Abstract □ 108

Introduction and aim: We have recently shown the presence of DNA fragmentation suggestive of apoptotic cell death in the brainstem of sudden infant death syndrome (SIDS) victims. (Pediatr. Res, 1999, In press). There is sample evidence that SIDS victims suffered repetitive episodes of hypoxemia and, there is also evidence that apoptosis can be triggered by hypoxemia. However, it is possible that another trigger is responsible for cell death, a trigger acting alone or in combination with hypoxemia: hypotension for example. The aim of this study was to determine whether DNA fragmentation typical of apoptosis could be found in a watershed area -the boundary zones between the irrigation by the anterior and middle cerebral arteries-, a brain region known to be particularly vulnerable to hypotension.

Methods: We used an in-situ end-labelling method that detects DNA fragmentation resulting from apoptosis (paraffin-embedded tissue). We studied 25 SIDS victims and 9 age-matched control cases who died in circumstances similar to the SIDS victims (sudden unexpected death in previously healthy infants) but of known pathologies, mostly infections.

Results: We found significant neuronal apoptosis in the watershed area between the frontal and parietal lobe in 68% of the SIDS victims. The distribution of apoptosis was mostly in layer III and IV Two control cases showed a much milder degree of neuronal apoptosis than the SIDS victims, the other being negative.

Interpretation: Our present results and the results of our previous work indicate the occurrence of an acute insult at least several hours before death, an insult from which the infants had apparently recuperated. We speculate that severe hypotension must have accompanied that episode because of the involvement of a specific area sensitive to hypotension. These findings might help us understand the sequence of events leading to SIDS and the pathophysiology of such events.