AL STRABISMUS Final- Dr Ahmad Lotfi

7/28/2019 AL STRABISMUS Final- Dr Ahmad Lotfi

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Ocular Motility and Strabismus

Introduction:

As the eyes can see only objects in front of them in their field of vision, they

have to move or rotate so that they can see wider fields. So for the function of

the eyes to see, they have to be able to rotate to follow the moving objects and

to see different objects in different locations in the environment. Visual

stimulation of the retina initiates ocular movements to follow the movingtargets and to stop the movements or fixate the eyes when the target objects

stop moving. The ocular motility is as essential as the function of vision

(imagine what would have been the situation if the eyes were fixed organs like

the nose and the ears). The eye rotates around three axes in three meridians;

the eye rotates horizontally (adduction and abduction) around a vertical axis

and rotates vertically (elevation and depression) around a horizontal axis and

torsionally (incyclotorsion and excyclotorsion) around an anteroposterior axis.

This ocular motility is the function of the extraocular muscles and their higher

cortical and supranuclear control. Each eye has six extraocular muscles, fourrectus muscles and two oblique ones. The twelve extraocular muscles (of both

eyes) act in a marvelous harmony through the higher central control moving

both eyes at one and the same time and for the same distance through the same

velocity. This is essential for what is called single binocular vision and that is

why nobody can move only one eye while fixating the other one (one can move

only one arm, only one leg but cannot move only one eye!!!! Can you??). So,

we can believe that we have only one seeing organ divided into two halves; the

right eye and the left eye.

The optical axis and the visual axis

The optical axis is an anatomical axis passing through the anterior pole of the

eye to the posterior pole. The visual axis on the other hand- is a physiological

axis. It starts from the fovea centralis (the most sensitive area of the retina) and

passes through the nodal point of the crystalline lens (the functional centre of

the lens) to cut the optical axis nasally making an angle of 5 degrees with it

(angle kappa). The eye rotates so that the visual axis is directed to the object of

regard. This small angle (angle kappa) solves the problem of having the eyes

anatomically parallel (simply look parallel) while the eyes are physiologically


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converging so that the visual axes can meet at the object of regard (parallel

lines simply do not meet at all). That is the advantage of having the fovea

centralis deviated in the temporal retina so that the two visual axes are

converging while the eyes are anatomically parallel. If the fovea centralis were

in the posterior pole, the eyes would have been ALWAYS converging lookinglike having convergent strabismus.

Fig 1: Optic axis and visual axis

The normal position of the eyes (orthotropia)

The eyes are normally placed so that the two visual axes are directed toward

the object of regard i.e. the two visual lines normally transect or cross at the

object of regard. Most of the time, the eyes are not parallel and that is normal

because the two eyes are directed to one object which means that the eyes are

converging towards that object. The eyes are only parallel while looking at a

distant object but not so when looking at a near one and both are normalpositions of the eyes. The corner stone is that the two visual axes are directed to

the object of regard and so they meet at that object.

Ocular motility; Herings law and Sherringtons law:

The eyes move freely in its place so that the cornea can be directed towards the

object of interest. The eyes can move horizontally, vertically and even

torsionally like the case of a ball and socket joint. That is why the optic nerve


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has a tortuous course in the orbit so that it is not stretched when the eyes

rotate.

Twelve extraocular muscles with their higher control are responsible for that

accurate ocular motility. That is why the extraocular muscles have very rich

nerve supply and sophisticated supranuclear and cortical control.According to Herings law; the yoke muscles receive equal and simultaneous

stimulation. The yoke muscles are one muscle from each eye that are

responsible for rotating the eyes in one direction of gaze e.g. the medial rectus

of the right eye and the lateral rectus of the left eye are responsible for moving

both eyes to the left side (left gaze) and they are called yoke muscles. It was

clearly stated for the first time by Alhacenin hisBook of Optics. Because of

this law one cannot move only one eye while fixating the other one. This is also

essential for the coordination of the movement of both eyes for maintenance of

binocular single vision.For the eyes to rotate in its place, contraction of one muscle should be

accompanied by relaxation of its antagonist e.g. to rotate the eye inwards, the

medial rectus should be stimulated while lateral rectus should relax.

