Diplopia Etiology, Evaluation, and Management: A 10-Step Guide to the Perplexed
Diplopia Etiology, Evaluation, and Management: A 10-Step Guide to the Perplexed on Seeing Double
Author: Izak F. Wessels, MMed, FRCSE, FRCOphth, FACS, Department of Ophthalmology, University of Tennessee College of Medicine, Chattanooga Unit.
Peer Reviewers: Victor J. Aaen, MD, Dph, Clinical Assistant Professor of Family Practice, University of North Dakota Family Physicians, Minot Air Force Base; and Jemison Bowers, MD, Associate Professor of Ophthalmology, University of Tennessee College of Medicine, Chattanooga Unit.
Editor’s Note—When patients complain about double vision, primary care physicians often tune out and simply refer these patients to an ophthalmologist. Izak Wessels, MD, outlines how to develop a differential diagnosis, distinguish an emergency or urgent condition from the more mundane, and know when to refer to the specialist. Internuclear ophthalmoplegia is also a not uncommon presentation of patients, and Dr. Wessels provides an algorithm for helping the practitioner sort out a differential diagnosis and management plan.
Normal binocular vision requires that all the ocular structures involved with movement and alignment (muscular and neurologic), as well as the intricate processes controlling conjugate gaze and cortical fusion, be intact. The not-so-uncommon complaint of double vision can simply be normal physiology or a serious omen with catastrophic significance.1,2 A good history and specific examination can greatly help resolve the problem.3-5 While the primary care provider should be able to refine the diagnostic possibilities, gatekeepers very poorly manage this symptom, overinvestigating as many as one in four patients, with an overcharge rate of more than 700%.6
Introduction
Diplopia is when one object appears double and is often the first manifestation of many systemic (muscular or neurologic) disorders.7,8 The primary care provider can greatly facilitate triage; a correct evaluation correlates well with appropriateness of urgent referral to neurology clinics.2
A systematic history and examination can help to delineate the specific anatomical (and often) pathophysiologic processes causing diplopia.3,4 This article presents some typical case histories in the context of a series of 10 questions.
Does the Diplopia Persist When Covering Either Eye?
Case 1. Mr. T, a very tall college senior, comes to see you for chest pains whenever he plays basketball. He reports seeing two blurry objects despite covering the left eye, but not when covering the right eye, which he blames on his contact lenses being dirty. Examination reveals a loud diastolic murmur over the precordium, and the blood pressure is 60/20 in the right arm and 140/85 in the left.
Diagnosis. Marfan’s syndrome, with a dissecting aneurysm of the ascending aorta, and partially dislocated crystalline lens.
Monocular diplopia is comparatively rare. Possible causes include:
• Severe astigmatism (e.g., keratoconus);8
• Additional openings in the iris that function as pupils;
• Cataracts or media opacities;9
• Dislocated or subluxated lens (e.g., Marfan’s syndrome, intraocular lens);10 and
• Retinal abnormalities (e.g., macular scarring)
Obviously, closing the affected eye will make the diplopia go away, but it will persist if the unaffected (other) eye is closed. Three, four, or more images may be seen, depending on the cause of the problem.11
Binocular diplopia (double vision only if both eyes are open) indicates mal-alignment of the eyes and inability to suppress the image from the deviating eye. A child with crossed eyes will not have double vision, since the developing brain can suppress the "wrong" image. If untreated, the vision in the deviating eye may be irreversibly damaged, called amblyopia.
Is the Diplopia Physiologic?
Case 2. Miss J, a 56-year-old spinster, complains of frequent diplopia and headaches. Her double vision is only for nearby objects, which she demonstrates by holding up one finger close to her face and explaining that it appears double when she looks across the room. When she then looks directly at her finger, she only sees one. Her new glasses also make everything double when she looks to either side.
Diagnosis. Physiologic diplopia.
