A white woman in her 30s presented with acute-onset sleepiness and decrease in consciousness. She had no history of neurologic disease and did not use tobacco, alcohol, or illicit drugs. She was afebrile, with blood pressure of 135/70 mm Hg, respiratory rate of 16 breaths/min, heart rate of 72 beats/min, and no vomiting or neck stiffness. The Glasgow Coma Scale score was 14, with confused conversation being the best verbal response. No cranial nerve palsy or lateralizing neurologic deficits were seen. The pupils were isochoric and normally reactive to light. The examination of vigilance and cognition revealed excessive drowsiness with recurrent consciousness fluctuations and executive dysfunction associated with initiative loss. A complete blood cell count, glucose level, and liver and kidney function test results were within reference limits; the sodium level was 139 mEq/L and the potassium level, 3.8 mEq/L (to convert both to millimoles per liter, multiply by 1.0). The alcohol level and toxic profile were unremarkable. Her 12-lead electrocardiogram revealed a normal sinus rhythm. Non–contrast-enhanced computed tomography of the brain had normal findings. Magnetic resonance imaging of the brain revealed patency of basilar and posterior cerebral arteries, internal cerebral veins, and venous sinuses and showed abnormal signals of both paramedian thalami that were hypointense on T1-weighted and hyperintense on T2-weighted images (Figure, A and B) and diffusion restricted (Figure, C and D). Electroencephalography disclosed a diffuse mild background slowing in absence of epileptiform activity. Thrombophilia screen, copper metabolism, and serum levels of vitamins B1, B6, and B12 were within reference limits. The vigilance disturbances resolved within a few days and the cognitive disturbances gradually improved during the next 3 weeks.
Lattanzi S, Provinciali L. Acute-Onset Sleepiness and Decrease in Consciousness. JAMA Neurol. 2016;73(1):117-118. doi:10.1001/jamaneurol.2015.2823