It is now apparent that the principal lesions of perinatal asphyxia--cerebral hypoxic-ischaemic damage and IVH--are pathogenetically interrelated, a fact that has long been suspected by pathologists (Pape and Wigglesworth, 1979). Prevention of such lesions would require, on the one hand, circulatory support to prevent hypotension and, on the other hand, the means to avoid excessive arterial pressure peaks in the early neonatal period together with experimental and clinical research to determine the optimal PCO2 level. It may therefore be concluded that neonatal ischaemia is a critical determinant for later neurological and intellectual development, and is probably the most important single factor known at present. Our consistent finding of hypoperfusion and, by inference, low metabolic activity supports the hypothesis that this ischaemia may cause minor structural changes in the white matter border zones between major arterial territories, leading to severe learning disorders in these children, who were examined with the 133Xe-inhalation computerized emission tomography technique (Lou et al, 1984).