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Prenatal cocaine exposure ( PCE ), theorized in the 1970s, occurs when a pregnant woman uses cocaine and thus exposes her fetus to the drug. " Crack baby " is a term coined to describe children exposed to crack (cocoa freebase in a smokable form) as a fetus; the concept of cracked babies emerged in the US during the 1980s and 1990s in the midst of crack epidemics. Other terms are " baby cocaine " and " child crack ". Early studies reported that people affected by cracks in the womb would experience severe emotional, mental, and physical disorders; this belief becomes common in the scientific and lay community. The widespread fear that cracking baby generations will put heavy pressure on society and social services as they grow older. Subsequent studies failed to prove the finding from earlier that PCE has severe paralyzing consequences; these earlier studies have been methodologically defective (eg with small sample sizes and confounding factors). Scientists have come to understand that the findings from the initial study are greatly exaggerated and that most people exposed to cocaine in the womb have no defects.

No specific disorder or condition is found in people whose mothers use cocaine while pregnant. Studies focused on children aged six years and younger have not demonstrated a long-term direct PCE effect on language, growth, or progression as measured by test scores. PCE also appears to have little effect on infant growth. However, PCE is associated with premature birth, birth defects, attention deficit hyperactivity disorder, and other conditions. The effects of cocaine on the fetus are considered to be similar to tobacco and less severe than alcohol. There is no scientific evidence demonstrating the difference in fetal harm between crack and cocaine powder.

PCE is very difficult to study because it is very rare in isolation: it usually coexists with other factors, which can disrupt the results of the study. Thus, studies have failed to show clearly that PCE has a negative cognitive effect, partly because the effect may be due to a concomitant factor. Pregnant women who use cocaine often use other drugs in addition, or they may be malnourished and lacking in medical care. Children in households where cocaine is abused are at risk of violence and neglect, and those cared for may experience problems due to unstable family situations. Factors such as poverty often associated with PCE have a much stronger influence on the intellectual and academic abilities of children than on cocaine exposure separately. Thus researchers have difficulty in determining the effects resulting from PCE and resulting from other factors in the history of children.


Video Prenatal cocaine exposure



Konteks historis

During the 1980s and 1990s, there was a surge in the use of crack cocaine in US cities: a cracked epidemic. During this time fears are emerging across the country that PCE will create a young generation with severe behavioral and cognitive problems. Early studies in the mid-1980s reported that cocaine use in pregnancy causes children to experience severe problems including cognitive, developmental, and emotional disturbances. This preliminary study has methodological problems including small sample size, confounding factors such as poor nutrition, and other maternal use of the drug. However, the results of this study sparked widespread media discussions in the context of the New Drug War. For example, a 1985 study showing the harmful effects of cocaine use during pregnancy created a huge media buzz. The term "crack baby" is generated from publicity around crack and PCE.

It is common in media reports to emphasize that infants affected by cracks in the womb will never develop normally. Children reportedly are inevitably destined to become physically and mentally disabled throughout their lives. Infants affected by cracks in the womb have been eliminated because they are destined to be severely disabled, and many are left in hospital. They are expected not to form a normal social bond. Experts predict the development of the "lower class biologist" of the born criminals who will prey on the rest of the population. The crime rate is expected to increase as the baby's generation exposed to crack grows (not they fall). It is thought that children will be difficult to entertain, irritable, and hyperactive, putting pressure on the school system. Charles Krauthammer, columnist for The Washington Post wrote in 1989, "[t] the heir will be a life of suffering, the possibility of perversion, of permanent inferiority." Boston University president at the time, John Silber, said "cracked baby... will never reach intellectual development to have an awareness of God." These biological inferiority claims are easily playable into existing classes and racial biases. Reporting is often sensational, supporting the worst predictions and getting rid of skeptics.

Reporting on the effects of PCE may have been affected by publication bias, a disproportionate study publication showed more severe results when a crack epidemic emerged. Scientific studies reporting that PCE has a significant effect may be more likely to be published than those that do not. Between 1980 and 1989, 57% of studies showed cocaine had an effect on the fetus received by the Society for Pediatric Research, compared with only 11% of studies that did not show any effect. The finding that other factors such as prematurity lag behind the symptoms indicated by infants exposed to cocaine does not "match the narrative of what has become a national fear" and received less attention. The idea of ​​a severe PCE effect may be easier to adhere to because they "fit in with cultural stereotypes".

