BRAIN ARTERIAL INFARCTS

Arterial infarcts due to cerebral hypoperfusion
Cerebral hypoperfusion is the most frequent cause of cerebral arterial infarcts. Cerebral hypoperfusion is due to systemic hypotension. Episodes of systemic hypotension lead to ischemia in the distribution of a given arterial territory. The local ischemia leads to cerebral infarct. Cerebral hypoperfusion produces border zone infarcts in premature and fullterm neonates.

Arterial infarcts due to cerebral embolism
Cerebral embolic infarcts are more common than thrombotic infarcts. The embolic material may arise from the placenta, heart, carotid artery (Figure 245.1), or from the vein in the lower extremities in neonates with cardiac malformation producing a right-to-left shunt.

A	B	C

Figure 245.1.—[A] MRI of the brain demonstrating a large infarct in the distribution of the left middle cerebral artery; [B] B-mode ultrasonography demonstrating a thrombus at the origin of the internal carotid artery; [C] MRA of the brain demonstrating a narrow internal carotid artery and absence of the middle cerebral artery.

Arterial infarcts due to cerebral thrombosis
Thrombotic arterial 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 antiphospholipid 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 proteins 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 and dehydration can also produce thrombotic arterial infarcts.