I think many of us reading this article might find the beginning overwhelming. unless you are very into complex neurobiology. I am nerdy and I still felt that way in the beginning. But if you skim along in the early parts and hang in there until you get to about page 10, from there on you can extract key little nuggets that can inform our practice. These little nuggets I hope will help us speak from a perspective of knowledge and advocate for intervention,  and make better sense of the infant’s/child’s history before us, seeing them through a different lense.  I hope these nuggets inform your feeding/swallowing practice, whether in the NICU, EI or even in the adult world—yes, there are enduring sequelae form prematurity. Even if you don’t work with preemies, our former preemies land on our doorstep as toddlers, children and indeed adults whose presentation may be related to early cerebellar  dysfunction.

Muehlbacher, T., Dudink, J., & Steggerda, S. J. (2025). Cerebellar Development and the Burden of Prematurity. The Cerebellum, 24(2), 39. (Full text available on Google Scholar)

Here are some takeaways I found when they finally highlight the implications for function:  particular co-comorbidities increase cerebellar risk; the connection between an increased incidence of autism in former preterms and cerebellar dysfunction; the association of h/o NEC with smaller cerebellar volume; that corticosteroids for CLD — often a common form of treatment in the NICU — slows cerebellar growth (and  clinically both in the NICU and beyond, our infants with CLD seem to have the most challenges with suck-swallow-breathe coordination); the potential correlation between hypoxia-induced  white matter injury affecting cerebellar volume and complexity of dendrite formation in animal models; large PDAs resulting in altered blood flow associated with cerebellar hypoplasia and changes in cerebellar micro-structure; a prospective study in very preterm infants showed that nutrition via  breast milk compared to formula-fed milk improved cerebellar volumes; that there is increasing evidence for the importance of early brain activity for development of neuronal survival and formation of brain networks;  a follow-up study of former preterm infants with isolated cerebellar injury demonstrated on MRI at three years of age an impaired growth of several cerebral regions affecting both gray and white matter— and the impeded remote cortical development after isolated cerebellar injury was linked to domain-specific functional deficits in neurodevelopment; intrauterine cerebellar growth reaches its peak during the third trimester, from 24 weeks to around term equivalent age  —after preterm birth, cerebellar growth is still rapid, but several studies using ultrasound or MRI have reported that postnatal cerebellar growth in very preterm or extremely preterm infants is impeded, resulting in a ‘cerebellar hypoplasia of prematurity’; several neurodevelopmental outcomes at seven years including IQ, receptive language and motor function were positively associated with cerebellar volumes at term equivalent age and at seven years, and increased cerebellar growth was correlated with better neurodevelopmental outcome at seven years;  A small study compared a cohort consisting of 22 preterm infants born between 28 and 33 weeks and without major comorbidities (considered as “low-risk” for neurodevelopmental impairment) with 24 term controls–the “low-risk” cohort still had smaller cerebellar and hippocampal volumes and a smaller corpus callosum on MRI at nine years of age which correlated with worse attention and executive functions in the preterm group;  autism spectrum disorder has a high prevalence in preterm infants and core autism symptoms are associated with regional volume changes in the cerebellum; perinatal cerebellar injury is the largest non-hereditary risk for autism with a 36-fold increase while prematurity < 32 weeks still increases the risk 7-fold;  adults formerly born preterm had  persistent cerebellar dysfunction up to adulthood  in a study, even in the absence of early direct cerebellar lesions.