Diplopia (Double Vision) Clinical Presentation

Updated: May 21, 2019
  • Author: Jitander Dudee, MD, MA(Cantab), FACS, FRCOphth; Chief Editor: Andrew G Lee, MD  more...
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Presentation

History

A clear and comprehensive history is the single most useful evaluation in treating patients with diplopia. The patient typically presents with a history of double vision, where single objects appear as double. Specific inquiry as to onset, progression, effects of distance of target, and variability with head posture or gaze direction, as well as previous similar episodes (especially if associated with other neurologic symptoms) and/or spontaneous resolution, is very helpful in the diagnosis and management of diplopia.

Three important symptoms should be elicited, as follows:

  • Does covering either eye make the diplopia disappear? This test helps to rule out monocular diplopia, which persists in one eye even if the other eye is covered. Simply asking about resolution of diplopia when covering one eye is insufficient and may be misleading because the patient may inadvertently cover the eye with the monocular diplopia. This may lead to the mistaken impression that the diplopia is binocular (resolves with covering either eye) rather than monocular.
  • Is the deviation the same in all directions of gaze or by tilting and rotating the head into different positions? A comitant deviation shows  minimal or no difference in separation of the images in all directions of gaze. When the extent of deviation changes (and indeed possibly disappears in a given direction), then the deviation is incomitant and suggests a problem with innervation, most likely a paretic muscle.
  • Is the second object displaced horizontally (side-by-side images) or vertically (images above each other)? Oblique diplopia (images separated horizontally and vertically) should be considered as a manifestation of vertical diplopia.

The traditional and detailed evaluation of the chief complaint includes onset (abrupt or slow), severity, duration, location, associated symptoms, and aggravating and relieving factors. A comprehensive and complete review of all these aspects, if necessary with a questionnaire, is more important than the appropriate physical examination or special tests.

Other significant aspects include a review of systems (eg, history of diabetes, vascular disease, or hypertension; headache and other neurologic complaints; muscle fatigue or weakness; medications and drugs being used [6] ), as well as a past medical and surgical history.

Inquire about recent trauma to the face and the head. Blunt injury to the cheek can result in a blow-out fracture of the orbit with hematoma or entrapment of the soft tissues and extraocular muscles, restricting upward and downward eye movement. Entrapment of the inferior rectus muscle can be confirmed by a forced duction test. Blunt head injury may also be associated with nonspecific sixth cranial nerve (abducens) weakness and severe diplopia when gazing to the affected side.

Evaluate old photographs, if available, to determine if a head posture (if present) is long-standing. Commonly, a congenitally weak superior oblique muscle can be compensated for by head tilt, but osteoarthritis of the neck or other mechanism can result in decompensation and sudden symptoms of a chronic subclinical condition.

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Physical

Evaluate the ocular system with respect to 2 specific aspects: first, physiologically (in turn also with 2 aspects, ie, sensory function and motor function), and, second, anatomically.

The first aspect of the evaluation includes the sensory component.

Confirm that the symptom is monocular or binocular. Does covering each eye in turn alleviate the problem, or does the diplopia persist despite covering the "good" opposite eye? Monocular diplopia is very uncommon. Possible causes include severe corneal deformity or marked astigmatism (keratoconus), multiple pupils or openings in the iris, refractive anomalies within the eye (early cataracts or partially displaced lenses as in Marfan syndrome), as well as retinal abnormalities (macular scarring and distortion).

Evaluate the magnitude of difference in spectacle correction required for each eye. Marked differences between the eyes (anisometropia) will frequently produce disabling diplopia, especially in extremes of gaze.

Determine the visual acuity in each eye separately, with and without spectacle correction and with a pinhole. Does a pinhole improve the visual acuity, or does it improve monocular diplopia? Major improvement in visual acuity with a pinhole suggests intraocular or refractive problems.

Evaluate the visual field by confrontation testing or formal visual field mapping to detect possible space occupying masses impinging on the visual pathways and/or cranial motor nerves. With severely constricted fields, the peripheral clues for fusion may be lacking, resulting in diplopia.

Determine how various directions of gaze modify the diplopia. Is the diplopia the same in the 9 cardinal directions of gaze? This includes straight ahead (primary gaze), to each side as well as up and down while looking toward that side, and straight up and down from the primary position. This evaluation can enhance subtle weaknesses of individual muscles that may not be apparent during testing of the range of movements.

Evaluate how tilting the head to the left or to the right alters the diplopia. The double vision will increase when the head is tilted to the same side if vertical diplopia is present due to weakness of the superior oblique muscle (innervated by the fourth cranial nerve [trochlear nerve]). Eliciting increases or decreases in the separation of the 2 images is an essential part of the Park three-step test. In addition, evaluating the ocular deviation in cases of vertical diplopia (along with the three-step test) in both supine and upright positions may help to differentiate between that caused by skew deviation versus a trochlear nerve palsy. If the vertical deviation  results from a skew deviation, it is more likely to improve with supine positioning than that caused by trochlear nerve palsy.

Evaluate the integrity of the other cranial nerves (eg, facial sensation [trigeminal nerve], facial muscle movements).

