Eye movement disorder with double vision

The presence of double vision in a patient with sufficient visual acuity implies the involvement of the eye muscles or oculomotor nerves or their nuclei in the pathological process. Deviation of the eyes from the neutral position (strabismus) is always noted and can be detected by direct examination or using instruments. Such paralytic strabismus can occur with the following three lesions:

A. Muscular lesion or mechanical damage to the orbit:

1. Ocular form of muscular dystrophy.
2. Kearns-Sayre syndrome.
3. Acute ocular myositis (pseudotumor).
4. Orbital tumors.
5. Hyperthyroidism.
6. Brown syndrome.
7. Myasthenia gravis.
8. Other causes (orbital trauma, dysthyroid orbitopathy).

B. Damage to the oculomotor (one or more) nerves:

1. Injury.
2. Compression by a tumor (often parasellar) or aneurysm.
3. Arteriovenous fistula in the cavernous sinus.
4. General increase in intracranial pressure (abducens and oculomotor nerves).
5. After lumbar puncture (abducens nerve).
6. Infections and parainfectious processes.
7. Tolosa-Hunt syndrome.
8. Meningitis.
9. Neoplastic and leukemic infiltration of the meninges.
10. Cranial polyneuropathies (as part of Guillain-Barré syndrome, isolated cranial polyneuropathies: Fisher syndrome, idiopathic cranial polyneuropathy).
11. Diabetes mellitus (microvascular ischemia).
12. Ophthalmoplegic migraine.
13. Multiple sclerosis.
14. Isolated lesion of the abducens nerve or oculomotor nerve of an idiopathic nature (completely reversible).

C. Lesions of the oculomotor nuclei:

1. Vascular strokes (cerebrovascular accidents) in the brainstem.
2. Brainstem tumors, especially gliomas and metastases.
3. Trauma with hematoma in the brain stem area.
4. Syringobulbia.

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A. Muscular lesion or mechanical damage to the orbit

Such processes may lead to disturbances in eye movements. When the process develops slowly, double vision is not detected. Muscle damage may be slowly progressive (oculomotor dystrophy), rapidly progressive (ocular myositis), sudden and intermittent (Brown's syndrome); it may be of varying intensity and localization (myasthenia).

The ocular form of muscular dystrophy progresses over the years, always manifesting itself as ptosis, and later involving the neck and shoulder girdle muscles (rarely).

Kearns-Sayre syndrome, which includes, in addition to slowly progressive external ophthalmoplegia, retinitis pigmentosa, heart blocks, ataxia, deafness, and short stature.

Acute ocular myositis, also called orbital pseudotumor (rapidly worsens during the day, usually bilateral, periorbital edema, proptosis (exophthalmos), pain are noted.

Orbital tumors. The lesion is unilateral, leading to slowly increasing proptosis (exophthalmos), limitation of eyeball movements, and later to disruption of pupillary innervation and involvement of the optic nerve (visual impairment).

Hyperthyroidism is manifested by exophthalmos (with pronounced exophthalmos, there is sometimes a limitation in the range of movements of the eyeball with double vision), which can be unilateral; a positive Graefe symptom; and other somatic symptoms of hyperthyroidism.

Brown's syndrome (strongrown), which is associated with a mechanical obstruction (fibrosis and shortening) of the tendons of the superior oblique muscle (sudden, transient, recurring symptoms are noted, the inability to move the eye upward and inward, which leads to double vision).

Miasthenia gravis (involvement of the eye muscles with varying localization and intensity, usually with pronounced ptosis, increasing during the day, usually involving the facial muscles and swallowing disorder).

Other causes: orbital trauma involving muscles: dysthyroid orbitopathy.

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B. Damage to the oculomotor (one or more) nerves:

Symptoms depend on which nerve is affected. Such damage causes paralysis, which is easily recognized. In case of paresis of the oculomotor nerve, in addition to strabismus, slight exophthalmos may be observed, caused by hypotonia of the rectus muscle with preserved tone of the oblique muscles, which contribute to the outward protrusion of the eyeball.

The following causes may result in damage to one or more oculomotor nerves:

Trauma (history helps) sometimes results in bilateral orbital hematomas or, in extreme cases, rupture of the oculomotor nerve.

Compression by a tumor (or giant aneurysm), especially a parasellar aneurysm, causes slowly increasing paresis of the oculomotor muscles and is often accompanied by involvement of the optic nerve, as well as the first branch of the trigeminal nerve.

Other space-occupying lesions, such as supraclinoid or infraclinoid aneurysms of the carotid artery (characterized by all of the above, slowly increasing involvement of the oculomotor nerve, pain and sensory disturbances in the area of the first branch of the trigeminal nerve, rarely calcification of the aneurysm, which is visible on a plain X-ray of the skull; later - acute subarachnoid hemorrhage).

Arteriovenous fistula in the cavernous sinus (a consequence of repeated trauma) eventually leads to pulsating exophthalmos, a synchronous noise with the pulse that is always audible, congestion in the conjunctival veins and in the fundus. With compression of the oculomotor nerve, an early symptom is mydriasis, which often appears before paralysis of eye movements.

General increase in intracranial pressure (usually the abducens nerve is involved first, later the oculomotor nerve).

