Part 9

That the squinting eye really possesses its full share of the visual field can easily be proved (especially in divergent squint) by the aid of a perimeter. The best eye is covered with a red glass, so that the objects projected from the fixation point, as well as the excentric field of vision of this eye, appear red. As soon as the test object moves towards the side of the squinting eye and enters the visual area covered by the latter, it appears in its natural white colour, and this in most cases before it has reached the centre of the retina of this eye.

Another proof that the squinting eye is really used for vision appears to me to lie in the fact that persons who squint, provided of course that the vision of the eye concerned is not very defective, do not show that uncertainty in the estimation of distance, which is apt to prove so troublesome to those who have only monocular vision.

If, then, the view of the constant suppression of the retinal images of the squinting eye is untenable, how is it to be explained that squint as the result of paralysis of the ocular muscles causes diplopia, while concomitant squint does not? The answer to this question is clear as soon as we abandon the supposition of a congenital retinal identity, and look instead upon the relation of the eyes to each other as harmonious; identity, or co-ordination as something acquired. Central fixation is congenital and depends upon anatomical conditions, for as the macula lutea is anatomically the most perfect part of the retina, it is natural that the new-born child soon learns to place this part of the retina opposite objects which attract its attention, and therefore those relations of the eyes to each other are naturally developed. For instance, if both eyes (Fig. 1) are directed to the distant point a, the image of point b, situated at the same distance, will fall on the inner half of the retina of the left eye; the left eye will now learn by experience to refer inner retinal images to objects lying to the left of the fixation point; at the same time, however, with binocular fixation, the right eye learns to seek the images of the temporal half of its retina in the left field of vision, and vice versâ. From this it is easy to trace the laws of binocular diplopia. For example, let a in Fig. 2 be the fixation point, while at the same time the image of b belongs in both eyes to the temporal half of the retina. Now, as we have already seen, the right eye has learnt to refer temporal retinal images, to objects lying to the left of the fixation point, while for the same reasons the left eye projects temporal images to the right. While then point a is seen binocularly singly, point b appears double, and certainly the image of the right eye is projected to the left of the fixation point, and that of the left eye to the right of it, in other words, crossed diplopia is present. But the eyes are divergent relative to point b; double images then which occur as a result of divergence (whether relative or absolute) must appear crossed, and one will easily be able to infer that for the same reasons those double images which occur in consequence of convergence, must be homonymous. All this, however, only with the presupposition, that the habit of binocular fixation is already fully developed; any disturbance of the same, in whatever way (by prisms, mechanical displacement of the eyes, paralyses of the ocular muscles, or by those forms of squint which arise after childhood is past) causes the double images to illustrate the law above explained. Certainly diplopia may be absent even then, but only in very rare instances. Now and then this happens in objectively proved ailments of the ocular muscles, where the patients complain of disturbed vision, which disappears immediately on the exclusion of one eye (see Case 12), a method of relief they usually discover for themselves; thus the indistinct vision is seen at once to be a disturbance of binocular vision. Many such patients learn to see the double images which formerly escaped them, after they have been instructed how to do so during the examination. With others, all efforts are in vain, it is impossible to render them conscious of the double images, notwithstanding that the presence of the binocular disturbance of vision proves that the habit of binocular fixation exists. This apparent contradiction is explained, if one reflects that the physiological basis of vision rests on a series of conclusions. The first thing which strikes us as a result of binocular fixation is, that the images of the centres of the retinæ may be referred to one and the same region of the room, and this experience will be retained, even if the images on the centres of the retinæ represent different objects in consequence of paralysis of the ocular muscles; the images are notwithstanding referred to one and the same part of the room, all objects are thrown together promiscuously, and the consequent embarrassment is of course removed directly one eye is shut. The experience of those patients whom it is impossible to render conscious of double images, despite the habit of binocular fixation, reaches up to this point. A second conclusion belongs to diplopia, and for that it is necessary to seek out from the confusion of objects, the two retinal images belonging to one and the same object, and the majority of people, though not all, take this second step also. It is seen at the same time that the opinion held by Donders, that diplopia is absent in squint, does not suffice, for this reason, because the image in the deviating eye is too excentric. What becomes then of the image lying in the centre of the retina?

The absence of diplopia in squint may be explained quite simply by the fact that the habit of binocular fixation has not been learnt or has been forgotten; one can learn nothing that cannot be again forgotten. The normal fusion of the visual fields can only develop in consequence of binocular fixation, and diplopia is only possible when some kind of binocular fusion exists. If no binocular fusion exists, then all possibility of diplopia is excluded. And why should those who squint from their earliest childhood not see well with both eyes, but yet with each separately, just as is the case with animals with laterally placed eyes? For example, in Fig. 3 there is convergent squint of the left eye, the right eye fixes the point a, whose retinal image is cast at a' in the left eye; the direction outwards in which these images are projected is discovered by drawing a straight line from a to c (the optical centre of the eye); suffice it to say that point a is seen by each eye in the direction in which it really stands.

But although both eyes see at the same time, yet the close relation which in binocular fixation develops between the centres of the retinæ does not occur in squint; firstly, because the retinal area in the squinting eye which corresponds to the fixation point is too excentric, and secondly, because the angle of the squint often changes. In binocular fixation, the fixation point of one retina answers to the corresponding point of the other; in squint, on account of the varying size of the squint angle, if a like relation develops between the eyes, the fixation point of one retina must correspond to a larger area of the other. Possibly this explains a fact that is often to be observed. In those cases of squint where diplopia can easily be caused by covering one eye with a red glass and the other with a vertically deviating prism, the double images disappear on rotation of the prism round the axis of vision, as soon as the angle of the prism reaches an angle of about 45°. The occurrence of double images shows that there exists for the upper and lower parts of the retinæ a community of vision by no means coinciding with the identity principle. The disappearance of the diplopia can be explained by the fact that the variations of the squint angle take place chiefly in the horizontal direction. Therefore the area in the squinting eye that corresponds to the fovea centralis of the fixing eye must be more extensive in the horizontal than in the vertical direction. Alfred Graefe has designated this phenomenon as "regional exclusion." Whilst then a sort of community of vision exists for the upper and lower parts of the retinæ, the sensations of the retinal area lying in the horizontal plane of the macula lutea of the squinting eye must be suppressed. The physiological occurrence of a suppression of the retinal images, as far as we are able to investigate it, always refers to the whole retina; however, the possibility of a "regional exclusion" should not be excluded to begin with; but in the inductive sciences it is for us to ask first, whether an incident really happens, and not whether it is possible. The fact from which Alfred Graefe draws his inference is not, as we have just seen, to be explained in any other way, and the ophthalmoscopic test described on p. 65 proves that also in these cases of "regional exclusion" both eyes are used for vision.

In many cases of periodic squint the condition of binocular vision is very interesting. Binocular fusion may be quite absent even in normal position of the eyes; on the other hand the non-occurrence of diplopia in squint does not prevent the occurrence of perfect binocular fusion with a normal position. In periodic outward squint I have sometimes seen binocular fixation without the existence of binocular fusion; the excluded eye deviates outwards, but as soon as it is free it puts itself into fixation, whilst neither with prisms nor stereoscope can anything other than alternating vision be proved, i. e. neither binocular diplopia nor fusion.

If squint arises when the habit of binocular single vision has become confirmed, diplopia is always present, at least at first; even children of six to seven years old make this statement uninvited, but they soon get accustomed to the new relations, and after a short time it is impossible to make them see double images (see Case 42). Habits cling more closely in adults, therefore that form of convergent squint in particular, which usually develops quickly in myopia of average degree, causes annoying diplopia to last for a longer time. For just when these patients want to employ binocular vision in order to estimate distance correctly, diplopia occurs to hinder and confuse them.

It is otherwise with the relative divergence which is developed in consequence of myopia. At first diplopia is present here for a short time; in this case circumstances are specially favorable to a temporary suppression of the deviating eye; the fixing eye receives large distinct images to which the attention is directed. Meanwhile the relatively divergent eye is usually turned to other more distant objects that furnish indistinct retinal images, from which the attention is easily diverted. The habit of suppression may become so dominant that binocular fixation continues to exist for distant objects and the presence of binocular fusion is easily traceable, while for near objects, which are monocularly fixed with relative divergence, it is impossible to render the patient conscious of the images of the deviating eye.

