To emphasize the diagnostic challenges in AOP infarction and its ability to imitate toxic-metabolic encephalopathies.

In the Artery of Percheron (AOP) vascular variant, a single perforator from the posterior cerebral artery supplies both paramedian thalami (and often the rostral midbrain). This variant is present in approximately 4–12% of individuals. AOP occlusion leads to bilateral paramedian thalamic infarction, often including the rostral midbrain, accounting for approximately 0.1–0.4% of ischemic strokes. Its clinical presentation often mimics toxic-metabolic encephalopathy, featuring altered consciousness, memory disturbance resulting from damage to the reticular activating system and ocular dysmotility from damage to the rostral midbrain's vertical gaze centers.

A 69-year-old woman with history of rheumatoid arthritis on tramadol was brought to the emergency department for decreased responsiveness. Initial examination revealed somnolence, pinpoint pupils, and transient improvement with naloxone. She exhibited mild confusion and reported binocular blurry vision. The initial working diagnosis was tramadol intoxication.

Neurologic examination demonstrated vertical gaze restriction more prominent on downward gaze with preserved horizontal movements (see video) and drowsiness. MRI revealed bilateral paramedian thalamic and rostral midbrain infarctions. MRA showed small linear focus of flow-related enhancement from the proximal P1 segment of the left posterior cerebral artery, consistent with variant anatomy and AOP thrombosis. 

The patient showed gradual improvement in alertness and memory. She was transferred to rehabilitation for persistent vertical gaze palsy.