Cranial Nerve & Brainstem Syndromes

Medial and lateral gaze coordination is controlled by input from CN III nucleus, CN VI nucleus and the medial longitudinal fasciculus (MLF). The nucleus for CN III is located within the midbrain, the nucleus for CN VI is located within the pons and the MLF is a tract that connects these nuclei and runs between the midbrain and pons.

An INO occurs from a lesion within the MLF and is a defect of lateral conjugate gaze in which the affected eye is not able to adduct and the contralateral eye is able to abduct, but with nystagmus.

Sagittal FLAIR and Axial DWI images at the level of the pons demonstrate a region of diffusion restriction (blue arrows) within the right hemipons involving the right medial longitudinal fasciculus (MLF) consistent with an infarct.

Differential Diagnosis for a lesion in the MLF is broad including stroke, demyelination, myasthenia gravis, etc.

The facial colliculi are paired small elevations (blue arrows) protruding from the dorsal pons into the fourth ventricle. They are formed by motor fibers from the facial nerve nucleus curving backward and laterally around the posterior aspect of the abducens nucleus prior to joining parasympathetic and special sensory fibers of the facial nerve and assuming an anterolateral course in the caudal pons.

A lesion affecting the facial colliculus will cause deficits of the abducens nerve and motor fibers of the facial nerve, leading to ipsilateral CN VI and VII palsies, manifesting as ipsilateral horizontal gaze palsy and lower motor neuron pattern facial weakness. This presentation has been termed the “facial colliculus syndrome”.

Sagittal T2-FLAIR, axial T2 and T1 weighted images at the level of the pons demonstrate a lesion that is T2/FLAIR hyperintense (white arrow) and T1 hypointense (orange arrow) involving the left facial colliculus, consistent with a demyelinating lesion in this patient with known multiple sclerosis.

Wallenberg syndrome is caused by an infarct of the lateral medulla due to compromise of the posterior inferior cerebellar artery (PICA). In younger patient’s this is commonly caused by vertebral artery dissection with secondary compromise of PICA. In older patient’s this can be caused by thromboembolic disease.

Classically, patient’s with Wallenberg syndrome present with a Horner syndrome (ipsilateral ptosis, miosis and anhydrosis), ipsilateral ataxia, and ipsilateral face and contralateral body sensory changes (so-called “crossed hemisensory deficits”), but they may present with varying combinations of deficits referable to the lateral medulla.

Axial pre-contrast T1-weighted and DWI images demonstrate a focus of restricted diffusion in the right dorsolateral medulla (red arrow), consistent with acute infarct. There is crescentic, intrinsically T1 hyperintense signal in the right vertebral artery (blue arrow), consistent with intramural hematoma related to a vascular dissection.