Considerable squint is by no means necessary for the cessation of normal binocular single vision; slight, frequently recurring deviations are quite sufficient, as in those cases where want of control renders physiological innervation for convergence more difficult. Double images are present here, although not in a troublesome way, as is usual in relative divergence, but binocular single vision does not exist even for distance. The reason for this does not lie in the impossibility of fixing the same object simultaneously with both eyes, for the objectively proved deviation may be extremely slight. A union cannot be obtained even by prisms. If crossed double images are present close together, a prism of a few degrees base inwards suffices to make them homonymous. The habit of binocular single vision is lost, in consequence of that disturbance to the innervation of the interni which is designated as insufficiency of the same.

The stereoscope, as well as the prism, is useful for testing binocular single vision, especially when it is suitably modified for the purpose. The prismatic glasses usually attached to stereoscopes are here quite superfluous. The advantage of the prismatic deviation consists solely in the fact that the centres of the images fixed for the macula lutea on each side can be removed farther from one another than the distance apart of the eyes amounts to, so that a greater extension of the visual area is rendered possible. Ordinary stereoscopic pictures are quite useless for testing binocular vision; it is a question here of employing diagrams, which contain on the one hand very prominent identical figures stimulating binocular fusion but which, on the other hand, offer for each eye special attractions not present in the visual field of the other. Further, it is desirable to regulate the stereoscope so that the glasses are not firmly inserted, but that glasses from the trial case may be applied according to the condition of refraction of the patient and the distance of the stereoscopic images.

The stereoscope is generally used with the greatest advantage in those cases where there is no conspicuous deviation, and by testing binocular vision conclusions may be drawn as to whether normal binocular fusion exists or has disappeared in consequence of the squint.

It is desirable to use both methods of investigation, that with the stereoscope as well as prisms, as each test has its own value. One who at once combines the stereoscopic fields of vision certainly has binocular single vision; in other cases this is only so far lost that the stereoscopic combination does not take place at once but only after some trouble. Care must be taken, especially when one eye has defective vision, that the corresponding visual field contains objects sufficiently large and easily recognisable, as very small objects which do not correspond to the lowered visual acuity are easily overlooked. It sometimes happens that both fields are seen at the same time, but that there is no fusion; finally it happens frequently that there is complete suppression of one visual field. In testing with prisms it may appear doubtful as to whether binocular fusion or suppression of one eye exists; however, the stereoscope at once gives us certain information. It must not be forgotten that the altered relations between the eyes, which are always possible in squint, also appear at the same time; he who sees double with prisms, may yet be able completely to suppress the stereoscopic visual field of one eye. Binocular fusion, suppression of the squinting eye and simultaneous vision with both eyes without binocular fusion can alternate in the same individual. Von Kries has come to the same conclusion, and if our colleague is unable to explain all the phenomena of binocular vision that he could observe in his own case, we need not be astonished if we sometimes hear from our patients statements that appear incomprehensible and unphysiological.

At any rate it is evident that the absence of diplopia in squint can easily be understood, without adopting the arbitrary idea of a constant, habitual suppression of the image of the squinting eye.

VISUAL ACUTENESS OF THE SQUINTING EYE.

Whether the state of refraction or the condition of the muscular equilibrium is held to be the chief cause of squint, defective vision of one eye will always have to be acknowledged as one of the most important favouring circumstances; in order to cure squint it is important to have regard to the visual acuity of both eyes, and not only to the defective condition. But this is no easy matter.

First it is to be observed, that most cases arise at an age when an objective determination of refraction is possible, but when the visual acuteness cannot be determined. Even in children who have received slight instruction, it is frequently difficult to distinguish whether imperfect knowledge of the letters or faulty visual acuteness is the cause of the non-recognition of the test-letters; when testing the vision of children it is often better to use figures than letters.

