Antenatal corticosteroids (ACS) are an established therapy for pregnant women at risk of preterm birth to help mature the fetus's lungs and reduce the chances of serious health issues. However, researchers at Nagoya University Graduate School of Medicine have found evidence that babies treated with ACS have smaller volumes of two key brain areas, the bilateral amygdalae and caudate nuclei, which are essential for emotion processing and motor control, respectively. Their findings were published in the European Journal of Obstetrics & Gynecology and Reproductive Biology.
ACS have revolutionised neonatal care, particularly for preterm infants. These steroids are commonly given to expectant mothers who are at risk of preterm delivery to speed up the development of the baby's lungs, significantly improving survival rates and reducing complications. However, while ACS has been shown to benefit respiratory health, concerns about its impact on brain development are increasing.
To address these concerns, a team of researchers from Nagoya University examined the relationship between ACS and the volumes of key brain areas in preterm infants at their term equivalent age, the development age when a preterm infant reaches the same level of growth and development as a full-term infant.
Dr. Kazuya Fuma and his team used clinical data of preterms at Nagoya University Hospital. Among the 59 babies studied, 46 were exposed to ACS before birth. They compared critical subcortical brain regions of those babies that had been exposed to ACS to those who had not. The brain regions included those important for emotions, memory, and motor control, such as the thalamus, hippocampus, amygdala, and caudate nucleus.
The study revealed that babies exposed to ACS had smaller subcortical segmental volumes in two key areas: the amygdala, crucial for emotional processing, and the caudate nucleus, associated with learning and motor functions.
Although this disparity was observed in infants born at 28 weeks or later, it was not observed in those born earlier. This suggests that the effects of ACS on brain development are dependent on gestational age.
The study does not assert that ACS is harmful. Rather, its purpose is to better understand the effects of ACS. Though ACS aids preterm survival, it may subtly alter brain structure. Understanding this tradeoff is vital for balancing short- and long-term health.
While corticosteroids are an essential treatment for preterm infants, it is not surprising that they may have side effects. However, rather than framing the discussion as to whether ACS is 'safe' or 'harmful', it is more important to consider the balance between risks and benefits instead."
Dr. Kazuya Fuma, Nagoya University
ACS therapy is crucial for handling premature births and notably raises survival rates. But doctors might need to fine tune its administration to reduce potential risks to brain development.
"In countries where ACS is well-established, the next challenge is optimization," Dr. Fuma said. "We identified varying impacts of ACS on different neonatal complications, and it is likely that these effects depend on gestational age. Moving forward, we need to closely examine the risks and benefits of ACS administration at each gestational week, including long-term outcomes."
While ACS remains an essential and life-saving therapy for preterm infants, there is an urgent need for more research into their long-term effects on brain development. The delicate balance between the undeniable benefits for respiratory health and the potential risks to neurological development must be better understood. By advancing our knowledge in this area, doctors can optimize ACS administration to save lives and ensure the healthiest possible outcomes for preterm infants as they grow and develop.
Source:
Journal reference:
Fuma, K., et al. (2024) Impact of antenatal corticosteroids on subcortical volumes in preterm infants at term-equivalent age: A retrospective observational study. European Journal of Obstetrics & Gynecology and Reproductive Biology. doi.org/10.1016/j.ejogrb.2024.08.034.