Sherrington describes this phenomenon in his law of reciprocal innervation. He

stated that; stimulation of one muscle is accompanied by equal and

simultaneous inhibition of its antagonist. So to look to the right side, both the

right lateral rectus and the left medial rectus muscles should have equal and

simultaneous stimulation (according to Herings law) and also both the right

medial rectus and the left lateral rectus muscles should receive equal and

simultaneous inhibition (according to Sherringtons law).

Binocular single vision

It is defined as the coordinated use of the two eyes in order to produce a single

visual mental impression leading to a full three dimensional vision or

stereopsis. This requires both sensory and motor coordination of both eyes.

Motor coordination of the two sets of extraocular muscles is essential so that

the eyes can be moved voluntarily or reflexly with great precision and perfect

alignment in any desired direction. Sensory coordination between the two

retinae is essential so that the corresponding retinal points are simultaneously

used and stimulated by the same object.

Corresponding retinal points are one point in the right retina and one point in

the left retina that have the same visual pathway and the same cortical destiny.

Each point of the retina of the right eye has a corresponding point in the retina

of the left eye. The most important two corresponding points are the two foveae.

The object of regard is fixated by the two foveae. Any object to the right side of

the object of regard stimulates a point nasal to the fovea of the right eye and a

point temporal to the fovea of the left eye. Those two points are correspondingretinal points. At the level of the optic chiasm, the nasal fibers of both sides
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cross to the opposite side so that they run with temporal fibers of the other

retina in the optic tract. So the optic tract carries the fibers of the

corresponding retinal points and this continues through the visual pathway till

the occipital cortex where fusion of the two images takes place. For the cortex

to be able to fuse the two retinal images of the same object, the object muststimulate two corresponding points otherwise the object will be seen double.

This is the case if one eye deviates because at that situation the objects will not

simulate corresponding retinal points.

Grades of binocular visionGrade I, simultaneous perception is the ability to see at one and the same time

two dissimilar images, one formed on each retina, but not necessarily

superimposed.

Grade II, fusion is the mental ability to blend two similar images falling oncorresponding retinal points, one image being formed on each retina, and

perceive them as one.

Grade III, stereopsis is the appreciation of depth brought about primarily by

the fusion of the two images received by slightly disparate points on the two

retina.

Following reflex and fixation reflex

The most important source of reflex tonus to the extraocular muscles comesfrom the visual impulses themselves. Changes in the visual field, even when

of slight attention value, can be shown to produce marked changes in the

extraocular muscle tone e.g. optokinetic nystagmus. So the following reflex

simply makes the eyes move to track the moving object of regard and keeps

it always fixated by the foveae of both retinae.

The fixation reflex comes into play after the object of regard has been

captured by the foveae by means of the following reflex. This reflex serves to

maintain the object on the fovea. The attention value of the object of regard

determines to a great extent how active this reflex will be. The stimulus of this

reflex is the sharp image of the object of regard when perceived by the fovea

centralis and the response is the fixation of the eye at that position. So, if a

child has a congenital disease affecting vision marked in both eyes, this reflex

will not develop normally due to the absence of the its stimulus which is the

sharp clear image. That is why cases with bilateral congenital dense cataract

develop searching nystagmus.

Fusional reflexes


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For the visual cortex to be able to blend the two images, both eyes should be

in a position so that objects are perceived by corresponding retinal points

otherwise objects will be seen double. Doubling of the images is the stimulus

for fusional reflexes. The response is reflex fine ocular movements till the

objects are seen by corresponding retinal points to eliminate diplopia. So, anydeviation of the eyes leads to capturing of objects by non corresponding

retinal points and so the visual cortex cannot fuse the two images with the

result of diplopia. This diplopia reflexly stimulates the fusional reflexes to

realign the eyes so that objects stimulate corresponding retinal points. Objects

are captured by corresponding retinal points only when the eyes are in a

normal position where the two visual axes are directed to the object of regard.

