infarcts due to cerebral hypoperfusion
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.
infarcts due to cerebral embolism
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.
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.
infarcts due to cerebral thrombosis
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
infarcts due to cerebral vasospasmodic phenomena
arterial infarcts occur in neonates exposed to cocaine and maternal
hypertension during pregnancy.