drug exposure & development

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February 2011 Dedicated to research, clinical training, and education in chemical addiction

INSTITUTIONAL ADVISORY BOARD

Glen W. Hanson, Ph.D, D.D.S

Utah Addiction CenterUniversity of UtahHealth Sciences Center410 Chipeta Way, Suite 280Salt Lake City, Utah 84108

ContaCt Us

University of UtahHealth Sciences Center410 Chipeta Way, Suite 280Salt Lake City, Utah 84108

Phone: (801) 581-8216Fax: (801) 587-7858E-mail: [email protected]: http://uuhsc.utah.edu/uac/

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Salt Lake City, Utah

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The Utah Addiction Center is based in the office of the University of Utah Senior Vice President for Health Sciences

TheUtahAddiction

ReportCenter

Volume 2 Issue 12

“Jonah’s mother was a heroin addict. Shortly after birth, it was obvious Jonah was in withdrawal. His jittery movements and crying persisted for the next 2 days and there was little anyone could do to console him. He scratched his face trying to get his hands to his mouth. His knees and elbows were rubbed raw from his agitated movement, and the muscles in his tiny legs were so stiff

that it was difficult to straighten his legs to diaper him” (Available: http://drugabuse.gov/consequences/prenatal/ ). This real-life account illustrates the disturbing impact of exposing a developing fetus to potent drugs of abuse during pregnancy. Most of the symptoms described above are due to the fact that the infant’s body is going through withdrawal from the effects of months of exposure to heroin. As difficult as it is to watch an innocent newborn suffer through this process, it is of some consolation to know that these withdrawal effects can be relieved with proper treatment and with time they will subside. However, effects of drugs of abuse during prenatal periods or exposure to these substances postnatally or even through adolescence can sometimes permanently affect a child’s development in dramatic or sometimes less obvious ways depending on the drug, the exposure pattern and environmental factors. Most people are aware that consumption of large quantities of alcohol through pregnancy frequently debilitates the offspring because expression of the resulting fetal alcohol syndrome (FAS) includes severe physical and emotional damage that compromises the intellectual, cognitive and motor functions of the afflicted child. Such damage can be evident during the pregnancy or immediately after birth. By comparison, the impact of other drugs of abuse is more difficult to identify and may be associated with subtle diminished capacity that doesn’t fully express until years after the drug exposure. For example, over the past two decades, particularly during the height of the cocaine epidemic in the United States, considerable scientific effort was focused on determining the adverse effects of this potent stimulant, especially in cocaine-exposed infants and toddlers. Early reports of severe damage in children exposed to crack cocaine lead to the stigmatizing label of so-called ‘crack babies.’ After conducting better controlled studies with improved elements of prospective designs, it was determined that exposure of these young children to cocaine per se was much

A. Lorris Betz, M.D., Ph.D.Louis H. Callister, J.D.Edward B. Clark, M.D.

M. David Rudd, PhD, ABPP Patrick Fleming, LSAC, MPARaymond Gesteland, Ph.D.

Jay Graves Ph.D.John R. Hoidal, M.D.

Glen W. Hanson Ph.D, D.D.S,Maureen Keefe, RN, Ph.D

Jannah Mather, Ph.D.Chris Ireland, Ph.D.

John McDonnell, Ph.D.Barbara N. Sullivan, Ph.D.

Ross VanVranken, ACSWKim Wirthlin, MPA

Drug Exposure and Development

» See Alcohol page 5

The Utah Addiction Center Report The Utah Addiction Center Report2 11

The Utah Division of Substance Abuse reported for 2009 that 6300 women

were admitted to public substance abuse treatment programs (Figure 1). On admission to the program, they are asked what their primary substance of abuse is. Methamphetamine was the most common, followed by alcohol. Of particular interest is that opiate addiction (which includes heroin and other opiates like oxycodone), is a significant problem. 357 (5.7%) of these women entering treatment were pregnant, indicating that their newborn has been exposed to these substances. What are the consequences of this exposure? This article will briefly review the medical literature about prenatal drug exposure and outcomes for the children.

Why is there specific concern about exposure to substances of abuse during gestation?

There is biologic plausibility that adverse events are happening to the fetal brain when exposed to these substances that exert their effects through the central nervous system. All substances of abuse work in the brain by changing the levels of naturally-occurring neurotransmitters, the chemicals that are an essential part of how nerve cells communicate. In the developing fetal brain, animal research has shown that neurotransmitters are not only there to move messages from one neuron to the next, but they also serve as trophic or growth factors in brain development. These molecules are capable of inducing and sustaining the growth and differentiation of nerve cells in the brain. If the neurotransmitters necessary for normal brain development are disrupted or altered by maternal substance use, structural changes may occur in the fetal brain that may have subsequent effects on later brain function and behavior. This is one major concern regarding in utero exposure. Another major concern about prenatal exposure is that the use of drugs that work on the central nervous system can alter the hormonal balance in the growing fetal brain. Barry Lester and colleagues at Brown University have hypothesized that substance abuse during pregnancy acts as an intrauterine stressor that can alter the expression of genes that are important to placental function. This, then, can lead to changes in the levels of important nervous system hormones in the fetal brain. They hypothesize that these changes could lead to enduring developmental and behavioral alterations in children with prenatal drug exposure.

