Venous brain infarcts may involve the veins or the venous sinuses. Venous brain infarcts occur more often in premature neonates than in fullterm neonates. Venous infarcts in premature neonates occur due to compression of the terminal vein by the mass effect of blood from germinal matrix bleeds. Venous infarct may be localized to the area drained by the medullary veins or may be more extensive and involve the areas drained by the medullary, thalamostriate, and choroidal veins (Figure 249.1). Venous brain infarcts are often hemorrhagic. In fullterm neonates, venous infarcts usually occur with dehydration and hypercoagulation states, and they involve the sinuses.

Figure 249.1.— Schematic representation of the brain (gestational age: 34-38 weeks) demonstrating angles on an axial cut (B-B: sagittal) and (C-C: coronal). The ventricles are represented in blue; the choroid plexus in pink. 1: medullary veins; 2: terminal vein; 3: internal cerebral vein; 4: vein of Galen; 5: straight sinus; 6: thalamostriate vein; 7: choroidal vein; 8: Heubner's artery; 9: striated branches of the middle cerebral aftery; 10: frontal poles; 11: frontal horn of the left lateral ventricle; 12: germinal matrix; 13: foramen of Monro; 14: third ventricle; 15: occipital poles.

A venous CNS infarct should be considered in patients with focal CNS deficits, abnormal movements or seizures, and in patients with predisposing conditions for venous or venous sinus involvements. Central nervous system deficits that should raise suspicion of the possibility of an infarct in a neonate are: monoparesis, hemiparesis, paraparesis, upper extremity diplegia, and quadriparesis. Conditions that predispose to a venous infarct are increased intracranial pressure, polycythemia, dehydration, hypotension, or a hypercoagulopathy.
The study of choice to diagnose infarcts varies. Brain ultrasonography is the study of choice in premature neonates with suspected brain venous infarct. Brain ultrasonography is highly effective in diagnosing periventricular infarcts due to terminal vein compression because the infarcts are directly beneath the fontanelle and are often hemorrhagic. On coronal projection, periventricular infarcts due to terminal vein compression often appear as asymmetrical globular or triangular-shaped echodensities irradiating from the external angle of the lateral ventricle. Periventricular infarcts due to terminal vein compression often resolve with or without cystic formation (Figure 249.2).

Figure 249.2.— Brain ultrasound demonstrating evolution of periventricular infarction. D: days of age; L GMH: left germinal matrix hemorrhage; PVHI: periventricular hemorrhagic infarct; B GMH: bilateral germinal matrix hemorrhage. There is a cyst in the area of the germinal matrix bleed.

In fullterm neonates suspected of having a venous infarct, the studies of choice are MRI, magnetic resonance venogram (MRV), or CT of the area in question (Figure 249.3). The study should be performed as soon as possible after the onset of clinical manifestations. Nevertheless, a normal MRI or CT within the first 24 hours after the onset of clinical manifestations does not eliminate the possibility of an ischemic venous infarct because ischemic central nervous system parenchymal changes may not be detected by MRI or CT studies during this period. Power Doppler ultrasound and MRV may demonstrate the flow abnormality earlier than MRI or CT. Power doppler ultrasound imaging is probably the study of choice to diagnose cerebral venous sinus thrombosis.

A	B

Figure 249.3.— [A] MRI and [B] MRV demonstrating a left transverse sinus thrombosis (complication of beta-streptococcal meningitis). TS: transverse sinus; IJV: internal jugular vein.