Eye Muscle Involvement in Strabismus

Binocular single vision may be defined as the coordinated use of the two eyes to produce a
single mental impression.
Grade1. Simultaneous macular perception
Images of the objects fall on the fovea of both eyes.
Grade 11. Binocular fusion: True fusion, with some amplitude, in which images are brought
together and held as long as the images are centered on the fovea of each eye.
Grade 111. Stereopsis: In-depth perception in three-dimensional vision, and thus evaluate the
object position relative to the environment
The monocular clue to depth perception includes Parallax, shading, size, perception, and
relative position to other objects. The object color appears bluer at distances relative to nearby
objects. The outlines of distant objects are less defined. The blurred outline could be due to
atmospheric haze.

Squint
In squint, the visual axes do not intercept at the point of regard. There are broadly two types: the
incomitant (Paralytic) strabismus and the concomitant strabismus.
Incomitant
This is when the mobility of the eyeball or balls is impaired as a result of paresis of one or more
extra-ocular muscles.
Acquired incomitant squints result in diplopia when the image of the object at a distance falls
on one eye and a dissimilar image falls on the macular of the squinting eye, which is often
suppressed to avoid confusion. The stimulation of vision in non-retinal corresponding areas in
both eyes results in diplopia, in a person with previous binocular vision.
The angle of deviation in a paralytic squint is greater if the deviating eye is fixating on the
object of regard than when the non-deviating eye is used. This is the cause of increased nervous
impulses transmitted to both eyes in synergy to overcome the squint. To further reduce the
diplopia, the patient may resort to compensatory head tilt, (compensatory head position). An
example is the case of palsy of the right lateral rectus muscle, the head may be tilted to the right
side, to maintain single binocular vision, with all eye movement to the left even in straight gaze.

Ocular Motility test

Use the broad H test
Some instruments used in testing Acquired deviation angles
1. Amblyoscope
2. Hess screen test

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 3. Electromyography

Types of extra-ocular muscle paralysis

Abducens Nerve paralysis

This is due to its long and tortuous intracranial pathway which may allow various
pathological processes along its line. It innervates the lateral rectus. The paresis of the
lateral rectus causes horizontal diplopia which is greater at a distance than near.
It is affected by
1. Any lesion that involves the nuclei and nerve with the brain stem
2. Lesions in the cavernous sinus and orbit including the vertebral basilar insufficiency,
3. Systemic hypertension, raised intracranial pressure, posterior fossa, and cavernous
sinus tumors
4. Trauma, middle ear diseases, meningitis and encephalitis
Trochlear nerve paralysis
Trochlear innervates the superior oblique muscle involved in the adduction of the eye. The
paralysis causes visual axes deviations and diplopia. The visual axis deviation and diplopia are
greater when the patient looks down in the direction away from the eye with paralyzed muscle.
Therefore, the left superior oblique paresis causes maximum vertical diplopia, while looking
down to the right; because the vertical action of the superior oblique muscle is greater in
adduction. The associated vertical diplopia is greater at near than at distance vision. The superior
oblique muscle has a torsional role in rolling in the eye, so the patient often develops a
compensatory head posture. The chin is often depressed, to overcome the depression action of
the muscles, it tilts away from the side of the paralyzed muscle to reduce the effect of extorsion
produced by the paralyzed muscle. The superior rectus and the superior oblique muscles are
torsional but antagonistic to each other’s action. Their action is to eliminate vertical movement
when the head is tilted. The muscles are affected by;
1. head trauma is the most common cause of the paralysis
2. Lesions of the nuclei, brain stem, cavernous sinus, and orbit

Oculomotor Paralysis
Because of the unopposed action of the lateral rectus supplied by the abducens nerve the affected
eye is rotated outwards (divergent squint). There is no depression of the eye because it is rotated
out of the position where the superior oblique muscle can act as a depressor. Diplopia may not be
a problem, because paralysis of the levator palpebrae superioris produces ptosis. A distinction is
made between complete oculomotor paralysis, in which all the eye muscles supplied by the
oculomotor nerve, including its parasympathetic component, are affected (total 3rd nerve palsy),
and situations in which the parasympathetic element is preserved.
Lesions involving the 3rd nerve nucleus alone are extremely rare, but the involvement of the brain
stem is by no means uncommon.
1. Oculomotor palsy associated with contralateral extrapyramidal signs indicates a lesion at the
level of the red nucleus.

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2. Oculomotor palsy combined with the crossed pyramidal signs locates a lesion at the level of
the cerebral peduncles.
3. Oculomotor palsy without any other neurological sign is suggestive of a disturbance between
the point where it leaves the brain stem and that at which it enters the posterior part of the
cavernous sinus, such as tumors and aneurysms that are located close to the posterior part of
the circle of Willis.
4. The 3rd, 4th, and 5th cranial nerve palsies may occur if there are lesions of these nerves in the
cavernous sinus and similar changes may also occur if the disturbance affects the orbital
apex but proptosis differentiates them because of the space it occupies at the orbital apex.

