It is now over half a century since Arthur Hertig first reported vascular pathology in the uterine arteries supplying the placenta in women suffering from preeclampsia. His pioneering histological studies have been validated and extended by many others, leading to the general concept that placental perfusion is compromised in these patients. More recent Doppler ultrasound studies have confirmed reduced intervillous blood flow in vivo, and so gradually a consensus has emerged that the placental lesions associated with preeclampsia arise from a state of chronic hypoxia. Whilst hypoxia may undoubtedly play a significant role in the generation of placental pathology, there is considerable evidence that another feature of the intervillous circulation, namely the constancy of the blood flow, may be a more important factor. In this review we propose that hypoxia-reoxygenation, secondary to intermittent perfusion of the intervillous space, is a more physiological approach to take to understanding the pathophysiology of both normal pregnancies, and those complicated by preeclampsia. We further propose that chronic reduction in placental perfusion alone may lead to fetal growth restriction, and that if the two phenomena are superimposed then preeclampsia with growth restriction will result.

Despite advances in both obstetrics and neonatology the perinatal mortality rate (PNMR) among twins still remains high, estimated as accounting for approximately 10% of all perinatal mortality. Perinatal mortality rates (PNMR) for England and Wales showed a dramatic reduction in perinatal deaths for multiple births over the 1950s to 1980s with a fall from approximately 90 to less than 50 per 1000 births. The Northern Region Perinatal Mortality Survey Steering Group also reported a significant reduction in twin PNMR between 1982 and 1994 from 55.4 to 44.4/1000 births. A similar decrease has also been noted in the Japanese twin population with a reduction in the PNMR between 1980 and 1998 from 91 per 1000 births to 31 per 1000. In Scotland between 1986 and 1990 PNMR for twins was 47 per 1000 approximately 4-5 times the rate in the singleton population. The higher preterm delivery rate in twins, either from spontaneous or induced labour, with its associated problems of prematurity remains the major cause of morbidity and mortality. Other factors, which contribute to the higher PNMR in twins include fetal growth retardation, intra-twin birth weight discordancy, fetal anomalies and problems specific to monochorionic twin gestations.

When an antenatal diagnosis of a fetal anomaly is made, the parents need accurate and clear information regarding prognosis and possible outcomes, to help them make decisions. The healthcare professionals, who are involved in their care and counselling, also need this information.

During gametogenesis in mammals, half of the parental chromosomes segregate to each gamete. Upon fertilization of two haploid gametes, the diploid number is restored (Figure 1A). Nondisjunction, malsegregation of the chromosomes during gametogenesis, can give rise to chromosomally unbalanced offspring (trisomies and monosomies) (Figure 1B). Genomic imprinting is an epigenetic phenomenon in which the activity of a gene is reversibly modified depending on the parent of origin. This leads to unequal, monoallelic expression of the maternal and paternal alleles of a diploid locus (Figure 1C). Thus, the normal state of an imprinted locus is an “imbalance”, not of chromosomes, but of the functional genetic content.