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Sudden Infant Death Syndrome
Is Serotonin the Key Factor?
in SIDS cases and begins to address the sex disparity in SIDSincidence. Recognizing that 5-HT influences a broad range of physiological systems including the regulation of breath- EUROPATHOLOGICAL STUDIES HAVE IDENTIFIED A KEYrole for the serotonin (5-hydroxytryptamine ing, the cardiovascular system, temperature, and the sleep- [5-HT]) pathways in sudden infant death syn- wake cycle, the study by Paterson et al4 extends the avail- drome (SIDS). Panigrahy et al1 reported a de- able literature in support of the underlying hypothesis that crease in 5-HT receptor binding in the arcuate nucleus, raphe´ SIDS is the result of 5-HT–mediated dysregulation of the au- obscurus, and other medullary regions that contain 5-HT cell bodies in SIDS cases in the United States. Similarly, Ozawa While the published neuropathological data are derived and Okado2 reported a decrease in 5-HT receptor binding from elegant studies, African American infants are one key in the dorsal nucleus of the vagus, solitary nucleus, and ven- group consistently underrepresented. Despite decreases in trolateral medulla in SIDS cases in Japan. Subsequently, Kin- the SIDS incidence in the United States with aggressive ney et al3 confirmed their prior observations of altered 5-HT Back to Sleep educational programs,5 the final 2003 receptor binding in medullary regions in Native American National Vital Statistics indicate a SIDS rate of 0.424 per Indians, a group at high risk for SIDS.
1000 live births for white infants but a rate of 1.152 per In this issue of JAMA, Paterson and colleagues4 report that 1000 live births for African American infants.6 These data “SIDS cases had a significantly higher number and density reflect a 2.7-fold higher incidence among African American of 5-HT neurons . . . and a significantly lower density of infants compared with white infants. Although this limita- tion of existing studies should not detract from the impor- 1A receptor binding sites . . . in regions of the medulla involved in homeostatic function compared with controls” tance of the results, and the study describing Native Ameri- and that “the density of [5-HT transporter] binding rela- can infants3 does represent an at-risk study population, it tive to the number of 5-HT neurons in the medulla was sig- suggests a need for expansion of the populations for future nificantly lower in SIDS cases compared with controls.” Fur- neuropathological studies from the primarily white and ther, Paterson et al4 demonstrate that male infants who Hispanic infants recruited from San Diego1,4 to those who more specifically represent the ethnicities of those who suc- sity in the raphe´ obscurus compared with female infants.
Taken together, the evidence strongly supports extensiveabnormalities in the 5-HT neuropathology of the medulla Author Affiliation: Department of Pediatrics, Pediatric Respiratory Medicine, Rush
University Medical Center, Chicago, Ill.
Corresponding Author: Debra Ellyn Weese-Mayer, MD, Department of Pediat-
See also p 2124.
rics, Pediatric Respiratory Medicine, Rush University Medical Center, 1653 W Con-gress Pkwy, Chicago, IL 60612 ([email protected]).
2006 American Medical Association. All rights reserved.
(Reprinted) JAMA, November 1, 2006—Vol 296, No. 17 2143
One solution is for medical examiners in regions with more bedding materials, overheating, and exposure to prenatal representative ethnicity for SIDS to join forces in provid- and postnatal cigarette smoke should be avoided. Despite ing autopsy specimens for neuropathological researchers.
remarkable progress made nationally in compliance with An alternative solution is to encourage development of young these known modifiable risk factors for SIDS, it is discour- neuropathological investigators (particularly in universi- aging that 65% of the infants who succumbed to SIDS in ties serving ethnically diverse populations, including Afri- the study by Paterson et al were in the prone or side sleep- can Americans) to pursue the study of SIDS in their own ing position at the time of death. These results emphasize laboratories. In so doing, the next generation of neuropatho- the critical need for reintroduction of the Back to Sleep cam- logical scientists studying SIDS will be secured, and infants paign to educate parents and caretakers of young infants.
