Pediatric Neuroradiology
Neonatal and pediatric neuroimaging rests on knowing the timetable of normal myelination, because the immature brain changes signal dramatically in the first two years. On T1-weighted images, myelin appears bright: the posterior limb of the internal capsule is normally bright by term, the splenium by about 4 months, and the genu by about 8 months. On T2, myelin becomes dark in a similar sequence. A common trap is calling normal T1 hyperintensity in neonatal white matter a hemorrhage or lipid lesion; in a neonate, symmetric T1 brightness in expected tracts is normal. Conversely, absence of the normal T1-bright posterior limb in a term infant with hypoxic-ischemic injury is a key sign.
Understand the patterns of neonatal brain injury. In preterm infants, germinal matrix hemorrhage originates at the caudothalamic groove; grade 1 is confined to the germinal matrix, grade 2 extends into the ventricle without hydrocephalus, grade 3 adds hydrocephalus, and grade 4 is intraparenchymal venous infarction, not simple extension. In term infants, hypoxic-ischemic injury favors the basal ganglia, thalamus, and cortex; in preterm infants it favors periventricular white matter. Also know the major malformations (Chiari II, Dandy-Walker continuum, holoprosencephaly, corpus callosal dysgenesis), posterior fossa tumors by age and location, and abusive head trauma findings.
Worked rule: In a neonate with seizures, obtain MRI with diffusion-weighted imaging; symmetric restricted diffusion in the basal ganglia and thalami after a sentinel event suggests profound perinatal asphyxia, while unilateral focal diffusion restriction suggests arterial ischemic stroke. Do not diagnose periventricular leukomalacia on an early cranial ultrasound before cystic change or volume loss appears.