What do the outcome studies say about prenatal exposure?

In order to know whether or not these hypothesized changes in fetal brain structure after in utero exposure to a particular substance of abuse manifest themselves as problems as the child grows up, outcome studies must be performed. When reviewing the published outcome studies, it is important to understand the difficulties of this type of research. The challenge is to relate the outcome measure of interest, for example, abnormal newborn behavior, to the variable of interest, say, in utero cocaine exposure while controlling for all the other variables that also may influence newborn behavior.

Assessing the effects of prenatal exposure to substances of abuse: What does current research tell us?Karen F. Buchi, MD, Professor, Chief, Division of General PediatricsDepartment of Pediatrics, University of Utah

• Pat Smith, [email protected]

• Susan Lewin, MD, Division of Medical Genetics U of Utah for diagnosis and management consultation and educational presentations. [email protected]. For appointments call Central Scheduling: 801 213-3599 or if urgent contact Heather 801 587-7563

• Support Group in Davis County: 2nd Thursday of the month - every other month and runs September through May as follows: September, November, January, March, May Time: 6:00 p.m. - 7:30 p.m., Davis Family Advocate Program 836 S. State Street Clearfield, Utah 84015. Contact Lynn Tanner (contact above)for more information.

There are many websites, including these official national sites:

• SAMHSA FASD Center for Excellence: fasdcenter.samhsa.gov

• Centers for Disease Control and Prevention FAS Prevention Team: www.cdc.gov/ncbddd/fas

• National Institute on Alcohol Abuse and Alcoholism (NIAAA): www.niaaa.nih.gov

• National Organization on Fetal Alcohol Syndrome (NOFAS): www.nofas.org

• National Clearinghouse for Alcohol and Drug Information: www.ncadi.samhsa.gov

Final notes

Due to the broad range of expression of ARND, if a provider is suspicious that a person has ARND but cannot confirm it, it is be worth treating the child as if this were the correct diagnosis, because management is then geared to the whole child who has permanent organic brain damage, and is more likely to be successful. This does not mean that other diagnoses or co-ocurring diagnoses should be forgotten.

And from a couple of parents:

To Label or to Diagnose

“Most parents of children with FAS/pFAS already feel that their children are labeled,-- as lazy, non-compliant, mean or stupid…We’d prefer an accurate diagnosis that describes what is happening with our children. A diagnosis of FAS (or ARND) makes REAL that our children experience, and that we experience raising them. We aren’t excusing our children’s behavior or imagining the difficulties they experience. An accurate diagnosis can motivate others to learn more about our children and how to work with them. At the very least, it helped me understand my son better, and I was able to learn strategies that made me a more effective parent for him.” --Don Adams, 1999

“We must move from viewing the individual as failing if s/he does not do well in a program

to viewing the program as not providing what the individual needs in order to succeed.”

—Dubovsky, 2000

To provide for our children successfully it is important to remember:

• FASD is a permanent lifelong condition

• Organic brain damage never goes away

• Diagnosis is helpful, label is not

• Progress continues throughout life

• Scaffold of support should never be removed

Utah Division of Substance Abuse Annual Report 2009

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One of the most problematic issues is poly-drug exposure. Researchers have not found a group of women and their babies to enroll in these studies who use one and only one substance of abuse (the one exception may be tobacco use). Most also use at least tobacco and/ or alcohol. The studies published in the late 1980s and early 1990s most often did not address the issue of poly-drug exposure.

The issue of controlling for confounders becomes increasingly difficult when looking at outcomes beyond the newborn period. These longer term outcome studies are trying to relate behavioral and cognitive function of the exposed child to the in utero exposure. To do this, one must control for a long list of confounders including maternal mental health, maternal education level, socioeconomic status, whether the child was raised in a stable home without substance use, in a home with continuing substance abuse, in foster care, and the list can go on and on.

Especially when looking at outcomes such as attention deficit disorder and learning disabilities, it is important to know if the biologic parents had these diagnoses, yet there are only a few studies that have attempted to address this confounder. When one reads a study about outcome of the drug-exposed child, one should read carefully the methodology to assess how good the attempt was to control for confounders. As a blanket statement, studies published in the early 90s did not do a good job of addressing these confounders and resulted in overstatements about the effects of in utero exposure.