Physiologic diplopia is a normal phenomenon because the visual axes cannot possibly intersect at all distances at the same time.11 Suddenly noticing the diplopia represents a disturbance of higher cerebral function, especially of attention.12 Other causes of "normal diplopia" include the edge effect of a bifocal lens, as well as a thick spectacle lens inducing a prismatic effect that convergence disparities notice more readily.13
Are the Eye Movements Normal?
Three cranial nerves dynamically balance the six extraocular muscles. (See Figure 1.) Four of the muscles are the recti—the medial recti adduct move the eyes inward horizontally, while the lateral recti abduct move the eyes outward horizontally and remain in dynamic balance.
The superior recti elevate and the inferior recti primarily depress the globe. However, because the superior and inferior recti both insert at 23° to the sagittal plane, they also intort and extort the eye (rotate the 12 o’clock position inward or outward). By slightly abducting the eye, the cornea will align with the superior and inferior recti and pure elevation or depression results.
The two remaining muscles (superior and inferior obliques) insert at 51° and counterbalance the torsional effects of the vertical recti. The superior oblique intorts and depresses, while the inferior oblique extorts and elevates. Therefore, in upgaze, the superior rectus and inferior oblique act in concert, and in downgaze, the inferior rectus and superior oblique act in concert. Neuronal reflexes achieve a remarkably stable interrelationship and dynamic balance between the different muscles in the various directions of gaze.
Inability of the eye to move in a certain direction will result in double vision when attempting to look in that direction. The cause may be neurologic or muscular.
Three cranial nerves control eye movements, III, IV, and VI. The Oculomotor (III) nerve supplies the lid elevator, pupil constrictor, and all but two of the six extraocular muscles. Therefore, classic III nerve lesions result in inability to elevate, adduct, or depress, and ptosis, as well as a dilated nonreactive pupil. Since the ptosis is usually total, the diplopia is often masked by the lid covering the pupil.
The abducens nerve (VI) only supplies the lateral rectus. Lesions of VI result in inability to abduct (lateral movements) with horizontal diplopia. The trochlear nerve (IV) supplies only the superior oblique. Lesions of IV result in vertical and torsional deviations and vertical diplopia.
Observe the range of movements of each eye separately as well as both together as the patient’s eyes fixate on the six cardinal positions, first, left and right, and then up and down in left or right gaze, like the lines of a capital letter "H." By observing up and down movements only when the eye is turned outward or inward, the superior and inferior recti as well as the inferior and superior obliques can respectively be isolated. (See Figure 2.) Note that the vertical muscles also have a torsional effect.
Is the Diplopia worse in any particular direction of gaze?
This evaluation is more sensitive than observing a decreased range of movement, since it relies on the dynamic balance between the muscles of both eyes. Attempting to move a weak muscle requires a greater neurologic stimulus that results in the opposite eye "overshooting" as the complementary muscle responds to a greater degree. For example, when looking toward the left, the left lateral rectus and right medial rectus contract equally due to equal innervation. If the left lateral rectus is weak, it requires greater stimuli but will contract less than it should. The right medial rectus receives the same excessive stimulation and will contract more. Thus, the patient may have normal vision when looking to the right, but intolerable diplopia to the left. The patient can usually tell in which direction the two objects are farthest apart. An oblique or vertical muscle weakness is more complex, as is described next.
Is There an Abnormal Head Posture?
Case 3. Mr. J, a 60-year-old male, complains of a worsening neckache due to a "slipped disk." There is no limitation or pain on neck movement, but he believes he has a "pinched nerve," causing him to see objects double or on top of one another.
He has a pronounced head tilt to the left. With the head held normally, the right eye is higher than the left and the deviation worsens when he tilts or turns the head to the right, or when both eyes look to the left.
Diagnosis. Right superior oblique weakness, trochlear (IV) nerve palsy.
A compensatory head, face, or chin posture minimizes the diplopia arising from a weak muscle. As discussed above, turning the eyes to the opposite side of the field of action of a weak muscle minimizes the need for that muscle to act. The head posture allows the patient to see straight ahead without moving the eyes from this "neutral position."14 The Parks three-step test may help elucidate which of the four muscles with a vertical effect (total of 8 in both eyes) is weak and, therefore, responsible for the vertical diplopia and compensatory head tilt.15 Although the test may appear impossibly complex at first, it follows a logical procession.
