Severe Asphyxia
Severe asphyxial events in term neonates result in a primarily central pattern of injury involving the
deep gray matter (putamina, ventrolateral thalami, hippocampi, dorsal brainstem, and lateral
geniculate nuclei) and occasionally the perirolandic cortex. These areas of the brain are actively
myelinating (an energy-intensive process) or contain the highest concentrations of NMDA receptors at term (4,13) and are, therefore, the most susceptible to neonatal HII. The remainder of the
cerebral cortex is generally spared or shows mild insults, since it is generally less metabolically active in the immediate perinatal period; however, with more prolonged insults, the remaining cortex
will become involved, a finding that generally portends a worse neurologic outcome (10).
Cranial US performed in the 1st week of life in term neonates has a fairly low sensitivity (50%)
for detecting abnormalities due to HII (14,15), but its sensitivity increases when it is performed
after 7 days. Early US findings include a global increase in cerebral echogenicity and obliteration
of the cerebrospinal fluid (CSF)– containing spaces, suggesting diffuse cerebral edema. Increased echogenicity in the basal ganglia, thalami, and brainstem can also be seen in the 1st week
but is more readily apparent after 7 days (15,16). The presence of thalamic echogenicity generally
suggests a more severe injury and correlates with a poorer outcome (17). Late findings include
prominence of the ventricles and extraaxial CSFcontaining spaces, likely due to atrophy. The use
of cerebral arterial Doppler US during US evaluation performed in the first few days of life may
improve sensitivity and specificity for brain injury, since the presence of diminished resistive indexes
(60) in the anterior and middle cerebral arteries has been associated with a poor clinical outcome,
even in the absence of other US abnormalities MR imaging is an accurate modality for evaluating neonatal HII. Diffusion-weighted imaging is sensitive for the detection of injury in the first 24
hours, during which time conventional T1- and T2-weighted images may appear normal. Diffusion-weighted images will demonstrate increased signal intensity in the region of the ventrolateral
thalami and basal ganglia (particularly the posterior putamina), in the perirolandic regions, and
along the corticospinal tracts (Fig 2). It should be noted that diffusion-weighted MR imaging performed during this period will often lead to underestimation of the ultimate extent of injury (18,19); indeed, normal findings at diffusionweighted imaging performed in the first 24 hours, although uncommon, have been reported (18). It
is believed that the prominent role of apoptosis in neonatal HII may explain why diffusion-weighted
imaging in the acute setting leads to underestimation of injury. Abnormalities seen at diffusionweighted imaging generally peak at 3–5 days and subsequently “pseudonormalize” by about the
end of the 1st week (4,6,10,20), although decreased ADC values can persist in injured regions
into the 2nd week (18,20). It should be noted that, although diffusion-weighted images seemingly improve and appear relatively normal by the end of the 1st week, this finding does not imply
that there has been improvement or reversal of underlying disease. Hence, we use the term
pseudonormalization to indicate the apparent resolution of signal intensity abnormalities on diffusion-weighted images. Because of the (admittedly unlikely) possibility of a false-negative diffusionweighted MR imaging study early in neonatal life, a negative MR imaging study performed for HII in the first 24 hours should prompt either repeat MR imaging at 2– 4 days, when diffusion abnormalities are expected to be greatest, or evaluationwith proton MR spectroscopy.Conventional T1- and T2-weighted MR images obtained on day 1 are frequently normaland are therefore less useful than diffusionweighted images obtained for the diagnosis of HII
in the acute setting. By day 2, injured areas may