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September 1941


Author Affiliations


From the Departments of Internal Medicine, Neurology and Psychiatry, University of Cincinnati College of Medicine, and the Cincinnati General Hospital.

Arch NeurPsych. 1941;46(3):509-512. doi:10.1001/archneurpsyc.1941.02280210135011

The cause of the coma and other neurologic manifestations which occur during insulin hypoglycemia has been a subject of some controversy among investigators in this field. The most striking and consistent effect of hypoglycemia on the brain is a diminished difference between the oxygen content of blood entering the skull (arterial) and that of blood leaving through the internal jugular veins.1 Some investigators2 have attributed this low arteriovenous difference during insulin hypoglycemia to a diminution in the oxygen uptake of the brain, while others have suggested that it may be due to an increased blood flow to the brain.3 After continuously recording the velocity of blood flow through the internal jugular vein with the Gibbs thermoelectric blood flow recorder4 in 2 cases, Loman and Myerson concluded that the volume flow of blood through the brain is slightly diminished during insulin hypoglycemia.5 On the other hand,

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