The Maternal Lifestyle Study and the Infant Development Environmental and Lifestyle Study

Because of the deficiencies in the research done in the early 90s, the major researchers in the area of outcome for drug-exposed newborns and children designed better and more comprehensive studies that addressed many of those deficiencies. The Maternal Lifestyle Study (MLS) and the Infant Development Environmental and Lifestyle Study (IDEAL) study are two multi-center longitudinal studies that are following cohorts of drug-exposed children. The MLS is a federal interagency collaborative effort and is the largest clinical prospective longitudinal study of acute neonatal events and long-term health and developmental outcomes associated with cocaine use during pregnancy. It was designed to address many of the methodological issues that limited the interpretability of prior studies, especially addressing the issues of polydrug use and the adequacy of the caregiving environment . Four institutions enrolled mothers and their infants between 1993 and 1995 and have been following them ever since. Those children are now entering adolescence and are continuing to be followed. The second study is the Infant Development Environmental and Lifestyle Study which again is a longitudinal prospective study, this time focusing on methamphetamine exposure. It follows many of the same methodologies of the MLS, in fact, it has some of the same lead investigators.

Next, a brief summary of the findings, when applicable, of the MLS and IDEAL study in regard to individual drugs.

Nicotine

The Maternal Lifestyle study did not look at nicotine effects, but one must never forget that tobacco smoking during pregnancy is the one of the leading causes of low birth weight in the United States. It is dose-related in that women can improve the birth weight of their babies by reducing the number of cigarettes they smoke each day. As for nicotine’s effect on the central nervous system, neonates born to mothers who smoke cigarettes have been shown to have neurobehavioral differences that begin shortly after birth. Importantly, maternal smoking while pregnant has emerged as a major risk factor in almost every epidemiologic study of SIDS. A review of nicotine outcome research published in the Journal of the American Academy of Child and Adolescent Psychiatry reported that in utero exposure to tobacco is associated with motor, sensory, and cognitive deficits in infants and toddlers. Findings in young children also seem to support a negative influence of in utero exposure to nicotine on behavior and cognitive function. There are many studies that have reported an increased rate of behavior disorders such as attention deficit disorder and conduct disorder among adolescents whose

Successful management is dependent upon making the right diagnosis. With a diagnosis, our percpetion of the child as having brain damage changes our expectations for the child. The characteristics that may enrage or frustrate before diagnosis are recognized as disability after.

Medication may be appropriate for many individuals, but the mainstay of management is about understanding the particular child, and modifying the environment so that he or she can succeed, and then learn. Trial and dose modification depending on symptoms takes time and patience/

Interpretation of Behaviors

Because of the patchy nature of the brain damage in ARND, some behaviors are typical and others are appropriate for much younger children. A helpful way to think of this is presented by Diane Malbin:

For an 18 year old:

SKILL EQUIVALENT DEVELOPMENTAL AGE (years)

Expressive Language 20

Comprehension 6

Money, time concepts 8

Emotional maturity 6

Physical maturity 18

Reading ability 16

Social skills 7

Living skills 11

A care provider or teacher must be alert to the potential range of abilities and it requires great skill to manage the behaviors in a single individual. Helpful management words are: SHOW me – they can parrot back words but may not understand the words.

Helpful concepts for care providers to reframe management include:

• Structure, structure, structure

• “Stretched toddlers”

• “10 second people in a 2 second world”

• They can talk the talk - can they really walk the walk?

These children are NOT competent adults at age 18, and if they are not provided structure and support as long as is necessary – often lifelong, they will fail, and will often end up in the criminal justice system where they deteriorate fast. FASD is a killing condition if we don’t provide adequate lifelong support.

Resources

Local Resources:

• www.utahfetalalcohol.org - has many references both local and national as well as local information and contacts. They also have a facebook page: Utah FASD Coalition

• Lynn Tanner, RN, 801 776-0054 [email protected]

At a Glance“ALARMS” or “ALARMMERS” helps us think about the behaviors

AdaptationMotorLearningExecutive functionADHDRegulation of stateReasoning (IQ)Speech/languageMemory Clarren et all 2005


mothers smoked during pregnancy. Most of these studies have methodologic problems such as not controlling for confounders such as parental IQ, psychiatric history, parenting style, etc. In reviewing the literature, there is no definitive study that confirms that in utero exposure to nicotine is responsible by itself for the differences in behavior and IQ seen between the exposed and unexposed groups. But with 25% of pregnancies exposed to nicotine through maternal smoking, even small differences between groups are significant, making prevention even more important.

Marijuana

Of the illicit substances, marijuana is the most frequently used by pregnant women. The Maternal Lifestyle Study reported that marijuana use was not significantly related to low birth weight or preterm birth. The IDEAL study also found that marijuana use was unrelated to gestational age-adjusted birth weight. While some behavioral differences have been observed in marijuana-exposed newborns compared with un-exposed newborns, there is little evidence that prenatal exposure to marijuana results in significant long-term difficulties in children.