Note which eye is higher: first with the head normally positioned, second with the head turned left or right, and, finally, with the head tilted to the left or right.
Step one. Which eye is higher in primary gaze? This reduces the possibilities from eight to four. A subtle deviation can be confirmed by covering one eye and watching whether the other moves up or down to take up fixation. By alternating the cover, the same effect will be evident in the eye just uncovered. Alternatively, ask the patient in which eye the image appears lower to identify the eye deviating upward.
If the right eye is higher, the weakness resides in the depressors on the right (right inferior rectus and right superior oblique) or in the elevators on the left (left superior rectus and left inferior oblique).
Step two. Is the deviation greater with left or right head turn? This halves the possibilities from four to two. If the right eye deviates greatest with the head turned to the right (both eyes are gazing to the left), the right superior obliques or the left superior rectus remain.
Step three. Is the deviation greater when tilting the head to the left or to the right? This is the Bielschowski head tilt and the final elimination step. It relies on the torsional balance provoked by tilting the head. The higher eye extorts (due to the inferior oblique), while the lower eye intorts (due to the superior oblique). If the diplopia is worse with head tilt to the right, then the weak muscle in the lower (right) eye is the superior oblique and in the higher (left) eye is the inferior oblique. Combining all three steps identifies the right superior oblique as affected.
Occasionally, the findings are subtle, which confuses the casual observer, more so if other nerves (e.g., III) are also partially affected. Vestibular diplopia can also cause confusion, since a head tilt may occasionally stabilize the dysfunction.16 However, typically these patients have symptoms of vertigo, hearing loss, and tinnitus.17
The astute clinician can "short cut" the process by realizing that of all the muscles, the superior oblique is most likely involved. A head tilt to the same side will exacerbate the diplopia, also the eye highest in adduction points at the affected muscle.
The IV cranial nerve emerges dorsally and has the longest brainstem course. Congenital weakness is often overlooked, and the patient may be unaware of a long-standing head tilt until old photographs (or the driver’s license) reveal the long-standing head tilt.
Is the Diplopia Variable or Does it Fatigue?
Case 4. Mr. P, a retired 68-year-old colonel with arthritis complains of excessive fatigue and weakness for the past few months. The labs are all normal except for a widened mediastinum on chest x-ray. He wants a "tonic" to relieve his fatigue that is causing droopy eyelids and double vision.
Diagnosis. Myasthenia gravis.
Ocular deviations that do not fit a clear-cut neurologic pattern are usually myogenic. Myasthenia is easily overlooked and can involve any eye muscle, including the lids (ptosis) but not the pupil. The symptoms are variable but usually worse in the evening, and a thymoma may be associated.18 To confirm the diagnosis, give a short-acting cholinesterase inhibitor ("Tensilon" edrophonium chloride 10 mg/mL) intravenously. First, inject 1 mg as a test dose and observe for possible hypersensitivity. If there has been no effect, inject the remaining 9 mg. A cholinergic response includes salivation, lacrimation, flushing, and a dramatic brief reversal of the weakness. Because the generalized cholinergic response includes an increased vagal tone, the patient may experience fainting or severe bradyarrhythmias. Atropine must be available as an antidote.19 Other myopathies (e.g., progressive external ophthalmoplegia, myotonia) may present similarly but will not respond to Tensilon.
Has There Recently Been Trauma to the Eye?
Case 5. Mr. T, a 21-year-old college quarterback, has a very bruised and swollen right eye after a fistfight. His cheek is allegedly totally numb, and when he lifts the lid, he has vertical double vision and the eye elevates and depresses very poorly.
Diagnosis. Classic blow-out fracture.
