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This section is being revised with new Publicantions to be added to those remaining below.

1. Ostfeld BM, Esposito L, Perl H, Hegyi T. (2010) Concurrent risks in sudden infant death syndrome. Pediatrics. March; 125(3):447-453.


BACKGROUND: Despite improved education on safe sleep, infants are still exposed to multiple risks for sudden infant death syndrome (SIDS). Variability among health care providers continues to exist regarding knowledge of risk factors and the provision of education to caregivers. OBJECTIVE: To enhance the content and delivery of SIDS risk-reduction initiatives by physicians and other health care providers and to provide them with a context for evaluating their discussions of risks and compensatory strategies, we sought to raise awareness of the frequency of risk factors in SIDS cases, patterns of co-occurrence, associations between modifiable and nonmodifiable risks, and the rarity of cases without risk. DESIGN and METHODS: In a population-based retrospective review of 244 (97%) New Jersey SIDS cases (1996–2000), we assessed the frequencies and co-occurrences of modifiable (maternal and paternal smoking, nonsupine sleep or prone status at discovery, bed-sharing, or scene risks) and nonmodifiable (upper respiratory infection or <37 weeks' gestational age) risks. RESULTS: Nonsupine sleep occurred in 70.4% of cases with data on position (159 of 226). Thirteen cases were of infants who were discovered prone, with an increased positional risk to 76.1%, in which 87% contained additional risks. Maternal smoking occurred in 42.6% (92 of 216) of the cases with data on this risk, and 98% among those cases had additional risks. At least 1 risk was found in 96% of the cases, and 78% had 2 to 7 risks. Of the 9 of 244 risk-free cases (3.7%), 7 lacked data on 2 to 5 risks per case. On the basis of the complete data, only 2 (0.8%) of all 244 cases were risk free. When nonmodifiable risks were excluded, 5.3% of the cases met this definition. CONCLUSIONS: Risk-free and single-risk SIDS cases are rare, and most contain multiple risks. Parent education should be comprehensive and address compensatory strategies for nonmodifiable risks.

2. Jhodie R. Duncan, PhD; David S. Paterson, PhD; Jill M. Hoffman, BS; David J. Mokler, PhD; Natalia S. Borenstein, MS; Richard A. Belliveau, BA; Henry F. Krous, MD; Elisabeth A. Haas, BA; Christina Stanley, MD; Eugene E. Nattie, MD; Felicia L. Trachtenberg, PhD; Hannah C. Kinney, MD (2010) Brainstem Serotonergic Deficiency in Sudden Infant Death Syndrome JAMA. Feb, 303(5):430-437.


BACKGROUND:  Sudden infant death syndrome (SIDS) is postulated to result from abnormalities in brainstem control of autonomic function and breathing during a critical developmental period. Abnormalities of serotonin (5-hydroxytryptamine [5-HT]) receptor binding in regions of the medulla oblongata involved in this control have been reported in infants dying from SIDS. OBJECTIVE: To test the hypothesis that 5-HT receptor abnormalities in infants dying from SIDS are associated with decreased tissue levels of 5-HT, its key biosynthetic enzyme (tryptophan hydroxylase [TPH2]), or both. DESIGN, SETTING AND PARTICIPANTS: Autopsy study conducted to analyze levels of 5-HT and its metabolite, 5-hydroxyindoleacetic acid (5-HIAA); levels of TPH2; and 5-HT1A receptor binding. The data set was accrued between 2004 and 2008 and consisted of 41 infants dying from SIDS (cases), 7 infants with acute death from known causes (controls), and 5 hospitalized infants with chronic hypoxia-ischemia. MAIN OUTCOME MEASURES:  Serotonin and metabolite tissue levels in the raphé obscurus and paragigantocellularis lateralis (PGCL); TPH2 levels in the raphé obscurus; and 5-HT1A binding density in 5 medullary nuclei that contain 5-HT neurons and 5 medullary nuclei that receive 5-HT projections. RESULTS: Serotonin levels were 26% lower in SIDS cases (n = 35) compared with age-adjusted controls (n = 5) in the raphé obscurus (55.4 [95% confidence interval {CI}, 47.2-63.6] vs 75.5 [95% CI, 54.2-96.8] pmol/mg protein, P = .05) and the PGCL (31.4 [95% CI, 23.7-39.0] vs 40.0 [95% CI, 20.1-60.0] pmol/mg protein, P = .04). There was no evidence of excessive 5-HT degradation assessed by 5-HIAA levels, 5-HIAA:5-HT ratio, or both. In the raphé obscurus, TPH2 levels were 22% lower in the SIDS cases (n = 34) compared with controls (n = 5) (151.2% of standard [95% CI, 137.5%-165.0%] vs 193.9% [95% CI, 158.6%-229.2%], P = .03). 5-HT1A receptor binding was 29% to 55% lower in 3 medullary nuclei that receive 5-HT projections. In 4 nuclei, 3 of which contain 5-HT neurons, there was a decrease with age in 5-HT1A receptor binding in the SIDS cases but no change in the controls (age x diagnosis interaction). The profile of 5-HT and TPH2 abnormalities differed significantly between the SIDS and hospitalized groups (5-HT in the raphé obscurus: 55.4 [95% CI, 47.2-63.6] vs 85.6 [95% CI, 61.8-109.4] pmol/mg protein, P = .02; 5-HT in the PGCL: 31.4 [95% CI, 23.7-39.0] vs 71.1 [95% CI, 49.0-93.2] pmol/mg protein, P = .002; TPH2 in the raphé obscurus: 151.2% [95% CI, 137.5%-165.0%] vs 102.6% [95% CI, 58.7%-146.4%], P = .04). CONCLUSION: Compared with controls, SIDS was associated with lower 5-HT and TPH2 levels, consistent with a disorder of medullary 5-HT deficiency.

