Department of Neonatology, Children's Hospital of Fudan University; Key Laboratory of Neonatal Disease, Ministry of Health, Shanghai 201102, China. chen6010@163.com
Abstract:The preterm birth has been increasing for the last decade. With the development of neonatal intensive care techniques, the survival rate of preterm infants is increased markedly. However, the brain of preterm infants is so vulnerable to injury that preterm brain injury has become an enormous public health problem. Hypoxia-ischemia and infection/inflammation are two main perinatal risk factors causing premyelinating oligodendrocyte and cortical neuron injury. Encephalopathy of prematurity is characterized by diffuse white matter injury and neuronal/axonal disruption, leading to neurological disabilities such as cognitive impairment and cerebral palsy. The advancement in imaging techniques, especially magnetic resonance imaging, provides more information for preterm brain injury and brain development, which contributes to the diagnosis and follow-up of the preterm infants. This article reviews the progress in encephalopathy of prematurity in order to open a new window to prophylaxis and management of this disease.
[1]Marlow N, Wolke D, Bracewell MA, Samara M. Neurologic and developmental disability at six years of age after extremely preterm birth[J]. NEJM, 2005, 352(1):919.
[3]Pierson CR, Folkerth RD, Billiards SS, Trachtenberg FL, Drinkwater ME, Volpe JJ, et al. Gray matter injury associated with periventricular leukomalacia in the premature infant[J]. Acta Neuropathol, 2007, 114(6): 619631.
[4]Ment LR, Vohr BR. Preterm birth and the developing brain[J]. Lancet Neurol, 2008, 7(5):378379.
[5]Volpe JJ. Encephalopathy of prematurity includes neuronal abnormalities [J]. Pediatrics, 2005, 116(1):221225.
[6]Kinney HC. The encephalopathy of prematurity: one pediatric neuropathologist′s perspective [J]. Semin Pediatr Neurol, 2009, 16(4):179190.
[7]Volpe JJ. The encephalopathy of prematuritybrain injury and impaired brain development inextricably intertwined [J]. Semin Pediatr Neurol, 2009, 16(4):167178.
[8]Volpe JJ. Brain injury in the premature infant: overview of clinical aspects, neuropathology, and pathogenesis [J]. Semin Pediatr Neurol, 1998, 5(3):135151.
[9]Back SA. Perinatal white matter injury: the changing spectrum of pathology and emerging insights into pathogenetic mechanisms [J]. Ment Retard Dev Disabil Res Rev, 2006, 12(2):129140.
[10]Back SA, Riddle A, McClure MM. Maturationdependent vulnerability of perinatal white matter in premature birth [J]. Stroke, 2007, 38(2): 724730.
[11]Back SA, Han BH, Luo NL, Chricton CA, Xanthoudakis S, Tam J, et al. Selective vulnerability of late oligodendrocyte progenitors to hypoxiaischemia [J]. J Neurosci, 2002, 22(2): 455463.
[12]Khwaja O, Volpe JJ. Pathogenesis of cerebral white matter injury of prematurity [J]. Arch Dis Child Fetal Neonatal Ed, 2008, 93(2): F153F161.
[13]Volpe JJ, Kinney HC, Jensen FE, Rosenberg PA. The developing oligodendrocyte: key cellular target in brain injury in the premature infant [J]. Int J Dev Neurosci, 2011, 29(4): 423440.
[14]Volpe JJ. Brain injury in premature infants: a complex amalgam of destructive and developmental disturbances [J]. Lancet Neurol, 2009, 8(1): 110124.
[15]Deng W. Neurobiology of injury to the developing brain [J]. Nat Rev Neurol, 2010, 6(6): 328336.
[16]Desilva TM, Billiards SS, Borenstein NS, Trachtenberg FL, Volpe JJ, Kinney HC, et al. Glutamate transporter EAAT2 expression is upregulated in reactive astrocytes in human periventricular leukomalacia [J]. J Comp Neurol, 2008, 508(2): 238248.
[17]Huang Z, Liu J, Cheung PY, Chen C. Longterm cognitive impairment and myelination deficiency in a rat model of perinatal hypoxicischemic brain injury [J]. Brain Res, 2009, 1301: 100109.
[18]Haynes RL, Billiards SS, Borenstein NS, Volpe JJ, Kinney HC. Diffuse axonal injury in periventricular leukomalacia as determined by apoptotic marker fractin [J]. Pediatr Res, 2008, 63(6): 656661.
[19]Billiards SS, Haynes RL, Folkerth RD, Borenstein NS, Trachtenberg FL, Rowitch DH, et al. Myelin abnormalities without oligodendrocyte loss in periventricular leukomalacia [J]. Brain Pathol, 2008, 18(2): 153-163.