Further, in these cases it is much to be desired that the habit of determining the refraction and visual acuteness at the same time should be discontinued, particularly in reduced visual acuteness, as the test-tables only contain a few letters, which have to be recognised at a distance of 5 to 6 metres. If they have once been read with one eye it may easily happen that in testing the second eye they are repeated from memory, without being clearly recognised; even a child soon learns the few letters by heart. Therefore, when it has been a case of determining the visual acuteness I have always conducted the examination at a distance of one metre, as the choice of letters or figures which can be employed at this distance is much larger than for greater distances. In every case the reading of test-letters must be used as an additional means of examination. We must never forget that the test of vision is a perfectly subjective examination, and that we are obliged first of all to accept the statements of patients as they are given without knowing what they are worth. I have met with patients in the most highly educated classes of society who, in intra-ocular troubles, for example, hæmorrhage of the retinal artery in the macula lutea, could not distinguish the largest type in the first examination, and the next day (perhaps with slight difficulty) could read small print.

Such inaccuracies may continue to exist during repeated examinations and for long periods. One of my patients, for instance, who first came under treatment in the year 1873, had extreme myopia in the left eye with good visual acuity; with the right eye, which was also myopic, and had suffered for several years from choroiditis of the macula lutea he could read only No. 20 Snellen, and a year later 7-1/2 was read with difficulty, word by word. Choroiditis of the macula lutea gradually developed in the left eye, and in the same proportion the statements as to visual acuteness of the right eye improved, so that finally at the end of 1881, 0·5 was read with difficulty with this eye, while the left still sufficed to read 0·4 (at about 5 cm.). As I tried to comfort the patient, who was very anxious about his left eye, with the fact that the right eye had considerably improved in the course of the year, he replied that he might previously have seen just as well with the right eye if he had only taken the trouble, this was certainly my own opinion.

The attention and intelligence shown by patients during examination materially influences its results, and one should never hold the first trial of vision to be conclusive. We must always remember, however, that all conclusions drawn from visual acuteness become more unreliable in proportion as the latter is slight. We must attend to some peculiar difficulties in testing the vision of those who squint or we shall be liable to make great mistakes. When testing the squinting eye, particularly in children, it is not sufficient merely to cover the other or to hold the hand over it, for they know how to bring the usual eye into fixation by holding the head on one side or peeping between the fingers; we must keep it carefully closed with a bandage.

It is still more frequently the case that visual acuteness is stated to be less than it is in reality. The result of always using the better eye for fixation is, that fixation is not learnt with the weaker one. Even where there is no squint we see very frequently that in one-sided hypermetropia the accommodation is only used in that proportion which has become habitual to the emmetropic eye and does not therefore suffice to produce clear retinal images, while good visual acuteness is obtained by means of the correcting convex glasses. In the case of squinters (even without difference of refraction) it happens very frequently that the first statements as to the visual power are considerably below the truth. Patients who assert that they can only read the largest print with difficulty, frequently read smaller, and even the smallest type without more trouble, and we must be careful to ascertain this at first. Accurate reports are usually obtained more quickly by means of convex glasses or eserine. In any case insufficient accommodation is, according to this, one of the difficulties, but not the only one, which has to be overcome before the squinting eye can be put into fixation. We can understand that the innervation necessary for distinct vision can be set aside even without loss of visual acuteness, just as we see the movement of convergence disappear without the interni losing their capacity for contraction.

In order to explain the relation between squint and defective vision, we must first consider the question hitherto neglected, or what is worse, answered with preconceived opinion, as to whether the same form of defective sight which is so common in squint also occurs without squint. No one doubts the existence of congenital amblyopia, nevertheless it has received but little attention in the handbooks on ophthalmology. Leber, for instance (in the well-known compilation, vol. v), does not mention it at all.

A more or less considerable reduction of visual acuteness, with good field of vision, normal sense of colour and normal ophthalmoscopic condition, are characteristic of congenital amblyopia. Colour-blindness may of course be present at the same time. I also hold as probable the very rare occurrence of congenital defects of the visual field in good central vision, but I will reserve for the present the few observations I possess on the subject.