Diseases causing oculomotor nerve palsies.

Encephalitis
Meningitis
Multiple sclerosis
Systemic hypertension
Diabetes
Tumors
Trauma
Migraine

Total ophthalmoplegia
It is a condition of total paralysis of all the extraocular muscles and is usually due to pathological
processes located in the cavernous sinus or the orbit. It can also be the result of myopathies.

Limitations of ocular movement due to causes other than nerve palsies

This can occur due to
1. Entrapment of the inferior rectus following blow-out fracture of the orbit.
2. Fibrosis of the inferior rectus muscle in dysthyroidism may mimic a superior rectus palsy.
However, a duction test under local anesthesia will determine that the mobility of the eye
is restricted in such circumstances.
3. Early manifestations of myasthenia gravis which causes the weakness of the extraocular
muscles because of the defect of neuro-muscular transmission.

Treatment
In many cases of extra-ocular muscle palsy there is spontaneous recovery, in most cases within
three months of the onset before surgery can be ordered. The objective of the surgery is to restore
binocular vision and gain a larger visual field.
The surgery is directed to either weakening the ipsilateral antagonist, or the contralateral
synergist or shortening the contralateral antagonistic muscles.

Diagnosis of Myasthenia gravis

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 1. Must always be considered for a patient presenting with a history of Diplopia which is
worse in the evening than in the morning
2. In a patient who on examination, a lesion attributable to paralysis cannot be established.
3. The administration of Tensilon injection will result in a transient restoration of the extra-
ocular muscle movements; therefore a positive Tensilon test is diagnostic of this
condition.

Other defects of Extra-ocular muscles

Gaze Palsies
This is due to disturbances in the partway of the brain stem or central to the extra-ocular motor
nuclei which control muscle movements. Lesions in the pathway that connects the frontal and
occipital cortex to the extra-ocular muscle motor nuclei in the brain stem cause defects in the
response to command and pursuit movements, respectively. However, the movements of the eye
are limited to the same extent and in the same direction, there is no diplopia.

Vertical Gaze Palsies

These are often caused by lesions affecting the upper aspects of the brain stem. Dorsal lesions
close to the pretectal nuclei produce disturbance of the upward gaze and more deeply located
lesions at the substantia nigari produce defects at the downward gaze.
Lesions such as tumors, arteriovenous malfunctions, degenerations, trauma, and encephalitis can
cause vertical gaze defects.
Disorders involving the pretectal region and the anterior part of the 3rd nerve complex can cause
upward defects, accommodation, and convergence (periaqueductal syndrome) paralysis.
Doll’s head phenomenon will be experienced, which is the eye movements involving head tilt
either up or down when the vestibular oculomotor pathways remain intact. Doll head responses
are observed when the eyes move in response to the head tilt. This may involve the supranuclear
gaze palsies and infranuclear gaze palsies.
Horizontal gaze palsies
Are caused by lesions adjacent to the lateral gaze centers in the pons.

Internuclear Ophthalmoplegia
Occurs because of the lesions involving the median longitudinal fasciculus and the adjacent
pontine reticular formation. This is characterized by the following: on horizontal gaze to the side
opposite to that of the lesion, the contralateral abducting eye shows jerky nystagmus, while the
ipsilateral adducting eye fails to adduct completely, even when the convergence movement
remains intact. During recovery from the lesion, the ipsilateral adducting eye tends to be slower
than the contralateral abducting eye. The abducting eye over-shoots and finally returns to the
final position, reaching the same fixation point at the same time.

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Nystagmus
This condition is commonly described as the involuntary to-and-fro oscillation of the eyes. The
movements can be horizontal, vertical, rotatory, or in other combined form. It can be either
acquired or congenital. In acquired nystagmus, the patient may be aware of the wobbling vision
(oscillopsia) unlike in the congenital condition. There are two main types of nystagmus, pendular
nystagmus and jerky nystagmus.

Pendular nystagmus
Pendular nystagmus appears earlier in life due to opacities in the ocular media, damage to the
retina, or the afferent visual pathways. Central fixation does not fully develop, and the eyes show
rapid oscillatory movements which are almost equal in both eyes.
Jerky nystagmus
In this condition the rates of movements of each eye are different. The direction of the fast
component movement determines whether the nystagmus is right, left, up, or down.
Nystagmus due to the disturbance of the peripheral vestibular apparatus tends to be transient, but
if there is destructive lesions of the central vestibular the nystagmus will be permanent. Any
damage to the peripheral vestibular apparatus on the left will cause nystagmus to the right vis-a-
vis. Patients with gaze palsies will show jerky nystagmus of larger amplitude and slower
frequencies than those with vestibular nystagmus.

