Brain stem abnormalities linked to SIDS, study shows

[Amish Country]

Fair use:

Brain stem abnormalities linked to SIDS, study shows
Published November 12, 2013 /
FoxNews.com

Underlying brain stem abnormalities may be responsible for the onset of sudden infant death syndrome (SIDS), a condition that causes babies to die unexpectedly in their sleep, Counsel and Heal reported.

In a study published in the journal Pediatrics, researchers reviewed the cases of 50 infants who died of SIDS. Though some of the infants studied were sleeping in unsafe environments – such as in a face-down position– the researchers discovered that regardless of sleep conditions, all of the babies studied showed abnormalities in their brain stem chemicals.

The researchers believe that these abnormalities prevented the infants from waking up when they experienced trouble breathing. However, the researchers said parents should still make every effort to ensure that their infants sleep in a safe environment.

“We have to find ways to test for this underlying vulnerability in living babies and then to treat it. Our team is focused now upon developing such a test and treatment,” said study author Dr. Hannah Kinney, a neuropathologist at Boston Children’s Hospital. “Safe sleep practices absolutely remain important, so these infants are not put in a potentially asphyxiating situation that they cannot respond to.”

http://www.foxnews.com/health/2013/11/12/brain-stem-abnormalities-linked-to-sids-study-shows/

 

[Emily]

Re: Brain stem abnormalities linked to SIDS, study shows

This is an article by the same researcher with insight into SIDS prevention:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3268259/

Annu Rev Pathol. Author manuscript; available in PMC 2012 January 30.
Published in final edited form as:
Annu Rev Pathol. 2009; 4: 517?550.
doi: 10.1146/annurev.pathol.4.110807.092322
PMCID: PMC3268259
NIHMSID: NIHMS347951
The Brainstem and Serotonin in the Sudden Infant Death Syndrome
Hannah C. Kinney,1 George B. Richerson,2 Susan M. Dymecki,3 Robert A. Darnall,4,5 and Eugene E. Nattie5
...
SUMMARY POINTS

The brainstem hypothesis in SIDS states that a majority of SIDS cases are due to a defect in brainstem-mediated protective responses to homeostatic stressors during sleep in a critical developmental period.
The brainstem hypothesis in SIDS is supported by several lines of evidence, including independent reports of subtle brainstem findings in SIDS cases at autopsy and reports of cardiorespiratory and arousal (subclinical) deficits in infants who subsequently die of SIDS, which are consistent with brainstem dysfunction.
The most reproducible and robust neurochemical findings in the SIDS brainstems studied to date involve abnormalities in the medullary 5-HT system, as detected by immunocytochemical, quantitative cellular, and tissue autoradiographic methods in brainstem tissues specially prepared at the time of autopsy.
Extensive experimental analysis indicates that the medullary 5-HT system is critical for the modulation and integration of a variety of homeostatic functions (e.g., respiration, chemosensitivity, autoresuscitation, blood pressure, temperature) that are state and age dependent, and underscores the possibility that deficits in this system could lead to sleep-related sudden death under stress in a critical developmental period.
State-of-the-art genetic mapping studies indicate that different subpopulations of 5-HT neurons originate from different progenitor pools in the embryonic brainstem, underscoring the possibility that these different populations may mediate different homeostatic functions.
A prenatal origin of medullary 5-HT abnormalities in SIDS is suggested by (a) the finding of deficits in the regulation of 5-HT cell number and differentiation in the medullae of affected cases, (b) epidemiologic data indicating that prenatal adverse exposures (e.g., alcohol and cigarette smoke/nicotine) are major risk factors for SIDS, and (c) autopsy data showing that prenatal exposure to cigarette smoke is associated with reduced 5-HT receptor binding in the arcuate nucleus in the postnatal period, irrespective of the cause of death...

Unfortunately the state I live in has used only a small fraction of money they got from the big lawsuit against tobacco companies for prevention and education.

There's some research being done on mitigating the effects of prenatal nicotine exposure:

Prenatal nicotine exposure in rhesus monkeys compromises development of brainstem and cardiac monoamine pathways involved in perinatal adaptation and sudden infant death syndrome: Amelioration by Vitamin C

It would be good if the research translated into a human application that prevented brain damage to fetuses exposed to smoking.