The presentations of cerebral arterial infarcts vary according to the vessels involved. Arterial infarcts in neonates have three presentations: (1) arterial border zone infarct, (2) single artery infarct, and (3) multi-artery infarct.

The presentation of arterial border zone infarcts varies in premature neonates and in fullterm neonates.

Brain arterial border zone infarct in premature neonates
Arterial border zone infarcts in premature neonates usually involves the end zones of irrigation of the long penetrating arteries of the anterior, medial, and posterior cerebral arteries. The border zone of irrigation of the long penetrating arteries is in the periventricular region (Figure 246.1).

Figure 246.1.— Schematic representation of arterial (A) and venous (B) brain systems; and of the common sites of arterial border zone infarcts (gray areas). 1: internal carotid artery; 2: anterior cerebral artery; 3: middle cerebral artery; 4: Heubner's artery; 5: striate branches of the middle cerebral artery; and 6: long perforating arteries of the anterior cerebral artery; arteries not labled are the long penetrating arteries of the middle cerebral artery.

The most common sites of involvement are the periventricular region adjacent to: (1) the lateral aspect of the trigone of the lateral ventricles, (2) the foramina of Monro, (3) the frontal horns of the lateral ventricles, and (4) the occipital horns of the lateral ventricles. Involvement of the centrum semiovale may occur in severe cases. Large arterial border zone infarcts in premature neonates often become hemorrhagic.
Arterial border zone infarcts in premature neonates selective involvement of oligodendrocytes. The selective involvement of oligodendrocytes in the periventricular region in premature neonates is due to the vulnerability of immature oligodendroglia to free radicals (mature oligodendroglia [Figure 246.2] are capable of neutralizing free radicals), and to being present in large numbers in the border zone of the irrigation field of the long penetrating arteries where the infarcts usually take place.

Figure 246.2.— Schematic representation of the major steps in free radical metabolism. Beneficial management of free radicals in the presence of sufficient enzyme activity. Superoxide dysmutase (SOD) converts superoxide anions (02) in the presence of hydrogen (H+) to hydrogen peroxide (H202). Hydrogen peroxide in the presence of cytoplasmic glutathione peroxidase (GLUT. PERO.) and peroxomal catalase (CATALASE) becomes water and oxygen.

Oligodenroglia damage is related to the production of free radicals during ischemic-reperfusion injury, the immaturity of the enzyme system involved in the detoxifications of free radicals, and the excess of iron store in immature oligodendroglia cells (Figure 246.3).

Figure 246.3.— Schematic representation of abnormal free radical metabolism. BAD: poor management of free radicals occurs because of decreased superoxide dysmutase (SOD) activity. Decreased superoxide dysmutase activity leads to an increase in superoxide anion (02-). WORSE: very poor management of free radicals occurs because of decreased glutathione peroxidase (GLUT. PERO.) and catalase activities (CATALASE), and increased iron content in the cytoplasm. Hydrogen peroxide in the presence of iron (Fe++) produces hydroxyl radicals by the Fenton reaction (FR).