At that time, the proposed mechanism by which cocaine harms the fetus is as a stimulant - it is predicted that cocaine will interfere with the normal development of the brain-related part of stimulation, resulting in problems such as bipolar disorder and attention deficit disorder. Reports from the mid-1980s to early 90s raised concerns about the relationship between PCE and slowing growth, limb defects, kidney defects and genitourinary and gastrointestinal systems, neurological damage, small head size, atrophy or cysts in the cerebral cortex, bleeding into in the ventricle of the brain, and obstruction of the blood supply in the central nervous system.

After a preliminary study reporting that PCE children will be severely deformed comes a study intended to show that exposure to cocaine in utero has no important effect. Nearly every prenatal complication was initially thought to be due directly to PCE found to be the result of confounding factors such as poor maternal nutrition, use of other drugs, depression, and lack of prenatal care. Recently the scientific community has begun to reach the understanding that PCE does have some important effects but they are not as severe as predicted in the initial study. PCE effects are very smooth but exist. Most people exposed to cocaine in utero are normal or close to it.

Maps Prenatal cocaine exposure



Pathophysiology

Cocaine, a small molecule, is able to cross the placenta into the fetal bloodstream. It may even be present in higher concentrations in the amniotic fluid than in the maternal bloodstream. The fetus's skin is able to absorb chemicals directly from the amniotic fluid until the 24th week of pregnancy. Cocaine can also appear in breast milk and affect breastfeeding infants. The severity of the effects depends on how many drugs are used, how often, and the stage in fetal development.

Cocaine prevents reuptake from neurotransmitters dopamine, serotonin, and norepinephrine. Thus they live in synapse longer, causing the excitement of the sympathetic nervous system and awakening the stress response. The euphoria experienced by cocaine users is thought to be largely due to the way to prevent neurotransmitter serotonin from being absorbed by the presinactic neurons that release them.

The use of cocaine during pregnancy can have a negative impact on the mother and fetus, but ways of affecting the fetus are not well understood. There are three main mechanisms in which exposure to cocaine harms the fetus: by altering brain chemistry, by altering the expression of certain genes, and by the constriction of blood vessels. The cocaine-influenced neurotransmitter is involved in the development of the fetus's brain, so the drug can affect fetal development directly by altering the development of the brain's monoaminergic system. The most important cocaine affecting fetal development is by binding to dopamine receptors.

Another possible mechanism in which cocaine harms the fetus may be partly by disrupting the blood supply to the uterus. Cocaine causes vasoconstriction (constriction of blood vessels) in the mother and fetus, which can cause hypoxia in the fetus. Limiting blood vessels causes the tissues to receive inadequate blood flow, killing cells, but this effect is less pronounced with cocaine than nicotine. Reduced blood flow to the uterus limits the delivery of oxygen and nutrients to the fetus. Cocaine also constricts blood vessels in the fetus, potentially linked to slowing fetal growth and abnormal development of the genitourinary, cardiovascular, gastrointestinal, and musculoskeletal systems. Cocaine causes changes in maternal blood pressure that are considered a cause of stroke in the fetus; one study found that 6% of cocaine-exposed infants had experienced one or more strokes. Such prenatal stroke may be the cause of the neurological problems found in some babies exposed to cocaine after birth. Contraction of blood vessels can also cause premature labor and premature birth. Cocaine has also been found to increase uterine contractility in utero, another factor that has been suggested as a possible mechanism for its contribution to an increase in prematurity rates. Increased uterine contractility may also lie behind the possibility of increased placental abruption (the placenta rips the uterine wall) which some findings are associated with PCE.

Specificity of prenatal cocaine on inhibition of locus coeruleus ...
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Diagnosis

The use of cocaine during pregnancy can be found by asking the mother, but sometimes women will not admit to having used the drug. Mothers may lie for fear of being sued or bring their children away, but even when they are willing to tell the truth, their memories may not be very accurate. It may also be impossible to ascertain the purity of the drugs they take. More reliable methods for detecting cocaine exposure include testing the newborn's hair or meconium (earliest stool). Hair analysis, however, can provide false positives for cocaine exposure, and newborns may not have enough hair to test. Newborn urine can be tested for cocaine and metabolites, but should be collected as soon as possible after birth. It is not known how long after exposure to markers will still appear in the urine of newborns. Mother's urine can also be tested for drugs, but can not detect drugs used too far in the past or determine how much or how often they are used. The test can not generally detect the use of cocaine more than a week before the sample collection. Mothers are more honest about the use of cocaine when their urine is also tested, but many users still deny it. Maternal and neonatal urine tests may provide false negative.

