Antenatal and Perinatal Antecedents of Moderate and Severe Spastic Cerebral Palsy
Authors: Dite Gillian S. , Bell Robin , Reddihough Dinah S. , Bessell Christine , Brennecke Shaun , BAppSci Mary Sheedy 
Published: February 2008

EDITORIAL COMMENT: Motor vehicle drivers know they can, inadvertently of course, with their vehicles, kill or maim; obstetricians, rightly or wrongly, largely believe that they can do the same — why else the emphasis on detection, interpretation and timely intervention (e.g. prompt delivery often by Caesarean section) when there is fetal distress (clinical or cardiotocographic) in labour, and employment of nontraumatic delivery when labour is obstructed. Is this analogy simplistic, false and/or naive? This journal has published a consensus statement (A) from an authoritative team of panel members from all the relevant disciplines that concluded that ‘while obstetric interventions in the presence of signs of possible hypoxia may prevent fetal death, there is no evidence that it will limit the prevalence or severity of cerebral palsy’ and that ‘all expert witnesses and the public, should recognize that the belief that Caesarean section will prevent many cases of cerebral palsy is incorrect?’ Where dear reader do you stand?. This paper unequivocally concludes that in cases of moderate and severe spastic cerebral palsy in nonmalformed infants of birth‐weights ≤2,500 g intrauterine hypoxia/birth asphyxia was associated with an increased risk of cerebral palsy (adjusted odds ratio 18.1). This finding was derived from the study of clinical items coded on perinatal forms, completed by midwives shortly after delivery, and gathered from the computerized data of the Victorian Perinatal Data Collection Unit, with appropriate matched controls from the same source. The authors have stressed that this set of data they have analyzed ‘was collected as part of routine data collection for perinatal morbidity and mortality surveillance not epidemiological research into aetiology of cerebral palsy’. They have stated that intrauterine hypoxia/birth asphyxia could reflect ‘a perinatal event, or unmasking of the effects of antenatal influences’. We encourage the authors' plan to collect data from the actual clinical histories of cases and controls to obtain more specific information on potential risk factors and to investigate ‘which are causal and which are the result of the event which caused the cerebral palsy?’

Norman A. Beischer Melbourne

(A) Maclennan A, Stanley F, Blair E et al. Consensus statement on the origins of cerebral palsy. Aust NZ J Obstet Gynaecol 1995; 35: 127–131.

Summary: Routinely collected perinatal morbidity data were abstracted for 204 cases of moderate and severe spastic cerebral palsy and 816 matched controls. Separate analyses were conducted for cases with birth‐weight ≥2,500 g and birth‐weight <2,500 g. The presence of a congenital abnormality was an important risk factor for cerebral palsy in both groups and further analyses were conducted after dividing the groups according to presence or absence of a congenital abnormality. In the <2,500 g group, resuscitation needed was clearly identified as a risk factor for cerebral palsy in the group with no congenital abnormalities (adjusted OR = 3.4; 95% CI = 1.6–7.5) while in the group with congenital abnormalities, none of the risk factors were clearly associated with an increased risk of cerebral palsy. Among the cases with birth‐weight 2,500 g, intrauterine hypoxia/birth asphyxia was clearly associated with an increased risk of cerebral palsy (adjusted OR = 18.1; 95% CI = 1.8–186) in the group with no congenital abnormalities while in the group with congenital abnormalities, none of the factors were clearly associated with an increased risk of cerebral palsy.