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(Double Vision)


Christopher J. Brady

, MD, Wilmer Eye Institute, Retina Division, Johns Hopkins University School of Medicine

Last full review/revision May 2021| Content last modified May 2021

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 of Diplopia

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 rest 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 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, or 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. Whether pain is present depends on the disorder. Other causes involve mechanical interference with ocular motion (which often cause pain) or a generalized disorder of neuromuscular transmission (which typically do not cause pain).

Some Causes of Binocular Diplopia


Suggestive Findings

Diagnostic Approach

Disorders affecting cranial nerves to extraocular muscles (presence of pain varies by cause)

Cerebrovascular disease affecting pons or midbrain

Older patients, risk factors (eg, hypertension, atherosclerosis, diabetes)

Sometimes internuclear ophthalmoplegia or other neurologic deficits

No pain


Compressive lesion (eg, aneurysm, tumor)

Often pain (sudden if caused by ruptured aneurysm) and other neurologic deficits

Immediate imaging (CT, MRI)

Idiopathic (usually microvascular)

Occurs in isolation (no other manifestations)

Ophthalmologic referral to check for other deficits

For isolated diplopia, 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


Wernicke encephalopathy

History of significant alcohol abuse, ataxia, confusion

Clinical diagnosis

Mechanical interference with ocular motion (pain is often present)

Graves disease (infiltrative ophthalmopathy usually associated with hyperthyroidism)

Local symptoms: Eye pain, exophthalmos, lacrimation, dry eyes, irritation, photophobia, ocular muscle weakness causing diplopia, vision loss caused by optic nerve compression

Systemic symptoms: Palpitations, anxiety, increased appetite, weight loss, insomnia, goiter, pretibial myxedema

Sometimes eye abnormalities precede thyroid dysfunction

Thyroid function testing

Orbital myositis

Constant eye pain that worsens with eye motion, proptosis, sometimes injection


Trauma (eg, fracture, hematoma)

Signs of external trauma; apparent by history


Tumors (near base of skull, in or near sinuses or orbit)

Often pain (unrelated to eye motion), unilateral proptosis, sometimes other neurologic manifestations


Neuromuscular transmission disorders (typically, pain is absent)


Sometimes preceded by gastrointestinal symptoms

Descending weakness, other cranial nerve dysfunction, dilated pupils, normal sensation

Serum and 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 repeated use of muscle

Ice pack test, single fiber electromyogram (EMG), anti–acetylcholine receptor antibody testing

Evaluation of Diplopia


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, such as weakness and sensory abnormalities, should be sought, noting whether these are intermittent or constant. Nonneurologic symptoms of potential causes are ascertained. They include 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 noting the initial position of the eyes, followed by 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 cover test and cover-uncover test can also be used to determine whether a deviation or strabismus is present with both eyes open (manifest/tropia), or only when one eye is open (latent/phoria). Both tests are done on both eyes. For the cover test, the patient is asked to fixate on an object with both eyes open, and one eye is covered. The other eye is observed for a refixation movement, which would indicate it had previously been misaligned, indicating a manifest deviation or tropia. The cover-uncover test is conducted similarly, except the eye being tested is covered for a few seconds and then the cover is removed. The same eye is observed for a refixation movement, which would indicate a latent deviation or phoria. The patient may also see the object "jumping" with the refixation movement during either test.

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

Relevant nonneurophthalmologic 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 cranial nerve is involved.

  • 3rd: Eyelid droop, eye deviated laterally and down, sometimes pupillary dilation
  • 4th: Vertical diplopia worse on downward gaze (patient tilts head to improve vision)
  • 6th: Eye deviated medially, diplopia worse on lateral gaze (patient turns head to improve vision)

Other findings help suggest a cause (see table 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). Patients 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.


Patients with monocular diplopia are referred to an ophthalmologist for evaluation of ocular pathology; no other tests are required beforehand.

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 is recommended to monitor the patient and help further delineate the deficit, particularly for a third nerve palsy, because it can also progress to involve the pupil.

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

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

Treatment of Diplopia

Treatment is management of the underlying disorder.

Key Points

  • Isolated, pupil-sparing single cranial nerve palsy in patients with no other symptoms may resolve spontaneously.
  • Imaging is required for patients with red flag findings.

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