Opiates/Opioids

The research on the effects of prenatal exposure to opiates isn’t as extensive as one may think given that opiate addiction has been around a very long time. Most studies of prenatal opiate (e.g. heroin or methadone) use show increased risk for low birth weight and preterm delivery, but few have controlled for associated risk factors, such as smoking tobacco. It is important to note that prenatal opiate use has not been associated with prematurity or birth defects. It is the well documented effect of opiate dependence on the neonate that sets prenatal opiate exposure apart from the other classes of drugs. Between 50 to 94% of prenatally exposed newborns will experience neonatal abstinence syndrome and require prolonged hospitalization. The physiologic effects of opiate withdrawal are more profound and troublesome to the newborn than any of the short term effects seen with exposure to the other drugs like cocaine or methamphetamine.

There is a paucity of studies addressing the issue of the long-term outcome of opiate exposed children. A study published in 2002 conducted in Norway followed heroin exposed children for 4 years. All of these children were either adopted or raised in foster care. They found that all children had normal cognitive scores at 4 years, but that a special weakness in the area of visual-motor and perceptual abilities was detected. There is a concern for differences on developmental testing between exposed and unexposed, but most studies did not control for polydrug exposure. There is a need for well-designed follow-up studies for these children.

Cocaine

Of all illicit substances, there are more outcomes studies concerning cocaine. There was a rapid rise in cocaine use in the 1980s and a great deal of cocaine research was funded. The MLS reported that cocaine use was associated with decreased birth weight, head size, and length among infants born at 33 weeks or more gestation adjusted for confounders such as other drug use, inadequate prenatal care, and medical risk factors. These were the same effects seen with tobacco. The MLS also reported that cocaine-exposed infants showed more neurologic “soft signs” and behavioral effects in the newborn period than non-exposed newborns.

The cohorts of cocaine-exposed children in research studies are now in late adolescence and are continuing to be followed. One can summarize that the current research suggests that, although there are effects of cocaine on child development, these effects are inconsistent and subtle and need to be understood in the context of polydrug use and the caregiving environment. There is concern that cocaine may affect areas of the brain that control behaviors such as substance use, psychopathology, antisociality, academic and cognitive problems. Research has yet to be conclusive regarding these concerns, however.

Evidence of CNS developmental abnormalities including at least one of the following:

• Decreased head size at birth

• Structural abnormalities e.g. microcephaly, agenesis of corpus callosum, cerebellar hypoplasia

• Hard or soft neurological signs

Complex pattern of cognitive or behavior abnormalities defined as:

• Inconsistent with developmental level

• Not explained by family background or environment alone

These cognitive or behavior abnormalities include difficulties with:

• Learning

• School performance

• Impulse control

• Higher level expressive and receptive language

• Social perception

• Abstraction or metacognition

• Math skills

• Memory

• Judgment

• Attention

Obviously this is a broad list and covers many aspects of behavior and learning problems. This also overlaps with many mental health diagnoses. As it is not possible to prove the diagnosis, a high index of suspicion is required to consider the ARND diagnosis as well as a reliable history of exposure. Red flags include:

• A diagnosis of reactive attachment disorder long after it is likely or if the child was too young

• The child repeatedly fails to progress with interventions provided at home and school that should be helping.

Diagnosis

1. Physical Diagnosis: The diagnosis of FAS and FASD should be made by a medical professional experienced with the disorder This is usually a medical geneticist, developmental pediatrician or neurologist or other interested physician. There is a differential diagnosis of conditions that look like FAS.

2. Neuropsychological Diagnosis: A psychologist and neuropsychologist needs to assess learning style and especially executive function, impulse control, memory and other frontal and prefrontal functions. Theses tests are not adequately covered in school psychological testing and many children may pass as able to function at school, when in fact they may have significant processing, memory and insight abnormalities in addition to ADHD. If this happens, the child may get blamed for not succeeding because disability is not recognized. Neuropsych testing should be undertaking after about age 5.

Management

A child with fetal alcohol syndrome, like children is recognizable has having special needs.

However for the majority of children exposed to brain damaging amounts of alcohol prenatally, there are no facial characteristics to draw attention to their needs.

“It is not the FACE that needs the services”

The Utah Addiction Center Report The Utah Addiction Center Report 58

Methamphetamine

Methamphetamine use among women is continuing to rise throughout the nation and many of these women are or will be pregnant. Although there are reports that have associated prenatal methamphetamine use with an increased incidence of premature delivery and placental abruption, the IDEAL study found no increase in maternal medical problems in 408 mothers who used methamphetamine during pregnancy. The study did find that methamphetamine exposure was associated with a decrease in birth weight and gestational age. Methamphetamine-exposed infants were found to have lower arousal and more stress signs, similar to cocaine. These subtle neurobehavioral findings are consistent with previous findings in cocaine and nicotine exposed children. The cohort of children in the IDEAL study is being longitudinally followed and the reports to date show no differences in mental development at ages 1, 2, and 3 years.

Conclusion

All drugs that work on the CNS have potential to affect fetal brain development when used by a pregnant mother. In the short-term, with the exception of opiates, drug-exposed newborns usually have no to minimal neurobehavioral problems in the newborn nursery.

