CT and MR in non-neonatal hypoxic–ischemic encephalopathy: radiological findings with pathophysiological correlations

Abstract

Non-neonatal hypoxic-ischemic encephalopathy is a clinical condition often related to cardiopulmonary arrest that demands critical management and treatment decisions. Management depends mainly on the degree of neurological impairment and prognostic considerations. Computed tomography (CT) is often used to exclude associated or mimicking pathology. If any, only nonspecific signs such as cerebral edema, sulci effacement, and decreased gray matter (GM)/white matter (WM) differentiation are evident. Pseudosubarachnoid hemorrhage, a GM/WM attenuation ratio <1.18, and inverted GM attenuation are associated with a poor prognosis. Magnetic resonance (MR) imaging is more sensitive than CT in assessing brain damage in hypoxic-ischemic encephalopathy. Some MR findings have similarities to those seen pathologically, based on spatial distribution and time scale, such as lesions distributed in watershed regions and selective injury to GM structures. In the acute phase, lesions are better depicted using diffusion-weighted imaging (DWI) because of the presence of cytotoxic edema, which, on T2-weighted images, only become apparent later in the early subacute phase. In the late subacute phase, postanoxic leukoencephalopathy and contrast enhancement could be observed. In the chronic phase, atrophic changes predominate over tissue signal changes. MR can be useful for estimating prognosis when other tests are inconclusive. Some findings, such as the extent of lesions on DWI and presence of a lactate peak and depleted N-acetyl aspartate peak on MR spectroscopy, seem to have prognostic value.

“Dazed and diffused”: making sense of diffusion abnormalities in neurologic pathologies

“…In adults, hypoxicischaemic injury most commonly occurs in the setting of cardiac arrest, whereas dehydration, perinatal anoxia and child abuse are the most common causes in children [1,2].…”

“…For instance, with carbon monoxide poisoning, where oxygen delivery to the brain is impaired but blood flow is preserved, diffusion abnormalities primarily involve the globus pallidus bilaterally [3,4]. By contrast, with cardiac arrest, where both oxygen delivery and blood flow to the brain are impaired, involvement of the cortex, watershed zones, basal ganglia, thalamus and hippocampus is more typical [1][2][3]. Whatever the cause, the diffusion abnormality is usually bilateral and symmetric [2].…”

“…By contrast, with cardiac arrest, where both oxygen delivery and blood flow to the brain are impaired, involvement of the cortex, watershed zones, basal ganglia, thalamus and hippocampus is more typical [1][2][3]. Whatever the cause, the diffusion abnormality is usually bilateral and symmetric [2].…”

“…Diffusion abnormalities caused by hypoxic-ischaemic injury can be seen within 1 hour of the acute insult, hours before CT or other MR sequences [1,2,5]. The abnormalities evolve before peaking approximately 2.0-4.5 days after the initial insult [6].…”

“…These diffusion abnormalities are thought to be caused, at least in part, by the glutamate excitotoxic pathway where reduced energy-dependent glutamate reuptake within the synaptic clefts results in cytotoxic oedema ( Figure 1). The glutamate receptors are concentrated in the dendrites of the cortical and deep grey matter, and this may explain the distribution of diffusion abnormalities in hypoxicischaemic injury [1,2]. DWI is useful for distinguishing cerebral abscesses, which can be rapidly fatal, from other less acute causes of peripherally enhancing lesions such as primary and metastatic malignancies [9] ( Figure 2).…”