Case Presentation A 61-year-old male with a PMHx of MI status post PCI, HTN, and HLD presented after being found unresponsive. On arrival to the ED, the patient had altered mental status with GCS of 8 and was intubated. The patient was not a thrombolytic candidate due to being outside the therapeutic window. On subsequent physical examination, he was found to have vertical gaze palsy on both upwards and downwards gaze. CT Head and CTA Head and Neck were negative for acute hemorrhage or LVO. However, MRI Brain WO showed bilateral thalamic infarcts with left thalamic hemorrhage making an occlusion of an Artery of Percheron neuroanatomical variant the most likely etiology. An extensive hypercoagulable workup showed the possibility of mild antithrombin 3 deficiency. Dual-antiplatelet therapy was initiated and the patient made substantial recovery.

Discussion Stroke is a frequent acute neurological presentation to an emergency department; however, strokes presenting as encephalopathy without clear lateralizing features require a high index of suspicion for appropriate recognition and management. The present case included altered mental status, memory impairment, and vertical gaze palsy, representing a triad consistent with artery of Percheron infarct, however given intact horizontal gaze, symptoms would have been non-lateralizing on NIHSS testing. Subsequent CT Head and MRI Brain demonstrated isolated bilateral thalamic infarcts with evidence of left thalamic hemorrhagic. These findings are a classic presentation for occlusion of the artery of Percheron, a neuroanatomical vascular variant of one artery arising from the Posterior Cerebral Artery supplying bilateral paramedian thalami. The Artery of Percheron is a rare entity, estimated to occur in 4% of the population with occlusion resulting in CVA even more rare (Lazzaro et al. 2010). It is important to consider bilateral ischemic pathology, even as might arise from a single artery, as a differential in cases of acute encephalopathy.

Conclusion The scientific relevance of the present case is to address various etiologies of bilateral thalamic stroke with special attention to single artery causes of bilateral strokes versus other causes of bilateral thalamic strokes. It is important to consider bilateral ischemic pathology, even as might arise from a single artery, as a differential in cases of acute encephalopathy. Reviewing the various etiologies of cerebral infarction can improve patient outcomes and provide a comprehensive understanding of the patients’ presenting symptomatology.

A practice gap exists in the identification and treatment of bilateral thalamic stroke etiologies. Given that these rare strokes typically present in the classic triad of AMS, memory impairment and vertical gaze palsy, it can be reasonable to miss the diagnosis in a high acuity setting such as a stroke alert that places high emphasis on criteria such as the NIHSS. As the NIHSS considers lateral gaze palsies, vertical extraocular movements may not be evaluated in the ED.

Disclosures S. Nittala: None. P. Mercho: None. S. Hussaini: None. P. Youssef: None. C. Oliu: None.