Vertical Diplopia: What is it? Symptoms, Causes, Diagnosis and Treatment

It usually indicates that there is a misalignment between the two eyes.

There are many different causes of vertical diplopia.

Some are benign, but others can be serious and require urgent evaluation, significantly if the onset is associated with a headache, a change in eyelid position, or an asymmetry of the pupil.

An ophthalmologist’s evaluation would be recommended as soon as possible.

Parts of your eye and how they work together

Cornea: the clear window in your eye. Its main job is to focus light.

If your double vision goes away when you cover one eye, you may have corneal damage in the uncovered eye.

If only one cornea is warped, you can only see twice as much in that eye. Glasses can probably fix the problem. The damage can be from:


  • Keratoconus, when your cornea becomes conical.
  • Infections, such as shingles or herpes.
  • Scars
  • Dryness.

Lens: It is located behind the pupil and helps focus light on the retina. Cataracts are the most common lens problem. Surgery almost always fixes them.

Muscles: control the movement of the eyes and keep the eyes aligned with each other. If a muscle in one eye is weak, it will not move in sync with the good eye.

You see double when you look in a direction controlled by the weak muscle. Eye muscle problems can be from:

A problem with the nerves that control them. Graves’ disease is a thyroid disorder that affects the eye muscles. It can cause vertical diplopia, where one image is on top of the other.

Nerves: they carry information from your eyes to your brain. You may see twice as much if it damages the nerves that control your eyes.

Guillain-Barre syndrome is a nervous condition that causes progressive weakness. Sometimes the first symptoms are in your eyes and include double vision. Diabetes can damage the nerves in the muscles that move the eyes.

Brain: The nerves that control your eyes connect directly to your brain, where images are processed. Many causes of double vision begin in the brain. They include:

  • Hits.
  • Aneurysms
  • Increased pressure within the brain due to trauma, bleeding, or infection.
  • Brain tumors.
  • Migraines

What are the symptoms?

Patients with binocular vertical diplopia may present with symptoms of recent or long-lasting appearance.

Others may not fully know that their eye symptoms are attributable to a duplicate vertical image.

Double vision can occur without other symptoms. Depending on the cause, you may also notice:

  • Misalignment of one or both eyes (“wandering eye” or “squinting” appearance).
  • Pain when you move your eye.
  • Pain around the eyes, such as the temples or eyebrows.
  • Headache.
  • Sickness.
  • Weakness in your eyes or anywhere else.
  • Droopy eyelids.

How is vertical diplopia diagnosed?

The diagnosis of acquired vertical strabismus is not always straightforward. There is no specific test that diagnoses vertical deviation.

The clinical presentation, signs, and symptoms are the driving forces that will help achieve a correct diagnosis.

The differential diagnosis of vertical diplopia includes ocular motor nerve palsy, superior oblique palsy, restrictive ophthalmopathy, myasthenia gravis, and oblique deviation.

This differential diagnosis is best used to classify signs and symptoms in a patient with vertical misalignment and diplopia.

Because most clinicians are more comfortable addressing the patient with complaints of horizontal diplopia.

One of the most effective tools for your doctor is the information you provide to make recognition more accessible, leading to more accurate diagnoses.

Think about these questions before your appointment:

  • When did double vision start?
  • Have you hit your head, fallen, or been unconscious?
  • Did you have a car accident?
  • Is double vision worse at the end of the day or when you are tired?
  • Have you had any other symptoms besides double vision?
  • Do you tend to tilt your head to one side? Look at old photos, or ask your family; you may not even know the habit.

Now focus on something in your field of view that does not move, like a window or a tree:

  • Are the two objects next to each other, or are they on top? Or are they slightly inclined? Which is higher or lower?
  • Both images are clear but not online? Or is one blurry and the other clear?
  • Cover one eye, then change. Does the problem go away when either eye is covered?

Pretend your field of vision is a clock face. Roll your eyes around the clock, from noon to six, and around 12 again.

  • Is your vision worse at any position on the watch?
  • Does any position make it better?

