Thread: Internuclear ophthalmoplegia with animated tutorial

Internuclear ophthalmoplegia is impairment of horizontal eye movements caused by damage to certain connections between nerve centers in the brain stem.


a. Normal primary position b. Left impaired adductionn on right gaze
c. Normal left abduction on left gaze d. Normal convergence


Left internuclear ophthalmoplegia

In internuclear ophthalmoplegia, the nerve fibers that coordinate both eyes in horizontal movements—looking from side to side—are damaged. These fibers connect collections of nerve cells (centers or nuclei) that the 3rd cranial nerve (oculomotor nerve) and the 6th cranial nerve (abducens nerve) originate from. In older people, the disorder usually results from a stroke, and only one eye is affected. In younger people, it usually results from multiple sclerosis, and both eyes are often affected. Less common causes include Lyme disease, tumors, and toxicity due to a drug (such as tricyclic antidepressants).

Horizontal eye movements are impaired, but vertical ones are not. The affected eye cannot turn inward, but it can turn outward. When a person looks to the side opposite the affected eye, the following happens:

The affected eye, which should turn inward, cannot move past the midline. That is, the affected eye looks straight ahead.
As the other eye turns outward, it often makes involuntary, repetitive fluttering movements called nystagmus That is, the eye rapidly moves in one direction, then slowly drifts in the other direction.
People with internuclear ophthalmoplegia may have double vision.

One-and-a-half syndrome results when the disorder that causes internuclear ophthalmoplegia also damages the center that coordinates and controls horizontal eye movements (horizontal gaze center). When the person tries to look the either side, the affected eye remains motionless in the middle. The other eye can turn outward but not inward. As in internuclear ophthalmoplegia, vertical eye movements are not affected.

In internuclear ophthalmoplegia and one-and-a-half syndrome, the eyes can turn inward when the person looks inward (as when focusing on a nearby object) even though the eyes cannot turn inward when the person looks to the side.

For internuclear ophthalmoplegia or one-and-a-half syndrome, treatment and outlook (whether the disorder abates or eventually resolves) depends on the disorder that caused it.

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The most common scenario in the examination is young female with history of multiple sclerosis.

However, it can also be seen in older patients with cerebrovascular accident. The main feature of this condition is impaired adduction. A favourite question is the site and side of the lesion.

In unilateral case, the affected eye shows failure (or impaired) adduction (failure of conjugate eye movement). The abducting eye shows jerk nystagmus with the quick phase towards the opposite side (this is called ataxic nystagmus but may not be obvious and can be absent). The horizontal saccade is abnormal with the affected eye lagging behind the normal eye. The vertical saccade and convergence are normal.
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Left saccade abnormality.

This may be the only sign present in patient with recovered internuclearophthalmoplegia.
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In the examination:

There may be strabismus in the primary position the internuclear ophthalmoplegia may be bilateral with or without asymmetry
if ask for further examination, mention that you would like to examine the patient for signs of demyelination:

Fundal examination for pale disc (from previous optic neuritis which may be in either eye)
Afferent pupillary defect (again from previous optic neuritis)
Cerebellar signs (for example scanning speech, disdianochokinesia, intentional tremor, past-pointing in finger nose test)

One and a half syndrome - Wikipedia, the free encyclopedia

Internuclear ophthalmoplegia is characterized by paresis of eye adduction in horizontal gaze but not in convergence. It can be unilateral or bilateral.

During horizontal gaze, the medial longitudinal fasciculus (MLF) on each side of the brain stem enables abduction of one eye to be coordinated with adduction of the other. The MLF connects the following structures:

6th cranial nerve nucleus (which controls the lateral rectus, responsible for abduction)
Adjacent horizontal gaze center (paramedian pontine reticular formation)
Contralateral 3rd cranial nerve nucleus (which controls the medial rectus, responsible for adduction)
The MLF also connects the vestibular nuclei with the 3rd cranial nerve nuclei.

Internuclear ophthalmoplegia results from a lesion in the MLF. In young people, the disorder is commonly caused by multiple sclerosis and may be bilateral. In the elderly, it is typically caused by stroke and is unilateral. Occasionally, the cause is neurosyphilis, Lyme disease, tumor, or drug intoxication (eg, with tricyclic antidepressants).

If a lesion in the MLF blocks signals from the horizontal gaze center to the 3rd cranial nerve, the eye on the affected side cannot adduct (or adducts weakly) past the midline. The affected eye adducts normally in convergence because convergence does not require signals from the horizontal gaze center. This finding distinguishes internuclear ophthalmoplegia from 3rd cranial nerve palsy, which impairs adduction in convergence (this palsy also differs because it causes limited vertical eye movement, ptosis, and pupillary abnormalities).

During horizontal gaze to the side opposite the affected eye, images are horizontally displaced, causing diplopia; nystagmus often occurs in the abducting eye. Sometimes vertical bilateral nystagmus occurs during attempted upward gaze.

Treatment is directed at the underlying disorder.

One-and-a-half syndrome: This uncommon syndrome occurs if a lesion affects the horizontal gaze center and the MLF on the same side. The eyes cannot move horizontally to either side except the eye on the side opposite the lesion can abduct; convergence is unaffected. Causes include multiple sclerosis, infarction, hemorrhage, and tumor.

With treatment (eg, radiation therapy for a tumor, treatment of multiple sclerosis), improvement may occur but is often limited after infarction.