Hypoglycaemia and cognitive function in diabetes.

Abstract

The human brain is almost totally dependent on a continuous supply of glucose, deprivation of which rapidly causes malfunction. In the brain there are regional differences in the susceptibility to neuroglycopenia with the cerebral cortex being most sensitive while deeper structures are more resistant. A fall in blood glucose provokes a hierarchy of responses including secretion of counter-regulatory hormones and development of warning symptoms which alert the individual to treat the hypoglycaemia. Symptoms are generated when blood glucose falls to specific threshold concentrations, although these are dynamic and can be modified by various factors. Symptoms can be classified as autonomic and neuroglycopenic, with the latter being related to altered cognitive functioning. Acute hypoglycaemia produces electroencephalographic (EEG) changes as well as neurophysiological abnormalities including increased latency and/or reduced amplitude of sensory evoked potentials. At blood glucose below 3 mmol/l cognitive functioning becomes impaired but the degree of dysfunction differs in various domains and a battery of psychometric tests are required to assess impairment of cognitive function during hypoglycaemia. Complex, attention-demanding and speed-dependent responses are most impaired with accuracy often preserved at the expense of speed. Cognitive function does not recover fully until 40-90 min after blood glucose is restored to normal. Hypoglycaemia also provokes changes in mood, increases anxiety and may induce depression and fear of further hypoglycaemia, which can modify behaviour and influence quality of glycaemic control. Recurrent severe hypoglycaemia may have long-term sequelae in the form of cumulative cognitive impairment and impaired awareness of hypoglycaemia.