Relationship of maternal substance abuse to subsequent sudden infant death syndrome in offspring

Kandall, Stephen R.; Gaines, Judith; Habel, Leo; Davidson, Georgia K.; Jessop, Dorothy Jones

doi:10.1016/s0022-3476(05)81554-9

Cited by 153 publications

(74 citation statements)

References 18 publications

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“…Abnormal respiratory control caused by chronic drug use has long been presumed to be the leading cause of an increased risk of sudden infant death syndrome [20,21]. Recent evidence shows that SIDS may result from a combination of prenatal vulnerability, postnatal stress and a critical developmental stage and may be caused by defiencies in breathing, autonomic and sleep-wake control [8].…”

Section: Discussionmentioning

confidence: 99%

“…In human infants, the methadone-induced neonatal abstinence syndrome (NAS) is characterized by hyperexcitability [46], abnormal REM sleep [17], increased sleep apnea [44], respiratory alkalosis [9], decreased sensitivity to hypercapnia [43], diarrhea, fever and central nervous system irritability, which in severe cases progresses to seizures [13]. In addition, opioid exposed infants are smaller at birth and have an increased incidence of sudden infant death syndrome (SIDS), which may in part be due to abnormal respiratory control [20,21].…”

Section: Introductionmentioning

confidence: 99%

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Respiratory effects of chronic in utero methadone or morphine exposure in the neonatal guinea pig

Nettleton¹,

Wallisch²,

Olsen³

2008

Neurotoxicology and Teratology

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This study uses a neonatal guinea pig model to compare the effects of in utero methadone or morphine exposure upon breathing control. We hypothesize that in utero methadone exposure will result in similar respiratory disturbances to those seen in morphine exposed neonates, but that the onset will be slower and the duration longer, due to methadone's longer elimination half-life. Pregnant DunkinHartley guinea pigs received once-daily injections of methadone, morphine, or vehicle (saline) during the last half of gestation and pups were studied 3, 7, or 14 days after birth. In utero methadone or morphine exposure resulted in decreased birth weight compared to vehicle, and pups experienced a withdrawal syndrome which included increased locomotor activity and respiratory disturbances but no change in rectal temperature. Both opioid exposures increased inspiratory minute ventilation during CO 2 challenge at 3 days after birth, but only in morphine exposed pups was this withdrawal effect still present on day 7. Surprisingly, only morphine exposure increased inspiratory minute ventilation during room air breathing. We conclude that in utero methadone exposure is not equivalent to in utero morphine exposure. With respect to neonatal respiratory control, methadoneinduced changes in respiration are only apparent during hypercapnia.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Respiratory effects of chronic in utero methadone or morphine exposure in the neonatal guinea pig

Nettleton¹,

Wallisch²,

Olsen³

2008

Neurotoxicology and Teratology

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“…These experimental observations have a human correlate. Infants that have been exposed to antidepressants or cocaine prenatally have a higher incidence of sudden infant death syndrome and autonomic disturbances, which appear to be due to a delayed maturation of noradrenergic neurons in the locus ceruleus and in the autonomic nervous system (Kandall et al, 1993;Hill and Tennyson, 1986). Surprisingly, NET is expressed ubiquitously in nonadrenergic neurons and in nonneuronal cells both in the avian and mammalian embryos, as determined by immunohistochemistry, in situ hybridization, and reverse transcriptase polymerase chain reaction (RT-PCR) (Ren et al, 2001(Ren et al, , 2003.…”

Section: A Role Of the Norepinephrine Transporter (Net) In Heart Devementioning

confidence: 99%

Cardiac neural crest stem cells

Sieber‐Blum

2003

Anat. Rec.

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Whereas the heart itself is of mesodermal origin, components of the cardiac outflow tract are formed by the neural crest, an ectodermal derivative that gives rise to the peripheral nervous system, endocrine cells, melanocytes of the skin and internal organs, and connective tissue, bone, and cartilage of the face and ventral neck, among other tissues. Cardiac neural crest cells participate in the septation of the cardiac outflow tract into aorta and pulmonary artery. The migratory cardiac neural crest consists of stem cells, fate-restricted cells, and cells that are committed to the smooth muscle cell lineage. During their migration within the posterior branchial arches, the developmental potentials of pluripotent neural crest cells become restricted. Conversely, neural crest stem cells persist at many locations, including in the cardiac outflow tract. Many aspects of neural crest cell differentiation are driven by growth factor action. Neurotrophin-3 (NT-3) and its preferred receptor, TrkC, play important roles not only in nervous system development and function, but also in cardiac development as deletion of these genes causes outflow tract malformations. In vitro clonal analysis has shown a premature commitment of cardiac neural crest stem cells in TrkC null mice and a perturbed morphology of the endothelial tube. Norepinephrine transporter (NET) function promotes the differentiation of neural crest stem cells into noradrenergic neurons. Surprisingly, many diverse nonneuronal embryonic tissues, in particular in the cardiovascular system, express NET also. It will be of interest to determine whether norepinephrine transport plays a role also in cardiovascular development. Anat Rec Part A 276A: 34 -42, 2004.

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“…12 However, the prevalence of sudden infant death syndrome (SIDS) is known to be higher in drug-exposed infants, with the highest rates in those exposed to opiates even when we control for prematurity, LBW, and perinatal infections such as HIV. 13,14 There is no evidence linking SIDS and CSTS failure, but the link between opiate exposure and SIDS does raise concern that opiate exposure may have adverse effects on cardiorespiratory status in neonates.…”

Section: Discussionmentioning

confidence: 99%

Car Seat Screening for Low Birth Weight Term Neonates

Davis

2015

Pediatrics

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BACKGROUND AND OBJECTIVE: Car seat tolerance screening (CSTS) is a common predischarge assessment of neonates. Almost half of nurseries and NICUs have low birth weight (LBW, ,2.5 kg) as an inclusion criterion, regardless of birth gestational age (GA). Little is known about the epidemiology of CSTS in this cohort. The objective of this study was to identify incidence and risk factors for CSTS failure in term LBW infants.

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Relationship of maternal substance abuse to subsequent sudden infant death syndrome in offspring

Cited by 153 publications

References 18 publications

Respiratory effects of chronic in utero methadone or morphine exposure in the neonatal guinea pig

Respiratory effects of chronic in utero methadone or morphine exposure in the neonatal guinea pig

Cardiac neural crest stem cells

Car Seat Screening for Low Birth Weight Term Neonates

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