Buy the Book PDA Download

Update Me E-mail alerts The Merck Manual Minute

Print This Topic Email This Topic

Diplopia is the perception of 2 images of a single object. Diplopia may be monocular or binocular. Monocular diplopia is present when only one eye is open. Binocular diplopia disappears when either eye is closed.

Etiology

Monocular diplopia can occur when something distorts light transmission through the eye to the retina. There may be > 2 images. One of the images is of normal quality (eg, brightness, contrast, clarity); the other(s) are of inferior quality. The most common causes of monocular diplopia are

• Cataract
• Corneal shape problems, such as keratoconus or surface irregularity
• Uncorrected refractive error, usually astigmatism

Other causes include corneal scarring and dislocated lens. Complaints also may represent malingering.

Binocular diplopia suggests disconjugate alignment of the eyes. There are only 2 images, and they are of equal quality. There are many possible causes of binocular diplopia (see Table 7: Approach to the Ophthalmologic Patient: Some Causes of Binocular Diplopia). The most common are

• Cranial nerve (3rd, 4th, or 6th) palsy
• Myasthenia gravis
• Orbital infiltration (eg, thyroid infiltrative ophthalmopathy, orbital pseudotumor)

Most commonly, the eyes are misaligned because of a disorder affecting the cranial nerves innervating the extraocular muscles (3rd, 4th, 6th cranial nerves). These palsies may be isolated and idiopathic or the result of various disorders involving the cranial nerve nuclei or the infranuclear nerve or nerves. Other causes involve mechanical interference with ocular motion or a generalized disorder of neuromuscular transmission.

Table 7
Some Causes of Binocular Diplopia Cause Suggestive Findings Diagnostic Approach Disorders affecting cranial nerves to extraocular muscles* Cerebrovascular disease affecting pons or midbrain Older patient, risk factors (eg, hypertension, atherosclerosis, diabetes) Sometimes internuclear ophthalmoplegia or other deficits No pain MRI Compressive lesion (eg, aneurysm, tumor) Often pain (sudden if caused by aneurysm) and other neurologic deficits Immediate imaging (CT, MRI) Idiopathic (usually microvascular) Occurs in isolation (no other manifestations) Ophthalmologic referral to ensure no other deficits If isolated, observation for spontaneous resolution Imaging (MRI, CT) if not resolved in several weeks Inflammatory or infectious lesions (eg, sinusitis, abscess, cavernous sinus thrombosis) Constant pain Sometimes fever or systemic complaints, facial sensory changes, proptosis CT or MRI Wernicke's syndrome History of significant alcohol abuse, ataxia, confusion Clinical diagnosis Mechanical interference with ocular motion† Graves' disease (hyperthyroidism causing infiltrative ophthalmopathy) Exophthalmos, eye pain or irritation, photophobia, goiter, pretibial myxedema Thyroid function testing (sometimes eye findings precede thyroid dysfunction) Orbital myositis Constant eye pain that worsens with eye motion, sometimes injection, proptosis MRI Trauma (eg, fracture, hematoma) Signs of external trauma; apparent by history CT or MRI Tumors (near base of skull, sinuses, orbit) Often pain (unrelated to eye motion), unilateral proptosis, sometimes other neurologic manifestations CT or MRI Neuromuscular transmission disorders‡ Botulism Sometimes preceded by GI symptoms Descending weakness, other cranial nerve dysfunction, dilated pupils, normal sensation Serum, stool testing for toxin Guillain-Barré syndrome, Miller Fisher variant Ataxia, decreased reflexes Lumbar puncture Multiple sclerosis Intermittent, migratory neurologic symptoms, including extremity paresthesias or weakness, visual disturbance, urinary dysfunction Sometimes internuclear ophthalmoplegia MRI of brain and spinal cord Myasthenia gravis Diplopia intermittent, often with ptosis, bulbar symptoms, weakness that worsens with repetition Edrophonium test *Presence of pain varies by cause. †Often painful. ‡Typically painless.

Evaluation

History: History of present illness should determine whether diplopia involves one or both eyes, whether diplopia is intermittent or constant, and whether the images are separated vertically, horizontally, or both. Any associated pain is noted, as well as whether it occurs with or without eye movement.

Review of systems should seek symptoms of other cranial nerve dysfunction, such as vision abnormalities (2nd cranial nerve); numbness of forehead and cheek (5th cranial nerve); facial weakness (7th cranial nerve); dizziness, hearing loss, or gait difficulties (8th cranial nerve); and swallowing or speech difficulties (9th and 12th cranial nerves). Other neurologic symptoms should be sought, such as weakness and sensory abnormalities, noting whether these are intermittent or constant. Nonneurologic symptoms of potential causes are ascertained, including nausea, vomiting, and diarrhea (botulism); palpitations, heat sensitivity, and weight loss (Graves' disease); and difficulty with bladder control (multiple sclerosis).