3. Moon RY, Horne RS, Hauck FR. (2007). Sudden infant death syndrome. Lancet. Nov 3; 370 (9598): 1578-87.


Despite declines in prevalence during the past two decades, sudden infant death syndrome (SIDS) continues to be the leading cause of death for infants aged between 1 month and 1 year in developed countries. Behavioural risk factors identified in epidemiological studies include prone and side positions for infant sleep, smoke exposure, soft bedding and sleep surfaces, and overheating. Evidence also suggests that pacifier use at sleep time and room sharing without bed sharing are associated with decreased risk of SIDS. Although the cause of SIDS is unknown, immature cardiorespiratory autonomic control and failure of arousal responsiveness from sleep are important factors. Gene polymorphisms relating to serotonin transport and autonomic nervous system development might make affected infants more vulnerable to SIDS. Campaigns for risk reduction have helped to reduce SIDS incidence by 50-90%. However, to reduce the incidence even further, greater strides must be made in reducing prenatal smoke exposure and implementing other recommended infant care practices. Continued research is needed to identify the pathophysiological basis of SIDS.

4. Esposito L, Hegyi T, Ostfeld BM.(2007) Educating parents about the risk factors of sudden infant death syndrome: the role of neonatal intensive care unit and well baby nursery nurses. Journal of Perinatal and Neonatal Nursing. Apr-Jun; 21(2):158-64.


Nurses in newborn nurseries and neonatal intensive care units are instrumental in educating parents about reducing the risk for SIDS. Nurse participation is acknowledged and encouraged in the current policy statement on SIDS Risk Reduction put forth by the American Academy of Pediatrics. Despite the decline in SIDS, it remains the leading cause of postneonatal infant mortality, and despite greater public compliance with the risk reduction guidelines there is room for improvement in how effectively and consistently they are disseminated. To facilitate nursing participation as educators, role models, and collaborators in the development of relevant hospital policies and procedures, we review the current recommendations, addressing issues that may serve as barriers to participation, describing the biological plausibility underlying risk-reducing practices, and presenting resources from which nurses may obtain teaching materials and model policies.

5. Ostfeld BM, Hegyi T, Denk C. Newborn sleep positions and SIDS Risk. New Jersey Department of heath and Senior Services, 2007,

6. Ostfeld BM, Perl H, Esposito L, Hempstead K, Hinnen R, Sandler A, Pearson PG, Hegyi T. (2006) Sleep environment, positional, lifestyle, and demographic characteristics associated with bed sharing in sudden infant death syndrome cases: a population-based study. Pediatrics.  Nov; 118(5):2051-9.