Long-term outcomes of in utero exposed children are being interpreted through the lens of the newest brain research. The NIH has sponsored research over the last several years involving MRI and functional imaging of the normally developing brain in children. This has led to a greater insight into how long it takes to fully develop and use the frontal cortex. In fact, it isn’t until the early 20s that the frontal cortex is fully developed. Researchers following cohorts of drug-exposed children into adolescence are seeing subtle yet significant differences in small subsets of their study populations in terms of frontal cortex processing. These differences were not noted when the children were younger because they weren’t yet able to use their frontal cortex. It is anticipated that as these children continue to be followed and evaluated, other differences in frontal cortex processing will be defined. The functional outcome of these subtle differences, in other words, do these differences have meaningful impact on how they live their lives, has yet to be defined. However even subtle effects can produce sizeable population level impacts on resource needs for educational intervention services. It should be noted, though, that the magnitude of observed outcomes of illicit substance use, to date, does not compare to the more established health and developmental risks of prenatal alcohol and tobacco exposure.

Even with the evidence that prenatal exposure to drugs of abuse can exert direct effects on the central nervous system that can potentially have long term consequences, the overwhelming evidence of all of the outcome studies is that the quality of the postnatal environment has a huge impact on the outcome of the child. Prenatal exposure is viewed as placing a child at biologic risk for problems in the future, similar to the way the child’s genetic profile can put them at risk. Whether these risks manifest themselves depends significantly on the way they are raised. Attention must be paid to the quality of the post-natal environment to ensure the best possible outcome.

very high incidence of evident fetal alcohol syndrome and partial FAS. In one orphanage in Russia, 40% of children were diagnosed with FAS by an American clinical geneticist who is a specialist in FAS. Clinicians working with children in these groups should have a high index of suspicion for FASD.

There is ongoing argument and discussion about diagnosing FAS and FASD. Some of the argument is because of no diagnostic test. However there is also an overlay. Twenty years ago, physicians would not consider or make a diagnosis of FAS. One of the stated reasons was that it hurt the child and family to have a “label”, and why do that because there was not treatment. Fortunately, this attitude has mostly disappeared, but many people still don’t think there is much to do to help people with FASD.

Alcohol is a teratogen - a substance capable of interfering with the development of a fetus, causing birth defects. This has been very well documented in animal studies. Teratogens vary in their toxicity. Some substances cause fetal damage at much higher levels than others. For instance isotretinoin, a medication used for acne is a highly teratogenic agent with a 30-50% incidence of congenital malformations. Evidence of prenatal alcohol use can only be seen in about 15-20% of exposed pregnancies. This does not include at this time the children who have functional brain damage without physical findings.

Thus not every person who drinks alcohol prenatally will have an affected baby. There are several modifying factors that play a role. However, at this time it is not possible to calculate the effects on any individual. These modifying factors include genetics, maternal age, social factors, and maternal nutrition. Dose, drinking pattern, gestational age are also important modifiers. Peak blood alcohol level is important. Thus a single binge (≥4 drinks per occasion) or multiple binges can have a significant impact on fetal brain development at the time of the binge. This is frequently a teen drinking pattern.

The problem is there is no way to assess who is at greater risk, so the surgeon general’s warning has been reiterated in recent years:

There is no known safe amount of alcohol exposure so women are urged not to drink any alcohol during pregnancy. This also applies to nursing mothers. Alcohol crosses into breast milk and the baby will be sharing the drink of the mother at a time of very rapid brain growth.

What is the clinical picture of FASD – specifically alcohol related neurodevelopmental disability? (ARND).

The Institute of Medicine defined ARND as a confirmed history of prenatal alcohol exposure associated with central nervous system abnormalities and cognitive abnormalities.

MATERNAL AND FETAL BLOOD ALCOHOL CONTENT (BAC)DIFFUSION OF ALCOHOL FOLLOWING SINGLE DRINK

HOURS

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%

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Fetal BAC

Diffusion from MOTHERto fetus

Diffusion from FETUS to mother

Equilibrium

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30

20

10

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less destructive than originally thought. It has since been concluded that high-stress emotional and compromised nutritional environments either alone or in combination with the cocaine accounted for many of the early findings of severe cognitive and emotional deficits in these ‘crack babies’. While these conclusions by no means suggest that exposure of infants and young children to cocaine during critical developmental periods is without potentially serious consequences, it does remind us that the impact of drugs during development is very complicated, can be subtle and often is profoundly influenced by an interaction between drugs and environment.

This Newsletter addresses these and other linked critical issues related to how early drug exposure influences development and how these consequences can be addressed.

» Alcoholcontinued from page 1


Prenatal Alcohol Exposure: Lifelong Consequences of an Invisible DisabilitySusan O. Lewin, MD, Associate Professor of Pediatrics, Division of Medical Genetics, U of Utah School of Medicine

It would seem that if a baby was brain damaged from alcohol exposure prenatally, it would be a straightforward medical, social and psychological condition that could be managed as any other

prenatal disorder with complex effects such as spina bifida or Down syndrome. Unfortunately for those affected and their families, it has not been so for a variety of reasons. Only recently, and still insufficiently, individuals with FASD are being diagnosed and offered treatment.