Past medical history should seek presence of known hypertension, diabetes, or both; atherosclerosis, particularly including cerebrovascular disease; and alcohol abuse.

Physical examination: Examination begins with a review of vital signs for fever and general appearance for signs of toxicity (eg, prostration, confusion).

Eye examination begins with measuring visual acuity (with correction) in each eye and both together, which also helps determine whether diplopia is monocular or binocular. Eye examination should note presence of bulging of one or both eyes, eyelid droop, pupillary abnormalities, and disconjugate eye movement and nystagmus during ocular motility testing. Ophthalmoscopy should be done, particularly noting any abnormalities of the lens (eg, cataract, displacement) and retina (eg, detachment).

Ocular motility is tested by having the patient hold the head steady and track the examiner's finger, which is moved to extreme gaze to the right, left, upward, downward, diagonally to either side, and finally inward toward the patient's nose (convergence). However, mild paresis of ocular motility sufficient to cause diplopia may escape detection by such examination.

If diplopia occurs in one direction of gaze, the eye that produces each image can be determined by repeating the examination with a red glass placed over one of the patient's eyes. The image that is more peripheral originates in the paretic eye; ie, if the more peripheral image is red, the red glass is covering the paretic eye. If a red glass is not available, the paretic eye can sometimes be identified by having the patient close each eye. The paretic eye is the eye that when closed eliminates the more peripheral image.

The other cranial nerves are tested, and the remainder of the neurologic examination is completed, including strength, sensation, reflexes, cerebellar function, and observation of gait.

Relevant non-neurophthalmologic components of the examination include palpation of the neck for goiter and inspection of the shins for pretibial myxedema (Graves' disease).

Red flags: The following findings are of particular concern:

• More than one cranial nerve deficit
• Pupillary involvement of any degree
• Any neurologic symptoms or signs besides diplopia
• Pain
• Proptosis

Interpretation of findings: Findings sometimes suggest which nerve is involved.

• Nerve III: Eyelid droop, eye deviated laterally and down, sometimes pupillary dilation
• Nerve IV: Vertical diplopia worse on downward gaze; patient tilts head to improve vision
• Nerve VI: Eye deviated medially, diplopia worse on lateral gaze; patient turns head to improve vision

Other findings help suggest a cause (see Table 7: Approach to the Ophthalmologic Patient: Some Causes of Binocular Diplopia).

Intermittent diplopia suggests a waxing and waning neurologic disorder, such as myasthenia gravis or multiple sclerosis, or unmasking of a latent phoria (eye deviation). Those with latent phoria do not have any other neurologic manifestations.

Internuclear ophthalmoplegia (INO) results from a brain stem lesion in the medial longitudinal fasciculus (MLF). INO manifests on horizontal gaze testing with diplopia, weak adduction on the affected side (usually cannot adduct eye past midline), and nystagmus of the contralateral eye. However, the affected eye adducts normally on convergence testing (which does not require an intact MLF).

Pain suggests a compressive lesion or inflammatory disorder.

Testing: Those with monocular diplopia are referred to an ophthalmologist to evaluate for ocular pathology, before which no other tests are required.

For binocular diplopia, patients with a unilateral, single cranial nerve palsy, a normal pupillary light response, and no other symptoms or signs can usually be observed without testing for a few weeks. Many cases resolve spontaneously. Ophthalmologic evaluation may be done to monitor the patient and help further delineate the deficit.

Most other patients require neuroimaging with MRI (CT may be substituted if there is concern about a metallic intraocular foreign body or if MRI is otherwise contraindicated or unavailable) to detect orbital, cranial, or CNS abnormalities. Imaging should be done immediately for those whose findings suggest infection, aneurysm, or acute (< 3 h) stroke.

Those with manifestations of Graves' disease should have thyroid tests (serum thyroxine [T₄] and thyroid-stimulating hormone [TSH] levels) done. Testing for myasthenia gravis and multiple sclerosis should be strongly considered for those with intermittent diplopia.

Treatment

Treatment is management of the underlying disorder.

Key Points

• Isolated, pupil-sparing nerve palsy in those with no other symptoms may resolve spontaneously.
• Imaging is required for those with red flag findings.
• Focal weakness (in any muscle) may indicate a disorder of neuromuscular transmission.

Last full review/revision April 2009 by Kathryn Colby, MD, PhD

Content last modified April 2009