The extraocular muscles

Each eye has six extraocular muscles, four rectus and two oblique muscles.

The four rectus muscles have common origins posteriorly from the annulus

of Zinn and they insert anteriorly into the sclera some millimeters from the

corneoscleral limbus. So when they contract they pull the insertion point

backwards. The oblique muscles -on the other hand- originate anteriorly (the

trochlea is the functional origin of the superior oblique and the anteromedial

aspect of the floor of the orbit is the origin of the inferior oblique) and insert

posteriorly. So when they contract they pull the insertion point forwards. Thisis essential to keep the eye in its place when the muscles contract as every

movement of the eye is caused by more than one muscle. If all the extra

ocular muscles were originating posteriorly and inserting anteriorly, any

ocular movement would have been associated with retraction of the eyeball

and narrowing of the palpebral fissure.

The medial rectus muscle originates at the apex of the orbit from theannulus of Zinn and inserts 5.5 mm from the limbus. It is supplied by

oculomotor nerve and acts as an adductor of the globe.

The lateral rectus muscle originates also from the annulus of Zinn andinserts 7.0 mm from the limbus. It is supplied by the Abducent nerve and acts

as an abductor of the globe.

b


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Fig 2: Extra ocular muscles

Fig 3: Extra ocular muscle actions (left) and measurements (right).


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Fig 4: Extra ocular muscles; from above and from below.The superior rectus muscle has the same origin and inserts 8.0 mm fromthe limbus. Its actions are; elevation, adduction and intorsion. It is supplied

by the oculomotor nerve. It is supplied by the oculomotor nerve.

The inferior rectus muscle also originates from the annulus of Zinn andinserts 6.5 mm from the limbus. Its actions are depression, adduction and

extorsion. It is supplied by the oculomotor nerve.

The superior oblique muscle originates above the annulus of Zinn andtravels anteriorly till the trochlear and then turns backwards and laterally to

be inserted in the upper lateral quadrant of the globe. Its actions areintorsion, abduction and depression. It is supplied by the trochlear nerve.

The inferior oblique muscle originates anteriorly from the bone of thefloor of the orbit anteromedially and travels posteriorly and laterally to be

inserted in the lower lateral quadrant of the globe. Its actions are extorsion,

abduction and elevation. It is supplied by the oculomotor nerve.

The extraocular muscles have special properties such as They have very rich nerve supply e.g. the lateral rectus has

special cranial nerve that supplies the lateral rectus only. They have very rich blood supply.

They have morel elastic fibers than the other striated

muscles so that muscle contractions and relaxations are

smooth.

They do not show signs of fatigue although they are

voluntary striated muscles. That is because only one tenth

of the muscle fibers is in action and the other nine tenths

are at rest.


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Strabismus or Heterotropia

DefinitionStrabismus is simply an ocular deviation. It can be defined as an extraocular

muscle imbalance, dysfunction or disturbance (not necessarily paralysis) so

that the two visual axes do not intersect at the object of regard. Normally the

two visual axes are directed to the object of regard and so the should meet at

the site of that object. If they do not meet there, strabismus exists.

Etiology

This includes any of those obstacles that may impede the development ormaintenance of the binocular perception and fusional reflexes. Those

obstacles may be optical, sensory, motor or psychological.

1) Optical obstacles : these obstacles prevent the formation of suitable

retinal images that can be successfully fused in the visual cortex into a

single mental impression. Those obstacles include high refractive

errors, anisometropia and aniseikonia. Opacities of the ocular media

also cause optical obstacles that interfere with the correct formation of

images on the retina leading, if bilateral to nystagmus, but if unilateral

to concomitant strabismus.

