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Aim: To evaluate the validity and potential value of the parent-completed Infant/Child Monitoring Questionnaire (IMQ) as a screening measure for developmental delay in high-risk infants., Methods: One hundred and forty-one term infants born with moderate or severe newborn encephalopathy (NE) and 374 randomly selected comparison infants were administered a Griffiths Mental Development Scales (GMDS) assessment and an IMQ concurrently. Concordance of classifications between measures was compared for agreement, sensitivity, specificity, positive predictive value, negative predictive value, false positives and false negatives., Results: Overall, sensitivity and specificity of the IMQ for infants with NE averaged across all age groups was 87%, positive predictive value 57% and negative predictive value 97%. The IMQ did not perform as well for comparison infants with a sensitivity of 50%, specificity 94%, positive predictive value 15% and negative predictive value 99% averaged across all age groups. Overall under-referral for infants with NE was 13%, compared with 50% for comparison infants., Conclusions: Use of the IMQ as an accurate screening measure in infants 'at risk' of developmental delay is supported. The low sensitivity of the IMQ for the comparison infants indicates a need for caution when considering its application for general population screening.

Between June 1993 and December 1996, 276 term newborn infants with encephalopathy and 564 randomly selected term controls were enrolled in a population-based study of moderate and severe term newborn encephalopathy (NE) in Western Australia. During comprehensive neurobehavioural and cognitive follow-up of all patients and controls at 3 years and again at 5 years of age we found an unexpected but strong association between NE and autism spectrum disorders (ASDs). A diagnosis of ASD by age 5 years was reached using criteria according of the Diagnostic Statistical Manual, 4th edition. Linking records to the Western Australian Disability Services Commission Register ensured that no child in the study with ASD was missed. By age 5 years, 37 (13.4%) infants with NE and one (0.2%) control had died. Among the 239 survivors of NE, 12 (5%) were diagnosed with an ASD. Of these, 10 (4.2%) met the full criteria for autism, one had pervasive developmental disorder-not otherwise specified, and one had Asperger syndrome. Among the 563 surviving controls, five (0.8%) were diagnosed with an ASD: three with autism, one with autism/possible Asperger syndrome, and one with Asperger syndrome. Compared with the controls, the children who had experienced NE were 5.9 times (95% confidence interval 2.0-16.9) more likely to have been diagnosed with an ASD.

Cerebral palsy (CP) can occur in term infants with or without preceding newborn encephalopathy. We compared the type and severity of CP and associated disability in these two groups. Participants from a population-based case-control study of term newborn encephalopathy were followed up for 6 years and linked to the Western Australian Cerebral Palsy Register. The remaining term infants with CP for the same period were also identified from the Cerebral Palsy Register. 13% of neonatal survivors of term newborn encephalopathy had CP, a rate of 116 per 1000 term live births. Overall, 24% of term infants with CP followed newborn encephalopathy. CP following newborn encephalopathy was more likely to: affect males (72% vs 56%); be severe (47% vs 25%); and be of spastic quadriplegia or dyskinetic types. Cognitive impairment was more common (75% vs 43%) and severe (41% vs 16%), as was epilepsy (53% vs 29%) in survivors of encephalopathy. These children were also more likely to: be non-verbal (47% vs 22%); have a severe composite disability score (47% vs 26%); and die between time of diagnosis of CP and age 6 years (5-year cumulative mortality 19% vs 5%). Children born at term who develop CP following newborn encephalopathy have a poorer prognosis than those with CP who were not encephalopathic in the first week of life.

This study was designed to investigate birth defects found in association with newborn encephalopathy. All possible birth defects were ascertained in a population-based study of 276 term infants with moderate or severe encephalopathy and 564 unmatched term control infants. A strong association between birth defects and newborn encephalopathy was found with defects affecting 27.5% of children with encephalopathy and 4.3% of control children (odds ratio 8.55; 95% confidence interval 5.25 to 13.91;p<0.001). In 11.8% of infants with a birth defect the defect was not diagnosed until after the newborn period, illustrating one of the difficulties in attempting to exclude infants with birth defects from studies of newborn encephalopathy. The majority of defects (89%) were not specific anomalies of the CNS. In 36.8% of children with encephalopthy who had a birth defect, the defect was considered to be the probable cause of the encephalopathy. Infants with birth defects who had encephalopathy had a poorer prognosis than those without: they were twice as likely to die by the age of 2 years and three times more likely to have cerebral palsy. This study catalogues the spectrum of birth defects associated with newborn encephalopathy and illustrates the importance of their inclusion when investigating both the aetiology and outcome of this condition.

