We present an index symptom  of  multiple sclerosis   with persistent left hemifacial spasm, direction changing nystagmus and blepharospasm. With a referable left pontine T2 hyperintensity, to identify a practice gap in an unusual presentation for multiple sclerosis. 

Multiple sclerosis results in demyelinating lesions of the central nervous system. The characteristically involved neuroanatomic tracts correlate to well defined typical symptom presentations¹.  In contrast, hemifacial spasm falls under the umbrella of movement disorders, with pathophysiology most commonly linked to peripheral  facial nerve mechanical irritation  in the subarachnoid space.²

The recognition of hemifacial spasm referable to multiple sclerosis represented a knowledge gap.  

On exam there was continuous L hemifacial spasm, blepharospasm and direction changing nystagmus on lateral gaze with limb ataxia and ataxic gait.

Contrasted brain MRI revealed bilateral non-enhancing ovoid shaped T2 hyperintensities in the infratentorial region, including adjacent to the fascicular portion of the left seventh cranial nerve.

There were additionally topographically and morphologically typical T2 hyperintensities   in the periventricular/juxtacortical region, with some lesions contrast enhancing, thus meeting 2024 McDonald’s criteria for multiple sclerosis. 

The left hemifacial spasm did not improve with high dose IV methylprednisolone. 

There is a knowledge gap in recognizing hemifacial spasm and direction changing nystagmus  as a clinical presentation of a central  demyelinating disease. In this case, it is posited to be secondary to demyelination of the fascicles of the seventh cranial nerve in the left hemi pons, but nuclear involvement has also been reported.⁴   Increasing recognition of this movement disorder secondary to an autoimmune demyelinating etiology may alert providers to obtain early neuro axis imaging.