It has been observed that a close temporal relationship exists between Sudden Infant Death Syndrome (SIDS) events and sleep. Most of the SIDS events are associated with night sleep, while most infants who are observed to die during the awake period have autopsy findings consistent with a non-SIDS etiology.
Sleep begins to coalesce from a series of naps to more prolonged night time sleep during the critical period for SIDS. However, the role of sleep in the pathogenesis of SIDS is still obscure. Melatonin, the hormone produced at night from the pineal gland, has a regulatory role in the timing and maintenance of sleep in humans. The few studies that exist on the ontogeny of melatonin in infants indicate that the production of melatonin commences at about 12 weeks of age. Since the production of melatonin by the pineal is under the regulation of the biological clock in the suprachiasmatic nucleus in the brain via sympathetic neurotransmission, the development of the melatonin rhythm may thus be a useful diagnostic tool to detect delays in the development of sympathetic neurotransmission in the autonomous nervous system. Pineal gland size and blood melatonin levels were reported to be significantly reduced in SIDS victims compared to age-matched control non-SIDS victims.
In our research we have hypothesized that in infants with SIDS, the electrical stability of the heart is reduced. This is expressed as an inability of the QT interval to decrease sufficiently as heart rate increases. It is also hypothesized that a delayed ontogeny of melatonin is a challenge facing infants who are epidemiologically at risk for SIDS due to immature cardiac responses. Deficient pineal melatonin function has been found to be associated with abundance of REM sleep during the first three months of infancy. As REM sleep is frequently accompanied by bradytachycardia, melatonin deficiency may potentially increase the challenge to the electrical stability of the heart during prolonged sleep.
By examining the electrical stability of the heart using RR and QT analysis and by studying the ontogeny of the 24 hour melatonin rhythms in full-term healthy and near-SIDS infants during the first six months of life, we are elucidating whether either one or both of these parameters can be potentially used to screen a large population of infants during the first weeks of life for the risk of SIDS.