Tilt your head to the right, then to the left.

  • Do any of these positions improve your vision or make it worse?

Red glass testing, double Maddox

The red glass and double Maddox subjective tests allow the patient to articulate the relative positions of the disparate images.

Assuming that the average, non-paretic eye is used for fixation, the image projected into the paretic eye will land on the extrafoveal retina.

The number of retinal mismatches increases as the eyes move further into the field of action of the involved eye muscle. The patient interprets this mismatch as double vision.

By placing a red lens in front of one eye, the locations of the two disparate and differently colored images can be described in the nine cardinal gaze positions and the tilt of the head towards the right and left shoulder.

The Maddox double rod test, a variation of the red glass test, uses a red and white Maddox lens to document torsional diplopia in a patient with suspected superior or inferior oblique muscle weakness.

As an example, a person with a paralysis of the right superior oblique muscle, in whom the red lens covers the right eye, will describe that the red line is lower than the white line and ingested because the right eye behind the red lens is relatively hypertrophic and extorted

The examiner or patient rotates the Maddox crystal until the two lines are parallel.

The magnitude of the cyclopropyl can be read out of the test frame, and the direction of the deviation is indicated by the displacement of the scratch mark on the Maddox bar from the 90-degree mark on the test frame.

As both tests involve a red lens, subjective diplopia can be induced iatrogenically by producing different images and breaking the fusion, allowing the heterophoria to manifest as a heterotrophy.

The Maddox Double Rod Test does not differentiate between a cyclophory and a cyclotropia and can mislead the unwary examiner into thinking that the patient has paralytic strabismus.

Both techniques are subjective. They depend on the patient’s ability to maintain fixation and accurately describe his diplopia.

Inaccurate conclusions can be related to poor vision in either eye or an unreliable sensory witness.

Duction and ocular version

When a patient follows their finger through the full range of eye movements, check the speed and extent of each eye as both eyes move together (version).

Then cover one eye and observe the monocular movements of the naked eye (duction).

If one eye shows limited vertical movement, for example, be careful not to assume that there is levator weakness or agonist muscles in the right eye.

Do not forget the other two possibilities, the antagonist’s anchorage or the contralateral antagonist’s inhibition.

Contralateral antagonist inhibition describes an ocular motility abnormality when a patient with extraocular muscle paralysis fixes with the paretic eye.

It most often causes confusion between true paresis of a superior oblique and apparent paresis of the contralateral superior rectus.

The pattern of the ductions and ocular versions in an 18-year-old woman who presented with vertical diplopia ten years after a car accident:

There was no history of strabismus, patches, or surgical treatment of the ocular muscles. On examination, visual acuity was 20/15 in the right eye and 20/25 in the left.

The ocular versions in the upward and left gaze showed a limitation of the elevation of the left eye, suggesting a paralysis of the left superior rectum. However, the left eye ducts to the left and up were full.

The coverage test revealed that she preferred to fixate with the right eye in the primary position.

The prism cover test showed a right hypertropia (RHT) of 16 D prisms (PD) in the primary position that increased in the left gaze and the correct head tilt, indicating a decreased right superior oblique muscle.

The example emphasizes several strabismus principles: the patient preferred to fixate with the eye that sees better, which in this case was the paretic eye.

According to Herring’s law, the fixing eye determines the nerve input to both eyes.

Thus, with true right superior oblique muscle paresis and fixation of the patient with the parasitic right eye, the antagonist of the right superior oblique, the right inferior oblique, requires less innervation to elevate the right globe to the primary position for fixation.

The subnormal innervation to the right inferior oblique is transmitted simultaneously to your eye muscle, the left sarcoplasmic reticulum in the left eye.

Therefore, with both eyes open and the proper eye fixation, the left eye is fully raised in gaze to the left and upward due to inhibition of the left sarcoplasmic reticulum.

The examiner should not rely solely on the versions in deciding to decrease the extraocular muscle. First, determine which eye is used for fixation and then check the eye ductions in addition to the eye versions.

