Value of the Dundee coronary risk-disk.

Abstract

proportion (55/932) of all cases of cerebral palsy in that period. The aetiology of cerebral palsy in low birthweight infants in multiple births is probably similar to that in singletons.In a few cases a cotwin died antenatally, with resulting brain damage in the surviving twin. This is seen in our data and has been known for many years.2 As rates of multiple births are rising it is important to keep monitoring the rates of cerebral palsy in these births.We agree with Judith Glynn and David Leon's comments. It is impossible from our epidemiological data to ascertain when brain damage occurred. We agree that in infants of 1500 g who develop cerebral palsy the sequence could have started antenatally, perinatally, or postnatally and the epidemiological picture would be similar. We recently reviewed this.3In normal birthweight infants it is also likely that there has been a shift from deaths to survivors with cerebral palsy, and possibly from survivors with cerebral palsy to non-handicapped survivors. We still believe that our data, in conjunction with other data to which we referred in our paper, can be interpreted as suggesting that birth asphyxia is not the main cause of cerebral palsy.