more representative of the SIDS population can be in- Alternatively, it may be time to introduce more innovative interventions that focus on the different ethnic groups af- Another key concern is the limited sample sizes for SIDS cases and controls in the published neuropathological stud- While the neuropathological studies in SIDS are provid- ies. The opportunity to perform these important studies is ing remarkable insight into the underlying mechanisms in dependent on access to the neuropathological tissue. That the 5-HT pathways, identification of the definitive cause for access has been made possible, in part, under a California SIDS will necessitate an expanded network of scientists and law7 that renders it unnecessary to obtain informed con- families working together toward the shared goal. They can sent from individual parents if tissue samples from their child join forces to influence legislation in their own states to rep- are to be used for research on sudden and unexpected in- licate the success of the California program. Likewise, cli- fant death. This statute was visionary and has allowed for nicians and researchers can gently inform parents who have remarkable progress in understanding the neuropathology lost an infant to SIDS about autopsy and the opportunity of SIDS. If it were possible for more states to follow the lead for their lost infant to contribute to the further understand- of California, sample size and ethnic diversity for these es- ing of SIDS. With 2162 infants dying from SIDS in the United sential SIDS studies would be expanded, controls could be States in 2003,6 there is no time to lose in determining if matched in a 1:1 ratio with SIDS cases, and the desperately serotonin is the key factor in the pathophysiology of SIDS.
sought answers as to why SIDS continues to occur mightbe elucidated at a faster pace.
Financial Disclosures: None reported.
Currently, controls used in the neuropathological stud- ies have typically died from a preceding illness or disease.
Because of the possibility that current controls had an un- REFERENCES
derlying susceptibility that increased their vulnerability to 1. Panigrahy A, Filiano J, Sleeper LA, et al. Decreased serotonergic receptor bind-
that illness, to death, or both, or that sequelae from the ill- ing in rhombic lip-derived regions of the medulla oblongata in the sudden infantdeath syndrome. J Neuropathol Exp Neurol. 2000;59:377-384.
ness might affect their neuropathological findings, it seems 2. Ozawa Y, Okado N. Alteration of serotonergic receptors in the brainstems of
possible that the reported controls may not reflect the “nor- human patients with respiratory disorders. Neuropediatrics. 2002;33:142-149.
3. Kinney HC, Randall LL, Sleeper LA, et al. Serotonergic brainstem abnormalities
mal” condition. By broadening geographic sources, more con- in Northern Plains Indians with the sudden infant death syndrome. J Neuropathol trols who died from trauma or other unintended events with- Exp Neurol. 2003;62:1178-1191.
4. Paterson DS, Trachtenberg FL, Thompson EG, et al. Multiple serotonergic brain-
out antecedent illness may be included.
stem abnormalities in sudden infant death syndrome. JAMA. 2006;296:2124-2132.
As Paterson et al4 clearly explain, data on infants in their 5. American Academy of Pediatrics Task Force on Sudden Infant Death Syndrome.
The changing concept of sudden infant death syndrome: diagnostic coding shifts,
study were collected after the successful implementation of controversies regarding the sleep environment, and new variables to consider in the Back to Sleep message recommending that infants reducing risk. Pediatrics. 2005;116:1245-1255.
younger than 1 year should be placed on their backs to sleep, 6. Hoyert DL, Heron MP, Murphy SL, Kung H-C. Death: final data from 2003.
Natl Vital Stat Rep. 2006;54:99.
that they should be sleeping on firm surfaces, and that soft 7. California Law Chapter 955, Statutes of 1989 (SB 1069).
2144 JAMA, November 1, 2006—Vol 296, No. 17 (Reprinted)
2006 American Medical Association. All rights reserved.

Source: http://s127133077.onlinehome.us/images/reading_material/Weese-Mayer.JAMA5HTeditorial.2006.pdf

Journal 30(2) 2009.pmd

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