Once diagnosed, the basic goals of diabetes therapy for children under the age of 6 years are similar to those recommended to all children and adolescents and include the avoidance of high and low blood glucose levels and the maintenance of normal growth and development. However, due to the continued development of the central nervous system, young children are particularly vulnerable to the debilitating consequences of recurrent hypoglycaemia.

There is a growing body of evidence supporting the negative consequences—mild cognitive deficits—resulting from overly aggressive attempts to normalize metabolism in young children. Ack et al?4 reported modest cognitive deficits in patients with a younger onset of type 1 diabetes. Others also reported brain damage as a result of severe hypoglycaemia, particularly in young children25'26. A series of studies by Ryan et al.27-29, using a battery of neurobehavioural tests, identified significant differences between youths with diabetes compared with control subjects on measures of verbal intelligence, visual-motor coordination and critical flicker threshold. Additionally, children diagnosed with diabetes under 5 years of age manifested significant cognitive deficits when evaluated during the adolescent years, probably resulting from symptomatic or asymptomatic hypoglycaemia occurring earlier in life, before final maturation of the central nervous system. In another study by Rovet et al.30, children diagnosed under 4 years of age scored lower than other children with diabetes diagnosed later in childhood, and lower than non-diabetic sibling controls on tests of visual-spatial orientation, but not on verbal ability. Hypoglycaemic seizures were found to occur in greater frequency in the group of children diagnosed under 4 years of age compared to those diagnosed at older ages, suggesting that severe hypoglycaemia may impair later cognitive functioning30.

Golden and colleagues31 collected longitudinal data on the frequency of hypoglycaemia from the time of diagnosis in a sample of 23 children with diabetes onset prior to the age of 5 years. Correlating this data with subscale scores on the Stanford-Binet Intelligence Scale yielded no significant findings between frequency of severe hypoglycaemia and any of the subscales. Importantly, it was the frequency of asymptomatic and mildly symptomatic hypoglycaemia that was significantly correlated with lower scores on the abstract/visual reasoning scale, indicating that even mild or asymptomatic episodes of hypoglycaemia can have a negative cumulative effect on cognitive functioning.

In the previously described studies, no measurements of neurocognitive functioning were made near the time of diagnosis to rule out the possibility that the metabolic decompensation of diabetes onset affected such functioning. Two studies have followed children with diabetes prospectively from diagnosis using neuropsychological assessments. The preliminary findings of Rovet and colleagues32 indicated no evidence of neurocognitive impairment in these children at diagnosis or 1 year later, but the authors reported that they may not have followed subjects long enough to observe any impairment. Northam and colleagues33 compared the performance of children with IDDM with the performance of control subjects on standardized measures of general intelligence, attention, speed of processing, memory, learning and executive skills. At 3 months post-diagnosis, there were no differences between the groups, but at 2 years post-diagnosis, children with diabetes demonstrated smaller gains, particularly in the areas of information-processing speed, acquisition of new knowledge and conceptual reasoning skills. The subset of the diabetes sample that performed worst were those children with early onset of diabetes, which further suggests an early onset effect33.

In light of these findings, suggesting that even asymptomatic hypogly-caemia in young children with developing nervous systems can be deleterious, prevention of severe and recurrent hypoglycaemia needs to be of paramount importance. In addition, infants and toddlers are unable to verbalize when they are suffering from hypoglycaemia, which can lead to delayed treatment and unconsiousness and/or seizures. The current trend of intensive insulin therapy, as advocated by the Diabetes Control and Complications Trial,1'2 for persons over 13 years of age must be aggressively avoided in these vulnerable young patients14'34-36. Therefore, age-specific blood glucose target ranges, with the provision for wide glycaemic excursions, should be the rule rather than the exception.

Achieving optimal glycaemic control in this age range is further complicated by the finicky eating habits, erratic physical activity and rapid growth of young children. Treatment goals, therefore, must be individualized to provide safe and effective medical treatment yet also permit the young child to master the normal developmental tasks of childhood. For example, the toddler who is a picky, pokey eater may be best suited to rapid-acting insulin analogue (Humulog) injections after meals, rather than prior to the meals, in order to avoid frantic parents who are unable to 'force their child to eat'.

Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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