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Non-perinatal hypoxic–ischaemic encephalopathy (HIE) has varying anatomical patterns dependent on the type of insult, the degree and duration of cerebral hypoxia, or presence and degree of hypoperfusion. Profound insults can affect the entire cerebral cortex or just the perirolandic cortex, the cerebellum and the deep grey matter structures. Less severe insults may affect only the watershed regions. The objective of this article is to review the anatomical patterns of non-perinatal HIEs by MRI.
Non-perinatal hypoxic–ischaemic encephalopathy (HIE) can be a devastating neurological injury and prompt recognition of it can result in significant changes in patient management. HIE insults develop in varying regions of the brain depending on the severity and duration of hypoperfusion or hypo-oxygenation . Brain parenchyma changes have corresponding MR signal characteristics that are often obvious but can be subtle . It is important for radiologists to be aware of the variations in the appearance of HIE in order to be alert to the diagnosis in subtle cases, recognise unusual patterns and be aware of the clinical ramifications.
This review shows cases of HIE beyond the perinatal period. Aetiological factors and timing of imaging findings are delineated. The cases involve the usual HIE-specific neuroanatomical locations: the cerebral cortex, cerebellum, hippocampus, basal ganglia and thalamus. In addition, cases of HIE showing damage to the cerebral white matter and limbic system are demonstrated. Also, cases that mimic the appearance of HIE are presented. It is critical for a radiologist to be aware of potentially confounding cases.
Mild cases of HIE, such as from mild or short-duration hypotension or brief cardiac arrest, are likely to demonstrate damage in the watershed zones (Figures 1 and and2)2) . The watershed pattern is well known but the changes in HIE can present asymmetrically and this needs to be understood to avoid misdiagnosis (Figure 1).
In moderate-to-severe cases of HIE, vulnerable areas are the perirolandic and occipital cortices (Figures 3 and and4)4) . The cortical injury is easier to see on diffusion-weighted imaging (DWI), but subtle changes can also be identified on T2 fluid-attenuated inversion–recovery (FLAIR) imaging (Figure 4). In more severe cases of HIE, the effects may cause the entire cerebral cortex to swell (Figures 5–7) and eventually become necrotic . In severe cases, the abnormality may be overlooked owing to the symmetric nature of the changes. This problem is well demonstrated on FLAIR imaging and DWI (Figure 5a,b). Visually, it should be noted that in these severe cases the apparent diffusion coefficient (ADC) maps demonstrate a pattern of very hypointense thickened grey matter (Figure 5c). The grey matter is mildly hyperintense to white matter on ADC maps in healthy individuals but this can flip-flop in cases of HIE (Figures 5c, ,7c7c and and8c).8c). Measuring the actual ADC values of the cortex can be useful when a patient has a potential history of a hypoxic–ischaemic insult and one is uncertain of the diagnosis. Of course, it is critical to know the time lapse between the event in question and the DWI acquisition, given that ADC values are time dependent in cases of stroke.
Though typical of HIE, the MR signal changes in the cortex are not specific to HIE and can be seen with other aetiologies such as recent seizure activity (Figure 8); encephalitis (Figure 9); Creutzfeldt–Jakob disease (CJD) (Figure 10); hypoglycaemia; hyperammonaemia; mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS); and hyponatraemia [6,7,8]. These cases usually have patchy non-symmetrical abnormalities that do not involve the perirolandic or watershed zones. Particular patterns of involvement (e.g. the temporal lobe in herpes encephalitis) can be suggestive of an alternative diagnosis. Also, laboratory values can be critical to differentiate cases of hypoglycaemia, hyperammonaemia and hyponatraemia. Microbiological and cerebrospinal fluid analysis can help to determine the aetiology of encephalitis and CJD. However, biopsy may be needed (brain biopsy or even a muscle biopsy for MELAS).
The cerebellum can show damage that is often limited to the watershed zones in mild cases of HIE (Figure 1) and can be widespread in severe cases. Cerebellar Purkinje fibres are hypermetabolic and therefore sensitive to hypoxic injury .
Infarction of the entire hippocampus can develop if the global ischaemic insult is severe (Figure 6) . The fornix, cingulum and hippocampus can be simultaneously involved in severe global ischaemia (Figure 11) . Fornix and hippocampal infarction can lead to memory deficits and amnesia .
When global ischaemia affects the basal ganglia, usually the caudate and putamen are the most vulnerable (Figure 5) . The globus pallidus can be affected selectively in unusual cases such as carbon monoxide poisoning and may also be affected in diffuse global damage (Figures 12 and and13)13) . The thalamus is often damaged in global ischaemia (Figures 2 and and5)5) .
Global ischaemia will sometimes lead to demyelination and destruction of cerebral white matter (Figure 14), especially when hypotension complicates intensive care . White matter involvement might be overlooked on conventional T2 weighted imaging because markedly oedematous grey matter may make the white matter appear to have relatively low signal intensity and to be normal in appearance. DWI and ADC mapping in this condition are helpful in recognising the white matter changes by clearly depicting the restricted diffusion (Figure 15). The white matter in unusual cases may also be affected after ischaemia without prominent grey matter involvement (Figure 11) . Delayed white matter infarction is possibly due to the development of post-anoxic leukoencephalopathy (Figure 14) . MRI of encephalitis in cases of severe white matter abnormality could be a confounding diagnostic consideration.
Our cases demonstrate that the anatomical site of tissue injury varies following a concept known as selective vulnerability. Particular sites with high energy demands face cytotoxic crisis when presented with mandatory anaerobic metabolism due to low oxygen delivery .
It is well known that DWI during the early phase after cerebral hypoxia is superior to conventional MRI for detecting ischaemia and can be used as a predictor of clinical outcome . However, even severe cases of HIE may have normal or subtle findings on DWI initially (Figures 7 and 14). That is why a radiologist must be very aware of the potential diagnosis, know the patterns that are seen and be able to detect subtle findings of diffuse HIE. However, measurement of ADC values and MR examinations over time when there is difficulty making the diagnosis initially can be crucial when evaluating HIE. Early detection will save time and provide more timely guidance to the clinical team concerning overall prognosis and give the patient and family better information about recovery .
Subtle imaging findings pointed out in this presentation aid the radiologist in making HIE diagnosis when the diagnosis might otherwise be missed.