Indian Journal of Ophthalmology

: 1960  |  Volume : 8  |  Issue : 1  |  Page : 16--24

The importance of scleral rigidity in ocular tonometry

J Francois 
 Ophthalmological Clinic of the University of Ghent, Belgium

Correspondence Address:
J Francois
Ophthalmological Clinic of the University of Ghent

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Francois J. The importance of scleral rigidity in ocular tonometry.Indian J Ophthalmol 1960;8:16-24

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Francois J. The importance of scleral rigidity in ocular tonometry. Indian J Ophthalmol [serial online] 1960 [cited 2020 Jul 6 ];8:16-24
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When the ocular tension is deter­mined with the aid of a SCHIOTZ tonometer the corneal indentation caused by the bar of the apparatus de­pends on two factors, viz.: the ocular tension on the one hand and the scle­ral rigidity on the other.

Rigidity and elasticity do not denote the same condition. The rigidity of a body is the resistance which it offers to a change in its shape, while its elasticity is its ability to undergo a change in its shape and to return to its previous shape.

The rigidity of the shell of the eye fundamentally results from physical characteristics of the sclera and, in addition, from corneal and uveal properties.

When a tonometer is applied to the eye, the indentation of the cornea causes displacement of fluid giving rise to scleral distention and a simul­taneous increase in ocular tension; the quantity of fluid driven from the eye­ball is negligible.

As the weight used is increased, the corneal indentation increases; thus, when ocular tension is determined with the aid of two different weights, two different tonometric readings are obtained.

The greater the difference between these two tonometric readings, the greater the scleral rigidity, as express­ed by FRIENDENWALD (1957) in the following equation


in which Pt 1 , and V 1 , represent the tonometric pressure and the volume of the indentation caused by the bar in the determination made with the first weight, whereas Pt 2 and V 2 re­present the respective values as ob­tained with the second weight; K re­presents the coefficient of ocular rigidity.

 Technique of Measuring Scleral Rigidity

If scleral rigidity is to be determined then it is necessary to use FRIEDEN­WALD's tables of calibration and a perfectly standardized tonometer, ass the least anomaly in the curvature of the bar or in the concavity of its in­ferior surface produces considerable errors.

To ensure that determination of ocular rigidity be of sufficient exact­ness it is necessary

1. To compare indentations of suf­ficiently different volume. The weights used should be 5.5 and 10 g. or, better even if possible, 5.5 and 15 g­

2. To make several determina­tions. In practice it is difficult to make a determination throughout 5-6 consecutive days but it is possible to take the average of three determina­tions made successively with the two weights; the arithmetical average of the three values of deviations obtain­ed with each weight is then calcula­ted.

The first average value is plotted on the curve of 5.5 g., and the second on the curve of 10 or 15 g, in FRIEDENWALD's monogram [Figure 1]. An oblique line AB is thus obtained, which is subsequently dis­placed parallel with its original posi­tion, by means of a square and a flat ruler until it passes through the intersection of ordinate and abscissa (CD). After this, the ocular rigidity can be read from the arc in the left lower corner of the monogram.

Subsequently, in order to determine the corrected ocular tension, the square is moved upward along the ruler again until it encounters on the 5.5 g. curve, the value of deviation obtained at the first of the three determinations of which the average was taken (line EF). The figure then indicated by the square on the ordinate is that of the ocular tension corrected by the rigi­dity factor.

Normally, the ocular rigidity varies, between 0.0200 and 0.0250, as shown in the [Table 1].

FRIEDENWALD's tables of cali­bration have been calculated for an average ocular rigidity of 0.0215, so that rigidities below 0.0215 affect to­nometric determinations by an insuffi­ciency error, while rigidities over 0.0215 affect the determinations by an error of excess.

If a glaucoma is suspected, for one reason or another, although ocular tension seems normal (below 22 mm. Hg), and particularly in the case of a tonometric reading above 22 mm. Hg, in the absence of any sign of glaucoma, then ocular rigidity must be determined.

If the coefficient of rigidity is nor­mal, the tonometric readings are correct.

If, however, the coefficient of rigi­dity is increased (over 0.0215), then the tonometric findings show an error of excess. The ocular tension would seem to be exaggerated, which evi­dently entails the risk of regarding a normal eye as a glaucomatous eye. We are familiar with several instances of this kind, in some of which there was even an operation. Yet it is only necessary to determine scleral rigidity to find that, after correction, ocular tension will have a normal average. The following case reports are eluci­dative in this respect

Case 1.D).,Cecile, aged 64, was exa­mined for conjunctival irritation. The eyeballs themselves seemed normal; the ocular fundus and the optic disc showed no anomaly.