History

Sometimes we have to relearn the lessons of history. In biblical times, “taking no strong drink’ was written in the Old Testament, Sparta and Carthage had regulations for newly-weds about not conceiving under the influence of alcohol. During the gin epidemic in London, many children were born “feebleminded” as depicted in Hogarth’s painting. There was the striking natural experiment of incarcerated women in Edinburgh whose children born were healthy if the mother was pregnant while in jail and the sibs born “outside’ while mothers were drinking, were affected by FAS

More recently, in the early 1970’s, the French, Germans, and then the Americans, published reports which describe children born to alcoholic mothers. These children had similar and characteristic physical findings. The common denominator was that the mothers were alcoholic and drank heavily during early pregnancy. The children were small (< 10th centile), have small heads (microcephaly) , and a characteristic facial appearance. The most striking findings are the small palpebral fissures (eye openings), a thin upper lip and a flat philtrum. There may be structural birth defects – heart, kidney and skeletal malformations; most importantly, there are abnormalities in brain development and/or function. These range from lethal brain malformations to subtle frontal lobe abnormalities, with executive function problems. They are “hard-wired” and permanent abnormalities if they are present, and unless we recognize them, the affected person is not offered care and may have lifelong maladaptive behaviors due to organic brain damage.

Terminology

Fetal alcohol syndrome (FAS) is readily recognizable as a syndrome – there are physical, growth and developmental components and children with FAS look more like each other than like their unaffected siblings. However, characteristic FAS can only occur if there is heavy drinking in the first 12 weeks of pregnancy. If a woman drinks heavily after that, the face and major organs have formed, and changes that occur will be more subtle. These changes are usually in the brain, and in growth. The result is a very wide range of possible outcomes. As there is no laboratory diagnostic test, recognizing “milder” forms as part of the clinical spectrum of FAS becomes very difficult. It remains a clinical diagnosis requiring a history of significant prenatal exposure and neuropsychological abnormalities with or without physical findings.

Fetal Alcohol Spectrum Disorder: This has resulted in the ironic situation that having a “milder” or less recognizable form of fetal alcohol syndrome, currently known as fetal alcohol spectrum disorder (FASD) may result in lack of diagnosis or wrong diagnosis, so that no or improper management is offered to the children and families. This can have catastrophic results and costs all of society significantly.

FASD is subdivided by the Institute of Medicine into several categories:

Fetal Alcohol Syndrome: 3 Categories

1. FAS with confirmed maternal exposure

2. FAS without confirmed exposure

3. Partial FAS with confirmed exposure

Alcohol Related Effects: Two categories may co-occur

1. Alcohol related birth defects (ARBD)

2. Alcohol related neurodevelopmental disorder (ARND)

For a diagnosis of ARBD or ARND, a history of substantial alcohol exposure must be obtained. If it is not available, the diagnosis can only be presumptive.

Scope:

“Of all the substances of abuse (including cocaine, heroin, and marijuana), alcohol produces by far the most serious neurobehavioral effects in the fetus.” — IOM Report to Congress, 1996

This remains true as shown in the annual national studies. Also, women continue to drink alcohol during pregnancy at a fairly steady rate. Although drug screens can be performed at birth, and the presence of many drugs can be detected in the baby at delivery, alcohol cannot be measured unless the mother consumed alcohol within a few hours before delivery. There are ongoing attempts to develop screening tools to assess alcohol exposure in the newborn, such has testing hair, but none have gained wide acceptance as yet. It is difficult to know how much to extrapolate and assume the use of alcohol if the drug screen is positive. Many

but not all women use alcohol along with methamphetamine and cocaine By self report, about 10-12% of US women will drink or binge drink during pregnancy, and are therefore at risk of having a baby damaged by the prenatal exposure. Peak blood alcohol level is important. A binge (≥4 drinks per occasion) can have a significant impact on fetal brain development at the time of the binge. Alcohol is a small molecule and crosses the placenta easily by diffusion. For a period of time, the blood alcohol level in the fetus is higher than in the mother, because of the immaturity of the fetal liver.

