Changing trends in cerebral palsy prevalence: an opportunity to consider etiological pathways.

Cerebral palsy (CP) is often accompanied by severe comorbidities and causes challenges to those affected, their families, and health services. Hence, any decreases in the prevalence of CP at the population level would be welcome news. Reports of a decreasing trend in CP prevalence in parts of Europe between the 1980s and the early 2000s were greeted with cautious optimism because prevalence could rebound in specific subgroups, including children born extremely preterm. Evidence of an overall prevalence decrease in other areas of the world in recent years would offer reassurance of a sustained decline. Smithers‐Sheedy et al. provide such evidence in a comprehensive description of pre‐ and perinatally acquired CP trends in Australia. Capitalizing on an excellent resource, the nationwide Australian Cerebral Palsy Register, the authors report a one‐third reduction in the prevalence of CP at 5 years of age between 1995 and 2014 in singleton children. The decline was evident in all gestational age groups, although it was somewhat more pronounced in children born extremely preterm. In this group, and among children born at term, there was a decrease in moderate to severe CP. While the prevalence of bilateral spastic CP, the most common type, decreased, the prevalence of both dyskinetic and hypotonic CP appeared to increase. Importantly, any concomitant changes in child mortality do not obscure these findings because deceased children with known CP were included in the numerators.

The authors attribute the declining trends in pre‐ and perinatally acquired CP prevalence to the concurrent implementation of measures that improve maternal and perinatal health. Among children born extremely preterm, who are at the highest risk of CP, measures may involve prenatal corticosteroids to enhance lung maturation, delayed cord clamping, magnesium sulfate to prevent brain injury, and specific changes in neonatal intensive care unit practices. Although the total and direct effects of these interventions on the incidence of CP may be challenging to prove at the population level, evidence on indirect effects is closer at hand since they are primarily aimed at preventing brain injury from asphyxia and asphyxia‐related neonatal morbidities mediate most of the effect of extremely and very‐preterm birth in CP. Among children born at term, who are the majority of those with CP, early detection of conditions leading to ischemic brain damage, and the advent of therapeutic hypothermia of infants with hypoxic–ischemic encephalopathy, may have played a role.

The increasing prevalence trends in dyskinetic CP, a type more common in children born late preterm and term rather than extremely preterm, are difficult to explain. Consideration of potential distal causes may offer clues. For example, dyskinetic CP is the motor type most strongly associated with maternal obesity in children born at term, and the prevalence of obesity in Australian females of reproductive age increased during the study years. This does not preclude other possible explanations including enhanced identification of children with dyskinetic CP, as the authors point out.

Documenting a decline in the prevalence of CP is salient from clinical, public health, and societal perspectives, and may also offer opportunities for research into the etiology. The potential effects of emerging interventions could be estimated using quasi‐experimental study designs. Continued surveillance and expanding research efforts on CP epidemiology in low‐ and middle‐income countries should remain important priorities in this field.