Loss of previously attained developmental milestones in an infant is often associated with central nervous system tumor, neuromuscular disease, or an inborn metabolic error. An infant with developmental regression and involuntary movements who was found to be vitamin B12 deficient on the basis of unrecognized maternal vitamin B12 deficiency is described. The infant had a dramatic neurologic recovery after receiving vitamin B12. The case and a review of similar cases is presented.

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Arachidonic acid (AA) metabolites have been implicated in neonatal pathologic states such as respiratory distress syndrome (RDS). Since free (nonprotein bound) AA is the substrate for synthesis of these compounds, a decreased capacity to bind AA in neonatal plasma could contribute to these disorders. AA binding was assayed by equilibrium dialysis in plasma samples from healthy adults and various infant groups. Plasma from these infant groups bound significantly less AA than adult plasma. Premature infants with RDS and premature infants receiving intralipid had the lowest capacity to bind AA. The increased availability of free AA may be important in neonatal pathophysiologic states involving arachidonate metabolites.