BRAINSTEM, AND SPINAL CORD ARTERIAL INFARCTS
Cerebellar, brainstem, and spinal
cord arterial infarcts are rare in the neonatal period. Cerebellar and
brainstem arterial infarcts involve the posterior cerebral circulation
Thrombosis is the most frequent mechanism of arterial infarcts
in these areas.
Cerebellar and brainstem arterial infarcts [A,B,C] in a patient that had
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.
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.
infarct in the neonatal period usually involves the brain. Venous infarcts
in the brainstem, cerebellum, and spinal cord are very rare.
CEREBELLAR, BRAINSTEM, AND SPINAL CORD VENOUS INFARCTS
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.
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.