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Internuclear ophthalmoplegia: pathophysiology and diagnosis
1Johns Hopkins Hospital, Baltimore, MD 21205.
Bailliere'S Clinical Neurology
|August 1, 1992
Summary
Internuclear ophthalmoplegia (INO) causes eye movement abnormalities like reduced adduction and nystagmus. Lesions in the medial longitudinal fasciculus (MLF) explain these findings, affecting conjugate gaze and vestibular reflexes.
Area of Science:
- Neuroscience
- Ophthalmology
- Neurology
Background:
- Internuclear ophthalmoplegia (INO) is a common neuro-ophthalmic disorder.
- It results from lesions affecting the medial longitudinal fasciculus (MLF).
- Understanding INO is crucial for diagnosing brainstem and cerebellar pathologies.
Purpose of the Study:
- To elucidate the primary clinical manifestations of unilateral and bilateral INO.
- To explore the underlying pathophysiology of INO, including abduction nystagmus.
- To correlate clinical findings with neuroanatomical pathways.
Main Methods:
- Clinical case review and analysis of neuro-ophthalmic findings.
- Review of neuroanatomical pathways involved in eye movement control.
- Pathophysiological correlation of lesion location with observed symptoms.
Main Results:
- Unilateral INO: adduction paresis (ipsilesional), abduction nystagmus (contralesional), possible skew deviation.
- Bilateral INO: bilateral adduction paresis, bilateral abduction nystagmus, impaired vertical gaze, vestibular responses, and smooth tracking.
- Abduction nystagmus often results from gaze-evoked nystagmus superimposed on adduction weakness or adaptation.
Conclusions:
- INO findings are largely explained by interruption of abducens internuclear neurons and vestibular nuclei projections.
- Lesions extending beyond the MLF or involving adjacent cell bodies can contribute to abduction nystagmus and saccadic slowing.
- Pathophysiology involves disrupted pathways for adduction, vestibular reflexes, and gaze control.