The relationship between the frequency of published recommended indications for placental pathological examination and the frequency of requests for such examination in a population-based study of term newborn encephalopathy was examined. Only 11.2% of placentas among 276 case infants and 0.7% of placentas among 564 term control infants were examined. Using the criteria set out in a consensus statement by the American College of Pathologists, all 276 cases fulfilled multiple maternal, fetal and placental indications for placental examination. Furthermore 43.3% of control infants fulfilled at least one criterion. Of the 25 case placentas that underwent pathological review, 16 were reported as having no diagnostic abnormality Six cases (24%) showed clinically important findings: four had evidence of infection, one had multiple chorangiomata and one had thrombosis and rupture of the umbilical vein. Of the three remaining placentas, one showed funisitis, one showed minor lymphohistiocytic villitis and one was from monochorionic twins. To our knowledge there are no agreed Australian guidelines for when a placenta should be submitted for pathological examination. We suggest that until guidelines based on properly designed studies are developed it may be appropriate to store all placentas for at least 72 hours. If the infant develops neurological symptoms or requires unexpected admission to a neonatal intensive care unit then placental examination may reveal important aetiological diagnostic and prognostic information.

Two previously published studies of term newborn encephalopathy showed that maternal thyroid disease to be a risk factor. From these studies we identified 13 case and three control mothers with thyroid disease and investigated them further. The majority of affected case mothers had idiopathic or autoimmune hypothyroidism. Compared with control mothers, case mothers had fewer thyroid function tests in pregnancy, were more likely to remain on the same dose of medication throughout pregnancy and to have experienced other pregnancy complications. The association between maternal thyroid disease and encephalopathy may be the result of a series of different causal pathways, some of which are suggested by our data.

Objective: To identify intrapartum predictors of newborn encephalopathy in term infants., Design: Population based, unmatched case-control study., Setting: Metropolitan area of Western Australia, June 1993 to September 1995., Subjects: All 164 term infants with moderate or severe newborn encephalopathy; 400 randomly selected controls., Main Outcome Measures: Adjusted odds ratio estimates., Results: The birth prevalence of moderate or severe newborn encephalopathy was 3.8/1000 term live births. The neonatal fatality was 9.1%. Maternal pyrexia (odds ratio 3.82), a persistent occipitoposterior position (4.29), and an acute intrapartum event (4.44) were all risk factors for newborn encephalopathy. More case infants than control infants were induced (41.5% and 30.5%, respectively) and fewer case infants were delivered by caesarean section without labour (3.7% and 14.5%, respectively). Operative vaginal delivery (2.34) and emergency caesarean section (2.17) were both associated with an increased risk. There was an inverse relation between elective caesarean section (0.17) and newborn encephalopathy. After application of a set of consensus criteria for elective caesarean section only three (7%) eligible case mothers compared with 33 (65%) eligible control mothers were sectioned electively. Of all the case infants, 113 (69%) had only antepartum risk factors for newborn encephalopathy identified; 39 (24%) had antepartum and intrapartum factors; eight (5%) had only intrapartum factors; and four (2%) had no recognised antepartum or intrapartum factors., Conclusions: The causes of newborn encephalopathy are heterogeneous and many relate to the antepartum period. Elective caesarean section has an inverse association with newborn encephalopathy. Intrapartum hypoxia alone accounts for only a small proportion of newborn encephalopathy. These results question the view that most risk factors for newborn encephalopathy lie in the intrapartum period.