Diplopia after blunt trauma to the cheek suggests an orbital floor fracture entrapping orbital soft tissue. This prevents up- or downward eye movement, and the parasthesia suggests damage to the infraorbital nerve as well. Urgent surgical release of the muscle and reconstituting the orbital floor is probably only necessary when there is severe enophthalmos.20 Waiting two weeks or more for the hematoma, tissue edema, and inflammation to subside will identify those patients absolutely needing surgery.21 The clear-cut history and typical findings rule out more serious intracranial pathology.22 The entrapped inferior rectus (a restrictive myopathy) resists upward eye movement, which can be confirmed by a forced duction test: Instill topical anesthetic, grasp the globe at the limbus (between the cornea and sclera) with forceps, and evaluate the ease of movement in all directions except upward. Although pushing the anesthetized eye in different directions with a moistened cotton-tip applicator applies much less force, similar information can be gained.23
Closed head injury can also be associated with nonspecific VI weakness.24 However, despite the eyes being misaligned, only about one-third of patients will experience diplopia after head trauma.25 Other "traumatic" causes include a misdirected dental local anesthetic injection or hematomas after a peribulbar block for cataract surgery.26,27
Is There any Proptosis or Orbital Mass?
Case 6. Miss M, a 50-year-old nervous white widow, successfully received radioactive iodine for acute hyperthyroidism 18 months ago and is well maintained on replacement therapy. She suffers from increasingly gritty, red, and watery eyes that see double whenever she looks up or down. The only positive findings are reduced upgaze, and the left eye appears proptosed.
Diagnosis. Early thyroid ophthalmopathy.
Although any orbital space-occupying lesion can cause ocular displacement and diplopia, the most common cause remains thyroid eye disease with enlarged muscles. Imaging studies can identify the pathological cause, including congenital defects (encephalocele); inflammation (orbital cellulitis and abscess, pseudotumor, thyroid eye disease); benign or malignant neoplasms (e.g., secondary metastases from breast, primary rhabdomyosarcoma, neurofibromatosis, optic nerve gliomata, etc.); and vascular abnormalities (arteriovenous fistulae, hemangiomata). Lesions may also arise from the paraocular sinuses.28 Diplopia and orbital pain may be the earliest signs of posterior communicating or basilar arterial aneurysm or a carotid-cavernous sinus fistula.29,30
Although laboratory tests can confirm an abnormal thyroid function, the diagnosis of thyroid eye disease is made clinically. The findings include ocular discomfort, lid retraction, and lag, diplopia, exophthalmos, and optic nerve dysfunction.31 Specific and classic signs include:
Lid lag. The upper lid follows the eye downward at the same rate. Lid lag shows as a delay in lid movement, making the sclera temporarily visible as the eye moves down.
Lid retraction. The upper lid margin overlaps the cornea by 2 mm (1/6 of the vertical diameter), while the lower lid margin lies at the lower limbus. Lid retraction causes both the upper and lower lids to pull away, creating a staring, "bug-eyed" appearance.
Proptosis. Evaluate protrusion of one eye by standing behind the seated patient with his or her head extended backward as far as possible and look along the face from the top of the head across the forehead toward the chin. Lift both lids up and note if one or both eyes stands out forward with respect to the eyebrows. Precise measurements require a Hertel exophthalmometer to quantitate the degree of proptosis and permit careful follow-up.32
Diplopia from thyroid disease usually follows inflammation and secondary fibrosis of the inferior recti, which forced duction tests will confirm.
A useful classification of the severity of thyroid ophthalmopathy has seven components (the mnemonic NO SPECS) that progressively indicate more serious disease.33
N. No signs or symptoms (the patient is dysthyroid, but the eyes are not yet involved).
O. Only signs (the patient shows some mild changes, without experiencing ocular irritation, redness, etc.).
S. Soft tissues: At this stage, there is lid lag and lid retraction. Although the eye may not be proptosed, there is a staring appearance.
P. Proptosis: The swelling of the orbital contents (lymphocytic infiltration of the muscles and fat of the orbit) results in a forward displacement of the eye. Tarsorrhaphy (suturing the lateral half of the eyelids together) and/or decompressing the orbital pressure into the ethmoid or maxillary sinus can help reduce the proptosis.