Although the versions may show limited eye movement, the ipsilateral ductions will be complete. The three-step test will correctly identify the weak eye muscle in a patient with inhibition of the contralateral antagonist.

Cover-discover test

The monocular ulnar coverage test can serve four purposes: it determines fixation preference, qualitatively identifies a heterotrophy, can be used to quantify the amount of deviation in various gaze positions and head position; and identify a phobia of the eye behind the occluder.

The patient is encouraged to fixate on a target binocularly while the examiner occludes one eye at a time. When one eye is covered, the movements of the uncovered eye are observed.

If there is no uncovered eye movement – and the eye has a good vision – it can be assumed to fix accurately. If the uncovered eye covers the fixation or fixates, it should not be aligned with the fixation under binocular conditions.

Such overt deviation under binocular conditions is called a tropia. The eye with a manifest tropia will make a rapid or saccadic eye movement to take fixation.

If the compensating movement is downward, the eye under binocular conditions is hypertrophic; if the movement is upwards, the eye is hypertrophic; if inwards, exotropia and, if external, esotropic.

The cover-uncover test can also identify an ipsilateral euphoria if the eye under the cover moves to the right, left, up, or down.

The most important use of the coverage test is to identify the eye used for fixation and the presence of a manifest deviation (tropia).

Remember that it does not determine which eye muscle is weak, as patients may prefer to fixate with their paretic eye. A noticeable deviation can be quantified with the prism coverage or the coverage/discovery test.

In the latter, the occluder is alternately moved from one eye to the next in rapid succession while the examiner adjusts the prism bar to neutralize eye movement.

The relatively rapid movement of the occluder prevents binocular fixation. Therefore, both euphoria and tropia are identified.

The coverage and alternative cover tests can quantify a tropia in the nine cardinal gaze positions and the tilt of the head towards the right and left shoulder.

Both exams are based on the excellent vision and cooperation of the patient.

These tests depend on good vision in each eye. Poor vision or inadequate cooperation diminishes its value.

A deviation of less than 1 degree may escape detection. Small-angle strabismus with eccentric fixation cannot always be diagnosed with these techniques, as the amblyopic eye may not make a detectable fixation movement when the healthy eye is covered.

The three-step test

The three-step test is simply a variation of the cover-discover test. It will quickly and accurately diagnose a weakened vertical eye muscle.

Each step halves the number of muscles that could be causing the vertical imbalance.

Paso 1

Determine if there is right or left hypertropia in the primary position.

With right hypertropia, the right globe is too high (hypertrophic) due to weakness of the depressor muscles of the right eye (right lower rectum and superior oblique), or the left eye is too low (hypertrophic) due to weak sarcoplasm left reticulum or inferior oblique.

Paso 2

Compare the amount of vertical deviation in the right and left gaze.

If the right hypertropia increases in the left gaze, the right superior oblique or the left sarcoplasmic reticulum decreases, as these two muscles mainly move the eyes vertically in the left gaze.

At this point, remember that the two muscles under suspicion are in different eyes, but both are intolerant.

If the right hypertropia in the primary position increased in the right gaze, the two muscles under suspicion would also be in different eyes (right inferior rectus and inferior oblique left), but both would-be extortionists.

In our example, the right superior oblique and the left sarcoplasmic reticulum on your globe when the head is tilted toward the ipsilateral shoulder.

That is to say, the right superior oblique penetrates the right eye when the head is inclined towards the right shoulder, and the left sarcoplasmic reticulum penetrates the left eye in the inclination of the left head.

Paso 3

Compare the vertical deviation in the right head’s tilt and the left head’s tilt.

Suppose the vertical deviation increases with the tilt of the right head (which reflects the incyclodeviation of the right eye and the eciclodeviation of the left eye). In that case, the right upper oblique should be decreasing.

If the hyper deviation increases in the tilt of the left head, the left superior rectus decreases.

The explanation is simple. When the head is tilted towards the right shoulder, the right globe typically comes into action from the actions of the right superior oblique and the right sarcoplasmic reticulum.

