Neuronal control of neonatal respiration - sleep apnea and the sudden infant death syndrome.

During the last decade evidence has been accumulated that there might be a continuum from normally occurring short spells of apnea during sleep to life threatening long lasting respiratory pauses with marked bradycardia or even cardiac arrest from which, however, the infant could be resuscitated - the so-called Near Miss for Sudden Infant Death Event - and finally, to the Sudden Infant Death Syndrome (SIDS). There are still many missing links between these three phenomena and it seems likely that the connection between all three is not a straight matter in degree of immature dysfunction of cardiorespiratory control mechanisms. However, no other concept has shead so much light on SIDS and - most probably - no other concept with its consequence of continuous home monitoring has already salvaged so many babies as research into the different sleep apnea syndromes during infancy. However, for the final evaluation of the above mentioned hypothesis two issues urgently need clarification: a) How much apnea is normal at different ages and in different risk groups of infants. b) Can "near miss infants" or future victims of SIDS be identified on the basis of the amount of apnea prior to the event. In the first part of this survey brain mechanisms possibly underlying both, sleep apnea and serious apneic events will be discussed. In the second part new normative data on the amount of apnea will be presented together with 2 extraordinary cases who could be studied by means of longterm polygraphic sleep recordings prior to a definitely serious near miss event in one case and a crib death in another.