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Central respiratory pattern deficiency

 

Ongoing research in the pediatric/neonatal community has begun to associate apnea-like breathing cessations in animal models with unusual neural architecture or signal transduction in central pattern generator circuits, including the pre-Bötzinger complex.[37]

 

Cervical spinal injury from birth trauma

 

During birth, if the infant's head is traumatically turned side to side, upper cervical spinal injury can result. Difficulty breathing is a classic sign of upper spinal cord and brainstem injury.[38] When infants with undiagnosed upper cervical spinal cord injury are continually placed on their stomachs for sleep, they are forced to turn their heads to the side to breathe.

 

Child abuse

 

Several instances of infanticide have been uncovered where the diagnosis was originally SIDS.[7][8] This has led some researchers to estimate that 5% to 20% of SIDS deaths are actually infanticides.[39][40][41][42] In 1997 The New York Times, covering the book The Death of Innocents: A True Story of Murder, Medicine and High-Stakes Science, wrote:

 

The misdiagnosis of infanticide as SIDS "happens all over," Ms. Talan, a medical reporter at Newsday, said. "A lot of doctors and police don't know how to handle it. They don't take it as seriously as they should." As a result of the book's revelations, people are starting to scrutinize possible cases of this "perfect crime," which involves no physical evidence and no witnesses.[43]

 

A United Kingdom pediatrician, Roy Meadow believes that many cases diagnosed as SIDS are really the result of child abuse on the part of a parent. During the 1990s and early 2000s, a number of mothers of multiple apparent SIDS victims were convicted of homicide to various extents, on the basis of Meadow's opinion. In 2003 a number of high-profile acquittals brought Meadow's theories into disrepute. Several hundred murder convictions were reviewed, leading to several high-profile cases being reopened and convictions overturned. Meadow's medical license was revoked in 2005,[44] after which he appealed to the High Court, which ruled in his favour in February 2006. The General Medical Council appealed to the Court of Appeal and in October 2006 by a majority decision, with the Master of the Rolls, Sir Anthony Clarke, dissenting, the Court of Appeal upheld the decision of the High Court in part, ruling that Meadow's misconduct was not sufficiently serious to merit the punishment which he had received.

 

The Royal Statistical Society issued a media release refuting the expert testimony in one UK case in which the conviction was subsequently overturned.[45]

 

Genetics

 

There is a consistent 50% male excess in SIDS per 1000 live births of each sex. Given a 5% male excess birth rate, there appears to be 3.15 male SIDS cases per 2 female, for a male fraction of 0.61.[3][4] This value of 61% in the US is an average of 57% black male SIDS, 62.2% white male SIDS and 59.4% for all other races combined. Note that when multiracial parentage is involved, infant "race" is arbitrarily assigned to one category or the other; most often it is chosen by the mother. The X-linkage hypothesis for SIDS and the male excess in infant mortality have shown that the 50% male excess could be related to a dominant X-linked allele, occurring with a frequency of 1⁄3 that is protective of transient cerebral anoxia. An unprotected XY male would occur with a frequency of 2⁄3 and an unprotected XX female would occur with a frequency of 4⁄9. The ratio of 2⁄3 to 4⁄9 is 1.5 to 1, which matches the observed male 50% excess rate of SIDS.



 

Although many researchers have found autosomal and mitochondrial genetic risk factors for SIDS, they cannot explain the male excess because such gene loci have the same frequencies for males and females. Supporting evidence for an X-linkage is found by examining other causes of infant respiratory death, such as suffocation by inhalation of food or other foreign objects. Although food is prepared identically for male and female infants, there is a similar 50% male excess of death from such causes, indicating that males are more susceptible to the cerebral anoxia created by such incidents in exactly the same proportion as found in SIDS.[46][original research?]

 

The 2006 JAMA study which indicated a relationship between fewer serotonin binding sites and SIDS noted that the boys "had significantly fewer serotonin binding sites than girls",[33] but the authors could not reproduce that result in their 2010 paper.[34] This neurological imbalance decreases with age, but the increased male SIDS risk of approximately 61% persists throughout each month in the first year of life.[47] Furthermore, this cannot explain the identical male overrepresentation in other respiratory mortality causes, such as respiratory distress syndrome or suffocation from inhalation of food or foreign objects cited above, that also exists for ages of 1–14 years in the U.S. from 1979 to 2005.[15][original research?]

