Visual Disturbancesdouble vision

Double vision (diplopia) is the simultaneous visualization of two images of one object. The symptom occurs with refractive errors, accommodation and convergence, neurological diseases, intoxication and injuries. Diagnostic methods for diplopia include visometry, computer autorefractometry, biomicroscopy, ophthalmoscopy, MRI, radiography, laboratory tests and pharmacological tests. For immediate elimination of diplopia, occlusion of one eye is indicated. Etiotropic treatment is determined by the underlying disease.

Causes of double vision


With astigmatic refraction, diplopia is monocular, so when one eye is closed, complaints do not disappear. Patients note a difference in the intensity of images in front of their eyes. One of them (usually true) looks clearer, and the second has the appearance of a shadow. It seems that the two objects partially overlap each other. When correcting astigmatism, double vision becomes less pronounced or disappears altogether.

Pathologies of convergence

Normally, due to convergence (simultaneous movement of the eyeballs in the direction of each other), binocular vision is preserved when viewing objects up close. If this mechanism is violated, the images from each of the eyes are incorrectly focused on the retina. Common causes of double vision:

  • Convergence excess. Diplopia appears when looking into the distance and may be accompanied by a decrease in visual acuity, discomfort or pain in the eyes. When trying to examine an object, the effect of its oscillation is created, which is caused by oscillopsia.
  • Insufficient convergence. Double vision occurs near. People have difficulty reading and writing. Prolonged work at close range leads to painful sensations, increased fatigue and the desire to “rub” the eyes.

Accommodation violations

Accommodation is the ability to see objects located at different distances from a person. Symptoms of deterioration of accommodation ability are usually nonspecific and require a detailed history collection. Double vision is characteristic of the following disorders:

  • Accommodation insufficiency. Patients complain about the deterioration of near vision, difficulties in focusing on an object that quickly changes location. Concomitant manifestations: monocular diplopia, headache, photophobia.
  • Excess accommodation. It is characterized by double vision and decreased visual acuity in the distance. The functions in the vicinity do not suffer at the same time. Patients note the periodic development of pain in the forehead, the appearance of micropsias.
  • Spasm of “near vision”. There is a spasm of accommodation, which reaches 8-10 dptr and pronounced miosis. Esotropia is combined with bilateral restriction of withdrawal. Horizontal diplopia persists both at a close and at a long distance.

Neurological disorders

Double vision is a common sign of diseases of the central and peripheral nervous system. The mechanism of development is based on an indirect lesion of one or more oculomotor muscles. Symptoms can be constant, transient or recurrent. The most common causes:

  • Paralysis of the abductor nerve. Esotropia develops due to paresis of the lateral rectus muscle. Horizontal diplopia is more noticeable at a great distance. Depending on the etiology, the dysfunction can be temporary or permanent.
  • Block nerve paralysis. Paresis of the superior oblique muscle provokes vertical, oblique or rotatory diplopia. Complaints of double vision occur when looking down. The contralateral tilt of the head is caused by a compensatory mechanism.
  • Intracranial hypertension. An increase in intracranial pressure (ICP) is accompanied by the development of asymmetric bilateral horizontal diplopia. Its severity correlates with the indicators of ICP.
  • Ocular neuromyotonia. An attempt to keep the eyes in an eccentric position potentiates episodic double vision. Patients develop involuntary, sometimes painful contractions of extraocular muscles.
  • Myasthenia gravis. The clinical picture is represented by single- or bilateral ptosis and diplopia, which are more noticeable in the afternoon than in the morning or after rest. Systemic manifestations often include dysphagia, dysarthria, dysphonia and shortness of breath.

Orbital myositis

Orbital myositis leads to diffuse damage to one or more oculomotor muscles, which limits the mobility of the eyes. Patients note the sudden appearance of diplopia, chemosis and injections of conjunctival vessels. Pain in the orbit is barely noticeable when one muscle is involved and unbearable with a common process. In severe cases, proptosis can be traced.

Thyroid ophthalmopathy

The lower rectus muscle is most often involved in the pathological process, so the direction of diplopia is vertical. Double vision is determined in the position of the head with the chin raised. It is possible to involve other external muscles of the eye. Symptoms worsen in the morning, which allows for differential diagnosis with orbital myositis. Dysfunction of the medial rectus muscle against the background of thyroid ophthalmopathy mimics the clinic of diverting nerve paralysis.


Traumatic damage to the walls of the orbit leads to displacement of the eyeball, which leads to diplopia, pain with eye movements and swelling of soft tissues. As the edema decreases with a fracture of the lower wall of the orbit, the severity of diplopia often increases. Double vision is unbearable, often accompanied by dizziness, headache. In order to eliminate it, patients close one eye.

Postoperative complications

Diplopia can occur after surgical treatment of strabismus, cataracts, retinal detachment. During cataract surgery, the causes are anisometropia, astigmatism, dislocation of the intraocular lens. Excessive correction of strabismus is complicated by double vision, which in childhood potentiates the development of amblyopia. Vitreoretinal interventions that lead to a change in the retinal profile are manifested by monocular diplopia, distortion of the image in front of the eyes.

Taking medications

Prolonged use of beta-blockers to reduce intraocular pressure leads to diplopia, ptosis, internuclear ophthalmoplegia and pronounced general weakness. Double vision is observed for several days or weeks after changing the dosage or type of glucocorticosteroids. Concomitant symptoms: nausea, vomiting, headache and increased drowsiness.