Together with congenital defective vision we must consider the depreciation in visual acuteness usually present in nystagmus, although it might be asserted that it can neither be the cause nor the result of the nystagmus, for we find very considerable degrees of congenital defective sight in both eyes without nystagmus, as well as nystagmus with remarkably good visual acuteness. Not to complicate the question, however, I have excluded all cases of nystagmus from the following investigation. All cases of myopia of higher degree (i. e. of more than 6 D.) have also been excluded, as in such cases for various well-known reasons the full visual acuteness is never present. In the case of individual patients who remained for years under my observation I have been able to convince myself that visual acuteness decreased in accordance with the increase of myopia; on the other hand, however, it appeared to me very probable that just those cases of myopia, which from the beginning do not possess full visual acuteness, have a special tendency to increase quickly.

For instance, if the examination of a hypermetropic eye, whose defect can be exactly determined by means of the ophthalmoscope, shows very faulty visual acuteness which is but slightly or not at all improved on correction of the hypermetropia, it is clear that the cause of defective sight is not to be sought in the hypermetropia. It is just the same with astigmatism. In defective vision with astigmatism proved by means of the ophthalmoscope, how frequently it is the case that not even the slightest improvement can be obtained with cylindrical glasses. This is usually attributed to the presence of an irregular astigmatism situated near the asymmetric meridian. If we illuminate the eye by means of a plane mirror, and observe one spot on the pupillary area which looks sometimes bright, sometimes dark, during slight rotations of the glass, this appearance can only be caused by the above-mentioned irregularity of the refraction of light, and it will be easy to determine whether the same takes place in the cornea or in the lens. But if this appearance is not present then irregular astigmatism cannot be proved. It is purely intentional, or a play upon words, if we refer an existing defective sight to an optic cause which cannot be proved. For instance, if haziness of the cornea exists, it is not difficult to learn to estimate by practical experience whether the amount of visual disturbance corresponds to the optic irregularities caused by the opacities and irregular refraction of the cornea. Slightly nebulous corneæ with disproportionately bad vision were therefore included in the following statistics; however, they do not influence the result as there are only ten cases in all. On the other hand, considerable opacity of the corneæ or cases which were complicated with anterior synechia, &c., were excluded from the statistics.

If then we find defective vision, the development of which has not been noticed by the patient, together with normal ophthalmoscopic condition and full visual field, and if it is further seen that the condition remains unchanged for years, we have every reason for considering the defective sight to be congenital. The statements of patients must of course be received with caution. If congenital amblyopia of moderate degree exists in both eyes, patients do not usually know that it is possible for anyone to see better; if the congenital defect is one sided, it is generally only casually noticed on closing the better eye. We can scarcely doubt that it is a case of congenital amblyopia if it happens in children. Acquired defective sight without ophthalmoscopic cause seldom occurs among children. I have seen a few cases as a result of severe cerebral disease (hydrocephalus, for example); so-called anæsthesia retinæ, or amblyopia marked by contraction of the visual field is not quite so rare. It is easy to avoid confounding both these cases with congenital amblyopia.

One must be more careful about drawing conclusions with regard to adults, for on the one hand it happens that gradually developed monocular visual disturbances are only accidentally observed by patients after they have reached a high degree, and it is very difficult then to persuade these attentive observers that it is not a case of sudden blindness of one eye. (Only a few people seem to be really aware that they have two eyes, and still fewer appear to suspect the existence of a visual field.)

In all these cases opportunity is hardly given for mistakes with reference to the diagnosis of congenital amblyopia, as slowly developed monocular defect scarcely occurs without ophthalmoscopic cause. On the other hand, ophthalmoscopic symptoms (such as hæmorrhage of the retinal artery in the macula lutea) may disappear without leaving a trace, while defective vision remains. The law of habit, however, usually helps us here. In congenital monocular defect patients are generally accustomed to this condition, and only notice it when special claim is made on the visual faculty of this eye,--he, on the other hand, who is accustomed to see with two equally good eyes, may not observe a gradually occurring blindness of one eye, if his talent of observation be faulty, but I have never had reason to suppose that a rapid depreciation of the central visual acuteness of one eye is also overlooked. Rapidly occurring monocular visual disturbances are noticed, whether detected with or without the ophthalmoscope.

Two peculiarities appear in isolated cases of congenital amblyopia, which may render the testing of vision difficult: rapid fatigue of the retina, and depreciation of the central visual acuteness in such a way, that an adjoining part of the retina possesses a better visual faculty than the centre.