With right superior oblique weakness, the right superior rectus acts only to achieve intorsion.

Right hypertropia becomes greater with correct head tilt because the right sarcoplasmic reticulum receives a more excellent supply of innervation to penetrate the right globe.

As the primary action of the right sarcoplasmic reticulum is to elevate the globe, the supernormal innervation not only helps to penetrate the correct globe but secondarily moves the globe upward since the weak right superior oblique does not oppose the elevating action of the upper straight.

Although the three-step test provides objective evidence of vertical muscle function, the results may be false for specific causes of vertical strabismus.

Example: A 52-year-old man complained of torsional and vertical diplopia after a minor head injury.

The results of the motility examination showed that 10 D prisms abandoned hypertropia in the primary position, which increased to 24 D prisms in the right gaze and 15 D prisms in the left head tilt, indicating a paralysis of the left superior oblique muscle.

However, due to long-standing amblyopia in the left eye, the patient preferred to fix it with the right eye.

When checking the eye rotations, the right eye did not rise well during the version, and the eye movement of the duction. The left eye movement was complete.

The forced ductions in the right eye were positive, and the orbital films showed a fracture in the right orbital floor with entrapment of the right inferior rectus muscle.

After surgical repair, the patient was orthotropic in the primary position. According to the three-step test, his mobility pattern no longer simulated paralysis of the left superior oblique muscle.

With entrapment of the right inferior rectus muscle and the patient’s preference for fixation with the right eye, the entrapped ipsilateral antagonist of the right inferior rectus, the right sarcoplasmic reticulum, prompts a supernormal immune signal to keep the right eye in the primary position for fixation.

As the fixation of the right eye determines the input of internal energy to both eyes, the supernormal innervation to the right sarcoplasmic reticulum is transmitted simultaneously to its contralateral yoke, the left inferior oblique.

Therefore, the left balloon moves upward in the primary position.

In the right gaze, the right sarcoplasmic reticulum exerts an even more significant strain against the right inferior rectus. The supernormal entrance to the left inferior oblique causes the left eye to elevate even more.

In the left head tilt, the left eye penetrates through the contraction of the left sarcoplasmic reticulum and the left superior oblique. The right eye is extracted through the right inferior rectus and the right inferior oblique.

The tied inferior straight rectus pulls the right eye down.

Therefore, the left eye is relatively taller, and the three-step test produces left hypertropia in the primary position that is worse with right gaze and left head tilt, a pattern that generally indicates weakness of the left superior oblique muscle.

Patients with an inferior rectus muscle anchorage may be misdiagnosed as paralysis of the superior oblique muscle in the unaffected eye if the examiner relies solely on the three-step test.

Using the same algorithm, contracture of an upper rectus muscle, for example, from thyroid ophthalmopathy, can produce contralateral inferior oblique “pseudo-weakness” using three-step criteria.

These diagnostic errors are more likely if the patient fixes with the eye “tied.”

This case again emphasizes the importance of establishing which eye has better vision and which is primarily used for fixation.

A simple test to determine fixation preference involves the principles of primary and secondary deviation.

Patients are asked to look at a fixation light while a red crystal is placed in front of either eye, and they are instructed to report whether the separation is more significant when looking with the right or left eyes.

Since the secondary deviation is always more significant than the primary deviation and occurs with paretic fixation of the eye, the patient’s observations betray the fixing eye.

The mercurial ophthalmoplegia of myasthenia gravis can confuse the most conscientious three-step examiner.

Myasthenic ophthalmoparesis can mimic various ocular motility disorders, including brainstem gaze palsy, cranial neuropathies, and primary orbital disease.

Further confusion may arise because extraocular muscle weakness tends to vary from one exam to the next.

Highly variable history of acquired diplopia, with or without ptosis, suggests the diagnosis of myasthenia. When in doubt, an intravenous Tensilon test should be performed.

Dissociated vertical divergence can have several characteristics similar to oblique muscle paralysis.

