Despite the fact that most perinatal and maternal complications are on the decline in diabetic pregnancies, the rate of congenital malformations has not changed over the past twenty years.1 In fact, congenital malformations have replaced asphyxia and respiratory distress syndrome as the leading cause of mortality in offspring born to mothers with insulin-dependent diabetes mellitus.2 The frequency of major congenital malformations has been estimated at 6 to 10% representing a three to five fold increase over the rate in the general population.3,4 Congenital malformations in the offspring of women with diabetes represent a significant social and financial burden to society.

Cerebral palsy has been defined as a group of non-progressive disorders of movement or posture due to a defect or lesion of the immature brain.1 Cerebral palsy is defined by clinical description only; there is no definitive test. It is not informative about aetiolgy, pathology or prognosis. The definition of cerebral palsy also lacks precision in that neither the age at which the brain is mature nor the severity of the disorder required are specified. Brain development is most rapid in utero and early childhood but continues at a diminished rate throughout life. There is therefore no biological rationale for choosing any particular age to define brain maturity. The defining age below whcih cerebral palsy may be recognised therefore varies between centres for pragmatic reasons usually associated with assertainment. For example, in Western Australia the criterion is set at 5 years,2 since by this age any central motor impairments of congenital or neonatal origin will be apparent and can usually be differentiated from progressive disorders or isolated motor delay. Thus the definition includes a group of children with post-neonatally acquired brain damage resulting in movement disorder. Post-neonatally acquired cerebral palsy differs from presumed congenital or perinatal cerebral palsy in that there is usually no doubt that it was caused by a specific post-neonatal event such as meningitis or head trauma. Although there is an excess of perinatal morbidity amoung children acquiring cerebral palsy post-neonatally,3 suggesting a prior vulnerability in some cases, post neonatally acquired cerebral palsy will not be considred further in this review.