucoma in the pig­mentary dispersion syndrome. Am J Ophthalmol 1989;108:223-9.

9. Campbell DG. Pigmentary dispersion and glaucoma. A newtheory. Arch OphthalmoI1979;97:1667-72.

10. Schenker HI, Luntz MH, Kels B, Podos SM. Exercise-in­duced increase of intraocular pressure in the pigmentarydispersion syndrome. Am J Ophthalmol 1980;89:598-600.

11. Epstein DL, Boger WP III, Grant WM. Phenylephrine pro­vocative testing in the pigmentary dispersion syndrome. AmJ Ophthalmol 1978;85:43-50.

12. Haynes WL, Johnson AT, Alward WLM. Inhibition of ex­ercise-induced pigment dispersion in a patient with the pig­mentary dispersion syndrome [letter]. Am J Ophthalmol1990;109:601-2.

13. Mitsui Y, Takagi Y. Nature of aqueous floaters due to sym­pathomimetic mydriatics. Arch Ophthalmol 1961;65:626­31.

14. Richardson TM, Hutchinson BT, Grant WM. The outflowtract in pigmentary glaucoma. A light and electron micro­scopic study. Arch Ophthalmol 1977;95:1015-25.

15. Lempert P, Cooper KH, Culver JF, Tredici TJ. The effectof exercise on intraocular pressure. Am J Ophthalmol1967;63:1673-6.

16. Marcus DF, Krupin T, Podos SM, Becker B. The effect ofexercise on intraocular pressure. I. Human beings. InvestOphthalmol 1970;9:749-52.

17. Marcus DF, Krupin T, Podos SM, Becker B. The effect ofexercise on intraocular pressure. II. Rabbits. InvestOphthalmol 1970;9:753-7.

18. Leighton DA. Effect of walking on the ocular tension inopen-angle glaucoma. Br J Ophthalmol 1972;56:126-30.

19. Myers KJ. The effect of aerobic exercise on intraocularpressure. Invest Ophthalmol 1974;13:74-7.

20. Shapiro A, WolfE, Ferber I, Merin S. The effect of physicalactivity on the intraocular pressure of glaucomatous patients.Eur J Appl Physiol 1983;52:136-8.

21. Epstein DL, Freddo TF, Anderson PJ, et al. Experimentalobstruction to aqueous outflow by pigment particles in livingmonkeys. Invest Ophthalmol Vis Sci 1986;27:387-95.

22. Smith DL, Kao SF, Rabbani R, Musch DC. The effects ofexercise on intraocular pressure in pigmentary glaucomapatients. Ophthalmic Surg 1989;20:561-7.

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