E. Extraocular muscles: The increasing chronic inflammatory process has resulted in muscle thickening (evident on MRI or CT scan) with restriction of globe movement. The inferior rectus, inferior oblique, and medial rectus muscles are affected in order of frequency. Treatment includes prisms in the glasses, radiation therapy, and, eventually, muscle surgery to remedy the fibrosed and contracted muscles. Carefully following the range of extraocular motion and diplopia fields is a relevant measure to determine the choice of therapy in clinical trials.34 The enlarged muscles may also be seen with idiopathic orbital myositis.35
C. Cornea: The proptosis, lid problems, and inability to roll the eyes upward during sleep (Bell’s phenomenon) all result in corneal exposure, drying, and ulcers. Lubricants (especially ointments at night) and possibly tarsorrhaphy and orbital decompression are urgently indicated.
S. Scotoma or sight: The increasing proptosis may damage the optic nerve that develops focal blind spots (scotomata) and decreased vision. Urgent orbital decompression may be required to save vision and is best managed by maxillofacial or ophthalmic plastic surgeons.36
Smoking worsens ocular symptoms, proptosis, and diplopia up to three-fold.37
Is the Diplopia Part of a Classic Neurologic Syndrome?
The classic pattern of neurological abnormalities allow recognition in most cases; establishing an etiology is not always simple.38 Causes for neurologic diplopia include interruptions of the blood supply (diabetes); inflammation and demyelination (multiple sclerosis and herpes zoster); tumors and aneurysms; or trauma. Lesions at or surgery to the skull base may result in diplopia, as well as oscillopsia.39 Intracranial hypertension can present with diplopia and papilledema, visual obscurations, tinnitus, etc.40
Possibly III Nerve?
Case 7. Mrs. S, a 48-year-old frail white female, has been confined to a wheelchair due to multiple sclerosis. She has been wearing an eye patch for a few weeks due to double vision whenever looking to the left. The only finding is an inability of the right eye to adduct, but there are no other signs of a III palsy since the pupil and eyelid move normally.
Diagnosis. Internuclear ophthalmoplegia.
This case demonstrates interruption of the connection between the brain stem nuclei.
The yoke muscles responsible for left gaze (left lateral rectus and right medial rectus) receive stimulation from the abducens (VI) and oculomotor (III) nuclei, respectively. The initial stimulus reaches VI first, which is then relayed to the opposite III via the medial longitudinal fasciculus (MLF), the internuclear connection (there is simply no direct connection to III for horizontal gaze). Damage to the MLF on the right (ischemia, MS, etc.) effectively denervates the right medial rectus only.41
Case 8. Mrs. M, a 55-year-old black female, has maturity onset diabetes that is poorly controlled by oral agents due to obesity. She recently developed a persistent headache, followed by diplopia and then a droopy left eyelid. The pupil responses are normal, but the eye can only abduct and intort.
Diagnosis. Pupil-sparing III palsy: Diabetic mononeuritis multiplex.
Diabetics especially may develop acute neuropathies of any nerve, including those supplying the eye. These almost invariably resolve completely over a six-week period. A diabetic III nerve neuritis spares the pupil because the pupillomotor fibers run on the surface of the nerve and are less affected by a microangiopathic ischemia. The headache is presumably vasculitic ischemia. Therapy includes patching the eye until spontaneous recovery has taken place.42
Pupil-sparing III nerve palsies are considered "medical." Usually, the ptosis causes more concern than the diplopia—simply because the lid covering the eye prevents them from seeing double. Management includes reassurance and control of blood pressure and blood glucose because, as a rule, they fully recover.