The motor aspect of the physiologic evaluation includes the following:

  • Determine the existence of a normal range of ocular movements. First observe each eye separately (ocular ductions), and then observe both eyes together (ocular versions). Careful consideration of the extraocular muscle anatomy clarifies the effect of each muscle and why one direction of gaze isolates each muscle's effects.

  • Determine that each eye is able to fully adduct (turn inward) and abduct (turn outward) and to fully elevate and depress in abduction and adduction (as if the eye is tracing a capital letter "H").

  • This helps to determine which eye muscle is responsible for diplopia; normal contraction of the medial rectus muscle produces adduction, while abduction is caused by the lateral rectus muscle. Because the vertical eye muscles diverge from their origination at the apex of the orbit to the insertion on the globe, the superior and inferior recti muscles can be evaluated best with the eye abducted.

  • With the eye abducted, the eye will move down by the inferior rectus muscle, while the superior rectus muscle will move it upward in abduction. Likewise, the oblique muscles can be isolated with the eye adducted; with the eye turned in, the inferior oblique muscle elevates and the superior oblique muscle depresses the eye. A simple rule for superior oblique weakness is "the eye that is looks highest in adduction is pointing at the affected superior oblique muscle."

  • Determine if diplopia worsens when the muscles are fatigued (eg, after strenuous use, at the end of the day). Myasthenia gravis can affect any muscle or group of muscles, and a common presenting symptom is variable diplopia. If myasthenia gravis is suspected, its diagnosis can be confirmed with a rest or sleep test or an ice test or after intravenously injecting a short-acting anticholinesterase (ie, 10 mg/mL edrophonium chloride [Tensilon]). Nonpharmacologic tests for myasthenia gravis have become more popular and more widely used clinically because of their ease of use and lack of significant adverse-effect profile compared with pharmacologic testing. See Other Tests.

Determine that other ocular motor functions are normal, as follows:

  • Is the lid in a normal position? (eg, lid retraction in thyroid eye disease or aberrant regeneration of the third nerve, ptosis, Cogan lid twitch sign, enhancement and variability in myasthenia gravis)

  • Is the pupil response normal and symmetric with the other pupil? Pupil asymmetry is a sinister sign when associated with diplopia because it indicates involvement of the third cranial nerve (oculomotor nerve). An important diagnostic clue is provided by detecting pupil sparing but otherwise complete third nerve palsy (eg, ptosis; inability to elevate, depress, or abduct the eye). A pupil whose function is spared, particularly if associated with complaints of headache or pain around the orbit, suggests diabetic third nerve palsy. This can avoid expensive and unnecessary imaging studies. Complete and spontaneous recovery after approximately 6 weeks is virtually the rule. Similar temporary mononeuritis multiplex processes can affect the sixth cranial nerve (abducens) with temporary loss of abduction.

The anatomical evaluation includes inspection, palpation, percussion, and auscultation.

Inspect the head position, eyes, eyelids, orbits, and face for symmetry or displacement (upward, downward; proptosis, enophthalmos). Ptosis of the upper eyelid indicates possible third nerve lesions, while eyelid retraction suggests thyroid ophthalmopathy. Abnormal head position (especially tilting the head to one side) suggests superior oblique muscle palsy.

Note inflammation or vascular congestion that may be suggestive of orbital cellulitis, orbital tumors (rhabdomyosarcoma), arteriovenous malformation (carotid cavernous fistula), and thyroid ophthalmopathy. Palpate the orbital rim for fractures and any absences (eg, encephalocele). Palpate soft tissues surrounding the eye for tumors. Gently push on the closed eyelid to determine increased resistance (fullness of the orbit), comparing one eye to the other eye. This may disclose orbital disorders (eg, fractures, tumors).

Perform percussion over the bony orbital rim to disclose focal tenderness from sinus inflammation.

Auscultate the closed eye for the bruit of a carotid cavernous fistula.

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Causes

Binocular diplopia caused by ocular misalignment can stem from supranuclear disease, nuclear disease, or infranuclear disease, which includes disease of the extraocular muscles, the nerves innervating these muscles, or the neuromuscular junction connecting the nerve and the muscle. It can be further classified as intermittent or constant. Common causes include the following:

  • Orbital disorders: Trauma, tumor, infection, thyroid-associated ophthalmopathy
  • Extraocular muscle disorders: Thyroid-associated ophthalmopathy, extraocular muscle injury or hematoma due to ocular surgery, congenital myopathies, mitochondrial myopathies, muscular dystrophy
  • Neuromuscular junction dysfunction: Myasthenia gravis, botulism
  • Palsies of the third, fourth or sixth cranial nerves: Microvascular ischemia, diabetic neuropathy, hemorrhage, tumor, vascular malformation, aneurysm, meningitis, multiple sclerosis
  • Central nervous system injury (pathways and cranial nerves nuclei): Ischemia, hemorrhage, tumor, vascular malformations, multiple sclerosis, hydrocephalus, syphilis, Wernicke encephalopathy, neurodegenerative disease

Less commonly, diplopia can be caused by drugs such as lacosamide, zonisamide, eslicarbazepine, botulinum toxin, rufinamide, pregabalin, sildenafil, gabapentin, topiramate, levetiracetam, amlodipine, adalimumab, lamotrigine, voriconazole, sertraline, and ciprofloxacin. [7]

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Complications

In infants and young children, diplopia can result in suppression and amblyopia of the nondominant eye.

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