PROLONGED COMA AND CEREBRAL METABOLISM

Abstract

The vulnerability of the brain to lack of either dextrose or oxygen is one of its outstanding characteristics. It has been previously demonstrated that the chief foodstuff of the brain is carbohydrate.¹ During insulin hypoglycemia, when the brain is deprived of its substrate, cerebral metabolism is necessarily depressed, with resulting changes in function.² The effects of a short period of hypoglycemia are readily reversible by the administration of carbohydrate. After prolonged hypoglycemia, however, permanent cerebral damage may occur, with irreversible functional changes, such as pareses of various types.³ When oxygen is not available for the utilization of dextrose the metabolism of the brain cannot proceed, and the symptoms of anoxia in many respects resemble those of hypoglycemia. When anoxia is of short duration the symptoms are entirely reversible;⁴ when it is more prolonged permanent damage may result.⁵ Different parts of the brain vary in susceptibility