title: Brain damage in preterm infants: etiological pathways.
abstract: Preterm newborns represent a high-risk population for brain damage, primarily affecting the white matter, and for related neurodevelopmental disabilities. Determinants of brain damage have been extensively investigated, but there are still many controversies on how these factors can influence the developing brain and provoke damage. The concept of etiological pathway, instead of a single determinant, appears to better explain pathogenetic mechanisms: the brain damage may represent the final outcome of exposure to several combinations of risk factors in the same pathway or in different pathways and can change according to the gestational age. The aim of this article is to review the current knowledge on the pathogenesis of brain damage in preterm infants, within the frame of two main theoretical models, the ischemic and the inflammatory pathway. The relationship between the two pathways and the contribution of genetic susceptibility to ischemic and/or inflammatory insult, in modulating the extent and severity of brain damage, is also discussed.
authors.affiliation: Unità di Neurologia Pediatrica, Università degli Studi Tor Vergata, Rome, Italy.
authors.forename: Carla
authors.initials: C
authors.lastname: Arpino
authors.forename: Luigi
authors.initials: L
authors.lastname: D'Argenzio
authors.forename: Carlo
authors.initials: C
authors.lastname: Ticconi
authors.forename: Ambrogio
authors.initials: A
authors.lastname: Di Paolo
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Stellin
authors.forename: Luisa
authors.initials: L
authors.lastname: Lopez
authors.forename: Paolo
authors.initials: P
authors.lastname: Curatolo
mesh_terms: D000328:Adult; D001720:Birth Injuries / Q000209:etiology; D001925:Brain Damage, Chronic / Q000151:congenital / Q000196:embryology / Q000453:epidemiology / Q000209:etiology*; D002547:Cerebral Palsy / Q000196:embryology / Q000209:etiology; D002821:Chorioamnionitis / Q000503:physiopathology; D016207:Cytokines / Q000378:metabolism; D002658:Developmental Disabilities / Q000209:etiology; D004827:Epilepsy / Q000196:embryology / Q000209:etiology; D005260:Female; D005315:Fetal Diseases / Q000503:physiopathology; D005311:Fetal Hypoxia / Q000503:physiopathology; D020022:Genetic Predisposition to Disease; D006801:Humans; D020925:Hypoxia-Ischemia, Brain / Q000150:complications / Q000151:congenital / Q000196:embryology / Q000503:physiopathology; D007230:Infant, Low Birth Weight; D007231:Infant, Newborn; D007234:Infant, Premature; D018836:Inflammation Mediators / Q000378:metabolism; D008607:Intellectual Disability / Q000196:embryology / Q000209:etiology; D007859:Learning Disabilities / Q000209:etiology; D008297:Male; D008959:Models, Neurological; D011247:Pregnancy; D011248:Pregnancy Complications; D011297:Prenatal Exposure Delayed Effects; D012307:Risk Factors
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators