Cocaine and development: mechanisms of fetal toxicity and neonatal consequences of prenatal cocaine exposure

Gingras, Jeannine L.; Weese‐Mayer, Debra E.; Hume, Roderick F.; O’Donnell, Karen

doi:10.1016/0378-3782(92)90011-5

Cited by 85 publications

(36 citation statements)

References 103 publications

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“…In fact, a growing body of evidence suggests that prenatal exposure to cocaine may have a significant impact on the development of regulatory processes in infants. These regulatory difficulties include poorer state regulation, more difficulty being calmed, increased physiological arousal, and differential physiological responding to sensory challenges, as measured by heart rate, heart rate variability, and cortisol levels, beginning in the neonatal period and persisting throughout the first year of life (Bard, Coles, Platzman, & Lynch, 2000;Bendersky & Lewis, 1998a,b;Brown, Bakeman, Coles, Sexson, & Demi, 1998a;DiPietro, Suess, Wheeler, Smouse, & Newlin, 1995;Gingras, Weese-Mayer, Hume, & O'Donnell, 1992;Karmel & Gardner, 1996;Mayes, Bornstein, Chawarska, & Granger, 1995;Mayes, Bornstein, Chawarska, & Granger, 1996;Regalado, Schechtman, Del Angel, & Bean, 1995;Regalado, Schechtman, Del Angel, & Bean, 1996;Schuetze & Eiden, 2006).…”

Section: Introductionmentioning

confidence: 99%

Prenatal cocaine and other substance exposure: Effects on infant autonomic regulation at 7 months of age

Schuetze

Eiden

Coles

2007

Developmental Psychobiology

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This study examined the association between prenatal exposure to cocaine and autonomic regulation at 7 months of age. Heart rate (HR) and respiratory sinus arrhythmia (RSA) were obtained from 154 (79 exposed, and 75 nonexposed) infants during baseline and tasks designed to elicit positive and negative affect. Cocaine-exposed infants had higher HR during the positive affect task. There was a significant suppression of RSA during the negative affect task for nonexposed infants but not for exposed infants. Fetal growth and maternal caregiving behavior did not mediate or moderate this association. These results provide additional support for an association between prenatal cocaine exposure and dysregulation during infancy.

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Section: Introductionmentioning

confidence: 99%

Prenatal cocaine and other substance exposure: Effects on infant autonomic regulation at 7 months of age

Schuetze

Eiden

Coles

2007

Developmental Psychobiology

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“…Whether the effects of cocaine on the developing brain are the consequence of prolonged episodes of hypoxia induced by this drug or result from a direct toxicity remains controversial (21,31). Cocaine can induce lasting contraction of the uterus and uterine arteries, thereby lowering the placental blood flow and the total oxygen supply to the fetus (reviewed in ref.…”

mentioning

confidence: 99%

Selective neuronal toxicity of cocaine in embryonic mouse brain cocultures.

Nassogne¹,

Evrard²,

Courtoy³

1995

Proc. Natl. Acad. Sci. U.S.A.

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Cocaine exposure in utero causes severe alterations in the development of the central nervous system. To study the basis of these teratogenic effects in vitro, we have used cocultures of neurons and glial cells from mouse embryonic brain. Cocaine selectively affected embryonic neuronal cells, causing first a dramatic reduction of both number and length of neurites and then extensive neuronal death. Scanning electron microscopy demonstrated a shift from a multipolar neuronal pattern towards bi-and unipolarity prior to the rounding up and eventual disappearance of the neurons. Selective toxicity of cocaine on neurons was paralleled by a concomitant decrease of the culture content in microtubuleassociated protein 2 (MAP2), a neuronal marker measured by solid-phase immunoassay. These effects on neurons were reversible when cocaine was removed from the culture medium. In contrast, cocaine did not affect astroglial cells and their glial fibrillary acidic protein (GFAP) content. Thus, in embryonic neuronal-glial cell cocultures, cocaine induces major neurite perturbations followed by neuronal death without affecting the survival of glial cells. Provided similar neuronal alterations are produced in the developing human brain, they could account for the qualitative or quantitative defects in neuronal pathways that cause a major handicap in brain function following in utero exposure to cocaine.

