Procedure
- Hold the light, or toy, at a distance of at least 40 cm.
- Keep it at eye level, exactly in front of the child’s nasal bridge.
- Starting from this position, move over a distance of approximately 30 cm in all directions of view.
- If needed, hold the child’s head.
- After this, repeat the examination in the horizontal directions with the right and left eye covered alternately (monocular following movement).
Figure 40
Findings
- Strabismus with a small squint angle: If one of the eyes makes a fixation movement during the brief covering of the other eye, there is no straight position of the eye [Figure 41].
Figure 41
- If the reflex images are asymmetrical, cover the straight eye and look what the initial squint eye does [Figure 42].
- Alternating Strabismus: If it makes a fixation movement, which remains after recovery of binocular vision [Figure 42a].
- Amblyopia: If the initial squint eye does not make a fixation movement. [Figure 42b].
Figure 42
- Exophoria/esophoria: After covering the eye for slightly longer, it makes a recovery movement to the neutral position that started from the outer or inner corner of the eye [Figure 43].
Figure 43
- Rejection by the child, when covering an eye for both the position or follow movement examination, may indicate amblyopia of the other eye. This eye will not follow the offered fixation object or light.
- When examining the following movements of the eye, you can check whether both eyes, the one positioned straight and the one affected by strabismus, follow the fixation object or light. Also check if the squint angle remains the same, regardless of the direction of view. If this is the case, then it is a non-paralytic squint.
- A second diagnostic option is when the eye affected by strabismus does follow in certain directions, but not in the opposite directions.
- In addition, the squint angle reduces when it remains at rest and increases when it looks into the opposite direction. In this case, it concerns a paralytic squint.
Strabismus, Paralytic And Non-Paralytic Squint
Strabismus
Strabismus is when the visual and anatomical axes of both eyes do not run parallel and the projection image is not formed in both central foveae during fixation. It is a secondary strabismus if an organic cause is the origin. In all other cases, it is a primary strabismus. With concomitant (non-paralytic) strabismus, “the squint exists in all directions of view”. This is in contrast to non-concomitant (paralytic) strabismus, where it usually only manifests itself in one direction and is dependent on the position of the eyes.
The squint may be present constantly (atropia) or intermittently (aphoria). It may be prevalent in various directions. If the eye axes in the horizontal direction are positioned away from each other, and the imaginary intersection is in the skull, we call this an exophoria or an exotropia. If they are towards each other, and the intersection falls in front of the head, this is called esophoria or esotropia. Abnormalities may also occur in a vertical direction. If one eye looks upwards, it is known as hyperphoria or hypertropia. Downwards is classed a hypophoria or hypotropia.
Paralytic Squint
The movements of the eye are produced by six external eye muscles per eye and directed by three different cranial nerves.
- Superior rectus muscle.
- Superior oblique muscle.
- Medial rectus muscle.
- Inferior oblique muscle.
- Inferior rectus muscle.
- Lateral rectus muscle.
Only the lateral rectus muscle and medial rectus muscle cause a straight singular movement of the eye (outside and inside in the horizontal plane). The other eye muscles move the eye independently from the starting position in two directions. They roll the eye around the vertical axis and they turn it around the horizontal axis. This is the result of the attachment sites of these muscles on the eye globe. When describing their action, the neutral position of the eye is used as the starting point (looking straight ahead). In this position, the superior rectus muscle moves the eye upwards and to the outside. The superior oblique muscle causes a downward and inward movement. The inferior oblique muscle is used to look upwards and inwards. The inferior rectus muscle is used to look downwards and outwards. A glance straight upwards is achieved by the joint efforts of the inferior oblique muscle and the superior rectus muscle. A glance straight downwards is a joint effort of the inferior rectus muscle and the superior oblique muscle.
When we look in a certain direction with both eyes, the eye muscles cooperate two by two [Figure 44]. These muscle pairs are sometimes called zygomatic muscles. In order to look to the right with both eyes, the right lateral rectus muscle and the left medial rectus muscle are used. For looking to the left, the left lateral rectus muscle and the right medial rectus muscle contract. For upwards right, the right superior rectus muscle and the left inferior oblique muscle are used. For upwards left, the left superior rectus muscle and the right inferior oblique muscle are used.
Figure 44
Both lateral rectus muscles are innervated by the abducens nerve. The superior oblique muscles are innervated by the trochlear nerve, whereas all other external eye muscles are innervated by the oculomotor nerve.
When one of these cranial nerves no longer functions, the muscle innervated by this nerve won’t be able to contract and the eye will be pulled to the other side by its ‘counterpart’. This is the underlying cause for paralytic squint. The angle of the squint will increase when looking in the direction where the eye is normally moved by the paralysed muscle and decrease when looking in the opposite direction.
Non-Paralytic Squint
Primary Non-Paralytic Squint: No demonstrable cause for the squint. The eye is simply positioned incorrectly in the socket.
Secondary Non-Paralytic Squint: There is a demonstrable cause for the squint.
To understand the most common causes for the development of this squint, we will first cover the development of vision in a child.
The diameter of a newborn’s eye is only three-quarters that of an adult eye. The growth will take place in the posterior part of the eye. The anterior structures, in which most of the refractory media are located, barely increase in dimension. To be emmetropic in adulthood, one would have to be hypermetropic as a baby, infant and toddler. It is estimated that a newborn’s vision is 5/100 and that of a 3-year-old child 5/7.5 to 5/5. This is achieved despite hypermetropia of 1 to 2 diopter.