  • It can increase adduction, mainly if there is an associated inferior oblique hyperactivity.
  • A spontaneous head tilt is often present to merge images.
  • Characteristically increased with forced head tilt (usually on the contralateral side).

To avoid a misdiagnosis of dissociated vertical divergence, the examiner should evaluate for hypertropia by a coverage test and not just by light reflection.

In the coverage tests, the decoupled nature of the deviation will be apparent.

In contrast to hyperphoria or hypertropia, in which the eyes move in different directions to refine again, each eye moves upward in a dissociated vertical divergence when the other eye is fixing.

Some patients with horizontal neurogenic strabismus show minor non-neurogenic vertical deviations in forced head tilt, with no evidence of true vertical muscle paresis.

Consider the example of an 11-year-old boy with a large 50-prism esotropia in the primary position.

After neutralizing the horizontal deviation, there was a right hypertropia of 4 D prisms that increased in the right gaze and the left head tilt.

However, the ductions and versions did not show any overacting or lack of action, and the Maddox double bar tests showed no signs of torsional weakness.

By three-step criteria, the findings of the vertical extraocular muscle were compatible with lowering the left inferior oblique.

However, this only represented a slight non-paralytic vertical deviation associated with significant horizontal strabismus.

Patients with esotropia have typically shown that each eye rises above the contralateral head tilt and depresses the ipsilateral tilt.

Patients with exotropia, in contrast, typically showed elevation in the ipsilateral tilt and depression in the contralateral tilt.

This type of deviation can be differentiated from true vertical muscle paresis in several ways:

  1. Ocular rotations do not show substantial limitations or over-performance of the vertical muscles of the eye, as seen with vertical muscle paresis.
  2. Patients with oblique muscle paralysis tend to have a substantial difference in a vertical deviation between right and left gaze.
  3. These patients do not spontaneously assume a head tilt to fuse and do not exhibit objective or subjective torsional diplopia.

Hirschberg and Krimsky tests

While the patient is asked to view an illuminated light source, the corneal light reflection deviation from the pupil’s center is estimated.

With the fixation lumen held 33 cm from the patient, a decentration of 1 mm corresponds to 7 degrees of ocular deviation.

Most examiners agree that if the abnormal pupillary reflex only touches the temporal pupillary border, that eye is approximately 15 degrees esotropic.

If it is in the center of the iris stroma, there are 30 degrees of esotropia, and if it is in the external limbic margin, there are 45 degrees of esotropia.

Using the same equipment, with the addition of a prism, the light reflections can be symmetrical.

Prisms of increasing power are placed before the fixing eye until the light reflection is focused on the deviating eye.

The prism with sufficient power to achieve centering of the light reflection indicates the magnitude of the deviation.

The examiner should sit directly in front of the deviating eye to avoid false readings caused by parallax. This is sometimes known as the Krimsky test.

These tests estimate the size of ocular misalignment by observing the deflection of corneal light reflections.

Its disadvantages are obvious: the lack of precision obtained with this methodology; deviations of up to 7 degrees can be ignored.

Anatomical alterations of the pupillary opening, such as ectopically positioned pupils and ectopic foveation, can also obscure normal fixation reflexes.

Forced duction, forced generation.

The forced duction test can differentiate between the ocular movement limitation of agonist eye muscle denervation and antagonist eye muscle anchorage.

If the examiner cannot move the globe in the direction of gaze limitation, the forced ductions are said to be positive, and it can be assumed that there is a mechanical or restrictive component.

The technique is essential in performing the forced ductions test.

It begins with a drop of topical anesthetic (proparacaine or tetracaine hydrochloride) on the conjunctiva. It then holds a swab moistened with 5 to 10% cocaine against the conjunctiva area for about a minute.

The patient is then asked to move his eyes as far as possible toward the suspected weakness.

Assuming abduction palsy of the right eye, the examiner, with fine-tooth forceps, grasps the conjunctiva of the right eye near the medial limbus and attempts to abduct the globe.

The forced ductions are harmful if no resistance is found, and the mobility defect is not restrictive.

