Cerebellar, brainstem, and spinal cord arterial infarcts are rare in the neonatal period. Cerebellar and brainstem arterial infarcts involve the posterior cerebral circulation (Figure 248.1). Thrombosis is the most frequent mechanism of arterial infarcts in these areas.

A	B	C

Figure 248.1— Cerebellar and brainstem arterial infarcts [A,B,C] in a patient that had ECMO.

Spinal cord arterial infarcts usually occur in the distribution of the artery of Adamkiewicz or the artery of the cervical enlargement. The artery of Adamkiewicz supplies the thoracolumbar spine. Occlusion of the artery of Adamkiewicz produces paraparesis. Occlusion of the artery of the cervical enlargement (Figure 248.1) produces quadriparesis, but it occasionally produces diplegia of the upper limbs. The most common mechanism of spinal cord arterial infarct is probably thrombosis or hypoperfusion.

A	B

Figure 248.1.— Median sagittal cervical spinal cord images. [A] T1-weighted image demonstrates an infarct in the cervical spine as an area of increased ecogenicity. [B] T2-weighted image demonstrates an infarct in the cervical spine as an area of increased ecogenicity.

Umbilical arterial placement has traditionally been associated with spinal infarcts but the association may not be causal.

Central nervous system venous infarcts are produced by thrombotic phenomena. The clinical manifestations of CNS venous infarcts vary according to the anatomical site involved. Venous infarcts in the brain usually produce seizures or paresis. Venous infarcts in other areas usually produce paresis.
The mechanism of cerebral venous infarct is thrombosis. Thrombotic venous infarcts may occur with hypercoagulation states such as proteins C and S deficiencies, antithrombin III deficiency, or the presence of Factor V-Leiden, anticardiolipins, and antiphospholipids antibodies. Protein C is a glycoprotein that inhibits factors V and VIII. Protein S is a glycoprotein that serves as a cofactor for protein C. The excess of factors V and VIII that occurs with protein C and S deficiencies and the excess of thrombin that occurs with antithrombin III deficiency leads to thromboembolic phenomena. Factor V-Leiden is a mutated Factor V. The mutation consists of the substitution of an aminoacid at a key position by the wrong aminoacid. The consequence of this substitution is that it renders Factor V (called Factor V-Leiden) resistant to protein C inactivation. The mechanism of thrombosis in neonates with anticardiolipins and antiphospholipids is not known. Polycythemia, sepsis, and dehydration can also produce thrombotic venous infarcts. Venous thrombosis due to compression occurs in premature neonates when the terminal vein is compressed by a ganglionic germinal matrix bleed. The presence of increased venous pressure contributes to the production of venous infarcts.