Through accommodation, the refractive capacity can be increased. However, the accommodating eye makes a simultaneous convergence movement. The degree of convergence is closely linked to the degree of dioptric increase of the refraction. For example, an emmetropic eye will have to accommodate 4 dioptrics to focus on an object that is 25 cm away from the eye. This accommodation is accompanied by a convergence of 14 degrees. Fixation at 33 cm will give an accommodation of 3 diopter and a convergence of 11 degrees. A hypermetropic eye of 1 diopter will have to accommodate 4 diopter to focus on an object that is 33 cm away from the eye. This is a convergence of 14 degrees [Figure 45].
Figure 45
When a child is not hypermetropic in both eyes (3 diopter in one eye and 2 diopter in the other); the more hypermetropic eye will have to accommodate and converge more. When examining the position of the eye using a fixation light, asymmetric reflex images are observed. This is known as an accommodative strabismus. This will eventually cause suppression of the worse eye and lead to suppression amblyopia. A second cause of secondary strabismus is a congenital cataract.
Background Information On Amblyopia
Animals that prey, oversee two adjacent areas with their right and left eye, through which different observations are registered [Figure 46]. At the cortical level, this does not cause any problems. There is no visual conflict and this is known as simultaneous vision. If we compare the skull of a prey animal with those of hunters, primates and humans; the deviating position of the eye socket is noticeable (lateral in the first group versus frontal in the latter groups). Because of this, the anatomical axes of both eyes run virtually parallel. Due to the limited distance between both eyes, they end up in almost the same location.
Figure 46
In the first 5 to 6 months of life, each eye looks independently, just as in prey. Because both eyes and the corresponding visual cortex develop independently of each other, this does not cause any problems at the cortical level. Therefore, humans see simultaneously at this stage of life.
In the healthy eye, the pupil, lens and central fovae lie on the axis of the eye and both eyes form an image of the same fixation point, albeit from a somewhat different angle: the retinal disparity.
As the cortical visual centres mature, the possibility develops for both images to merge into one. This is known as sensory fusion. The same phenomenon occurs with images that originate from the peripheral retina. The sensory fusion is maintained by the motor fusion, the capacity to position the eyes in such a manner that both look to the same fixation point. As soon as development has reached this stage, binocular single vision, stereopsis and depth perception is possible. This normally happens in the fifth or sixth month of life.
Retinal Correspondence
If, in a hypothetical experiment, a two-eyed being were to turn into a one-eyed being, both eyes would move medially until they merge, and the central fovae of both eyes would converge. The nasal peripheral retina of the right eye would overlap with the temporal of the left eye and vice versa. In other words, images that are projected as nasal in the left eye are projected as temporal in the right eye. In the one-eyed being, the eye ends up in the same spot. This is referred to as the normal retinal correspondence [Figure 47].
Figure 47
Diplopia
When we hold two fingers at different distances, in the middle of our eyes, and fixate on the nearest finger, we will see the furthest finger double in our peripheral visual field. Because of convergence during fixation on the nearest finger, the furthest finger projects in the nasal retina halves. Our brains interpret this information as one finger being present in the temporal visual field of each eye. This is known as diplopia [Figure 48]. Something similar happens when the eye sockets do not run parallel and only one of the eyes fixates on a subject. The image of the object is projected onto the macula lutea in the fixating eye. In the non-fixating eye, it is projected on the nasal or temporal retina half. At the cortical level, this is interpreted as if the object, for that eye, is located in the temporal or nasal visual field.
Figure 48
Confusion
The world around us is full of ‘objects’. One of these objects will be projected onto the central visual field of the non-fixating eye. Hence, centrally, two different images are projected, that cannot be made to overlap at the cortical level. This is called confusion [Figure 49].
Figure 49
Adjustment Mechanisms
If one foveal and one peripheral projection image is formed of a fixated object, this will be perceived as a double image, and the images are considered to ‘interfere’ at the cerebral level. A second interfering factor is the confusion that appears because of the different foveal images. To avoid this, various adjustment mechanisms are possible. If we were to carry out the previous-mentioned one-eyed experiment with one strabismic eye and one straight eye, the fovea of the straight eye will coincide with a section of the peripheral retina of the strabismic eye.
A possible adjustment is that the peripheral retinal area (where the image is formed) will cooperate with the central fovea. It will take over the function of the fovea. An abnormal retinal correspondence will develop. This is accompanied by a complete reorganisation at the cortical level, facilitating a fusion of the projection image from the peripheral retina with the foveal image. The result is binocular vision of poor quality and an inferior depth perception. The earlier in life that this phenomenon takes place, the harder it is to reverse it. Because the fovea in the strabismus eye regresses to a central scotoma here, correction of the position of the eye will have to be properly considered in this situation.
A second adjustment mechanism is the suppression of the qualitatively inferior image produced by the strabismic eye (it originates from the peripheral retina which is more light sensitive, but it is not as focused). When this happens constantly in the same eye, it will not develop any further than where it was when the suppression started. As a result of this, the eye becomes more or less amblyopic. Because this is the result of suppression by the image produced in this eye, we call this suppression-amblyopia. If this happens at a very young age and is not noticed in time, the loss of vision will be markedly more severe than if this happens in a 4 to 5-year-old child (due to the fact that the eye is more mature in this age group). On the other hand, a timely detection of suppression at a very young age will mean a better prognosis than when it is diagnosed in an older child. The neurological system, and also the eye and the optic nerve, has much more plasticity and recovery potential at a young age.