BACKGROUND: In 2005, the American Academy of Pediatrics Task Force on Sudden Infant Death Syndrome recommended that infants not bed share during sleep. OBJECTIVE: Our goal was to characterize the profile of risk factors associated with bed sharing in sudden infant death syndrome cases. DESIGN/METHODS: We conducted a population-based retrospective review of sudden infant death syndrome cases in New Jersey (1996-2000) dichotomized by bed-sharing status and compared demographic, lifestyle, bedding-environment, and sleep-position status. RESULTS: Bed-sharing status was reported in 239 of 251 cases, with sharing in 39%. Bed-sharing cases had a higher percentage of bedding risks (44.1% vs 24.7%), exposure to bedding risks in infants discovered prone (57.1% vs 28.2%), and lateral sleep placement (28.9% vs 17.8%). The prone position was more common for bed-sharing and non-bed-sharing cases at placement (45.8% and 51.1%, respectively) and discovery (59.0% and 64.4%, respectively). In multivariable logistic-regression analyses, black race, mother <19 years, gravida >2, and maternal smoking were associated with bed sharing. There was a trend toward less breastfeeding in bed-sharing cases (22% vs 35%). In bed-sharing cases, those breastfed were younger than those who were not and somewhat more exposed to bedding risks (64.7% vs 45.1%) but less likely to be placed prone (11.8% vs 52.9%) or have maternal smoking (33% vs 66%). CONCLUSIONS: Bed-sharing cases were more likely to have had bedding-environment and sleep-position risks and higher ratios of demographic and lifestyle risk factors. Bed-sharing subjects who breastfed had a risk profile distinct from those who were not breastfed cases. Risk and situational profiles can be used to identify families in greater need of early guidance and to prepare educational content to promote safe sleep.

7. Paterson DS, Trachtenberg FL, Thompson EG, Belliveau RA, Beggs AH, Darnall R, Chadwick AE, Krous HF, Kinney HC. Multiple serotonergic brainstem abnormalities in sudden infant death syndrome. JAMA. 2006 Nov 1;296 (17):2124-32 “Copyright © 2006, American Medical Association. All Rights reserved.”


CONTEXT: The serotonergic (5-hydroxytryptamine [5-HT]) neurons in the medulla oblongata project extensively to autonomic and respiratory nuclei in the brainstem and spinal cord and help regulate homeostatic function. Previously, abnormalities in 5-HT receptor binding in the medullae of infants dying from sudden infant death syndrome (SIDS) were identified, suggesting that medullary 5-HT dysfunction may be responsible for a subset of SIDS cases. OBJECTIVE: To investigate cellular defects associated with altered 5-HT receptor binding in the 5-HT pathways of the medulla in SIDS cases. DESIGN, SETTING, AND PARTICIPANTS: Frozen medullae from infants dying from SIDS (cases) or from causes other than SIDS (controls) were obtained from the San Diego Medical Examiner's office between 1997 and 2005. Markers of 5-HT function were compared between SIDS cases and controls, adjusted for postconceptional age and postmortem interval. The number of samples available for each analysis ranged from 16 to 31 for SIDS cases and 6 to 10 for controls. An exploratory analysis of the correlation between markers and 6 recognized risk factors for SIDS was performed. MAIN OUTCOME MEASURES: 5-HT neuron count and density, 5-HT(1A) receptor binding density, and 5-HT transporter (5-HTT) binding density in the medullary 5-HT system; correlation between these markers and 6 recognized risk factors for SIDS. RESULTS: Compared with controls, SIDS cases had a significantly higher 5-HT neuron count (mean [SD], 148.04 [51.96] vs 72.56 [52.36] cells, respectively; P<.001) and 5-HT neuron density (P<.001), as well as a significantly lower density of 5-HT(1A) receptor binding sites (P < or=.01 for all 9 nuclei) in regions of the medulla involved in homeostatic function. The ratio of 5-HTT binding density to 5-HT neuron count in the medulla was significantly lower in SIDS cases compared with controls (mean [SD], 0.70 [0.33] vs 1.93 [1.25] fmol/mg, respectively; P = .001). Male SIDS cases had significantly lower 5-HT(1A) binding density in the raphé obscurus compared with female cases (mean [SD], 16.2 [2.0] vs 29.6 [16.5] fmol/mg, respectively; P = .04) or with male and female controls combined (mean [SD], 53.9 [19.8] fmol/mg; P = .005). No association was found between 5-HT neuron count or density, 5-HT(1A) receptor binding density, or 5-HTT receptor binding density and other risk factors. CONCLUSIONS: Medullary 5-HT pathology in SIDS is more extensive than previously delineated, potentially including abnormal 5-HT neuron firing, synthesis, release, and clearance. This study also provides preliminary neurochemical evidence that may help explain the increased vulnerability of boys to SIDS.

8. Ostfeld BM, Esposito L, Straw D, Burgos J, Hegyi T. (2005) An inner-city school-based program to promote early awareness of risk factors for Sudden Infant Death Syndrome. Journal of Adolescent Health. 2005 Oct; 37(4):339-41


Adolescent, nonwhite women with less than high school education have infants at higher risk for Sudden Infant Death Syndrome (SIDS) but face barriers to risk reduction education. We implemented a novel school-based health education program (grades 4 to 12) and found an association between exposure and awareness of risk factors.