Specificity of prenatal cocaine on inhibition of locus coeruleus ...
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Effects and prognosis

Research has produced very diverse reports on the impact of PCE: some claim severe and common physical defects, others find specific effects, others not at all. The dose of the drug is an important determinant of the outcome, in addition to how much is used, for how long, and what treatment is given after birth. Drug use in the first trimester is the most harmful to the fetus in terms of neurological and developmental outcomes. The later PCE effects in a child's life are not well understood; there is little information about the effects of exposure to cocaine in utero in children over the age of five. Several studies have found differences associated with PCE in height and weight while others do not; these differences are generally missing or small at school-age children. Much remains unknown about what factors might exist to help children exposed to cocaine in utero . It is not known whether the effects of PCE increase after the children reach adolescence, or whether the neural rewiring that occurred during this period of development weakens the effect. A review of 27 studies conducted between 2006 and 2012 found that cognitive development was mild to moderate in PCE adolescents, but it was not clear how important this effect was in practical terms.

Unlike fetal alcohol syndrome, no characteristic is found that results uniquely from exposure to cocaine in utero . Cocaine exposure in utero can affect the structure and function of the brain, affecting children for developmental problems later on, or this effect can be explained by children of mothers who use cracks that are at higher risk for domestic violence , parenting deadbeat, and maternal depression. When researchers can identify PCE effects, these effects are usually small.

Pregnancy and birth

Research has found after controlling for other factors that some effects present in pregnancies involving cocaine: placenta abruptio, prematurity, low birth weight, and small size compared to infants from the same gestational time. The newborn's PCE has a smaller head and a shorter body. The PCE effect is more severe when the amount of cocaine is greater. As many as 17-27% of pregnant women use cocaine to deliver prematurely. In association with prematurity, uterine growth is reduced, and low birth weight is connected to PCE. There is also data showing that spontaneous abortion is associated with cocaine use. Cocaine reduces appetite and has been linked to maternal weight loss during pregnancy; In addition, narrowing of blood vessels may further limit the supply of nutrients to the fetus. Using cocaine while pregnant also increases the likelihood of maternal and fetal vitamin deficiencies, respiratory distress syndrome for infants, and intestinal infarction. Initial reports found that babies were exposed to high-risk cocaine for sudden infant death syndrome; However, by itself, exposure to cocaine during fetal development has not been identified as a risk factor for the syndrome. Some, but not all, PCE children have hyponal (excessive muscle tone), and decreased reflexes and motor function have been found in infants aged four to six weeks.

While newborns exposed prematurely to drugs such as barbiturates or heroin often have drug withdrawal symptoms (neonatal abstinent syndrome), this does not occur in infants exposed to cracks in utero; at least, such symptoms are difficult to separate in the context of other factors such as prematurity or prenatal exposure to other drugs.

Mental, emotional, and behavioral results

Studies have shown a small deficit in the behavior, cognitive, attention, emotional, and functional language of PCE infants, children, and adolescents. However, other studies linked findings to negative effects on cognitive development with confounding factors. Studies show that the environment in which a child grows makes a more important contribution to results in cognitive, behavioral and other outcomes than the exposure to cocaine itself. School performance is slightly affected in older children. In the IQ study, children exposed to cocaine did not seem to score lower than others. Although PCE correlates with a low IQ score, scientists generally believe that PCE alone does not cause this effect; more likely due to related factors. At school age and younger children, PCE does not appear in studies to influence children for worse intellectual performance. Poor performance on an IQ test can actually be caused by problems by maintaining attention if the tests fail to take this factor into account separately.

Cocaine causes a fetal brain growth disorder, the most obvious effect with high cocaine levels and prolonged exposure duration across all three trimesters of pregnancy. Studies using neuroimaging such as magnetic resonance imaging (MRI) and FMRI have shown differences in the brain structure of PCE children, for example in the cerebral cortex and limbic system. PCE children who have slowed brain growth because the fetus is at higher risk for brain and motor growth disorders, language and attention problems after they are born. Studies have found that children are exposed to cocaine during fetal development problems with language, behavior, development, and attention. But this effect is small, especially when the research controls other factors such as exposure to other drugs. Cognitive and attention skills may be affected by PCE, possibly because of effects on areas of the brain such as the prefrontal cortex. The areas of the brain in the frontal lobes involved in dealing with stress, attention, and impulsivity appear to be particularly influenced by PCE, as evidenced by neuroimaging studies that show abnormalities in this area of ​​the brain. The PCE baby has proven to be more agitated and excited and has lower arousal and self-regulation; Such behavioral effects can persist or worsen after the age of 12 months. Children whose mothers use cocaine during pregnancy may develop symptoms similar to attention deficit disorder, and a connection has been found between the disorder itself and PCE. A mild deficit in language has been found in older PCE children. Language development is disrupted, may be the last teenager, but adolescents up to age 17 can improve their receptive language skills.

