Glucose is the predominant metabolic fuel of the brain, yet the brain cannot synthesize glucose, nor can it store more than a few minutes' supply in the form of glycogen. As a result, survival of the brain, and thus of the individual, is dependent on a continuous supply of glucose from the circulation-a dependence evident in the consequences of hypoglycemia. These include neurogenic (autonomic) warning symptoms (such as sweating, palpitations, hunger, and tremor), followed sequentially by neuroglycopenic manifestations (including cognitive dysfunction) and, finally, coma and death. It is hardly surprising that physiologic mechanisms to prevent or correct hypoglycemia have evolved (Figure 1). The mechanisms are so effective that hypoglycemia is a distinctly uncommon clinical event, except in persons who use drugs intended to lower the plasma glucose concentration, such as insulin and the sulfonylureas employed to treat diabetes mellitus. More problematic hypoglycemic substances include alcohol. The cause of a hypoglycemic episode is usually apparent. Nevertheless, the differential diagnosis of clinical hypoglycemia is extensive. It includes a number of major illnesses that cause hypoglycemia in the setting of hepatic, renal, or cardiac failure. It also includes hormonal deficiencies, tumors (insulinoma or certain extrapancreatic tumors), and autoimmune disorders. Correct diagnosis is sometimes challenging.
|State||Published - Jan 1 1992|