Objective: To ascertain antepartum predictors of newborn encephalopathy in term infants., Design: Population based, unmatched case-control study., Setting: Metropolitan area of Western Australia, June 1993 to September 1995., Subjects: All 164 term infants with moderate or severe newborn encephalopathy; 400 randomly selected controls., Main Outcome Measures: Adjusted odds ratio estimates., Results: The birth prevalence of moderate or severe newborn encephalopathy was 3.8/1000 term live births. The neonatal fatality was 9.1%. The risk of newborn encephalopathy increased with increasing maternal age and decreased with increasing parity. There was an increased risk associated with having a mother who was unemployed (odds ratio 3.60), an unskilled manual worker (3.84), or a housewife (2.48). Other risk factors from before conception were not having private health insurance (3.46), a family history of seizures (2.55), a family history of neurological disease (2.73), and infertility treatment (4.43). Risk factors during pregnancy were maternal thyroid disease (9.7), severe pre-eclampsia (6.30), moderate or severe bleeding (3.57), a clinically diagnosed viral illness (2.97), not having drunk alcohol (2.91); and placenta described at delivery as abnormal (2.07). Factors related to the baby were birth weight adjusted for gestational age between the third and ninth centile (4.37) or below the third centile (38.23). The risk relation with gestational age was J shaped with 38 and 39 weeks having the lowest risk., Conclusions: The causes of newborn encephalopathy are heterogeneous and many of the causal pathways start before birth.

Objective: To compare cardiotocograph (CTG) records during labour in cases of neonatal encephalopathy and matched controls., Design: Case-control study., Setting: Metropolitan area of Perth, Western Australia., Subjects: Term deliveries complicated by neonatal encephalopathy and controls matched for sex, hospital, time of birth, day of week of birth and maternal health insurance., Main Outcome Measures: Low fetal heart rate (FHR) variability, FHR accelerations, late decelerations, total Kreb's score and FIGO classification of CTG records., Results: The neonatal encephalopathy group had significantly more abnormal CTG records (89%) classified according to FIGO, although 52% of control CTG records were also abnormal. CTG records from cases developed significant differences in terms of absence of FHR accelerations and low FHR variability, but not late decelerations, prior to delivery., Conclusion: Given the low incidence of neonatal encephalopathy in this study (7 per 1000) the predictive value of an abnormal CTG record is clinically unhelpful. However, the changes in the FHR in such cases suggest a greater disturbance of fetal (rest-activity) behaviour during labour.

Objective: Preliminary investigation of the contribution of adverse antepartum and intrapartum factors to neonatal encephalopathy in singleton neonates born full term., Design: Matched case-control study based on incidence density sampling of controls., Setting: Two major teaching hospitals (one paediatric and one obstetric) and three peripheral maternity hospitals in Perth, Western Australia (population 1.2 million)., Subjects: 89 cases, all the full term singleton neonates born during an eight month period in 1992 who fulfilled one or more of six criteria during the first week of life (seizures, abnormal conscious state, persistent hypertonia or hypotonia, and feeding or respiratory difficulties of central origin). One full term control infant without neonatal encephalopathy was matched to each case by sex, hospital of delivery, time of day and day of the week of birth, and maternal health insurance status., Main Outcome Measures: Odds ratio estimates of relative risk of neonatal encephalopathy associated with antepartum and intrapartum factors., Results: Estimated incidence of moderate or severe encephalopathy in first week of life was 3.75 per 1000 full term live births. Thirteen cases and no controls had evidence suggestive of important intrapartum hypoxia, and in only five of these cases was the neurological condition at birth attributed to events during the intrapartum period. Univariate conditional logistic regression analysis identified significant differences between cases and controls for maternal vaginal bleeding in pregnancy, maternal thyroxine treatment, congenital abnormalities, induction of labour, interval from membrane rupture to delivery, maternal pyrexia in labour, augmentation of labour, abnormal intrapartum cardiotocograms, and meconium in labour. Family history of convulsions also approached significance., Conclusions: Our preliminary results suggest that intrapartum hypoxia, according to currently used criteria, was not the cause of neonatal encephalopathy in most cases in this population. Our findings suggest that many aetiologies of neonatal encephalopathy originate in the antepartum period.