B48-40 From Stroke to Silence: A Case of a Partial Locked-in Syndrome Due to Isolated Ventral Pontine Ischemic Stroke

Locked-in syndrome occurs in the setting of damage to the ventral pons and midbrain caused by ischemia, trauma, mass, myelinolysis. The hallmark presentation is quadriplegia and bulbar palsy with preserved cognition, vertical eye movement, and hearing. We present a rare case of a bilateral pontine ischemic stroke. We present a case of a 54-year-old male with history of untreated hyperaldosteronism and hypertension who presented with sudden onset right sided weakness and slurred speech. After non-contrast CT head and CTA were unremarkable, he received tenecteplase (TNK) for presumed ischemic stroke. Shortly thereafter, he developed progressive quadriplegia, aphasia, and required intubation. Subsequent CTH was negative for hemorrhage. MRI showed central pontine diffusion restriction. He had no acute metabolic derangements that would have precipitated osmotic demyelination so this is attributed to pontine ischemia with resultant locked-in syndrome. He retains sensation despite flaccid paralysis and is able to communicate through eye and subtle head movements. The severity of his deficits did necessitate tracheostomy. Of note, he had a recent self-diagnosis of “Bell’s Palsy” suspected to represent sequela of brainstem stroke that ultimately progressed until his hospitalization. He is now anticipating inpatient rehab though his degree of expected neurologic recovery remains uncertain. This case highlights not only the rarity of pontine infarctions, but those significant enough to result in locked in syndrome, which carries a 70-80% mortality rate. Ischemic locked-in syndrome is most commonly caused by large ventral pontine lesions, typically due to basilar artery atherosclerotic disease, resulting in complete occlusion of the basilar artery.1 Pontine infarctions are rare, accounting for approximately 7% of all ischemic strokes with involvement of collateral vessels being exceptionally unusual.2 In a study including 30 cases of pontine artery infarction, three were bilateral, with one of the three having hemiplegia with contralateral hemiparesis.3 Our patient reported self-diagnosis of “Bell’s Palsy” and eye movement abnormalities in the months leading up to hospitalization. Basilar artery occlusion often presents with prodromal symptoms of vertigo or headaches,4 so this may have represented insidious ischemia which was exacerbated after TNK. TNK administration is not associated with increased risk for locked-in syndrome, although clot migration is possible. We suspect this case may represent stepwise ischemia in a patient with vertebral artery occlusion secondary to dynamic clot movement.