A 44-year-old man was admitted to the neuroscience intensive care unit with subarachnoid hemorrhage due to the rupture of a giant basilar terminus aneurysm. On admission he followed simple commands, had a complete left third nerve palsy, exhibited severe dysarthria, and showed no evidence of hemiparesis. The next day he underwent a cerebral angiogram that demonstrated a basilar terminus aneurysm measuring 3 × 3 × 3 cm (Figure, B). This aneurysm was nearly completely embolized with 17 bare platinum helical coils. Two days later he became stuporous and anarthric and developed a complete right third nerve palsy. Magnetic resonance imaging at this time demonstrated bilaterally symmetric, extensive edema without restricted diffusion, located primarily in the gray matter and extending from the midpons rostrally to the inferior thalamus (Figure, C and D). The aneurysm had not changed in size and there was no hydrocephalus. Intravenous dexamethasone, 4 mg every 8 hours, was administered with coincident mild improvement in his level of arousal for 2 days. Thereafter, his neurologic function again declined. By hospital day 9, he was stuporous and anarthric, rarely followed commands, had bilateral ophthalmoplegia and mydriasis, and was markedly bradykinetic. Slow improvement occurred during the subsequent 3 weeks. On discharge on hospital day 28, he was fully alert and oriented, had only a partial left third nerve palsy, and was mildly dysarthric and bradykinetic. Improvement of the brainstem and thalamic edema paralleled the clinical course and, at the time of discharge, only minimal edema in the tegmentum of the pons and midbrain remained (Figure, E and F).