After lumbar puncture (after which, a picture of damage to the abducens nerve is sometimes noted, but with spontaneous recovery).

Infections and parainfectious processes (spontaneous recovery is also observed here).

Tolosa-Hunt syndrome (and paratrigeminal Raeder syndrome) are very painful conditions characterized by incomplete external ophthalmoplegia and sometimes involvement of the first branch of the trigeminal nerve; spontaneous regression is characteristic within a few days or weeks; steroid therapy is effective; relapses are possible.

Meningitis (includes symptoms such as fever, meningism, general malaise, damage to other cranial nerves; it can be bilateral; cerebrospinal fluid syndrome).

Neoplastic and leukemic infiltration of the meninges is one of the known causes of damage to the oculomotor nerves at the base of the brain.

Cranial polyneuropathies as part of spinal polyradiculopathies of the Guillain-Barré type; isolated cranial polyneuropathies: Miller Fisher syndrome (often manifests itself only as bilateral incomplete external ophthalmoplegia; ataxia, areflexia, facial paralysis, and protein-cell dissociation in the cerebrospinal fluid are also noted), idiopathic cranial polyneuropathy.

Diabetes mellitus (an uncommon complication of diabetes, observed even in its mild form, usually involving the oculomotor and abducens nerves, without pupillary disorders; this syndrome is accompanied by pain and ends with spontaneous recovery within 3 months. It is based on microvascular ischemia of the nerve.

Ophthalmoplegic migraine (a rare manifestation of migraine; a history of migraine helps in the diagnosis, but other possible causes must always be excluded).

Multiple sclerosis. Oculomotor nerve damage is often the first symptom of the disease. Recognition is based on generally accepted diagnostic criteria for multiple sclerosis.

Idiopathic and completely reversible isolated lesion of the abducens nerve (most commonly found in children) or oculomotor nerve.

Infectious diseases such as diphtheria and botulism intoxication (swallowing paralysis and accommodation disorder are noted).

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C. Lesion of the oculomotor nuclei:

Since the oculomotor nuclei are located in the brainstem among other structures, damage to these nuclei manifests itself not only as paresis of the external eye muscles, but also as other symptoms, which allows them to be distinguished from damage to the corresponding nerves:

Such disorders are almost always accompanied by other symptoms of damage to the central nervous system and are usually bilateral.

In nuclear oculomotor palsy, the various muscles innervated by the oculomotor nerve rarely show the same degree of weakness. Ptosis usually appears only after the extrinsic eye muscles have become paralyzed (the "curtain falls last"). The intrinsic eye muscles are often spared.

Internuclear ophthalmoplegia results in strabismus in a certain direction of gaze and diplopia when looking to the side. The most common causes of nuclear eye movement disorders are:

Stroke in the brainstem (sudden onset, accompanied by other brainstem symptoms, mainly cross symptoms and dizziness. Brainstem symptoms, usually including nuclear oculomotor disturbances, manifest themselves in the known alternating syndromes.

Tumors, especially stem gliomas and metastases.

Traumatic brain injury with hematoma in the brain stem area.

Syringobulbia (does not progress for a long period, symptoms of damage along the length axis, dissociated sensitivity disorders on the face) are observed.

Double vision may also be observed in some other disorders such as chronic progressive ophthalmoplegia, toxic ophthalmoplegia due to botulism or diphtheria, Guillain-Barré syndrome, Wernicke's encephalopathy, Lambert-Eaton syndrome, myotonic dystrophy.

Finally, diplopia is described in cases of lens opacity, incorrect refractive correction, and corneal diseases.

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D. Monocular diplopia (double vision when looking with one eye)

Monocular diplopia is always intriguing for a neurologist. This condition can often be either psychogenic or caused by a refractive error in the eye (astigmatism, corneal or lens transparency disorder, dystrophic corneal changes, iris changes, foreign body in the eye, retinal defect, cyst in it, defective contact lenses).

Other possible causes (rare): occipital lobe damage (epilepsy, stroke, migraine, tumor, trauma), tonic gaze deviation (concomitant), disruption of the connection between the frontal gaze field and the occipital region, palinopsia, monocular oscillopsia (nystagmus, mokimia of the superior oblique muscle, eyelid twitching)

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Double vision in the vertical plane

This situation is rare. Its main causes are: orbital base fracture involving the inferior rectus muscle; thyroid orbitopathy involving the inferior rectus muscle, ocular myasthenia, third (oculomotor) cranial nerve lesion, fourth (trochlear) cranial nerve lesion, skew deviation, myasthenia.

Less common causes include: orbital pseudotumor; extraocular muscle myositis; primary orbital tumor; inferior rectus entrapment; third nerve neuropathy; aberrant reinnervation in third nerve injury; Brown's syndrome (strongrown) - a form of strabismus caused by fibrosis and shortening of the tendon of the superior oblique muscle of the eye; double elevator palsy; chronic progressive external ophthalmoplegia; Miller Fisher syndrome; botulism; monocular supranuclear gaze palsy; vertical nystagmus (oscillopsia); superior oblique myokymia; dissociated vertical deviation; Wernicke's encephalopathy; vertical one-and-a-half syndrome; monocular vertical diplopia.