The evidence suggests that cocaine exposure in utero causes problems with sustained behavior and attention, possibly by affecting parts of the brain that are susceptible to toxins during fetal development. School-age PCE children found difficulty regulating their behavior and retaining their attention. Children exposed to high levels of cocaine in utero show inhibition of behavior worse than those with lower exposure levels or unexposed children. Changes in attitudes and concerns caused by PCE can be measured on a standard scale; But the effect of this behavior seems mild. Children exposed to cocaine in the first trimester are less able to mingle, more withdraw, and exhibit more anxious and depressed behavior. Those exposed to higher cocaine doses have been reported to exhibit aggressive and disruptive behavior. PCE girls are seven times more likely to experience naughty behavioral problems, but PCE boys are no more likely than other boys. Studies from the 2000s and 2010s contradict on whether PCE adolescents have a greater risk of using drugs such as cocaine, alcohol, and marijuana. A 2010 study found that PCE girls were more likely to suffer from anxiety than their unexposed peers.

Physical results

Slow growth is well documented in the fetus, but it is unclear whether older children remain smaller or catch up with their peers. Some studies show that growth remains slow for ten years. PCE can also disrupt the way motor systems become mature. Documented motor effects include poor reflexes and movement quality in infants. PCE may have an effect on the neuroendocrine system, but further studies are needed to determine if it is and what the effect is.

The literature review reports that cocaine use causes congenital defects between 15 and 20% of the time; But other large-scale studies found no difference in the birth anomaly levels in PCE and non-PCE infants. It has been suggested that some birth defects can be caused by cocaine disorders in the growth of blood vessels. Most PCE defects are found in the brain, heart, genitourinary tract, arms and legs. The use of cocaine by pregnant women can directly or indirectly contribute to defects in the formation of the circulatory system and is associated with abnormalities in aortic development. Cardiac malformations may include missing ventricles and defects with the cardiac septum, and may result in lethal congestive heart failure. Genital malformations occur at a higher level than normal with PCE. Liver and lung are also at higher risk for abnormalities. The Cloverleaf skull, a congenital malformation in which the skull has three lobes, the brain is deformed, and hydrocephalus occurs, also associated with PCE. Such as birth defects, small head size, and stroke are risks in PCE.

Prenatal Antidepressant Exposure: Clinical and Preclinical ...
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Epidemiology

Of all cocaine users, women of childbearing age comprise 15-17%. It is estimated that 0.6 to 3% of pregnant women in developed countries use cocaine. A 1995 survey in the US found that between 30,000 and 160,000 cases of prenatal exposure to cocaine occur every year. With one estimate, in the US 100,000 babies are born every year after exposure to cocaine crack in utero . It is estimated that 7.5 million PCE children live in the US. Pregnant women in urban areas of the United States and those with low socioeconomic status are more likely to use cocaine. However, the prevalence of real cocaine use by pregnant women is unknown.

Prenatal Alcohol Exposure, FASD, and Child Behavior: A Meta ...
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Legal and ethical issues

Damage to a child from the PCE has implications for public policy and law. Several US states have put pressure on pregnant women who use drugs, including assaults with deadly weapons, underage corruption, child killings, child abuse, and the distribution of drugs to minors. But this approach has generally been rejected in court on the grounds that the fetus is not legally a child. Between 1985 and 2001, more than 200 women in over 30 US states face demands for drug use during pregnancy. In South Carolina, a woman who used cracks in her third trimester of pregnancy was sentenced to eight years in jail when her son was born with cocaine metabolites in her system. The South Carolina Supreme Court upholds this belief. By 2013, all but one woman sued in the US for drug use while pregnant have won their case on appeal.

From 1989 to 1994, amid public condemnation of baby cocaine, the University of Medicine of South Carolina tested pregnant women for cocaine, reporting those tested positive to the police. The US Supreme Court found that the policy was unacceptable on constitutional grounds in 2001. Some advocates argue that the punishment for pregnant women using crack as a means to treat their addiction is a violation of their privacy rights. According to the study, the fear of prosecution and children taken is related to the refusal to seek prenatal care or medical care.

Some nonprofit organizations aim to prevent PCE by birth control. One such initiative, Prevention Project, offers women addicted to cocaine money as an incentive to undergo long-term birth control or, often, sterilization - an approach that has caused public outcry from those who regard this practice as eugenics.

