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 versa_. 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 retinae 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 retinae
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?
[Illustration: FIG. 2.]
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.
[Illustration: FIG. 3.]
But although both eyes see at the same time, yet the close relation
which in binocular fixation develops between the centres of the retinae
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 deg. The occurrence of double images shows that there exists for
the upper and lower parts of the retinae 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 retinae, 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,
haemorrhage 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 corneae 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 corneae
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
anaesthesia retinae, 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.