Prenatal cocaine exposure
[2] Pregnant mothers who use cocaine often use other drugs in addition, may be malnourished and lacking in medical care, are at risk of violence, and may neglect their children.
Factors such as poverty that are frequently associated with PCE have a much stronger influence on children's intellectual and academic abilities than does exposure to cocaine in isolation.
[7] Studies focusing on children of six years and younger have not shown any direct, long-term effects of PCE on language, growth, or development as measured by test scores.
[8] Early studies reported that people who had been exposed to crack in utero would be severely emotionally, mentally, and physically disabled; this belief became common in the scientific and lay communities.
[10][11] Early studies in the mid-1980s reported that cocaine use in pregnancy caused children to have severe problems, including cognitive, developmental, and emotional disruption.
[12] These early studies had methodological problems, including small sample size, confounding factors such as poor nutrition, and use of other drugs by the mothers.
[7] Charles Krauthammer, a columnist for The Washington Post wrote in 1989, "[t]heirs will be a life of certain suffering, of probable deviance, of permanent inferiority.
"[14][16] The president of Boston University at the time, John Silber, said, "crack babies ... won't ever achieve the intellectual development to have consciousness of God.
[8] Reports from the mid-1980s to early '90s raised concerns about links between PCE and slowed growth, deformed limbs, defects of the kidneys and genitourinary and gastrointestinal systems, neurological damage, small head size, atrophy or cysts in the cerebral cortex, bleeding into the brain's ventricles, and obstruction of blood supply in the central nervous system.
[20] The euphoria experienced by cocaine users is thought to be largely due to the way it prevents the serotonin from being reabsorbed by the presynaptic neuron that released it.
[15] Cocaine also constricts the blood vessels in the fetus, which is potentially linked to slowed fetal growth and abnormal development of the genitourinary, cardiovascular, digestive, and musculoskeletal systems.
[15] Cocaine has also been found to enhance the contractility of the tissue in the uterus, another factor that has been suggested as a possible mechanism for its contribution to increased prematurity rates.
[36] More reliable methods for detecting cocaine exposure involve testing the newborn's hair or meconium (the infant's earliest stool).
[19] A review of 27 studies performed between 2006 and 2012 found that cognitive development was mildly to moderately affected in PCE adolescents, but how important these effects were in practical terms was unclear.
[22] As of 2013, studies had found after controlling for other factors that some effects are present in pregnancies involving cocaine: abruptio placenta, prematurity, low birth weight, and small size compared to babies of the same gestational time.
[39] Using cocaine while pregnant also heightens the chances of maternal and fetal vitamin deficiencies, respiratory distress syndrome for the baby, and infarction of the bowels.
[40] Some PCE children experience hypertonia (excessive muscle tone),[41] and reduced reflexes and motor function have been found in babies four to six weeks old.
In behavior, cognition, memory, grasping of information, and attention are areas that are common struggles for children that were exposed to cocaine in the womb.
Long-term studies have shown that there are alterations made in the structure and function of the brain occur when exposed to these drugs with cause change in the behaviors of the individual over time and they develop and grow.
[1] Studies that use neuroimaging such as magnetic resonance imaging (MRI) and FMRI have shown differences in brain structure of PCE children, for example in the cerebral cortex and limbic system.
[3] PCE infants have been shown to be more jittery and excitable and have lower arousal and self-regulation; such behavioral effects may persist or worsen after 12 months of age.
[1] Evidence suggests that in utero cocaine exposure leads to problems with behavior and sustained attention, possibly by affecting parts of the brain that are vulnerable to toxins during fetal development.
[19] A review of the literature reported that cocaine use causes congenital defects between 15 and 20% of the time; however another large-scale study found no difference in rates of birth anomalies in PCE and non-PCE infants.
[44] Cocaine use by pregnant mothers may directly or indirectly contribute to defects in the formation of the circulatory system and is associated with abnormalities in development of the aorta.
[40] In South Carolina, a woman who used crack in her third trimester of pregnancy was sentenced to prison for eight years when her child was born with cocaine metabolites in its system.
One such initiative, Project Prevention, offers women addicted to cocaine money as an incentive to undergo long-term birth control or, frequently, sterilization—an approach which has led to public outcry from those who consider this practice to be eugenics.
[44] PCE is very difficult to study because of a variety of factors that may confound the results: pre- and postnatal care may be poor; the pregnant mother and child may be malnourished; the amount of cocaine a mother takes can vary; she may take a variety of drugs during pregnancy in addition to cocaine; measurements for detecting deficits may not be sensitive enough; and results that are found may only last a short time.
[34] When researchers control for use of other drugs, many of the seeming effects of cocaine on head size, birth weight, Apgar scores, and prematurity disappear.
[57] Animal studies in various species have found that cocaine impacts brain structure, function, and chemistry, and causes long-term changes at the molecular, cellular, and behavioral levels.
[34] Adult rats that were exposed to cocaine prenatally have deficits in learning, memory, and motor skills, and may have abnormalities in dopamine processing.
