Romanian JouRnal of PediatRics – Volume 71, suPPl. 2, 2022 69 Current therapies to reduce the risk of brain damage associated with preterm birth Eliza Clotea 1 , Roxana Georgiana Bors 1 , Vlad Dima 2 , Mihaela Plotogea 3 , Valentin Varlas 1,4 1 Department of Obstetrics and Gynecology, Filantropia Clinical Hospital, Bucharest, Romania 2 Department of Neonatology, Filantropia Clinical Hospital, Bucharest, Romania 3 “Nicolae Malaxa” Clinical Hospital, Bucharest, Romania 4 “Carol Davila” University of Medicine and Pharmacy, Bucharest, Romania ABSTRACT Premature birth is an important public health problem associated with increased perinatal morbidity and mortality rates. Due to the triggering mechanisms of premature birth as well as the immaturity of the fetal brain, it is more prone to in- jury. Thus, these premature babies have an increased risk of immediate neurological complications as well as late neu- rodevelopmental abnormalities, which can have lifelong repercussions. Prompt identification of fetal brain injury and their treatment, as well as the supervision at regular time intervals of the neurodevelopment of children born prema- turely, are a real challenge for the medical system. Ref: Ro J Pediatr. 2022;71(Suppl2) DOI: 10.37897/RJP.2022.S2.15 ABSTRACT Keywords: preterm birth, brain injury, follow-up, neurological outcomes, therapy Corresponding author: Article History: Roxana Georgiana Bors Received: 01.09.2022 E-mail: borsroxanag@gmail.com Accepted: 10.09.2022 INTRODUCTION Premature birth is defned as birth before com- pleting 37 weeks of gestation. According to WHO, across the world, the rate of preterm birth is rising and varies from 5% to 18%. While the mortality asso- ciated with preterm birth has declined steadily in the last years, complications of prematurity are the main cause of death among children aged 5 and below and continue to lead to high rates of neurodevelopmental disability, including cerebral palsy [1]. Cortical maturation begins in intrauterine life, from 34 weeks of pregnancy, and progresses until the age of 30. Oligodendrocytes are the cells most respon- sible for myelination and are cellular targets in pre- mature brain injury. Neurodevelopment depends on cortical maturation as well as connectivity of cortical structures. The morphometric and structural modif- cation of the cortex is associated with developmental, neurological, and behavioral disorders [2,3]. Thus, due to the immaturity of the brain, premature ba- bies are at risk of developing neurological disorders throughout their lives, a risk inversely proportional to their maturity at birth [2]. Etiological factors for neurodevelopmental dis- ability in preterm babies are still only partially un- derstood, and the dysfunction is considered to be multifactorial. These factors affect the development of oligodendrocytes, thus infuencing the myelination of the white matter and the cortical gray matter [3]. Among the factors that increase the susceptibility of a premature baby’s brain to injury are: vascular fragility, effects on the function of the blood-brain barrier, decreased functioning of developing neuro- glial cells, damage to the process of oligodendroglial maturation, and the selective vulnerability of certain brain regions [4]. Hypoxia-ischemia in the perinatal period is known to cause brain injury in preterm infants at the level of the white matter, subsequently affecting the gray matter, with neurodevelopmental impair- ment. Antenatal hypoxia can be found in fetuses with growth restriction or those small for gestational age, these disorders are predisposing factors for cerebral palsy and developmental disorders. Also, during the delivery, they can be exposed to acute asphyxia. Post- natal hypoxia can occur secondary to apnea associat- ed with prematurity or bronchopulmonary dysplasia (BPD) [5,6]. The vascularization of the premature brain is un- derdeveloped, thus the germinal matrix, the most vascularized structure, is also the most prone to hem- orrhages, especially in premature infants under 32 weeks, hemorrhage that progresses to the level of the lateral ventricles and can even cause periventricular hemorrhagic infarction [7]. PAPER 15