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Hypoxic-ischaemic encephalopathy: MRI findings
  1. Alder Hey Children’s Hospital
  2. Eaton Road
  3. Liverpool L12 2AP

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    Editor—Rutherford et al diagnosed type I hypoxic-ischaemic encephalopathy (HIE) from MRI scans showing high signal intensity in periventricular white matter.1 Figure 1 shows a T2 weighted spin-echo sequence with high signal in the posterior periventricular white matter in a 1 year old child.

    We believe that these MRI findings occur in normal children and should not be interpreted as evidence of HIE.

    Areas of high signal intensity in the white matter dorsal and superior to the ventricular trigones occur in many children on long TR/TE images. These have been attributed to the known physiological delay in myelination of fibre tracts involving parietal and temporal association areas, and have been called “terminal zones.”

    Distinction between these periventricular areas of high signal and mild periventricular leucomalacia is difficult,2 but is facilitated by preservation of a layer of myelinated white matter between the ventricle and the areas of high signal in normal subjects. This layer is absent in periventricular leucomalacia.3Figure 1 clearly shows that this layer is preserved.

    We conclude that the authors’ criteria for type I HIE would lead to overdiagnosis, and would have serious medico-legal implications.


    Dr Rutherford et al reply: The authors state that we have diagnosed type I HIE on the basis of MRI findings. Needless to say, HIE is a clinical (Sarnat and Sarnat, 1976) and not an MRI diagnosis. We described MRI changes in infants who had already been diagnosed with HIE.

    The authors state that the findings in fig 1 can occur in healthy children. We agree, and clearly stated this in the study: “It is sometimes difficult to differentiate periventricular changes from those due to immature white matter in infants under a year old.”

    Perhaps we could have shown these abnormalities with a more obvious example, but in any infant it is difficult to display all the abnormalities present using one image at one level. However, the periventricular changes we have seen in these mildly asphyxiated infants fall outside the normal range for infants over 1 year. They were also often present in frontal as well as posterior periventricular white matter.

    The authors describe the MRI findings in infants with PVL and how these changes differ from those shown in fig 1. We do not dispute this, but we did not claim that our changes were suggestive of PVL. The changes we showed may be secondary to a delay in myelination, although in some infants they seem to become more obvious with time. This can be clearly shown using the fluid attenuated inversion recovery (FLAIR) sequence. We are continuing to monitor these particular infants, and hope to combine follow up imaging with a detailed fine motor examination at the age of 5 years.

    Finally, the statement about medico-legal issues is rather sensationalist, in our opinion. An increase in T2 in the posterior periventricular white matter is a very common and non-specific finding (albeit an abnormal one) in children referred for MRI of the brain for a variety of developmental problems.