Yet the Schiotz tonometer (weight 7.5 g.) indicated increased ocular ten­sion, viz.: 31.8 mm. Hg in both eyes, which did not prevent visual acuity from being perfect (0.8 on the right, and 1.0 on the left) and the field of vision from being complete (Gold­mann, tests 5/4, 1/4 and 1/3).

In view of these findings, determi­nations of ocular regidity were resort­ed to. The average of six deter­minations in each eye (RE : 3.08 for weight 5.5 g. and 7.16 for weight 10 g.; LE : 2.02 for 5.5 g. and 6.60 for 10 g.) gave a coefficient of 0.033 on the right, and 0.037 on the left. The corrected tension was therefore 19 mm. Hg on the right and 15.5 mm. Hg on the left - values to be considered entirely normal.

Case 2.-C., Jean, aged 54, was exa­mined for progressive loss of vision in the course of 18 months. The examination showed a discrete disturbance in the anterior one-third of the corneal parenchy­ma and an incipient nuclear cataract. The other refractive media, the ocular fundus and the optic disc., pupil reflexes and motility' were normal. Visual acuity was 3/10 in both eyes.

The ocular tension was increased as determined on the Schiotz tonometer, viz.: 27.3 mm. Hg on the right, and 25.3 mm. Hg on the left.

Tonography, however, yielded a normal result, viz.: on the right R = 4.8 (C - 0.020), and on the left R = 4.2 (C = 0.021). The field of vi­sion was likewise normal in various tests.

Determination of scleral rigidity (average of 6 determinations) gave a coefficient of 0.038 on the right, and 0.043 on the left, i.e. a markedly in­creased coefficient, so that the cor­rected ocular tension was actually 15.5 mm. Hg on the right, and 10 mm. Hg on the left. The increased ocular tension was therefore only apparent.

Whereas an increased rigidity may give rise to a pseudo increase in ocu­lar tension, a low rigidity, on the other hand can mask, a genuine hy­pertension. In such a case an ap­parencly normal ocular tension can prove -- after correction - to be increased.

This is particularly frequent in cases of myopia and endocrine exophthalmos.

I. Myopia.

In marked myopia (exceeding 5 D), there is a considerable diminution of scleral rigidity due to thinning of the sclera. This fact, first observed by FRIEDENWALD (1931) and con­firmed by GOLDAIANN & SCH­A4IDT (1957), was also verified by WEEKERS et al. (in 1957). These authors found an average rigidity of 0.0214 which corresponds with the normal value in 26 subjects suffer­ing from myopia (-1 to -5 D.) In 48 cases of myopia exceeding --5.50 D., however, the average rigidity was no more than 0.0151. This difference is statistically significant.

Determination of scleral rigidity in cases of marked myopia makes it possible to reach the following conclusions

1. Contrary to common belief, the myopic eye is not hypotensive.

2. Ocular hypertension may remain unrecognizable in cases of myopia.

3. In the case of recognizable signs glaucoma in myopic subjects, the condition is sometimes incorrectly referred to as glaucoma "without hypertension".

4. Ocular hypertension as shown by the Schidtz tonometer is as a rule more marked than is indicated by simple tonometric determination.

The following is a report on a case of myopic glaucoma, apparently with­ hypertension.

Case 3-Mrs. K., Marcel, aged 49, lost the right eye following detachment of the retina. The left eye was examined and showed the following particulars

1. very marked myopic choroiditis with atrophic plaques and Fuchs spot.

2. The optic disc was pale and seemed a little excavated.

3. The ocular tension according to the Schiotz method was normal, viz.: 18.5 mm Hg.

4. The visual acuity was 0.4 (6/15) after correction (-17 D. sph. -0.5 D. cyl. axis at 172º).

5. The field of vision showed a nasal de­ficiency, characteristic of glaucoma [Figure 2].

6. Determination of scleral rigidity yield­ed a coefficient of 0.012, so that the corrected tension was -24 mm. Hg (i.e. considerably- higher than it ap­peared to be at tonometry).

The diagnosis of glaucoma was therefore obvious.

Since the introduction of determi­nation of scleral rigidity, glaucomata without hypertension have become exceptional. Yet they do exist, as de­monstrated by the following observa­tion:

Case 4.-B., P almyre, aged 57, com­plained of visual difficulties over a two­ year period.

Objective examination of the eyes only revealed a hollow disc, slightly atrophic, in both eyes.

The visual acuity was 10/10 in both eyes. The field of vision showed the nasal deficiencies characteristic of glaucoma [Figure 3].

In no case did the ocular tension exceed 21.8 mm.. Hg in either eye throughout a year of observations; it always varied between 14.3 and 21.8 mm. Hg.

Tonographic results were variable right eye R = 4-10, left eye R= 4.5 -10.

Gonioscopy showed an iridocorneal angle which was open and normal in both eyes.

