Double Trouble: How to Diagnose Diplopia

This approach can help you determine if a patient’s complaint is muscular or neurogenic, and if it’s an annoyance or a threat to vision and life.

True double vision is one of the most troubling symptoms a patient encounters. Some causes are as benign as an uncorrected refractive error. Others may be life-threatening. 

Identifying the cause is extremely important—and extremely challenging—when you consider that 12 extraocular muscles (six per eye) contribute to eye movement. And, since the cause may be neurological, you also must understand the relationship between the third, fourth and sixth cranial nerves and these muscles.

In this sixth installment of our "Review of Symptoms" series, we provide an algorithm of sorts to help you determine the cause of your patient’s double vision. We’ll look at how to narrow down which muscles are involved and how to determine cranial nerve involvement.

History

A thorough history is perhaps the most important part of the exam when a patient presents with diplopia. The answers to five questions will help you narrow your search for the cause: 

• Is the diplopia real? Patients may mistakenly describe visual aberrations as diplopia. They commonly see a ghost image from an uncorrected refractive error and report this as double vision. You can quickly rule out this etiology with refraction and/or pinhole occlusion. 

Patients who experience true diplopia naturally are quite troubled by this symptom and nearly always present this as their chief complaint. Rarely will you elicit diplopia as an incidental complaint. 
• Is the diplopia monocular or binocular? Ask the patient to cover each eye alternately and report whether the diplopia disappears with occlusion. If the diplopia ceases while covering either eye, the problem is binocular; there’s a balance disturbance between the two eyes. If the diplopia persists when only one eye is covered, then the patient has monocular diplopia. 

Monocular diplopia indicates a problem within the ocular media, particularly the cornea and lens. Monocular diplopia is not neurogenic; it does not involve cranial nerves III, IV and VI.
On rare occasions, the patient may report monocular and binocular diplopia that occur simultaneously. This usually results from two different entities. 
• Is the diplopia horizontal or vertical? The patient’s answer will further help you narrow the problem down to one of two muscle groups. Four recti muscles—two lateral, two medial—control horizontal eye movements. We can attribute horizontal diplopia to one of these muscles. 

The remaining eight muscles—two each of inferior and superior recti, and superior and inferior oblique—control vertical eye movements. One of these eight muscles is involved in vertical diplopia. 
• Does the diplopia increase in any direction of gaze? Diplopia that does not increase in a particular direction of gaze generally points to a muscle-balance problem such as convergence excess or insufficiency.

Diplopia that increases in a particular direction of gaze will further narrow your diagnosis. Horizontal diplopia that increases in left gaze indicates a problem with the right medial rectus or the left lateral rectus. If vertical diplopia increases on left gaze, then the right inferior oblique, right superior oblique, left inferior rectus or left superior rectus is the cause. 
Diplopia that increases in a particular direction of gaze also indicates a non-comitant strabismus that may be muscular or neurogenic in nature 
• Is the diplopia greater at distance or near? The former points toward the medial recti and the oblique muscles. It excludes the lateral, superior, and inferior recti muscles, whose primary action is in abduction. For example, horizontal diplopia that is greatest at distance and in right gaze implicates the right lateral rectus.

Once you’ve identified the paretic muscle or muscles, these examination techniques will determine if the paresis is muscular or neurogenic.