Double vision is common in the abuse of narcotic substances, alcoholic beverages or medications for the purpose of suicide. Regardless of the root cause, the clinical picture of intoxication syndrome is represented by headache, confusion, dizziness. Specific signs are determined if poisoning provoked:

  • Cocaine. The leading symptoms of overdose: diplopia and a feeling of excessive anxiety. The skin becomes pale, moist, cold to the touch. Marked mydriasis is noted. There may be an increase in body temperature, the development of nausea and vomiting. Clonic-tonic seizures appear.
  • Ethylene glycol. Acute poisoning is manifested by double vision, dilation of retinal veins and paling of optic nerve discs. Pupils react sluggishly to light. With prolonged exposure to vapors, the mucous membrane of the eyes and upper respiratory tract is affected.
  • Gelsemium evergreen. All parts of the plant contain toxic alkaloids associated with strychnine – gelzemin and gelzeminin. Along with diplopia, skin irritation is observed. The most common cause of intoxication is the sucking of nectar from a flower, which is mistaken for honeysuckle.


At the initial examination of an ophthalmologist, the type of diplopia is first established. If the symptoms disappear when one eye is closed, then we are talking about the binocular form. In the monocular variant, double vision persists when the second eye is closed. To establish the etiology of diplopia, specific examination methods are performed:

  • Visometry. Visual acuity is measured in the distance and at the working distance of the patient with and without correction. At the same time, it is necessary to find out at what distance double vision occurs and whether its characteristics change in glasses or when the head is tilted.
  • Computer autorefractometry. Subjective refraction is studied with the selection of a trial correction. After instillation of cycloplegics, the study is repeated to obtain objective refraction indicators.
  • Biomicroscopy of the eye. It is necessary to examine the anterior segment of the eye in detail and assess the condition of the refractive media of the eyeball. In case of articulation, the position of the intraocular lens should be determined.
  • Ophthalmoscopy. Examination of the fundus reveals signs of intracranial hypertension (stagnation of the optic disc, dilated convoluted veins, narrowed arteries). After vitreoretinal interventions, distortion of the retina surface is possible.
  • MRI of the orbits and optic nerves. The technique makes it possible to visualize the thickening of the oculomotor muscles, which is observed in orbital myositis and thyroid ophthalmopathy. With concomitant proptosis, it is important to exclude pathological changes in fiber.
  • Radiography of the orbit. It is performed in a straight and lateral projection in the presence of a fracture clinic of the bone walls of the eye socket. In case of difficulties in diagnosis, computed tomography is recommended.
  • Blood test. If thyroid ophthalmopathy is suspected, measurement of TSH, T3, free T4 and the level of antibodies to thyrotropin receptors is indicated. In myasthenia gravis, it is necessary to assess the level of autoantibodies to the muscle acetylcholine receptor.
  • Pharmacological tests. The essence of the tests is reduced to subcutaneous administration of an anticholinesterase drug in the clinical picture of myasthenia gravis. The test is considered positive with full or incomplete compensation of clinical signs.


Help before diagnosis

Unilateral occlusion is used to eliminate diplopia and concomitant symptoms at the diagnostic stage. It should be remembered that these are temporary measures that are recommended before determining the etiology. There are different options for occlusion: an eye patch, matte lenses for glasses, contact lenses with an opaque center, special occluders.

If there are signs of intoxication, it is necessary to call an ambulance immediately. The patient is transported in a sitting position or on his side. It is important to perform gastric lavage in a timely manner and introduce an antidote. In acute poisoning with narcotic analgesics, naloxone hydrochloride is used. The universal antidote is sodium dimercaptopropanesulfonate monohydrate (unithiol).

Conservative therapy

An important role is given to timely etiotropic therapy of the underlying disease. With thyroid ophthalmopathy, treatment is carried out by an ophthalmologist together with an endocrinologist and is aimed at achieving euthyroidism. Patient management tactics are developed individually, but in most cases involves the use of synthetic analogues of thyroid hormones and glucocorticosteroids.

In myasthenia gravis, drug treatment is aimed at compensating for neuromuscular transmission disorders and correcting immune disorders. The administration of immunoglobulin G, anticholinesterase agents and glucocorticosteroids is shown. Also, the complex of therapy includes the intake of potassium chloride and spironolactone.

Double vision often occurs against the background of refractive anomalies. When they are detected, the appointment of eyeglass correction or soft contact lenses is shown. In case of convergence violation, orthoptic treatment is recommended. If the diplopia persists, it is advisable to apply prismatic correction.

Surgical treatment

Surgical interventions on extraocular muscles are carried out if positive dynamics has not been observed for at least 6 months, and the cause of diplopia is paralysis of the cranial nerves. In case of vision-threatening thyroid ophthalmopathy, decompression is performed. Fractures of the bone walls of the orbit require reconstructive interventions. If there is a residual diplopia after the operation, the use of Fresnel lenses is recommended.


  1. Binocular diplopia. A practical approach/ Janet С. Rucker. – 2005. link
  2. Diplopia and eye movement disorders/ C Danchaivijitr, C Kennard// Journal of Neurology, Neurosurgery, and Psychiatry. – 2004.
  3. Thyroid ophthalmopathy/ S. Schultz, L. Maun, E. Cherni.// Ophthalmological Vedomosti, Volume 5. – 2012. – No. 2.

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