Review Article

Modeling the Encephalopathy of Prematurity in Animals: The Important Role of Translational Research

Table 2

Major histopathology features of the encephalopathy of prematurity in the human brain.

(1) White matter
 (a) Periventricular leukomalacia of the telencephalic white matter
   (i) Periventricular focal necrosis in different stages (acute, organizing, and macro- and/or microcysts)
   (ii) Gliosis and microglial activation in the surrounding white matter
   (iii) Early loss of pre-OLs
   (iv) Expression of markers of oxidative and nitrative stress by pre-OLs
   (v) Possible maturation arrest of OLs
   (vi) Impaired myelin formation
   (vii) Upregulation of cytokines in macrophages, activated microglia, and reactive astrocytes
 (b) Widespread axonal damage within and distant from the necrotic foci
 (c) Deficit of neurons within necrotic foci, surrounding white matter distant from the necrotic foci, and subplate region
 (d) Postmitotic migrating neurons as possible reparative event
 (e) Gliosis of the cerebellar white matter
(2) Gray matter
 (a) Neuronal loss and/or gliosis of the cerebral cortex, thalamus, globus pallidus, hippocampus, cerebellum, and brainstem in different combinations and to different degrees, with preferential involvement of thalamus and basal ganglia
(3) Hemorrhages
 (a) Subpial
 (b) Subarachnoid
 (c) Germinal matrix (with suppression of cell proliferation)
 (d) Cerebellum
(4) Infarcts
 (a) Microinfarcts of the thalamus
 (b) Focal infarcts of the cerebral cortex