Article Highlights

• Internuclear ophthalmoplegia (INO) results from disruption of the medial longitudinal fasciculus (MLF), impairing coordinated horizontal gaze.
• Affected patients demonstrate ipsilateral adduction weakness with contralateral abducting nystagmus due to disconnection between the abducens and oculomotor nuclei.
• Etiology is age-dependent, with multiple sclerosis more common in younger patients and stroke the leading cause in older adults.
• Acute INO warrants neuroimaging (CT followed by MRI) to localize demyelinating or ischemic lesions along the MLF.
• Pseudo-INO, particularly from myasthenia gravis, should remain in the differential when similar ocular motility findings are present.

 

Like the respiratory system or primary motor cortex control, coordinated horizontal eye movement is one of those important bodily functions we rarely notice or appreciate — until something goes wrong.

Eye movement disorders such as internuclear ophthalmoplegia (INO) occur when the medial longitudinal fasciculus (MLF) pathway is damaged, causing double vision, loss of vision and dizziness, among other concerns.

"Internuclear ophthalmoplegia looks complicated, but it's really just a lesion between two nuclei that have to talk to each other for the eyes to move together," says Dr. Andy Lee, neuro-ophthalmologist and chair of the Blanton Eye Institute at Houston Methodist.

In a new whiteboard video about the condition, Dr. Lee explains that the abducens nucleus in the pons controls the lateral rectus muscle, while the oculomotor nucleus in the midbrain drives the medial rectus. Their connection via the MLF ensures both eyes track in tandem. A lesion disrupting that link prevents the affected eye from adducting, while the contralateral eye develops a horizontal abducting nystagmus.

In younger patients, internuclear ophthalmoplegia is most often caused by multiple sclerosis. In older patients, stroke is the leading culprit. Acute presentations require neuroimaging — typically CT followed by MRI — to identify a demyelinating lesion or vascular infarct along the MLF.

Dr. Lee cautions against overlooking pseudo-INO, which presents with similar motility deficits but stems from neuromuscular junction pathology such as myasthenia gravis. "If you see adduction weakness with nystagmus, you can't stop at the MLF," he says. "You have to keep pseudo-INO in your differential."

Ultimately, a true INO points to a lesion in the medial longitudinal fasciculus — a critical insight that underscores the value of careful neuro-ophthalmic evaluation. By recognizing its characteristic ocular motor findings, physicians can more quickly narrow the diagnostic pathway and identify the underlying neurologic disease.