CT of generalized gray matter infarction due to hypoglycemia.

A 35-year-old man was found unconsc ious at home by his roommate. On arriva l at a nearby hospital emergency room , he demonstrated decorti ca te posturing , an absent pupillary light reflex bilaterall y, and was unresponsive to painful st imuli . A serum glucose drawn on arri va l was 26 mg / dl. Hi s initial laboratory studies , inc lud ing elec trolytes and a drug screen, were oth erwi se unremarkable. An ad mission CT scan of th e head was considered norm al. He had no history of diabetes mellitus, and was taking no known medications. He had been diagnosed c linically as having " hypoglycemia" some 8 months before , but this was apparently never documented chemically. He was reported to have engaged in ep isodic bouts of heavy drinking, but hi s medical history was oth erwi se unremarkable. He was initially treated with intravenous glucose, and maintained sati sfac tory se rum g lucose levels for th e res t of his hospital course. Subsequen t laboratory studies yielded a minimally dec reased T 4 of 2.3 ,ug / dl (normal, 4 .5-1 2 ,ug / dl) and decreased plasma cortisol of 2 ,ug / d l (normal, 5-25 ,ug / dl) . Th e rest of hi s endocrine workup was normal, inc luding a normal fas tin g serum insulin level. A repeat CT head scan 1 week after admission (fig s. 1 A and 1 B) , demonstrated patchy corti ca l enhancement after contrast administration . He was treated with supplementallevothyrox ine and hyd rocorti sone and nasogastric tube feedings. Repeat CT on hospital day 26 (figs . 1 C 1 G) demonstrated intense enhancement of much of his cerebral gray matter after intravenous contrast administrat ion. Despite treatment, he never regained co nsc iousness and died on hospital day 27. An autopsy was performed with partic ular attenti on to th e endoc rine system. However, no abn orm alities were demonstrated in th e th yroid or adrenals , and ca reful sec tion ing of th e pancreas showed no evidence of an insulinoma. Sections of th e cerebral cortex revealed diffuse and severe laminar necrosis of gray matter accompanied by g liosis. Sections of th e basal gang lia, ce rebellum, and pons also showed anox ic changes. Th e white matter was unremark able, other than mild edema seen in some secti ons. Th e final diagnosis was diffuse g ray matter encephalopath y due to hypog lycemia, etiology unknown.