Sudden infant death syndrome (SIDS) is a mysterious phenomena that has managed to confound science so far. SIDS is defined as the sudden death of any infant or young child that is unexpected by history and in which a thorough post mortem examination fails to demonstrate an adequate cause (Hunt & Brouillette, 1987). It is the leading cause of death in infants in developed countries occurring at a rate of almost 2 per 1000 births. It most often occurs in infants between the ages of one month and eight months with the highest occurrence in the 4-6 month range. Several behaviors have been associated with this syndrome such as prolonged sleep apnea, increased risk of breath inspiration pause, excessive periodic breathing, diminished ventilatory sensitivity to hypoxia, and impaired arousal response to hypoxia, but none of these have stood out as the definitive cause or as a screening device (Hunt & Brouillette, 1987). Instead it appears SIDS may be the result of a collection of factors that in the right circumstances results in infant death. This paper will examine some of the factors that appear to be associated with SIDS as well as some hypotheses on the cause.

Recent findings have shown that one cause of what has been labeled SIDS is suffocation or carbon dioxide rebreathing (Kemp et al, 1993). Technically this is not SIDS but it is often misdiagnosed as the cause of death if the physical scene is not examined, and it may also be a significant cause of SIDS. It seems that the practice of placing infants in the prone position, common in America and Europe, may be detrimental to the infant’s well-being. Studies of rabbits placed in this position on various surfaces have shown death to ensue as a result of expired air becoming trapped creating a rebreathing scenario, suffocating the animal (Ponsonby et al, 1993). The study also found that the type of surface contributed to this result with soft and natural fiber mattresses having higher incidence of suffocation than firm synthetic ones. These findings do not find a solution but do provide information on how some deaths attributed to SIDS may have been prevented by placing these infants on their sides or backs. It also raises the question as to why the infants do not arouse from the hypoxic state created, or react as is normal in older children and adults.

One hypothesis that for a long time received much focus, was that SIDS was the result of recurrent apneic episodes. Today this idea has been rejected as the main cause, as many infant’s first apneic experience results in death and many that experience frequent apneic episodes never die. Still it can not be eliminated as it is most likely an associated factor with SIDS, that in unison with others results in death.

The leading mechanism that is being examined now is the failure to arouse. Arousal from sleep is in all likelihood the most important defense mechanism against danger stimuli such as hypoxia or airway obstruction. It appears that this mechanism does not function properly resulting in the infant’s death. The brainstem is most likely involved somehow but the reasons for the failure to arouse are many.

One idea is that hypoxia creates the problem. Studies have shown that physical stimuli restricting breathing, such as airway obstruction, are a fairly strong stimulus for arousal. Hypoxia on the other hand appears to act as only a mild stimulus in infants. It was also found that repetitive exposure to hypoxia can lead to habituation in which the individual responds even less to the stimulus (Ward et al,1992). This may be the result of the hypoxia affecting the hypothalamus, which may facilitate arousal, by acting as a depressant. Another theory behind this, is that there is a deficiency in peripheral chemoreceptors, such as in the carotid body. It is not sure if it is the chemoreceptor which is at fault or if the neural pathway may be insufficient because of lack of myelination ,which has also been found.

Another theory is that SIDS infants have altered sleep patterns. It appears that these infants have more REM sleep leading to fewer movements during sleep, especially in the early morning hours when SIDS deaths most often occur. Included in this is a difficulty in reaching the awake state, which ties into a failure to arouse (Schechtman et al, 1992). This alteration in sleep may help explain some of the reasons why infants do not adjust when in a position that is conducive to rebreathing as occurring during REM, the body is often paralyzed to prevent injury during dreams.

A final reason for the failure to arouse may be neurochemical in nature. High amounts of GABA, an inhibitory neurotransmitter, has been found in the cerebral spinal fluid and brains of SIDS infants. In addition the levels of excitatory neurotransmitters such as aspartate have been found to be low in infants (Lagercrantz & Ranold, 1991). These two factors may work by there not being enough excitation elicited when a stimulus is detected to trigger the arousal response, or that the large presence of inhibitory neurotransmitters suppresses the response leading to a larger chance that the need to arouse will not be met. Another neurotransmitter that is found in large quantities is dopamine, which has been found to suppress the response of the peripheral chemoreceptors. A hypoxic state may be detected but it is not relayed to the brain, resulting in death.

Another area of interest in SIDS, is that it may be caused by a problem in development. This idea is supported in part by the fact most deaths occur in the first six months. One study found that there is delayed myelination in pathways concerned with arousal and cardiorespiratory functions (Kinney et al, 1991). This lack of myelin would cause a failure in the proper conduction of signals along these pathways. The study also found myelin abnormalities in the visceromotor regions of the cerebellum and prefrontal-temporal-limbic systems, which may lead some research away from the brain stem to higher centers of the brain which have been ignored. Yet another study found that in about one half of the SIDS cases it examined, there was an abnormal proliferation of astroglial fibers in the lateral reticular formation of the medulla and also hypomyelination present (Naeye et al). The astroglial fibers are basically scar tissue in the brain, leading to the conclusion that development never finished in this location which is associated with the wake state. They also found there were deficits in the hypoglossal nucleus which would lead to lack of tongue control and may contribute to airway obstruction which has been postulated as a cause of death in SIDS cases.

Most of the ideas concerning SIDS are related to the idea of a failure to arouse. The main problem is trying to identify why this failure occurs. The idea of rebreathing or suffocation causing many deaths when taken with the other ideas presented. The infant in the prone position has itself in a dangerous situation which because of problems in its ability to arouse or adjust position lead to its inability to overcome hypoxia episodes and it succumbs. This failure may be due an excess or lack of specific neurotransmitters, delayed myelination, or developmental abnormalities, with all having an equal chance of being responsible.

It is hard to believe that SIDS is caused by one phenomena, but instead it is the additive result of various small things that happen to be present at the same time. This presents problems for treatment and/or prevention, as many different responses would be needed and would the correct one be given. Evidence has shown that sleeping in the prone position can lead to suffocation and hypoxia. This should be used to change the patterns of child placement to at least try to eliminate this factor. This won’t end SIDS, but may remove some cases while science tries its best to find a clear cut cause, or at least a way to identify accurately those at greatest risk, and eventually a preventative method.

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