2) Sensory obstacles : they include all causes of uniocular defective vision

especially in infants and young children. These include failure of

development or disease of the macula or other parts of the visual

pathway. Prolonged uniocular activity as in occupations such as watch

makers or microscopists may also lead to development of strabismus.

Care should be taken in cases of unilateral congenital severe ptosis and

also in cases of corneal ulcers in infants as prolonged occlusion of one

eye may develop strabismus.

3) Motor obstacles : these prevent the adequate coordination of the two

eyes. These include any disease of the muscles, myoneural junctions,motor nerves or the supranuclear or cortical control

4) Psychological obstacles : any severe mental or physical trauma is liable

to convert pre-existing latent strabismus into a manifest one.

Classification of StrabismusStrabismus may be

1) True or

2) Apparent. Apparent strabismus is simply a false or pseudo strabismus.

Pseudo strabismus may be due to epicanthus, wide interpupillarydistance or high errors of refraction.


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True strabismus may be1) Manifest or

2) Latent.

Manifest strabismus may be1) Concomitant (where the angle of deviation is equal in all directions of

gaze) or

2) Incomitant (where the angle of deviation is not equal in all directions

of gaze) as in cases of paretic or restrictive strabismus.

Concomitant strabismus may be1) Accommodative,

2) Nonaccommodative or

3) Partially accommodative.

Accommodative strabismus may be1) Refractive,2) Non refractive or

3) Mixed.

I. Heterophoria (latent strabismus)

Heterophoria or latent strabismus is defined as tendency of one or both eyes

to deviate but this tendency is controlled by the fusional reflexes to maintainbinocular single vision and to avoid diplopia. When one eye deviates, the

images of the object of regard are not formed on corresponding retinal points.

At this situation the visual cortex will not be able to fuse or blend the two

images and so the object is seen double. This diplopia stimulates the fusional

reflexes to readjust the extraocular muscle tone to keep the visual axes

directed to the object of regard to maintain binocular single vision and

eliminate diplopia. If one eye is covered, diplopia will not be perceived if the

covered eye deviates. To summarize, there is tendency of one or both eyes to

deviate but this deviation leads to diplopia. Diplopia stimulates fusionalreflexes to realign the eyes and correct the deviation.

So if the controlling reflexes are inhibited by any means, the latent deviation

will be manifest. Covering one eye eliminates the binocular diplopia and so

the controlling fusional reflexes will not act. In such a case the deviation of

one eye will be manifest.

Types of heterophoria Esophoria; a latent tendency of visual axis to deviate inwards i.e.

toward the nose.

Exophoria; a latent tendency of the visual axis to deviate outwards i.e.away from the midline.


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Hyperphoria; a latent vertical deviation in which the visual axis of one

eye tends to deviate upwards as compared with that of the other eye.

Hypophoria; a latent tendency of the visual axis of one eye to deviate

downwards as compared with that of the other eye.

Cyclophoria; a latent tendency of the vertical meridian of one eye towheel-rotate inwards (incyclophoria) or outwards (excyclophoria) from

the vertical position. Cyclophoria is usually associated with hyper and

hypophoria.

Symptoms and signs of heterophoriaHeterophoria may be symptomless but symptoms may arise when the effort,

required to maintain the eyes in orthotropia, becomes a conscious effort.

Symptoms of heterophoria include;

Headaches or eye aches

Intermittent diplopia

Intermittent strabismus usually noticed by the relatives

Blurring of vision or running of the words into one another while

reading

Nausea and giddiness

Feeling of heavy lids, redness of the conjunctiva

Etiology of heterophoria High errors of refraction where myopia leads to exophoria while

hyperopia leads to esophoria

Wide orbits

Minor weakness of one or more of the extraocular muscles

Diagnosis of heterophoria

1. Cover- uncover test; by covering one eye, the binocular diplopia will

not be seen and so controlling reflexes will not be initiated. So, if thereis a tendency for deviation, it will show itself in the form of deviation

of the eye under cover. When the cover is removed, binocular diplopia

is perceived and in no time the fusional reflexes will correct the

alignment of the eyes and so, the uncovered eye will be seen moving

from the deviating position to the normal one. If the covered eye is

deviating under cover and then corrects its position when uncovered,

there is heterophoria.

2. Ocular movement testing; they are found to be normal.

3. Worths four dot test; five dots are seen, namely two red and threegreen in cases of heterophoria.


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4. Maddox rod and tangent scale test; the Maddox rod is placed in trial

frame before one eye with its cylinders horizontally aligned, the other

eye remaining uncovered. The patient then looks at a spot white light

in the tangent scale. If the patient is normal, a red light appears to go

vertically through the spotlight. In the event of exophoria oresophoria, the red line appears to be at one side of the spotlight. Then,

the Maddox rod is rotated so that its cylinders become vertical. Here

the red light appears horizontal. In orthophoria, the red light appears

horizontally through the spotlight. In cases of Hyperphoria or

hypophoria, the red line appears to be below or above the spotlight

respectively. The amount of latent deviation is measured on a tangent

scale.

Fig 5: Maddox rod test (right) and tangent scale (left)

5. The Maddox wing test; this is a test to measure the latent deviation for

near fixation.

Fig 6: The Maddox wing test


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6. Assessment of binocular functions using Titmus fly stereotest is found

to be normal in most cases. In a minority of cases it is found to be

subnormal.

Fig 7: Titmus fly stereotest

Treatment of heterophoria:

1. Cases without symptoms; sometimes heterophoria is discovered

accidentally during routine examination where it is not noticed by the

patient or his relatives. In such a case, no treatment is needed even it is

wise not to mention it to the patient.

2. Cases with symptoms;

Accurate correction of any refractive error may alleviate the symptoms.

Orthoptic training for horizontal phorias may be tried before prisms.

The use of prisms. A prism of an appropriate strength may beincorporated with the glasses of the patient. The power of prism

diopters needed is divided between the two eyes. Prisms are more

beneficial for vertical phorias.

Surgical correction is indicated when the other modalities fail to

correct the latent deviation.

II. Manifest StrabismusII.1. Paralytic strabismus


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If the ocular deviation is due to paralysis (complete loss of movement) or

paresis (partial loss of movement) of one or more of the extraocular muscles,

it is called paralytic or incomitant strabismus. Incomitance means that the

angle of deviation is not the same in all directions of gaze. In such a case the

eyes may be orthotropic in one direction of gaze and heterotropic of differentdegrees in the other directions. The deviation increases in the direction of

action of the affected muscle and decreases in the direction of action of its

antagonist.

Etiology

It is due a lesion anywhere the nuclei of the third, fourth and sixth cranial

nerves and the muscles themselves. The lesions may be due any of the

following causes;

1. Congenital absence of the nerve nucleus or absence of the muscle orits malinsertion.

2. Traumatic, either affecting the muscle or its nerve supply.

3. Inflammatory, encephalitis, neuritis or DS.

4. Vascular, cerebral hemorrhage or thrombosis.

5. Toxic, alcohol, lead poisoning or diphtheria toxins.

6. Neoplastic, a tumor pressing on the nerve supply of the muscle.

7. Myogenic, myasthenia gravis, thyrotoxic myopathy or ocular

myopathy.

Symptoms1. Binocular diplopia; the patient sees everything double when using both

eyes and sees normal when closing one eye. In cases of horizontal

deviations, diplopia is crossed (heteronymous) in cases of exotropia and

uncrossed (homonymous) in cases of esotropia.

2. Deviation of one eye and the deviation increases in certain direction.

3. Vertigo, nausea and uncertain gait. These symptoms disappear when

the patient closes one eye to avoid diplopia, so these symptoms are due

to diplopia.