Physiological forms of Nystagmus

These are end-point forms of nystagmus induced in healthy individuals often observed at the
extremities of the lateral gaze, optokinetic nystagmus is commonly observed by persons in a
moving car looking out at electric poles, and vestibular nystagmus (Labyrinthine) when the body
is rotated in a chair, and in response to caloric stimulation.

Concomitant strabismus
Forms of concomitant strabismus:
1. Convergent squint
2. Esotropia
3. Divergent squint or exotropia
4. Vertical squint or hypertropia
Concomitant strabismus has the same visual axis deviation angle in all directions of gaze
and there is no limitation to the movement of the eyes when tested separately. The
secondary and the primary deviations are equal in magnitude.
Many children develop squints before the age of 3 years, and if not treated, amblyopia
may develop in some of them, which may affect their adult life as they are barred from
some occupations that do with driving, flying, etc.

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 Note:
Concomitant squints are commonly present in these conditions:
1. newborns immediately after birth and are associated with brain damage
(e.g. spastics and atheloids, Mongols, etc.
2. children who were born prematurely or suffered respiratory embarrassment in the early
postnatal period are also liable to develop manifested deviation.
3. Are often an associated family history of squint
4. where there is history of meningitis or cerebral trauma to the child
5, common in hypermetropic children

Monocular Strabismus
This occurs when only one eye is used for fixation. Visual function in the deviating eye
becomes progressively impaired. Initially, it is a facultative suppression of the macula,
but if suppression is maintained, it may later become obligatory. Diplopia is not obvious
because the extra-macular point in the squinting eye, to which the object of regard is
projected, is also suppressed. A child with a monocular squint macula may fail to develop
the full range of central connection in the squinting eye and if not treated early the vision
may be permanently impaired (amblyopic). The child who develops amblyopia may be
grossly deficient in discrimination sense in the affected eye and their fixation on the
object of gaze is parafoveal, paramacular, or even eccentric. They cannot read fine prints,
but movement appreciation, night vision, and color vision remain intact. However,
amblyopia does not develop in squints acquired after 6 years of age.

Some causes of amblyopia in children in preschool age,

1. Prolonged periods of occlusion of one eye such as when a child is wearing a bandage
for a long time after surgery, because of congenital ptosis.
2. Child with marked anisometropia
3. Sever astigmatism

Ophthalmoscopic features in Amblyopia

1. No abnormalities or disturbances are visible
2. Pupillary light reflexes are normal

Alternating Strabismus
 Either eye is used to fixate alternatively
 Suppression of the macula remains facultative
 This kind of squint does not give rise to amblyopia
Pseudo-Strabismus
 Occurs when the interpupillary distances are abnormal either too large or too small
(apparent esotropia or exotropia)
 Abnormality of the orbit is present
 Where a child has prominent epicanthic folds
 Pseudo strabismus can be differentiated from true strabismus with a cover test.

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Eye Examination for Squints
Identify manifest squint by performing a cover test. The result is the movement of the
deviating eye. If squint is present it takes up fixation provided eccentric fixation is not
present, On removal of the occlusion the deviating eye takes up fixation position. In
alternating squint, the previous fixation is continuous and there is no movement.

Measure the angle of deviation of the squinting eye, by determining the corneal reflection
of the source light on both eyes. The light reflection should be normally situated
symmetrically on the cornea of the children with normal fixation and on pseudo-
strabismus, but asymmetrical in the presence of squint. If the light reflex is central to the
fixating eye and the reflex is at the pupil edge of the squinting, the angle of deviation is
approximately 15o. If the reflection is at the corneoscleral junction, the angle of deviation
is about 45o. More accurate measurements are obtained using a tangent scale Maddox
cross, while older children can be measured with an amblyoscope and stereoscope The
angle of deviation can also be measured using prisms in conjunction with a cover test.

Testing for central fixation

This is carried out using a fixation target and the ophthalmoscope, if the image of the
fixation target falls on the fovea, central fixation exists. Fixation can also be paramacular
or eccentric, depending on where the fixation target image is in the fundus. The Worth
four-dot test can also be used in testing for simultaneous macular perception. This is by
presenting two different targets with the patient wearing a red/ green filter spectacle e.g.
the right eye sees the red star and a white square target while the left eye sees the two
green circles and the square. If there is a concomitant squint, only one eye sees a pattern,
and if there is a paralytic element the target may run together.
For children, the two eyes must be assessed independently. Children with amblyopia are
often happy when the squinting eye is occluded, but turn the head if the fixating eye is
occluded.