Nonaneurysmal cranial nerve compression as cause of neuropathic strabismus: evidence from high-resolution magnetic resonance imaging.

PURPOSE: To seek evidence of neurovascular compression of motor cranial nerves (CNs) in otherwise idiopathic neuropathic strabismus using high-resolution magnetic resonance imaging (MRI).

DESIGN: Prospective, observational case series.

METHODS: High-resolution, surface coil orbital MRI was performed in 10 strabismic patients with idiopathic oculomotor (CN III) or abducens (CN VI) palsy. Relationships between CNs and intracranial arteries were demonstrated by 0.8-mm thick, 162-μm resolution, heavily T2-weighted MRI in fast imaging using steady-state acquisition sequences. Images were analyzed digitally to evaluate cross-sectional areas of extraocular muscles.

RESULTS: In one patient with CN III palsy, an ectatic posterior communicating artery markedly flattened and thinned the ipsilateral subarachnoid CN III. Cross-sections of the affected medial, superior, and inferior rectus muscles 10 mm posterior to the globe-optic nerve junction were 17.2 ± 2.5 mm(2), 15.5 ± 1.3 mm(2), and 9.9 ± 0.8 mm(2), significantly smaller than the values of 23.6 ± 1.9 mm(2), 30.4 ± 4.1 mm(2), and 28.8 ± 4.6 mm(2), respectively, of the unaffected side (P < .001). In 2 patients with otherwise unexplained CN VI palsy, ectatic basilar arteries contacted CN VI. Mean cross-sections of affected lateral rectus muscles were 24.0 ± 2.3 mm(2) and 29.8 ± 3.1 mm(2), significantly smaller than the values of 33.5 ± 4.1 mm(2) and 36.9 ± 1.6 mm(2), respectively, in unaffected contralateral eyes (P < .05).

CONCLUSIONS: Nonaneurysmal motor CN compression should be considered as a cause of CN III and CN VI paresis with neurogenic muscle atrophy when MRI demonstrates vascular distortion of the involved CN. Demonstration of a benign vascular cause can terminate continuing diagnostic investigations and can expedite rational management of the strabismus.