 

Inner ear damage

 

Records of hearing tests (oto-acoustic emissions/OAEs) administered to certain infants show that those who later died of SIDS had differences in the pattern of these tests compared with normal babies. The OAE signal-to-noise ratio was reduced in the right ears of SIDS babies (Rubens DD et al. Early Human Development 84, 225-9 (2008)).[48] It should be noted this was a small study (n=31 cases and 31 controls) with serious limitations (several significant factors were not controlled), and has been criticised from various perspectives.[49] The authors' suggestion for the cause of SIDS is that the deaths are caused by disturbances in respiratory control other than suffocation. The vestibular apparatus of the inner ear has been shown to play an important role in respiratory control during sleep; this inner ear damage could be linked to SIDS. The authors speculate that the damage occurs during delivery, particularly when prolonged contractions create greater blood pressure in the placenta. The right ear is directly in the "line of fire" for blood entering the fetus from the placenta, and thus could be more susceptible to damage. If the findings are relevant, it may be possible to take corrective measures. Researchers are beginning animal studies to explore the connection.[50]

 

Nitrogen dioxide

 

A 2005 study by researchers at the University of California, San Diego, found that "SIDS may be related to high levels of acute outdoor NO2 exposure during the last day of life."[51] While nitrogen dioxide (NO2) exposure may be one of many possible risk factors, it is not considered causal, and the report cautioned that further studies were needed to replicate the result.

 

Toxic gases

 

In 1989, a controversial piece of research by UK scientist Barry Richardson claimed that all cot deaths were the result of toxic nerve gases being produced through the action of fungus in mattresses on compounds of phosphorus, arsenic and antimony. These chemicals are frequently used to make mattresses fire-retardant.[citation needed]

 

Support for this hypothesis was based on the observation that the risk of cot death rises from one sibling to the next.[citation needed] Richardson claimed that parents are more likely to buy new bedding for their first child, and to reuse that bedding for later children. The more frequently used the bedding, the more chance that fungus has become resident in the material; thus, a higher chance of cot death. A paper by Peter Fleming and Peter Blair[52] references evidence from other studies that both supports and refutes the increasing occurrence of SIDS with mattress sharing, suggesting that this is still inconclusive.

 

Dr. Jim Sprott recommends new parents either buy bedding free of the toxic compounds or wrap the mattresses in a barrier film to prevent escape of the gases. Sprott claims that no case of cot death has ever been traced to a properly manufactured or wrapped mattress.[53]

 

However, a final report of "The Expert Group to Investigate Cot Death Theories: Toxic Gas Hypothesis", published in May 1998, concluded that "there was no evidence to substantiate the toxic gas hypothesis that antimony- and phosphorus-containing compounds used as fire retardants in PVC and other cot mattress materials are a cause of SIDS. Neither was there any evidence to believe that these chemicals could pose any other health risk to infants."[54] The report also states that "in normal cot-like conditions it is not possible to generate toxic gas from antimony in mattresses" and that "babies have also been found to die on wrapped mattresses."

 

According to Dr. Sprott, as of 2006, the New Zealand government has not reported any SIDS deaths when babies have slept on mattresses wrapped according to his method. While the Limerick report claims that babies have been found to die on wrapped mattresses, Dr. Sprott argues that a chemical analysis of the bedding should be performed. He additionally claims that this part of the report was flawed:

 

In February 2000 Dr. Peter Fleming (a co-author of the Limerick Report and principal author of the UK CESDI Report) conceded that the claim that three babies in the United Kingdom had died of cot death on polythene-covered mattresses could not be substantiated.[55]

 

Vaccination

 

Vaccination does not increase the risk of SIDS, and may reduce the risk slightly.[56][57]

 

According to the US Centers for Disease Control and Prevention:

 

From 2 to 4 months old, babies begin their primary course of routine vaccinations. This is also the peak age for sudden infant death syndrome (SIDS). The timing of these two events has led some people to believe they might be related. However, studies have concluded that vaccines are not a risk factor for SIDS.[57]

 

Vitamin C

 

In the 1970s, high doses of vitamin C were touted as a preventive measure for SIDS,[58] although the claim was controversial even then.[59][60] Subsequent studies failed to support a preventive role for vitamin C in SIDS.[61] To the contrary, a 2009 study found that high levels of vitamin C were strongly associated with SIDS, possibly through a pro-oxidant interaction with iron.[62]

 


Date: 2015-12-17; view: 618


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