[20]Andiman SE, Haynes RL, Trachtenberg FL, Billiards SS, Folkerth RD, Volpe JJ, et al. The cerebral cortex overlying periventricular leukomalacia: analysis of pyramidal neurons [J]. Brain Pathol, 2010, 20(4): 803-814.
[21]Leviton A, Gressens P. Neuronal damage accompanies perinatal white-matter damage [J]. Trends Neurosci, 2007, 30(9): 473-478.
[22]Zubiaurre-Elorza L, Soria-Pastor S, Junque C, Segarra D, Bargallo N, Mayolas N, et al. Gray matter volume decrements in preterm children with periventricular leukomalacia [J]. Pediatr Res, 2011, 69(6): 554-560.
[23]Haynes RL, Xu G, Folkerth RD, Trachtenberg FL, Volpe JJ, Kinney HC. Potential neuronal repair in cerebral white matter injury in the human neonate [J]. Pediatr Res, 2011, 69(1): 62-67.
[24]Talos DM, Fishman RE, Park H, Folkerth RD, Follett PL, Volpe JJ, et al. Developmental regulation of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor subunit expression in forebrain and relationship to regional susceptibility to hypoxic/ischemic injury. I. Rodent cerebral white matter and cortex [J]. J Comp Neurol, 2006, 497(1): 42-60.
[25]Lee JD, Park HJ, Park ES, Oh MK, Park B, Rha DW, et al. Motor pathway injury in patients with periventricular leucomalacia and spastic diplegia [J]. Brain, 2011, 134(Pt 4):1199-1210.
[26]Wachtel EV, HendricksMunoz KD. Current management of the infant who presents with neonatal encephalopathy [J]. Curr Probl Pediatr Adolesc Health Care, 2011, 41(5): 132-153.
[27]Glass HC, Bonifacio SL, Chau V, Glidden D, Poskitt K, Barkovich AJ, et al. Recurrent postnatal infections are associated with progressive white matter injury in premature infants [J]. Pediatrics, 2008, 122(2): 299-305.
[28]Anjari M, Counsell SJ, Srinivasan L, Allsop JM, Hajnal JV, Rutherford MA, et al. The association of lung disease with cerebral white matter abnormalities in preterm infants [J]. Pediatrics 2009, 124(1): 268-276.
[29]Malin GL, Morris RK, Khan KS. Strength of association between umbilical cord pH and perinatal and long term outcomes: systematic review and meta-analysis [J]. BMJ, 2010, 340: c1471.
[31]O′Shea TM, Counsell SJ, Bartels DB, Dammann O. Magnetic resonance and ultrasound brain imaging in preterm infants [J]. Early Hum Dev, 2005, 81(3): 263-271.
[32]van Wezel-Meijler G, Steggerda SJ, Leijser LM. Cranial ultrasonography in neonates: role and limitations[J]. Semin Perinatol, 2010, 34(1): 28-38.
[33]Benavente-Fernandez I, Lubian-Lopez PS, Zuazo-Ojeda MA, Jimenez-Gomez G, Lechuga-Sancho AM. Safety of magnetic resonance imaging in preterm infants[J]. Acta Paediatr, 2010, 99(6): 850-853.
[35]Ment LR, Hirtz D, Huppi PS. Imaging biomarkers of outcome in the developing preterm brain[J]. Lancet Neurol, 2009, 8(11): 1042-1055.
[36]Inder TE, Huppi PS, Warfield S, Kikinis R, Zientara GP, Barnes PD, et al. Periventricular white matter injury in the premature infant is followed by reduced cerebral cortical gray matter volume at term[J]. Ann Neurol, 1999, 46(5): 755-760.
[37]Shah DK, Doyle LW, Anderson PJ, Bear M, Daley AJ, Hunt RW, et al. Adverse neurodevelopment in preterm infants with postnatal sepsis or necrotizing enterocolitis is mediated by white matter abnormalities on magnetic resonance imaging at term[J]. J Pediatr, 2008, 153(2): 170-175.
[40]ElDib M, Massaro AN, Bulas D, Aly H. Neuroimaging and neurodevelopmental outcome of premature infants [J]. Am J Perinatol, 2010, 27(10): 803-818.
[41]Kawai N, Maeda Y, Kudomi N, Yamamoto Y, Nishiyama Y, Tamiya T. Focal neuronal damage in patients with neuropsychological impairment after diffuse traumatic brain injury: evaluation using 11C-flumazenil positron emission tomography with statistical image analysis [J]. J Neurotrauma, 2010, 27(12): 2131-2138.