4. Abnormal head posture. This posture is adopted to avoid diplopia andits distressing effects and in the interest of maintaining binocular single

vision. Abnormal head posture is simply moving the head instead of the

eye. When the right lateral rectus is paralyzed, the right eye cannot

move to the right, so the head is turned to the right. Abnormal head

posture may be horizontal (in the form of face turn to the right or to the

left), vertical (in the form of chin elevation or depression) or torsional

(in the form of head tilt to the right shoulder or to the left one).

5. Past pointing; the patient does not see objects in their correct locations

and so he cannot point to them correctly e.g. the patient complains thathe cannot catch a pen on the desk, he might put his hand in front,


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behind or beside the pen.

Signs1. Deviation of one eye; misalignment is obvious in one direction and

less obvious in another direction. Deviation may disappear incertain direction (the direction of action of the antagonistic muscle).

This is called incomitant strabismus.

2. Limitation of ocular movement; limitation is seen in the direction of

action of the affected muscle i.e. limitation of abduction in cases of

lateral rectus palsy.

3. The secondary angle of deviation is greater than the primary angle

of deviation. The primary angle is the deviation elicited when the

patient fixes with the sound normal eye and the secondary angle is

the deviation elicited when the patient fixes with the affected eye.Considering Herings law explains this fact.

4. Compensatory head posture; in the form of face turn, chin elevation

or depression or in the form of head tilt to one shoulder.

5. False projection; the paralysed eye does not see objects in their

correct location due to increased innervation conveyed by the nerve

supplying the paralysed muscle in an effort to force it to act. False

projection can be demonstrated by asking the patient to close his

sound eye and telling him to point quickly to an object in front of

him. The finger will be directed to one side of the object depending

on the direction of the main action of the affected muscle.

Pathological sequelae of paralysis of individual extraocular muscles Contracture of the direct antagonist; this takes place because

the contraction of the direct antagonist becomes unopposed.

Overaction of the contralateral synergist; this is due to

overstimulation of the affected muscle to force it to contract.

According to Herings law, the contralateral synergist

receives also overstimulation leading to its overaction.

Inhibitional palsy of the contralateral antagonist; accordingto Sherringtons law when the contralateral synergist receives

overstimulation its antagonist receives over-inhibition.

Paralysis of individual ocular muscles

Clinical picture of lateral rectus palsy (Abducent nerve palsy)

Esotropia in the primary position

Limitation of abduction


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Esotropia increases on looking to the affected

side

Secondary angle of deviation is greater than the

primary angle

Uncrossed diplopia Face turn to the side of the affected muscle

Fig.8: Right Abducent nerve palsy. There is esotropia of the right eye in

the primary position (A) and limitation of abduction of the right eye onright gaze (B)

2. Clinical picture of third nerve palsy Ptosis is present and may mask diplopia if the lid covers the

pupillary area.

Limitation of elevation, depression and adduction

Large angle exotropia

Pupil may be dilated and fixed

Paralysis of accommodation with difficult near work

Crossed diplopia


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Fig.9: Third nerve palsy of the right eye (the ptosed upper lid is elevated by

the examiner to show exotropia)

3. Clinical picture of trochlear nerve palsy Head tilt to the opposite shoulder

Limitation of downward and inward movement

Hypertropia if the head is forced to tilt to the same side shoulder

Hypertropia when looking to the opposite side

Fig. 10: Trochlear nerve palsy of the right eye where there is Hypertropia in the primary

position (A) that increases when looking to the left (B) and decreases when looking to the

right(C). Hypertropia increases when tilting the head to the left (D) and decreases when

tilting the head to the left shoulder (E).


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Treatment of paralytic strabismusThe aim of treatment is as follows:

To restore comfortable binocular single vision over as a large an area

as possible.

To make the ocular movement as symmetrical and equal as possible.

General principles in management of paralytic strabismus:

Treatment of the cause should be tried at first. It is wise to allow enough time

for spontaneous recovery. It is advised to wait for 6 months before deciding to

correct the deviation surgically. Surgical treatment is indicated when there is

no hope of recovery (after 6 months of stability of the condition) and before

development of the secondary changes as direct antagonist contracture.