Failure to passively move the globe is considered positive forced duction, indicating a mechanical limitation of eye movement.

Several types of positive forced duction tests have been described:

  1. If the globe can be rotated no further than voluntary gaze, the restriction, in the author’s opinion, is due to tissue scarring or stiffness of the muscle opposite the gaze limitation, that is, the antagonist.
  2. Forced ductions can also be positive, on rare occasions, with restrictive conditions of the agonist extraocular muscle.
  3. In patients with long-standing extraocular muscle paralysis, wherein there may be antagonist shortening, forced ductions may reveal that the balloon rotates beyond the patient’s voluntary gaze but does not reach full and free excursion.

Forced Duct Test Errors: Various technical errors can invalidate the conclusions of the forced duct test.

When rotating the globe, following the natural arc of rotation is essential, as this is the best way to detect increased resistance compared to rotations in uninvolved directions.

If one unintentionally pushes the balloon inward, the examiner can simulate complete rotations by retracting the balloon.

It is essential to grasp the balloon as close to the limbus as possible, where Tenon’s conjunctiva and connective tissue meet in a single layer.

If the globe is held further back, the conjunctiva may stretch, and the force of the forceps does not effectively rotate the globe.

Good patient cooperation is mandatory.

Suppose the patient does not voluntarily look in the requested direction. In that case, the antagonist muscle may continue to be innervated, causing the examiner to feel resistance that does not represent an actual mechanical restriction.

There are also clinical situations where the forced duction test can provide spurious information.

For example, when there is a contraction of the extraocular muscles, as in aberrant third nerve regeneration or Duane syndrome. In the latter, the effect of forced ductions is certainly variable.

While the forced ductions test provides clinically sound information on the presence of restrictive ophthalmopathy.

That is, the state of the antagonist extraocular muscle, the active forced generation test helps establish the “force” or amount of active force exerted by an agonist extraocular muscle.

One author has described using an oculomicodynamic to measure the force of an extraocular muscle.

Subsequent modifications and research led the researchers to conclude that 60 to 80 g of force was produced by a normal rectus muscle during intense horizontal or vertical gaze.

When studying patients with paralytic and restrictive ophthalmoparesis, 7, it was found that a paretic muscle generated only a fraction of this normal force, and muscles that functioned against a tied extraocular muscle appeared to generate supranormal forces.

These test results have been used to determine the amount of residual inferior rectus paresis after an orbital floor fracture8 and for surgical planning.

If forced active generations reveal signs of complete extraocular muscle paralysis, for example, the surgeon may choose to perform a muscle transposition procedure rather than a simpler resection and recession.

Understand the causes of vertical diplopia

To confidently assess a patient with vertical diplopia, it is essential to understand several concepts:

The biomechanics and neuroanatomy of vertically acting extraocular muscles

The reward asks the patient a few informative questions that can locate the diminished extraocular muscle even before the physical exam begins.

Also, the convenience and pitfalls of various time-honored clinical testing techniques routinely used to assess the primary complaint of viewing two images one above or diagonally apart from one another.

Extraocular Muscles: Anatomy and Biomechanics

The eyes are located in the orbits, two symmetrical bony cavities of the skull on each side of the nasal root. The standard six extraocular muscles (MOEs) move the eye in the horizontal, vertical, oblique, and rotary planes.

The internal rectus (MR) and lateral rectus (RL) advance from the orbital apex along with the medial and lateral aspects of the globe, respectively, to adduct and sequester the globe in all positions of the globe. Horizontal gaze.

The superior and inferior rectus muscles and the superior and inferior oblique eye muscles have more complicated actions, depending on the initial position of the eye in orbit.

It advances at a 23-degree angle to the medial wall of the orbit and joins the globe superiorly. With the eye sequestered at 23 degrees, the sarcoplasmic reticulum (SR) plane is parallel to the anterior vertical anterior plane of the globe.

In this position, the contraction of the sarcoplasmic reticulum elevates the eye. With the balloon adducted at 67 degrees, the plane of the sarcoplasmic reticulum muscle becomes perpendicular to the visual axis, and its contraction penetrates the eye.