On the other hand, III nerve palsies involving the pupil are considered "surgical" because a compressive lesion (aneurysm of the posterior communicating artery of the circle of Willis, brain tumor, other space occupying lesion, etc.) is often associated. Other physical signs (loss of consciousness, meningismus, etc.) may make the presentation more serious and dramatic, such as the familiar "Hutchison’s" dilated pupil on the side of an expanding intracranial mass.43
Diplopia can also be associated with ischemia from giant cell arteritis, but the optic neuropathy and visual loss usually dominate.44 An atypical "migraine" episode may show the same signs, and only by very careful specific history and subtle examination (as well as neuroimaging) can a more sinister cause be excluded.45
| Table 1. Diplopia Algorithm60 |
| 1. Is it monocular? |
| Check for corneal or lenticular opacities and for extra openings in the iris by the red reflex using a direct ophthalmoscope. A dislocated lens will be evident in the pupil. |
| 2. Is it physiologic? |
| 3. Are the eye movements normal? |
| Isolate the weak muscle by tracing an H pattern. |
| 4. Is it worse in any direction of gaze? |
| 5. Is there an abnormal head posture? |
| Possible oblique muscle (IV) dysfunction. Which eye is
higher in:
Step one: In primary gaze? Step two: With the head turned left or right? Step three: With the head tilted left or right? |
| 6. Does it vary during the day? |
| Possible myasthenia gravis. 10 mg IV Tensilon test. |
| 7. Has there recently been trauma to the eye? |
| Is there loss of sensation over the
cheek?
Probably blow out fracture: X-ray the floor of the orbit and the maxillary sinus. |
| 8. Is there any proptosis or signs of an orbital mass? |
| Use Werner classification: NOSPECS
to determine severity
Probably thyroid ophthalmopathy. Confirm muscle enlargement by CT scan of orbit. |
| 9. Is it part of a classic neurologic syndrome? |
| Possible III nerve: Pupil sparing:
medical third nerve lesion: observe
Pupil involved: Surgical third nerve. Tumor, aneurysm likely. Possible IV: Evaluate head posture Possible VI |
| 10. Are any other factors present? |
| Infections, metabolic diseases. |
Possibly IV Nerve (Trochlear)?
This has been discussed above. The Bielschowski head tilt test identifies the affected superior oblique muscle and nerve.46 The head turn and tilt frequently decompensate in middle age, when degenerative joint disease restricts neck mobility, or after head injury, fever, or intoxication.
Possibly VI Nerve (Abducens)?
The abducens (VI) nerve supplies only the lateral rectus. Weakness causes the eye to be adducted and unable to abduct. The head is usually turned toward the side of weakness (i.e., with a left VI weakness the head will be turned to the left). (Note that a IV weakness tilts the head to the opposite side.) The forced duction test shows easy and full lateral movements, proving the medial rectus is not tight. Only 16% of nontraumatic IV palsies failed to recover, and, of these, 40% had serious underlying pathology.47
The localizing value of an abducens palsy is limited, since it is a nonspecific sign of other problems, including increased intracranial pressure and pineal tumors.48,49
Are any Other Factors Present?
Infrequently, other diseases, including epilepsy, can adversely affect eye movements.50
Case 9. A 9-year-old white patient on total parenteral nutrition fell out of bed but did not suffer a head injury. The patient now has an ataxic gait, diplopia, and nystagmus.
Diagnosis. Classic Wernicke’s encephalopathy.
Diplopia was the first indication of a nutritional deficiency in a series of patients on total parenteral nutrition when there was a temporary shortage of appropriate multivitamin infusions.51 It may also develop during pregnancy as a result of increased metabolic demand.52 Other rare metabolic diseases include Wilson’s disease, malabsorption, and vitamin B1 deficiency.53,54
Infections can also cause diplopia: Black tar heroin injections may result in wound botulism, causing diplopia, dysphagia, dysponia, and descending paralysis.55 Opportunistic infections in HIV-positive patients can result in diplopia, a sign of severe disease.56
Conclusion
This particular outline can guide evaluation and management of most cases of diplopia. If the cause (e.g., IV palsy, thyroid disease, etc.) results in permanently abnormal ocular alignment, then surgical intervention may be successful to reduce symptoms.57,58 In other cases, an opaque contact lens is less cosmetically significant than wearing a patch.59
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