Severe hypoplasia of medullary arcuate nucleus: quantitative analysis in sudden infant death syndrome.

The human arcuate nucleus (ARCn) is postulated to be homologous to ventral medullary cells involved in chemoreception, and respiratory and blood pressure responses. Abnormalities in central respiratory control may result from dysfunction of this anatomic ventral area. We evaluated the changes of the neuronal population of the medullary ARCn in infants victims of the sudden infant death syndrome (SIDS). In this study we tested the hypothesis that anatomical deficiency of the ARCn is associated with SIDS. The volume and neuronal density of the ARCn were morphometrically quantified with an image analyzer in 36 cases of SIDS and 12 age-matched controls. We found a marked hypoplasia in the SIDS ARCn compared to controls and, particularly, in 11 SIDS cases (30%) in which the ARCn exhibited a severe hypoplasia, being almost totally absent. Three-dimensional reconstructions and morphometric measurements of ARCn confirmed this marked hypoplasia in all the serial sections examined (P = 0.0001) and the reduced neuronal density (P = 0.0025) in relation to control cases. In conclusion these abnormalities observed in the ARCn are consistent with the idea that ARCn dysfunction plays an important role among the causative factors of sudden infant death. The hypoplasia of the ARCn represents the most frequent congenital abnormality in our experience, and can be a plausible morphological substrate for a subset of SIDS.