Scleral rigidity was normal: 0.020 on the right and 0.021 on the left; the corrected tension was therefore 15 mm. Hg on the right, and 13.5 mm. Hg on the left.

This, therefore, was a genuine case of glaucoma "without hypertension".

II. Endocrine exophthalmos.

Distinction is made between two types of endocrine exophthalmos, viz. thyrotoxic or hyperthyroid exophthal­mos, and thyrotropic or ophthalmo­plegic, oedematous exophthalmos.

A. Thyrotoxic exophthalmos. This is the exophthalmos seen in Graves disease. It is associated with retrac­tion of the superior palpebra by a spasm of the palpebral levator muscle. This spasm explains all the other changes usually seen, and particularly the Von Graefe sign, characterized by failure of the superior palpebra to fol­low a downward movement of the eyeball.

These manifestations, which would seem to depend on an increase in tonus of the sympathetic system, are not associated with either chemosis or diplopia, although heterophoria or a deficiency in convergence are not un­common.

B. Thyrotropic exophtalmos . This exophthalmos is seen either in hyper­thyroids treated by medication or surgery, or spontaneously in subjects apparently free of any thyroid symp­tom.

This exophthalmos, which may be very marked and give rise to lagoph­thalmos, is associated with ocular paresis and more oz less marked che­mosis.

It has been attributed to pituitary secretion of an exophthalmic substance related to thyrotropic hormone and producing an increase in the water con­centration of various tissues (WYBAR, 1957).

ALBERT (1945) was able to induce exophthalmos in a minnow by inject­ing an anterior pituitary extract. DOBYNS and WILSON (1954) de­monstrated that injection of serum from subjects suffering from thyrotro­pic exophthalmos produced exoph­thalmos in goldfish, whereas serum from normal subjects had no such effect.

The two types of exophthalmos can be combined, and it is not uncommon to find that a thyrotoxic exophthal­mos, when treated, becomes a thyro­tropic exophthalmos.

Differential diagnosis between these two forms of exophthalmos can be based on an injection of the patient's serum into a goldfish; it is far more simple, however, to differentiate by determining the ocular rigidity.

WEEKERS & LAVERGNE (1958) have demonstrated that scleral rigidity is normal in thyrotoxic exophthalmos, whereas it is considerably diminished in thyrotropic exophthalmos. We have been able to confirm this.

In 26 cases of thyrotoxic exoph­thalmos, WEEKERS & LAVERGNE (1958) found an average rigidity of 0.0226. In all our cases we likewise obtained a normal rigidity value.

In 8 cases of thyrotropic exophthal­mos, however, ocular rigidity was con­siderably diminished (3 cases by WEEKERS & LAVERGNE, and 5 personal observations) ; the average coefficient for 16 eyes was 0.0106, with a minimum of 0.0080 and a maximum of 0.0155. [Table 2]

Of these 8 patients, 6 were hyper­thyroid and under treatment (radio­active iodine, antithyroid substances) ; the other two showed no goitre or any sign of Graves' disease; they were not treated.

The diminution in scleral rigidity would seem to be in accordance with imbibition of the sclera by water, which alters its physical properties. This change is clinically revealed by more or less marked chemosis which accompanies thyrotropic exophthalmos.

The diminution in scleral rigidity seen in thyrotropic exophthalmos is not only a diagnostic aid but also makes ii possible to demonstrate ocular hy­pertension, which is relatively fre­quent: 4 patients out of 8 showed an increased ocular tension. Yet this hy­pertension may well remain unre­cognized if ocular tension is not cor­rected by means of rigidity values.

It is true that this hypertension is as a rule hardly marked; it can, how­ever, give rise to changes in the field of vision (WEEKERS & LEVERGNE, 1958). It is not associated with any change in the iridocorneal angle. Its development parallels that of the ex­ophthalmos and it disappears as the exophthalmos disappears. It is un­doubtedly because of its short stand­ing at the time of the first examina­tions that its functional symptoms are not as a rule very marked.

The hypertension is favourably influenced by any therapy which reduces the secretion of aqueous humour (diamox, neptazane, adrena­lin). Myotics, however, hardly affect it.

In exceptional cases there may be an acute crisis, with closure of the iridocorneal angle (' WEEKERS & LAVERGNE, 1958) ; medication is then, insufficient, and an operation must be resorted to.

It is still impossible to decide whe­ther ocular hypertension in thyrotro­pic exophthalmos is due to an increaed resistance or to increased secretion of aqueous humour: the diminution in scleral rigidity makes it impossible to interpret the tonographic curves. It seems, however, that an increase in resistance following an increase in in­trascleral venous tension is involved.

It must be pointed out once again that the ocular tension is normal in thyrotoxic exophthalmos.

