LAUSR

Acute hypersomnia is a rare presentation of bilateral paramedian thalamic strokes (PTS). The typical symptoms of vertical gaze palsy, memory impairment, and even coma, do not include acute hypersomnia. Hypersomnia can be normal in appropriate settings. However, acute hypersomnia from a wake state is abnormal and should alert observers to a potential stroke, making timely intervention consequential to patient’s outcome. A 59-year-old right-handed female, who was a passenger in a car, suddenly fell asleep and started snoring. Her sister, as the driver, was not able to arouse her. The patient was taken to the Emergency Department for further evaluation. Initial head CT was normal. Follow up MRI of the brain demonstrated bilateral PTS with extension to rostral midbrain (Axial images are available with DWI/ADC windows). Throughout her five-day-hospitalization, she remained somnolent without improvement. Her neurological exam was significant for decreased alertness, impaired short-term memory recall, vertical gaze palsy, and difficulty with two-step commands. She had no focal weakness or numbness. Electroencephalogram (EEG) showed generalized theta slowing background without seizure or epileptiform discharges. Cerebral and neck vessel images, cerebrospinal fluid studies, echocardiogram, and hypercoagulable tests were normal. Outpatient workup revealed atrial fibrillation, which was the strokes’ presumed etiology. She was also diagnosed with obstructive sleep apnea (Apnea-Hypopnea Index of 9.6) and was treated with CPAP. Despite compliance, her hypersomnia (Epworth Sleepiness Scale of 24) and cognitive dysfunction persisted, making a resumption of her prior employment not feasible. Bilateral PTS commonly stem from the artery of Percheron (AOP), which is a rare vascular variation where a single artery arises from the posterior cerebral artery to supply both thalami and midbrain.1 Ischemic disruption of the thalami’s dual role in sleep-wake regulation can lead to decreased daytime arousal and increased nighttime sleep disturbance with subsequent hypersomnia.2,3 Vertical gaze palsy is due to disruption of descending pathway of vertical gaze center. Bilateral PTS have deleterious long-term clinical consequences. Increased recognition of acute hypersomnia as the presenting symptom for PTS can enhance acute stroke treatment with tPA and/or mechanical thrombectomy, and thereby improve the odds for recovery.