ABSTRACT
Both Type 1 and Type 2 diabetic adults have a greatly increased risk of developing mild cognitive impairments. Individuals in poor metabolic control who have a long history of hyperglycaemic-associated biomedical complications (e.g., peripheral neuropathy; retinopathy) may manifest a variety of cognitive deficits. These range from a subtle reduction in mental efficiency (e.g., Ryan et al., 1992) through relatively circumscribed memory impairments (Reaven et al., 1990) to a true “diabetic encephalopathy” characterized by widespread central nervous system (CNS) damage and gross dementia (Reske-Nielsen et al., 1965). Yet the micro- and macrovascular complications of hyperglycaemia are not the only causes or correlates of cognitive impairment in the diabetic adult. Insulin-induced hypoglycaemia can also produce significant neuropsychological dysfunction. Although it has long been known that a single episode of severe hypoglycaemia may be sufficient to cause extensive CNS damage in humans (Chalmers et al. 1991; Kalimo & Olsson, 1980) and animals (Auer, 1986), a number of recent reports have suggested that repeated episodes of mild to moderately severe hypoglycaemia may also produce detectable cognitive deficits that are thought to be permanent (Langan et al., 1991; Wredling et al., 1990).