Modifying factors:

Prevalence of FASD in the US: varies depending upon the source

• Mostreport0.5-3/1000

• FASD(notFAS)morecommon:upto15/1000

• 6-22infantsborndailyinUSwithFAS

• 87-103infantsbornwithFASD

• Utahestimate:1bornwithFASDevery3-6days

Some populations have a higher prevalence of FASD. Foster children are up to 10x more likely to have FASD. Children from Russia and Eastern European countries, especially from the orphanages, have a

MMWR May 22, 2009 / 58(19);529-532

1991 1993 1995 1997 1999 2001 2003 2005

Any use, not pregnant

Binge drinking, not pregnant

Any use, pregnant

Binge drinking, pregnant

PE

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YEAR

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50

40

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0.7

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ALCOHOL

COCAINE

ANY ILLICIT DRUG

MARIJUANA

The Utah Addiction Center Report The Utah Addiction Center Report 58

Methamphetamine

Methamphetamine use among women is continuing to rise throughout the nation and many of these women are or will be pregnant. Although there are reports that have associated prenatal methamphetamine use with an increased incidence of premature delivery and placental abruption, the IDEAL study found no increase in maternal medical problems in 408 mothers who used methamphetamine during pregnancy. The study did find that methamphetamine exposure was associated with a decrease in birth weight and gestational age. Methamphetamine-exposed infants were found to have lower arousal and more stress signs, similar to cocaine. These subtle neurobehavioral findings are consistent with previous findings in cocaine and nicotine exposed children. The cohort of children in the IDEAL study is being longitudinally followed and the reports to date show no differences in mental development at ages 1, 2, and 3 years.

Conclusion

All drugs that work on the CNS have potential to affect fetal brain development when used by a pregnant mother. In the short-term, with the exception of opiates, drug-exposed newborns usually have no to minimal neurobehavioral problems in the newborn nursery.

Long-term outcomes of in utero exposed children are being interpreted through the lens of the newest brain research. The NIH has sponsored research over the last several years involving MRI and functional imaging of the normally developing brain in children. This has led to a greater insight into how long it takes to fully develop and use the frontal cortex. In fact, it isn’t until the early 20s that the frontal cortex is fully developed. Researchers following cohorts of drug-exposed children into adolescence are seeing subtle yet significant differences in small subsets of their study populations in terms of frontal cortex processing. These differences were not noted when the children were younger because they weren’t yet able to use their frontal cortex. It is anticipated that as these children continue to be followed and evaluated, other differences in frontal cortex processing will be defined. The functional outcome of these subtle differences, in other words, do these differences have meaningful impact on how they live their lives, has yet to be defined. However even subtle effects can produce sizeable population level impacts on resource needs for educational intervention services. It should be noted, though, that the magnitude of observed outcomes of illicit substance use, to date, does not compare to the more established health and developmental risks of prenatal alcohol and tobacco exposure.

Even with the evidence that prenatal exposure to drugs of abuse can exert direct effects on the central nervous system that can potentially have long term consequences, the overwhelming evidence of all of the outcome studies is that the quality of the postnatal environment has a huge impact on the outcome of the child. Prenatal exposure is viewed as placing a child at biologic risk for problems in the future, similar to the way the child’s genetic profile can put them at risk. Whether these risks manifest themselves depends significantly on the way they are raised. Attention must be paid to the quality of the post-natal environment to ensure the best possible outcome.

very high incidence of evident fetal alcohol syndrome and partial FAS. In one orphanage in Russia, 40% of children were diagnosed with FAS by an American clinical geneticist who is a specialist in FAS. Clinicians working with children in these groups should have a high index of suspicion for FASD.

There is ongoing argument and discussion about diagnosing FAS and FASD. Some of the argument is because of no diagnostic test. However there is also an overlay. Twenty years ago, physicians would not consider or make a diagnosis of FAS. One of the stated reasons was that it hurt the child and family to have a “label”, and why do that because there was not treatment. Fortunately, this attitude has mostly disappeared, but many people still don’t think there is much to do to help people with FASD.

Alcohol is a teratogen - a substance capable of interfering with the development of a fetus, causing birth defects. This has been very well documented in animal studies. Teratogens vary in their toxicity. Some substances cause fetal damage at much higher levels than others. For instance isotretinoin, a medication used for acne is a highly teratogenic agent with a 30-50% incidence of congenital malformations. Evidence of prenatal alcohol use can only be seen in about 15-20% of exposed pregnancies. This does not include at this time the children who have functional brain damage without physical findings.

Thus not every person who drinks alcohol prenatally will have an affected baby. There are several modifying factors that play a role. However, at this time it is not possible to calculate the effects on any individual. These modifying factors include genetics, maternal age, social factors, and maternal nutrition. Dose, drinking pattern, gestational age are also important modifiers. Peak blood alcohol level is important. Thus a single binge (≥4 drinks per occasion) or multiple binges can have a significant impact on fetal brain development at the time of the binge. This is frequently a teen drinking pattern.

The problem is there is no way to assess who is at greater risk, so the surgeon general’s warning has been reiterated in recent years:

There is no known safe amount of alcohol exposure so women are urged not to drink any alcohol during pregnancy. This also applies to nursing mothers. Alcohol crosses into breast milk and the baby will be sharing the drink of the mother at a time of very rapid brain growth.

What is the clinical picture of FASD – specifically alcohol related neurodevelopmental disability? (ARND).

The Institute of Medicine defined ARND as a confirmed history of prenatal alcohol exposure associated with central nervous system abnormalities and cognitive abnormalities.

