<h3>Objective:</h3> To describe a case of lateral medullary syndrome (LMS) presenting with ipsilateral hemiparesis and upper motor neuron (UMN)-type facial palsy. <h3>Background:</h3> LMS is a classical vascular syndrome involving the posterior inferior cerebellar artery, which presents typically with ipsilateral Horner syndrome, ipsilateral ataxia, and contralateral hemianesthesia. Motor weakness and facial palsy are not traditionally presented in LMS. <h3>Design/Methods:</h3> Case report. <h3>Results:</h3> A 62-year-old male with poorly controlled hypertension presented with sudden onset left hemiparesis. On presentation, initial blood pressure was 178/95 mmHg. The neurological exam showed dysarthria, left facial palsy sparing the forehead, left facial hypoesthesia, and left hemiparesis (NIHSS 8). Diffusion-weighted MR Brain showed acute infarct in the left lateral medulla. FLAIR sequence showed chronic infarct in the right thalamus. CT arteriogram revealed non-opacification of the left vertebral artery at the level of C2–C3 with opacification of the distal left V4 via retrograde flow, severe stenosis of the right M1 segment, and multifocal atherosclerosis of the bilateral internal carotid arteries. Initial labs showed elevated LDL (213 mg/dl) and normal hemoglobin A1c. Right hemianesthesia was reported during his hospitalization; dysphagia, frequent hiccups, and left dysmetria out of proportion to weakness were noted during the recovery. After acute interventions, he was started on dual antiplatelet treatments for 90 days and a single antiplatelet afterward given concerns of large vessel disease as stroke etiology. <h3>Conclusions:</h3> Atypical clinical presentation in this LMS case included the combination of ipsilateral hemiparesis and ipsilateral UMN-type facial palsy. LMS with ipsilateral hemiparesis is known as Opalski’s syndrome, which is explained by involving the post-decussating pyramidal tract at the lower medulla and upper cervical spine. The explanation of ipsilateral UMN-type facial palsy in our case remains unclear. One possible explanation is the aberrant caudal looping of facial corticobulbar fibers into medulla oblongata prior to synapsing with the pontine facial nucleus. <b>Disclosure:</b> Dr. Yu has nothing to disclose. Mr. Bluntson has nothing to disclose. Dr. Sharma has nothing to disclose.
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