In the primary gaze position, the movement is combined elevation and more slight intorsion adduction; adduction results from the midline of the muscle belly medial to the center of rotation of the globe with the eye in the primary position.

The superior oblique (SO) muscle originates from the orbital apex and advances along the superior medial wall of the orbit to the trochlea, where it becomes tendinous.

After passing through the trochlea, the tendon is reflected temporarily at a 51-degree angle to the medial wall of the orbit.

It passes dorsally over the globe, ventral to the sarcoplasmic reticulum muscle, and inserts into the posterotemporal sclera.

As the reflected tendon delivers the direction of force to the scleral surface, the eye’s movement varies concerning the plane of the tendon insertion of the superior oblique.

Starting from a position of 51 degrees of adduction, where the plane of the superior oblique muscle tendon is parallel to the visual axis, the superior oblique pulls the eye downward.

In the primary position, the movement is combined with intorsion and slight abduction; tendon abduction results are posterior to the center of rotation of the globe.

Starting from an eye position of 39 degrees of abduction, where the visual axis is perpendicular to the plane of the superior oblique muscle, the superior oblique will penetrate the globe.

The course of the inferior rectus is parallel to the sarcoplasmic reticulum muscle, and the inferior oblique is parallel to the tendinous portion of the superior oblique muscle.

The superior and inferior rectus muscles play a more critical role in eye movement in the vertical plane. The upper and lower oblique muscles have a more decisive twisting action on the globe.

 A single vertical paretic muscle

Image projection law

This law states that an object that forms its image at any point on the retina is projected towards a point in visual space directly opposite. The visual axes are parallel when a distant object is seen with two eyes that generally see.

The conjugate gazes upward and, for example, is achieved by conjugate movement of the eyes to the right and the simultaneous and equal innervation of the right sarcoplasmic reticulum and the left inferior oblique muscles.

Each extraocular muscle moves the eye at the same distance and speed to achieve precise “foveation.”

If there is an interocular difference in the speed or extent of eye movement, the fixation target falls at non-corresponding points in the retina, and diplopia results.

It follows that conjugated eye movement further into the field of the weakened eye muscle will increase the amount of retina mismatch and thus increase the distance between disparate images.

History taking

Using the Law of Imaging, the collection of the patient’s history should include these four questions:

  • Is your double vision present in a straight gaze?
  • Are the images more separated when you look to the right or left?
  • If it gets worse with the correct gaze, does it get worse when looking to the right and up or to the right and down?
  • What happens if you tilt your head to the right or left shoulder?

An affirmative answer to question 1 limits the differential diagnosis of double vision to the four pairs of extraocular muscles that move the eyes vertically.

These include the right and left sarcoplasmic reticulum, the inferior rectus, the superior oblique, and the inferior oblique.

If diplopia worsens on correct gaze, the number of suspicious extraocular muscles narrows from eight to four.

Since only the right sarcoplasmic reticulum, the right inferior rectus, the left inferior oblique, and the left superior oblique move the eye vertically in the right gaze.

The greater diplopia with the eyes turned to the right. It upward involved the right sarcoplasmic reticulum, or the left lower oblique, while the worsening of the diplopia to the right and down points to the lower proper rectum or the left upper oblique.

If diplopia worsens with correct head tilt, right eye critical or left eye extorters are decreasing; quite the opposite applies if diplopia worsens on left head tilt.

A critical point is not to assume that an eye movement limitation is related to extraocular muscle weakness.

Always use the word “diminishing” instead of ocular muscle weakness to remember that incomplete excursion of the globe may result from agonist extraocular muscle weakness, antagonist extraocular muscle anchorage, or contralateral antagonist inhibition.

Abnormal postures of the head. Since binocular diplopia worsens or improves in different gaze positions, the symptomatic patient may adopt a compensatory posture of the head, face, or chin that provides the best binocular simple vision (VSB).