Frontiers | Effective Connectivity within the Mesocorticolimbic ...
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Social stigma

Children exposed to social stigma encountered prematurely as infants and school-age children; some experts say that the stigma "crack baby" is more dangerous than PCE. Teachers are influenced by this cultural stereotype; Such biases can negatively impact children's educational experiences resulting in stigmatization. Teachers who know that certain children have been exposed to cracks in the womb may expect these children to become disruptive and experience delayed development. Children exposed to cocaine may be ridiculed by others who know about exposure, and these children's problems may be misdiagnosed by doctors or others as a result of PCE when they may actually be caused by factors such as illness or abuse.

The social stigma of the drug also complicates PCE research; researchers work under the awareness that their findings will have political implications. In addition, the perceived despair of 'crack baby' may have caused researchers to ignore the possibility of early intervention that may help them. Social stigma can turn into self-fulfilling prophecy.

Brain Development Effects: Prenatal Exposure to Drugs and Alcohol ...
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Research

The confounding factor

A number of effects have been thought after the initial study to be associated with prenatal exposure to cocaine actually due in part or entirely to other factors, such as exposure to other substances (including tobacco, alcohol, or marijuana) or the environment in which the child was raised.

PCE is very difficult to investigate because of various factors that can disrupt the results: pre and postnatal care may be poor; pregnant women and children may be malnourished; the amount of cocaine consumed by the mother may vary; she may take medications during pregnancy other than cocaine; measurements to detect deficits may not be sufficiently sensitive; and the results found can only last a short time. Studies differ in how they define the use of heavy or light cocaine during pregnancy, and the period of exposure during pregnancy in which they focus (eg the first, second, or third trimester) The use of drugs by the mother places the children at high risk for exposure to toxins or if not a hazardous environment, and PCE does not present many risks beyond these risk factors, the PCE is clustered with other risk factors for children, such as physical abuse and neglect, domestic violence, and prenatal exposure to other substances. children in the same area being studied in connection with PCE Most women who used cocaine while pregnant took other drugs as well, one study found that 93% of those who used cocaine or opiates also used tobacco, marijuana or alcohol. use of other drugs, many effects of cocaine that appear on the size of the head, birth weight, score Apgar, and prematurity disappears.

Addiction to any substance, including cracks, may be a risk factor for child abuse or abuse. Crack addiction, like other addictions, distracts parents from children and leads to less caring care. Mothers who continue to use drugs once their babies are born have difficulty forming normal parental bonds, more often interacting with their infants in a flat, unenthusiastic, and flat manner. Conversely, low-pressure environments and responsive parenting can have a protective effect on the child's brain, potentially compensating for the negative effects of PCE. Many drug users do not get prenatal care, for various reasons including that they may not know that they are pregnant. Many drug addicts do not get medical treatment at all and have very bad diets, and children living around smoked crack are at risk of inhaling secondary smoke. Cocaine using mothers also has higher rates of sexually transmitted infections such as HIV and hepatitis.

In some cases, it is unclear whether PCE direct results lead to behavioral problems, or whether environmental factors are wrong. For example, children who have caregiver instability may have more behavioral problems as a result, or perhaps behavioral problems manifested by PCE children lead to greater turnover in caregivers. Other factors that make learning PCE difficult include the reluctance of the mother to tell the truth about the history of the drug, the uncertainty of the dose of street drugs and the high level of attrition (loss of participants) of the study.

Animal model

One way to solve the problem with uncertainty about cocaine effects due to confounding factors is to use animal models; this allows researchers to study the effects on a particular dose and time. Studies have used mice, other rodents, rabbits, and primates. However, the difference between physiology and gestation of species means that animal findings may not apply to humans. Mice, rats, and rabbits have shorter gestation times, so researchers should continue to give the drug after they are born to get closer to modeling a human pregnancy; But this introduces more difference. Animals and humans metabolize drugs at different rates, and highly teratogenic drugs in animals may not be present in humans and vice versa. Animals can not be used to measure differences in abilities such as reasoning only found in humans. Research on animals in various species has found that cocaine affects the structure, function, and chemistry of the brain, and causes long-term changes at the molecular, cellular, and behavioral levels. In a study study in pregnant mice, injected cocaine was less damaging to the cells than the injected nicotine, and more recovery occurred between doses. Adult mice exposed to cocaine prematurely have a deficit in learning, memory, and motor skills, and may have abnormalities in dopamine processing. Animal studies have also shown that male offspring who use cocaine while their sperm are formed may continue to have abnormalities later in life.

Altered Neural Processing of the Need to Stop in Young Adults at ...
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References

Bibliography


Prenatal Antidepressant Exposure: Clinical and Preclinical ...
src: pharmrev.aspetjournals.org


External links

  • Crack Babies: A Tale from the Drug Wars, a documentary from The New York Times

Source of the article : Wikipedia

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