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Current Perspectives in SIDS

Published in SIDS Horizons -June 1996
Written by: Ronald Harper, Ph.D.,
Professor of Anatomy and Cell Biology,
Department of Neurobiology and the Brain Research Institute,
University of California, Los Angeles.

Dr. Harper is world renowned as a basic neuroscientist, and has been involved in SIDS research for over 25 years.

Researchers have gathered a large body of physiological and anatomic information in their search to determine what causes Sudden Infant Death Syndrome. The collective data suggest that the underlying cause for SIDS may pre-exist in fetal life, and that signs of risk are apparent from the first week of life, and continue for at least two months. The data also suggest that the underlying defect involves some aspect of the interactions between breathing and cardiovascular mechanisms.

The data have been acquired from studies of infants who later succumb to the syndrome, and from subsequent siblings of infants who have died. On rare occasions, some records of heart rate and breathing have also been obtained during, or in close proximity to the fatal event. Anatomical evidence from the brain has also been gathered from infants who died, and compared with carefully matched controls of infants who succumbed to other causes.

The evidence suggests that infants who succumb to SIDS show signs of some deficit in the part of the brain that controls heart rate, breathing, and alterations in blood pressure as they interact with one another and with outside influences. It is normal for infants to pause while breathing during sleep and for their heart rate to change as they are breathing in and out. Infants who succumb to SIDS pause less often during respiration, and have fewer changes in heart rate than those who do not succumb. This may be the result of the recently described loss, in SIDS victims, of brain cell components that use a particular chemical for transmitting information. In addition, recordings from infants during a fatal event can show a profound slowing of the heart not preceded by apnea (although often accompanied by apnea), and continued heart rate slowing even while artificial ventilation (CPR) was maintained.

It appears that some infants who succumb undergo cardiovascular collapse. To maintain blood circulation, the brain must send signals to the muscular walls of the arteries to (relatively) constrict, and thus maintain blood pressure. A loss of these signals to constrict the arteries results in vessel dilation and a marked loss of blood pressure; the loss of blood pressure leads to insufficient pumping of blood though vital organs, and eventual death.

The brain maintains blood pressure through a system called the "sympathetic" nervous system. In some SIDS victims, that system appears to be momentarily activated (which incidentally results in profuse sweating) and then inactivated or suppressed during events. The inactivation component of this scenario, together with the heart rate slowing, is remarkably similar to the "decompensatory" phase of shock usually triggered by a large loss of blood, deep pain, or a variety of other phenomena. Infants who succumb to SIDS do not appear to have fluid loss or to experience deep pain prior to the event; thus, it would seem that some other sensory signal may be triggering the shock-like process in the fatal sequence.

Since a structural deficit appears to be present in the brains of SIDS victims, the "trigger" may be a normal sensory event (for example, signals from the small rise in blood pressure that usually accompanies a body movement) that is not interpreted correctly by the brain. In addition, SIDS victims tend to remain asleep, rather than momentarily wakening throughout the course of a night; The failure to arouse during the course of such a trigger may contribute to the fatal outcome.

Researchers have focused on failure in the breathing mechanism as the underlying cause of SIDS, rather than cardiovascular mechanisms. This is due principally because of reports of repeated apneic events in SIDS victims, and because of the petechiae found above the diaphragm in a large proportion of infants who succumb. The latter finding suggests the occurrence of an obstructed airway, since the negative pressure caused by a descending diaphragm with an obstructed upper airway would generate such petechiae. However, the conditions under which petechiae are generated are not completely understood, and breathing events associated with cardiovascular collapse may well contribute to petechiae development.

There are some obvious "first-step" efforts which must be taken to find the mechanisms of SIDS. These are:

1) Determination of brain mechanisms which can trigger the sequences leading to cardiovascular changes associated with shock.

2) Description of the functions associated with nerve cells lacking particular neurotransmitters in SIDS victims. And,

3) assessment of the effect of sleep states on events which can lead to cardiovascular collapse.

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