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Topographical Differences

The age-dependent topographical differences can be explained as follows (cf. Marín-Padilla 1996, 1997).

The periventricular zone in younger preterm infants is vascularized by numerous arterioles and venules and has a variable venous drainage system (Marín-Padilla 1996). Early periventricular hemorrhages are small, multifocal, and caused by direct injury of the vascular endothelium, i.e., by endothe-lial cell necrosis, rupture of the vessel wall, or focal thrombosis. The hemorrhagic site fills with microg-lia/macrophages in the first hours after insult. There is a local proliferation of fibrous astrocytes, giving rise to a periventricular scar (Cherian et al. 2004). Throughout the injured site, residual periventricular gliotic scarring may develop and consists of closely packed fibrous astrocytes with interwoven fibers running parallel to the ependymal surface, possessing a few blood vessels. Glial nodules alternating with scattered foci of ependymal epithelium line the ependymal surface. Mineralized and/or calcified cellular elements and hemosiderin-laden macrophages may persist indefinitely in the scar (Gould et al. 1987). The sequelae include post-hemorrhagic hydrocephalus (i.e., hydrocephalus ex vacuo), periven-tricular gliosis, and distinct changes in the superimposed developing gray matter. Associated with the residual lesion are thinning of the neocortex, peri-ventricular leukomalacia plus significant secondary structural and functional alterations of the overlying gray matter.

The external glial limiting membrane (subpial) is a second highly vulnerable area in younger premature infants. It consists of closely apposed glial end-feet covered by basal lamina. During vascularization of the developing neocortex, meningeal capillaries progressively perforate this membrane, penetrating the nervous tissue. The glial endfeet and their perforating capillaries are vulnerable to perinatal

atrophy of the cerebrum and d cerebellum obviously caused by brain hypoxia/ischemia with the clinical features of spasticity, seizures and severe mental retardation

Fig. 22.3a-d. Perinatal brain injury without knowledge of the cause: a severe type of motor (spastic) paralysis with joint contraction and deformity; b slight to distinct external and c internal

atrophy of the cerebrum and d cerebellum obviously caused by brain hypoxia/ischemia with the clinical features of spasticity, seizures and severe mental retardation asphyxia, which often induces layer I (subpial) hemorrhages. The earliest morphological change in cases of asphyxia is swelling of the glial endfeet (edema). If the edema persists, the glial endfeet disintegrate, the subpial membrane undergoes focal disruption, and the perforating vessels rupture and cause a lay er I hemorrhage. The necrotic debris and blood are scavenged by macrophages. Regeneration of the glial cells and proliferation of fibrous astrocytes create permanent marginal heterotopias at a level slightly above the neocortex.

White matter lesions are also seen in older premature infants. The white matter is rendered vulnerable by its vigorous metabolic rate, rapid growth, and increasing distance from new perforating vessels caused by the expansion of the intervening gray matter. Perinatal white matter injury can result from a combination of edema, hypoxia, ischemia (vascular compression), impaired perfusion (border zones), and vascular injury with or without hemorrhages.

Acute white matter lesions are hard to recognize. They can vary from small subcortical lesions to large lesions extending from periventricular to subcortical regions. Their salient feature is local axonal destruction, which is followed by tissue necrosis (infarction), edema, liquefaction, disintegration, reabsorption by macrophages, and early cavitation. The cystic cavities are lined by minimal reactive gliosis. The principal pathologic feature of healing white matter lesions is the capacity of the overlying gray matter to continue its development.

Gray matter lesions acquired perinatally are associated with respiratory difficulties, premature birth, etc. They often result from hemorrhagic and/ or hypoxic-ischemic injuries, or a combination of both. The pathological picture is characterized by acquired cortical dysplasias, such as reactive gliosis (acquired microgyrias, leptomeningeal heterotopias, multicystic encephalopathies, ulegyrias, porenceph-alopathies, and hydranencephalopathies). All cases exhibit scarring as characterized by a subpial gliosis and a gliosis of the subcortical white matter.

Microgyria are characterized by astrocytosis of the gray matter in association with islands of gray matter tissue. Ulegyria result from severe damage to the gray matter in the depth of a sulcus while the corresponding gyral crest is spared. The surviving gyral crests are isolated by the almost total destruction of their corresponding sulci.

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