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 moving targets 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, four rectus 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

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 looking like 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 normal positions 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

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 Alhacen in his Book 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 corresponding retinal points. At the level of the optic chiasm, the nasal fibers of both sides

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 must stimulate 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 vision

Grade 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 on corresponding 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 comes from 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

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, any deviation 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. This is 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 the annulus 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 and inserts 7.0 mm from the limbus. It is supplied by the Abducent nerve and acts as an abductor of the globe. b

Fig 2: Extra ocular muscles

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

Fig 4: Extra ocular muscles; from above and from below. The superior rectus muscle has the same origin and inserts 8.0 mm from the 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 and inserts 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 and travels anteriorly till the trochlear and then turns backwards and laterally to be inserted in the upper lateral quadrant of the globe. Its actions are intorsion, abduction and depression. It is supplied by the trochlear nerve. The inferior oblique muscle originates anteriorly from the bone of the floor 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.

Strabismus or Heterotropia
Definition
Strabismus 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 or maintenance 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 Strabismus
Strabismus may be
1) True or 2) Apparent. Apparent strabismus is simply a false or pseudo strabismus. Pseudo strabismus may be due to epicanthus, wide interpupillary distance or high errors of refraction.

True strabismus may be

1) Manifest or 2) Latent.

Manifest strabismus may be

1) 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 be

1) Accommodative, 2) Nonaccommodative or 3) Partially accommodative.

Accommodative strabismus may be

1) 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 maintain binocular 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 fusional reflexes 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.

 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 to wheel-rotate inwards (incyclophoria) or outwards (excyclophoria) from the vertical position. Cyclophoria is usually associated with hyper and hypophoria.

Symptoms and signs of heterophoria

Heterophoria 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 there is 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 three green in cases of heterophoria.

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 or esophoria, 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

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 be incorporated 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 Strabismus

II.1. Paralytic strabismus

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 different degrees 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 or its 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.

Symptoms
1. 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 and its 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 that he cannot catch a pen on the desk, he might put his hand in front,

behind or beside the pen.

Signs
1. Deviation of one eye; misalignment is obvious in one direction and less obvious in another direction. Deviation may disappear in certain 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; according to 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

 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 on right 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

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).

Treatment of paralytic strabismus

The 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, nonaccommodative 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 diopter of accommodation.

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 between accommodation 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

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 (refractive accommodative 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.

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 Amblyopia
Amblyopia (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.

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 when the 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.