Table 3

Chronological magnetic resonance imaging findings in anoxic/hypoxic encephalopathy

Acute phase (<24 hours)

Early subacute phase (24 hours to day 13)

Late subacute phase (days 14 to 20)

Chronic phase (>21 days)

Characteristics

Brain swelling

Brain swelling

Absence of brain swelling

Diffuse atrophy and dilatation of the ventricles

DWI

Hypersignals in the cortex, in the thalamus and in the basal ganglia

Hypersignals in the cortex, in the thalamus and in the basal ganglia

Progressive disappearance of hypersignals found previously

Normal

T2

Hypersignals in the cortex, in the thalamus and in the basal ganglia

Hypersignals in the cortex, in the thalamus and in the basal ganglia. Possible subcortical hyposignals

Hypersignals of the cortex, the thalamus, the basal ganglia and the pons

Normal or possible hypersignals of the cortex, the thalamus, the basal ganglia and the pons

T1

No abnormalities

No abnormalities

Possible spontaneous subcortical and basal ganglia hypersignals

Can be normal

T1 with gadolinium enhancement

No abnormalities

Possible subcortical enhancement suggestive of cortical laminar necrosis

Possible subcortical enhancement suggestive of cortical laminar necrosis

No abnormalities

Comments

DWI seems more sensitive to mild hypoxic/anoxic injury in the first hours, and the hypersignal in cerebral cortex seems more precocious than in the basal ganglia

Hypersignals on both DWI and T2 become more intense, particularly in the thalamus and the basal ganglia

In some cases, appearance of diffuse white matter, abnormalities of delayed anoxic leukoencephalopathy on both DWI and T2

In some cases, hypersignals of the cortex and hyposignals in the subcortical zone on both T2 and T1, suggestive of cortical laminar necrosis

DWI, diffusion weighted imaging; T1, T1 weighted sequence; T2, T2 weighted sequence. Adapted from [66,67].

Weiss et al. Critical Care 2007 11:230   doi:10.1186/cc6107