A few remarks on non-inflammatory exophthalmos are appropriate here. It is generally understood that an orbital tumor is suggested by unilat­eral exophthalmos, whereas bilateral exophthalmos indicates hyperthyroid­ism. The problem, however, is not quite so simple. The following facts must be taken into account:

1. The exophthalmos can be only apparently unilateral. Generally speak­ing, the apex of the cornea is localized about 12 mm. in front of the temporal orbital margin. There are, however, a great many exceptions to this rule. And an exophthalmos of 18 mm. is therefore not necessarily pathological.

On the other hand, the impression may be that the exophthalmos is uni­lateral whereas in fact it is bilateral, although more marked on one side than on the other (e.g. 24 mm. on the right, and 20 mm. on the left).

2. Another important fact is that even a unilateral exophthalmos can be due to hyperthyroidism, pituitary hy­perfunction or chronic orbital myositis.

In an attempt at differential diagno­sis, let us first consider the symptoms of an orbital tumour :

1. The chief symptoms - exoph­thalmos - is progressive and irredu­cible.

2. There is often more or less marked ptosis with paresis of one or several ocular muscles. The internal muscles (pupillary sphincter and ciliary muscle) are hardly ever affected.

3. According to the localization, there is sometimes papilloedema or atrophy of the optic disc, which obvi­ously involves functional disturbances.

4. Corneal sensitivity may be dim­inished.

The clinical diagnosis can then be confirmed by the following examina­tions :

1. Radiography or, better even, tomography of the orbit.

2. Radiography after :

a) Injection of air, which does not penetrate the tumour mass and therefore clearly delimits the growth.

b) Injection of a contrast medium, which fills the free spaces and outlines their con­tours.

3. Arteriography.

4. A biopsy.

I. It has been pointed out that uni­lateral exophthalmos may be due to orbital myositis. The following case is an example

Case 5. - The patient was a man aged :12 who underwent a sympathectomy for arteritis 4 years previously. In September 1956 the right eye became exophthalmic. An orbitotomy revealed no tumour. The patient was examined in March 1957, when he showed the following symptoms :

1. Exophthalmos, marked on the right (27.5 mm.) and less marked on the left (22.5 mm).

2. In repose, the gaze was directed straight ahead but the right eyeball turned down.

3. On the right there seemed to be com­plete paralysis of the superior rectus mus­cle, and paresis of the internal and the external rectus muscle; the inferior rectus muscle retained its normal function.

4. The conjunctival and episcleral veins of the right eye were dilated, but there was no chemosis properly speaking.

General examination was negative. There was no sign of hyperthyroidism, emaciation, tachycardia or asthenia. The BAIR was normal (+3%)

The thyroid was slightly hypertro­phic. Absorption of radioactive iodine was accelerated. These two signs indicated overstimulation.

The question may be raised whether this case was one of thyrotropic ex­ophthaloms.

Verification of the passive move­ments of the eyeball, however, showed that it was impossible to displace the eye in upward direction. This excluded paralysis of the superior rectus muscle and indicated myositis of the inferior rectus muscle. This diagnosis was con­firmed by the fact that the eyeball, even in repose, was turned down.

The cause of this myositis was pro­bably hypophyseal, as the exophthal­mos was bilateral, and as the metabol­ism was not increased.

This case (and other similar cases) shows that the following measures should be taken in the case of exoph­thalmos :

1. Verification of the position of the eyeball, recording its possible de­viation in one direction or another.

2. Verification of the passive mobi­lity of the eyeball; when it is impossible to displace the eye within the region of action of an apparently paralysed muscle it must be concluded that there is a lesion of the antagonist muscle (which cannot be extended due to myositis); the diagnosis of paralysis should then be rejected.

II. Exophthalmos, even when uni­lateral, may be of endocrine origin, in which case:

1. The exophthalmos is only ap­parently unilateral (it is simply more marked on one side than on the other).

2. There is retraction of the sup­erior palpebra, which does not follow the eyeball in its downward movement.

3. There is often white chemosis with dilation of episcleral veins and orbital myositis.

It has thus been shown how a dif­ferential diagnosis can be made bet­ween thyrotoxic exophthalmos and thyrotropic exophthalmos.


The technique of measuring scleral rigidity is described in detail.

The importance of measuring scleral rigidity in arriving at the true tension state in an eye is discussed. Apparent­ly high but normo-tensive and appar­ently hypo-tensive but really glaucom­atous cases can be unmasked. This is illustrated by 3 cases.

One case is described of glancoma with low-tension even after correction for rigidity.

The role of myopia and thyrotropic states in lowering scleral rigidity are discussed.

A differential diagnosis between thyrotropic and thyrotoxic exophthal­mos is fully discussed.[13]


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