• Ductions and versions. Version testing helps identify an underacting muscle. Have the patient fixate the non-paretic eye upon the test target. When the patient reaches the paretic field of gaze, cover this eye and instruct him to refixate with the paretic eye. If the patient can refixate and further move the paretic eye, the paresis is neurogenic. Otherwise, there must be a muscle restriction. 
• Saccadic eye movements. A normal eye has a slow pursuit and fast refixation on saccades. Compensatory refixation will be slow and gliding if the paresis is neurogenic, and abnormally fast and of limited amplitude if muscular. 
• Alternate cover testing in the paretic field of gaze. Normal eyes refixate symmetrically during an alternate cover test. In neurogenic paresis, the alternate cover test will cause the patient to alternate fixation between the normal and paretic eyes. So, the normal non-paretic eye will have a refixation exaggerated in speed and amplitude; the paretic eye will pick up fixation more slowly. Asymmetry on refixation indicates a neurogenic etiology. 
• Forced duction testing. Ask the patient with ophthalmoplegia to look in the paretic field of gaze. Using an anesthetic-soaked cotton-tipped applicator, try to gently push the eye into the paretic field. If you’re able to move the eye (negative test), the paralysis is neurogenic. If not (positive test), muscle restriction is causing the paresis. 
• Tensilon and ice pack testing. Myasthenia gravis (MG), one of the neuromuscular diseases, can cause ophthalmoplegia and diplopia, and mimic any cranial neuropathy. Tensilon (edrophonium chloride) inhibits the enzyme acetylcholinesterase at the neuromuscular junction. This allows endogenously released acetylcholine a longer opportunity to achieve neurotrans- mission and subsequent action. If injection of this drug brings with it subsequent improvement in ocular motility, then MG has been causing the paresis. 

Presentation and Clinical Course 

Patients with diplopia and ophthalmoplegia often present with diagnostic clues that point to the etiology. If the patient presents with sudden onset of both, the likely cause is a cranial nerve infarction. This is especially likely if the patient is elderly and has ischemic vascular disease, and if his ocular motility improves spontaneously.

Slowly worsening diplopia and ophthalmoplegia typically indicate a neoplasm compressing the involved nerve. If the diplopia and ophthalmoplegia are variable and worsen later in the day as the patient fatigues, MG may be the cause. 

Diplopia, particularly the intermittent kind, in patients older than 60 may be secondary to giant cell arteritis. If the patient experiences severe head pain at the onset of diplopia and ophthalmoplegia, an aneurysm may be compressing the nerve. Ischemic vascular infarcts may also be painful.

Cranial Nerve Palsies 

Once you’ve determined that the cause of the patient’s diplopia is neurogenic, you’ll then need to determine the cranial nerve that’s involved. Here’s where your under- standing of the ocular anatomy is important. Diplopia may be attributed to one of the following cranial nerve (CN) palsies:

• CN III. This patient will present with ptosis and a "down-and-out" eye position. Curiously, the patient may not initially report diplopia due to the ptosis. However, when the patient raises the lid mechanically, he will have vertical diplopia with a strong horizontal component, and difficulty elevating, depressing, and adducting the eye. 

The pupil may be normal in size and reactivity, or it may be larger and sluggish. Pupil involvement strongly indicates a subarachnoid aneurysm—a medical emergency. 
• CN IV. This patient will complain of vertical diplopia worse at near. On alternate cover testing with the Parks Three-Step Test, you’ll notice the patient will have a hyperdeviating eye. The hyperdeviation increases on opposite gaze and head tilt to the same side. In cases of longstanding CN IV palsy, the patient typically adopts a com- pensatory head tilt to the opposite side in order to ameliorate the diplopia. 
• CN VI. If the patient complains of horizontal diplopia that’s worse at distance than near and worse when looking to the right or left, investigate the possibility of a CN VI palsy. The patient will demonstrate an abduction deficit that worsens when he looks into the paretic field of gaze. 
• Multiple cranial nerve palsies. Patients who manifest diplopia from multiple CN palsies simultaneously are likely to have a lesion within the cavernous sinus—CN III, IV and VI are in close approximation within the cavernous sinus—or within the orbit. You must meticulously study these locations. Multiple nerve palsies can also occur with widespread systemic diseases such as myasthenia gravis and giant cell arteritis.

Drs. Sowka and Kabat are on faculty at the Nova Southeastern University College of Optometry, Fort Lauderdale, Fla. 
 

Causes of Monocular Diplopia Uncorrected astigmatism or other refractive error  Spectacle aberrations  Dry eye and other ocular surface disorders  Corneal scars  Iridectomy or iridotomy  Cataracts  Ectopia lentis  Cystoid macular edema

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July 15, 2000