Etiology

Lack of oxygen to the brain can be categorized as anoxic anoxia, anemic anoxia, and ischemia. Anoxic anoxia consists of reduced arterial oxygen content and tension. This may be secondary to decreased oxygen in the environment or an inability for oxygen to enter the circulatory system such as during cardiac arrest or during pulmonary disease. Anemic anoxia consists of low oxygen content in the blood secondary to decreased hemoglobin content. Ischemic anoxia describes a state of insufficient cerebral blood flow. Such decreased flow states may be secondary to cardiovascular collapse or conditions of increased vascular resistance, such as in stroke or migraine.

The brain normally consumes approximately 3.5 ml of oxygen for each 100 g of brain tissue per minute. When this rate declines to 2.5 ml, delirium and subsequent coma can develop. Rates of cerebral oxygen metabolism below 2 ml/100 g per minute are incompatible with a conscious state. The brain cannot store oxygen and survives only for minutes after its oxygen supply is reduced below critical levels. In acute anoxia, consciousness is lost within 15 sec. Pyramidal cells in the CA1 sector of the hippocampus, Purkinje cells of the cerebellum, and pyramidal cells of the third and fifth layers of the cerebral cortex are vulnerable to even moderate degrees of anoxia. Widespread necrosis of the cortex with the brain stem intact produces a vegetative state. More severe anoxia affecting the cortex, basal ganglia, and brain stem results in coma and subsequent death.

Under physiologic conditions, glucose is the brain's only substrate and crosses the blood-brain barrier by facilitated transport. During each minute, the normal brain uses approximately 5.5 mg (31 mmol) of glucose per 100 grams of tissue. If there is hypoglycemia, defined in adults as a blood glucose concentration of less than 40 mg/dl, signs and symptoms of

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