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To the Editor: We read with interest the report by Gottfried et al.1 on delayed posthypoxic demyelination, in which they demonstrated by proton MR spectroscopy elevated choline and lactate and reduced N-acetyl aspartate signal in the affected white matter, consistent with demyelination and shift to anaerobic metabolism. In addition, arylsulfatase A activity from peripheral leukocytes was recorded at approximately 50% of normal, consistent with a "pseudodeficiency" phenotype. The authors pointed out that relative arylsulfatase A deficiency is a predisposing factor for delayed hypoxic leukoencephalopathy.
We would like to present a similar case of delayed hypoxic leukoencephalopathy following successful resuscitation after cardiac …
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