With horizontal ocular muscle weakness, the patient tends to turn his face to the side of the horizontal rectus muscle that is not working to relieve diplopia.

A turn of the face to the right involuntarily casts the eyes to the left and avoids the diplopia in the right gaze caused by the descent of the right lateral rectus muscle.

The inflection of the superior or inferior rectus muscles, which mainly moves the eye in a vertical plane, is compensated by the flexion or extension of the chin.

To avoid the gaze position generated by the paretic right sarcoplasmic reticulum, that is, elevation in abduction, lift the chin back and to the right (towards the action of the right sarcoplasmic reticulum).

The vestibule-ocular reflex moves the eyes downward and to the left, away from the maximum field of action of the paretic right sarcoplasmic reticulum. The noon point of the cornea is conventionally taken as the vertical pole.

If the noon point is stretched nasally, the eye’s movement is called intorsion or incision; When the noon point is turned outward, the balloon is said to be ex-cycled or extorted.

Torsional diplopia is characterized by one image rotating clockwise or counterclockwise, away from the other.

It is almost always caused by the inactivity of an upper or lower oblique eye muscle since the main action of these extraocular muscles, at least in the primary gaze position, is too intricate and extorts the globe respectively.

Torsional diplopia can be relieved by an angular tilt of the head to the right or left shoulder. Usually, when the head is tilted towards the left shoulder, the left eye is opened, and the right eye is exceeded.

In this case, intorsion of the left eye is achieved by co-contraction of the left upper oblique and the left sarcoplasmic reticulum, and extortion of the right eye by contraction of the lower rectum right lower oblique.


This will depend on the underlying cause.

Treatment for monocular double vision

Treatment will depend on the cause.

Astigmatism: refers to an abnormally curved cornea. Corrective glasses or contact lenses can often counteract curvature and correct the passage of incoming light to the eye.

Laser surgery is another option. This treatment consists of reshaping the cornea with a laser.

Cataracts – Surgery is generally the best option. The surgical procedure removes the clouding and the cause of double vision. Complications include infection, pain, and possibly continued blurred or double vision, but prompt treatment can resolve them.

Dry eye: If the eyes do not produce enough tears or dry out too quickly, they can become inflamed and painful. This can result in double vision. Often, a prescription for tear replacement eye drops will relieve symptoms.

Treatments for double binocular vision

Depending on the cause, treatments for binocular vision vary but include:

  • Use glasses.
  • Eye exercises.
  • Wear an opaque contact lens.
  • Botulinum toxin (botox) injections into the eye muscles, causing them to remain relaxed.
  • Wearing an eye patch.
  • Surgery on the muscles of the eye to correct their position.

An adhesive prism, placed between the eyes in the center of the glasses frame, can also help realign the images from each eye.

Eye exercises

Exercises cannot treat many of the conditions that cause double vision. However, some exercises can help with convergence insufficiency.

Smooth convergence

Focus on a clear goal, perhaps a thin stick or small text in a magazine. Hold this at eye level, an arm’s length away from you.

Try to keep the image as a single image for as long as possible. Move the lens towards the nose slowly and steadily.

When the single image becomes two images, your eyes have stopped collaborating. Concentrate intensely on stitching these images together. Once they come together, bring the target close to your nose.

Once you cannot rejoin the images, return your hand to its original position and start the exercise again.

The usual range of convergence is 10 centimeters (cm) away from the nose. Try to keep the image as a single image up to the 10 cm mark.

An orthoptist can provide a tool known as a point card to assist in these steps.

Convergence jump

Pick a target similar to that in the smooth convergence exercise. Start the target at a distance of 20 cm from the nose. Fix your gaze on the target for 5 to 6 seconds.

Switch to looking at a fixed object about 3 meters (m) away for about 2 to 3 seconds. Shift your vision to the closest target.

Repeat this, gradually moving the lens closer until you can focus on the object when it is 10 cm away without double vision.

The effectiveness of these exercises is primarily limited to the treatment of convergence insufficiency. If symptoms do not improve, visit a doctor for further tests.