Surgical treatment is in the form of weakening of the direct antagonist and

contralateral synergist. The contralateral antagonist might be strengthened.

For example, in cases with lateral rectus paralysis, the direct antagonist that

is the medial rectus should be recessed and the contra lateral synergist that is

the medial rectus of the other eye should be also recessed. Resection of the

affected muscle may be of help if the paralysis is not complete. In cases with

complete paralysis, resection of the affected muscle might not be of help and

in such cases muscle transposition is indicated.

II.2. Concomitant strabismus

It is a type of strabismus where the angle of deviation is constant in all

directions of gaze. Concomitant strabismus may be accommodative, non-

accommodative or partially accommodative.

II.2.a. Accommodative strabismus

It is a type of concomitant strabismus that is caused by accommodation.

Accommodation is the ability of the eye (mainly the crystalline lens) to

change its diopteric power to focus objects at different distances from the eye.

As the object of regard approaches the eyes, the eyes have to do two things;

first, the eyes have to converge to direct the visual axis to the object and

second the eyes have to accommodate to focus the near object on the retina.

There is a relationship between accommodation and its accompanying

convergence where the eyes converge for 3-5 prism diopters for each diopterof accommodation.


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Accommodative strabismus has the following criteria:

1. It has a late onset (around the age of 2-5 years). The late onset is due to

the late development of accommodation reflex.

2. There is a high error of refraction (in the refractive and mixed types)3. It starts as an intermittent esotropia then becomes manifest

4. It is corrected by glasses

Fig 11: Accommodative esotropia (above) corrected with glasses (below).

There are three types of accommodative esotropia:

1. Refractive type; where the deviation is due to the high refractive error.

In such cases, when the error of refraction is corrected by glasses, the

deviation is corrected both for distant and for near fixation.

2. Non-refractive type; where the deviation is due to high AC/A ratio. The

AC/A ratio is the ratio between accommodative convergence (AC) and

accommodation (A). Normally there is equilibrium betweenaccommodation and its convergence to keep the eyes directed at the

object of regard (convergence) and at the same time to keep the object

sharply focused on the retina (accommodation). If this equilibrium is

disturbed with over convergence, the eyes will deviate with normal

accommodation. In such cases there is minor error of refraction and

the eyes are orthotropic in distant fixation and esotropia appears only

in near fixation. Such cases are treated by bifocal glasses where there

are two lenses in front of each eye, one upper lens and one lower lens.

The lower segment lens has a power of 3 diopters more than the upper


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segment lens. The lower segment functions to stop accommodation at

near fixation which is the cause of overconvergence.

3. Mixed type; where there is an error of refraction causing refractive

accommodative esotropia and also there is high AC/A ratio. In such

cases, there is a small esotropia for distant fixation (refractiveaccommodative esotropia) that increases markedly with near fixation

(non refractive accommodative esotropia). In such cases, bifocal

glasses are prescribed where the upper segment corrects the error of

refraction (corrects the refractive element) and the lower segment has a

power of extra 3 diopters (to stop accommodation for near that is

responsible for the marked increase in the esotropia for near fixation

due to the high AC/A ratio).

II.2.b. Non accommodative concomitant strabismus

It is a type of concomitant strabismus not related to accommodation and so

not corrected by glasses. It may start congenitally or at early infancy where it

is called essential infantile esotropia. It may start later in life where it is

usually due to decompensated latent strabismus or due to marked loss of

vision in one eye .

Essential infantile esotropia

Essential infantile esotropia is the convergent strabismus that dates since

birth or since early infancy. It is characterized by

Large angle of esotropia

Cross fixation where the infant fixates objects in the right

side of its field of vision by the left eye and objects in the

left side of the field by the right eye.

Small usual error of refraction

Oblique muscle dysfunction A- and V- pattern deviation

Dissociated vertical deviation.

Latent or manifest-latent nystagmus

It is treated surgically by weakening of the two medial rectus muscles with

-sometimes- strengthening of one or both lateral rectus muscles.

