Address the challenges of diagnosis and management of pediatric oculomotor nerve palsy through a case presentation of a 5-year-old boy with acute left oculomotor palsy and review of the literature.
The most common causes of pediatric oculomotor nerve palsy are congenital (hypoplasia, agenesis, or focal thinning), traumatic (basilar skull fracture, orbital trauma, intracranial hemorrhage), and neoplastic (schwannoma, neuroma, meningioma). Less common but important considerations include inflammatory etiologies—specifically post-infectious or inflammatory neuritis.
A previously healthy 5-year-old male presented with sudden onset diplopia, anisocoria (L ~ 8 mm, R ~ 4mm), left pupil nonreactivity to light, ptosis and deficits in left adduction and vertical upward gaze. History was negative for any prior trauma, but parents endorsed a recent viral infection that had resolved a week prior to presentation.
CT head was negative for intracranial bleed, mass lesion, or fracture. MR angiography showed no evidence of aneurysms. MRI of the brain including FLAIR and T1 post contrast images showed subtle but clear thickening and enhancement of the left oculomotor nerve at the superior orbital fissure consistent with demyelinating neuropathy (images will be shown). Lumbar puncture was unsuccessful. Serum antibody testing for myasthenia gravis, neuromyelitis optica, MOGAD, and diverse peripheral neuropathies (i.e. GBS variant, Miller-Fisher syndrome) were unrevealing. Viral panel was negative. IVIG and 2 courses of steroid with taper were prescribed. Right eye patching was initiated. Over the next three months, the patient experienced gradual and complete symptom resolution.
This case emphasizes the diagnostic challenge of pediatric oculomotor nerve palsy. The most common etiologies were excluded, while imaging findings and therapeutic response indicate an inflammatory or post-infectious mechanism. Early recognition and management remain critical in minimizing the risk of developing amblyopia and preserving visual function.