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“…It is precipitous to make any definitive statement; however, some physiologi- cal properties of phenytoin, cardiodepression and hypotension, for example (Danielson et al, 1992), may more severely affect the placental blood flow in some women and, as a consequence, interfere with normal fetal development, resulting in this rare malformation complex featuring gastroschisis and absence of one limb. Nevertheless, in utero exposure to cocaine could also result in vascular disruption; some evidence of it is gastroschisis and limb anomalies, as stated in the works by Viscarello et al (1992) and Gingras et al (1992). Through different means, cocaine and phenytoin may cause vascular disruption and, in this manner, induce some common malformations.…”

Section: Discussionmentioning

confidence: 99%

“…There appears to be an inverse association (as pregnancy progresses) between time of CVS and limb reduction defects (Firth, 1997). Several anomalies, like microcephaly (Volpe, 1992), limb reduction anomalies, gastroschisis, neural tube defects (Gingras et al, 1992), and body wall complex (Viscarello et al, 1992), have been detected in fetuses whose mothers used cocaine during pregnancy. All these abnormalities might also be associated with vascular disruption.…”

Section: Introductionmentioning

confidence: 99%

A case of prenatal diagnosis of fetal hydantoin syndrome by ultrasound

Gollop

Salzo

1999

Genet. Mol. Biol.

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Fetal hydantoin syndrome (FHS) is a set of disruptions occasionally present in fetuses exposed in utero to phenytoin or other anticonvulsants. Administration of phenytoin in early pregnancy may impair proper psychomotor performance expected for children's development. Several combined phenotypic markers delineate the syndrome, but the presence of single clinical signs is more common. There is controversy about the etiology of FHS. Associated disruptions may be related to a deficiency in a detoxifying enzyme (epoxide hydrolase), vascular problems, and/or factors not yet known. Genetic causes are believed to influence susceptibility to the drug. This text reports an unusual pattern of malformations detected in an ultrasound scan (gastroschisis, sacral meningomyelocele, and absence of the right lower limb) and in the anatomopathological study (left-side gastroschisis, sacral meningomyelocele, scoliosis, left clubfoot, absence of the right lower limb, and pectus carinatum) of a fetus whose mother took phenytoin. These defects may have been provoked by exposure to the drug during embryogenesis. In view of similar malformations observed in cases of prenatal exposure to cocaine, a recognized vasoconstrictor, it is suggested that vascular disruptions of hemodynamic origin constituted the event leading to some of the anomalies caused in the developing embryo. A complication of the chorionic villus sampling procedure, used for cytogenetic analysis, is another possibility.
A síndrome da hidantoína fetal consiste em um conjunto de disrupturas por vezes observadas em fetos expostos à fenitoína ou outros anticonvulsivos no período pré-natal. A administração de fenitoína em fase precoce da gravidez pode prejudicar o desempenho psicomotor esperado no desenvolvimento infantil. Diversos indicadores fenotípicos, em conjunto, caracterizam a síndrome, mas a presença de sinais clínicos isolados é mais comum. Há controvérsia quanto à sua etiologia. As disrupturas associadas podem estar relacionadas à deficiência de uma enzima desintoxicante (epóxide-hidrolase), a problemas vasculares e/ou a fatores ainda desconhecidos. Acredita-se haver causas genéticas conferindo susceptibilidade à substância. Este texto relata um padrão distinto de malformações detectadas no período pré-natal ao ultra-som (gastrosquise, meningomielocele sacral, escoliose, ausência do membro inferior direito), bem como posteriormente ao exame anatomopatológico (gastrosquise à esquerda, meningomielocele sacral, escoliose, pé esquerdo torto, ausência do membro inferior direito e pectus carinatum) de feto cuja mãe fez uso de fenitoína. Os defeitos podem ter se originado da exposição à droga durante a embriogênese. Em vista de malformações semelhantes observadas em casos de exposição pré-natal à cocaína, um conhecido vasoconstritor, sugere-se que rupturas vasculares de origem hemodinâmica constituíram o evento por trás de algumas das anomalias causadas no embrião em desenvolvimento. Uma complicação do procedimento de coleta de amostra de vilo corial utilizado para anál...

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Cocaine and development: mechanisms of fetal toxicity and neonatal consequences of prenatal cocaine exposure

Cited by 85 publications

References 103 publications

Prenatal cocaine and other substance exposure: Effects on infant autonomic regulation at 7 months of age

Prenatal cocaine and other substance exposure: Effects on infant autonomic regulation at 7 months of age

Selective neuronal toxicity of cocaine in embryonic mouse brain cocultures.

A case of prenatal diagnosis of fetal hydantoin syndrome by ultrasound

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