II.2.c. Partially accommodative strabismus

It is a type of concomitant strabismus. It is due in part- to accommodation

and so can be partially corrected by glasses both for distant and near fixation.


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For example, if the patient has an angle of 30 degrees without glasses and an

angle of 20 degrees (both for distant and near fixation) with glasses, the

patient has partially accommodative strabismus. Such cases need both optical

(glasses) and surgical treatments.

Surgical treatment of concomitant strabismus

To correct a concomitant deviation, one should weaken the muscle pulling

the eye in the direction of deviation and strengthen its antagonist e.g. in

esotropia the medial rectus should be weakened and the lateral rectus should

be strengthened. Weakening of a muscle can be achieved through recession

of its insertion. Strengthening can be achieved through resection of some

millimeters of the muscle tendon. Resection of a muscle leads to its stretching

and so increases its contractility according to Starlings law. On the other

hand, recession of a muscle decreases its stretching and so decreases its

power of contraction. Weakening can be achieved also through partial

tenotomy or in some rare cases complete tenotomy. Strengthening can also be

performed via tucking or folding of the muscle tendon and also via

advancement of the tendon (the opposite to recession). The amount of

resection and recession is determined according to the degree of deviation;

the higher the degree of deviation in prism diopters the more the amount of

resection and recession in millimeters.

Strabismic AmblyopiaAmblyopia (lazy eye) denotes diminished visual acuity due to

impairment of foveal vision without demonstrable clinical or structural

anomaly of the eye or the visual pathway. Strabismic amblyopia

denotes reduced foveal vision as a result of manifest deviation in one

eye. Amblyopia develops easier in younger children and also can be

corrected easily in the younger ages. As the child is getting older,

amblyopia develops with difficulty and at the same time is corrected

with difficulty. That is why early development of strabismus (in infants)

leads to deeper amblyopia than that which develops as a result of

deviations starting in older children.

Strabismic amblyopia can be corrected by means of what is called

occlusion therapy. Occlusion of the sound non amblyopic eye forces

the brain to perceive images coming from the amblyopic eye. By

repetition of occlusion for a long time the relationship between the

amblyopic eye and the visual cortex is getting better and the functional

loss of vision is corrected either completely or partially.


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Nystagmus

It is an involuntary rhythmic oscillatory movements of the eyes. It is usually

bilateral; however it might be unilateral in an amblyopic squinting eye whenthe sound eye is occluded.

Clinical types:1. Jerking nystagmus; oscillations consist of two phases, a slow movement

in one direction followed be a quick correcting jerk in the opposite

direction. Nystagmus is described as right, left, up or down according to

the direction of the quick correcting phase.

2. Pendular nystagmus ; both phases are of equal speed i.e. to and- fro

movements like a pendulum. This is usually of ocular origin due to

defective central vision and is called searching nystagmus.3. Rotatory nystagmus ; here the oscillatory movements occur around the

optic axis (intortions and extortions).

Etiology of nystagmus:Nystagmus may be due to causes in the eyes (ocular nystagmus), in the

labyrinth or due to central causes.

1. Ocular nystagmus ; it may be physiological (as end-gaze nystagmus,

optokinetic nystagmus and latent nystagmus) or pathological (as

searching nystagmus, congenital idiopathic nystagmus and spasmus

nutans).

2. Vestibular or labyrinthine nystagmus; may be physiological in cases of

caloric stimulation or Galvanic stimulation or with rotation of the

head. It may be pathological in cases with labyrinthitis or Meniere

disease. It is usually of the jerking type.

3. Central nystagmus; this is typically jerking nystagmus. It may be due

to disturbance of the complex mechanism coordinating the sensations

coming from the labyrinth and the eyes and controlling the orientation

of the eye movements. It may be due to lesions of the brain stem, the

cerebellum or the spinocerebellar tract.

Documents

AL STRABISMUS Final- Dr Ahmad Lotfi