MATERNAL AND FETAL BLOOD ALCOHOL CONTENT (BAC)DIFFUSION OF ALCOHOL FOLLOWING SINGLE DRINK

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less destructive than originally thought. It has since been concluded that high-stress emotional and compromised nutritional environments either alone or in combination with the cocaine accounted for many of the early findings of severe cognitive and emotional deficits in these ‘crack babies’. While these conclusions by no means suggest that exposure of infants and young children to cocaine during critical developmental periods is without potentially serious consequences, it does remind us that the impact of drugs during development is very complicated, can be subtle and often is profoundly influenced by an interaction between drugs and environment.

This Newsletter addresses these and other linked critical issues related to how early drug exposure influences development and how these consequences can be addressed.

» Alcoholcontinued from page 1


mothers smoked during pregnancy. Most of these studies have methodologic problems such as not controlling for confounders such as parental IQ, psychiatric history, parenting style, etc. In reviewing the literature, there is no definitive study that confirms that in utero exposure to nicotine is responsible by itself for the differences in behavior and IQ seen between the exposed and unexposed groups. But with 25% of pregnancies exposed to nicotine through maternal smoking, even small differences between groups are significant, making prevention even more important.

Marijuana

Of the illicit substances, marijuana is the most frequently used by pregnant women. The Maternal Lifestyle Study reported that marijuana use was not significantly related to low birth weight or preterm birth. The IDEAL study also found that marijuana use was unrelated to gestational age-adjusted birth weight. While some behavioral differences have been observed in marijuana-exposed newborns compared with un-exposed newborns, there is little evidence that prenatal exposure to marijuana results in significant long-term difficulties in children.

Opiates/Opioids

The research on the effects of prenatal exposure to opiates isn’t as extensive as one may think given that opiate addiction has been around a very long time. Most studies of prenatal opiate (e.g. heroin or methadone) use show increased risk for low birth weight and preterm delivery, but few have controlled for associated risk factors, such as smoking tobacco. It is important to note that prenatal opiate use has not been associated with prematurity or birth defects. It is the well documented effect of opiate dependence on the neonate that sets prenatal opiate exposure apart from the other classes of drugs. Between 50 to 94% of prenatally exposed newborns will experience neonatal abstinence syndrome and require prolonged hospitalization. The physiologic effects of opiate withdrawal are more profound and troublesome to the newborn than any of the short term effects seen with exposure to the other drugs like cocaine or methamphetamine.

There is a paucity of studies addressing the issue of the long-term outcome of opiate exposed children. A study published in 2002 conducted in Norway followed heroin exposed children for 4 years. All of these children were either adopted or raised in foster care. They found that all children had normal cognitive scores at 4 years, but that a special weakness in the area of visual-motor and perceptual abilities was detected. There is a concern for differences on developmental testing between exposed and unexposed, but most studies did not control for polydrug exposure. There is a need for well-designed follow-up studies for these children.

Cocaine

Of all illicit substances, there are more outcomes studies concerning cocaine. There was a rapid rise in cocaine use in the 1980s and a great deal of cocaine research was funded. The MLS reported that cocaine use was associated with decreased birth weight, head size, and length among infants born at 33 weeks or more gestation adjusted for confounders such as other drug use, inadequate prenatal care, and medical risk factors. These were the same effects seen with tobacco. The MLS also reported that cocaine-exposed infants showed more neurologic “soft signs” and behavioral effects in the newborn period than non-exposed newborns.

The cohorts of cocaine-exposed children in research studies are now in late adolescence and are continuing to be followed. One can summarize that the current research suggests that, although there are effects of cocaine on child development, these effects are inconsistent and subtle and need to be understood in the context of polydrug use and the caregiving environment. There is concern that cocaine may affect areas of the brain that control behaviors such as substance use, psychopathology, antisociality, academic and cognitive problems. Research has yet to be conclusive regarding these concerns, however.

Evidence of CNS developmental abnormalities including at least one of the following:

• Decreased head size at birth

• Structural abnormalities e.g. microcephaly, agenesis of corpus callosum, cerebellar hypoplasia

• Hard or soft neurological signs

Complex pattern of cognitive or behavior abnormalities defined as:

• Inconsistent with developmental level

• Not explained by family background or environment alone

These cognitive or behavior abnormalities include difficulties with:

• Learning

• School performance

• Impulse control

• Higher level expressive and receptive language

• Social perception

• Abstraction or metacognition

• Math skills

• Memory

• Judgment

• Attention

Obviously this is a broad list and covers many aspects of behavior and learning problems. This also overlaps with many mental health diagnoses. As it is not possible to prove the diagnosis, a high index of suspicion is required to consider the ARND diagnosis as well as a reliable history of exposure. Red flags include:

• A diagnosis of reactive attachment disorder long after it is likely or if the child was too young

• The child repeatedly fails to progress with interventions provided at home and school that should be helping.

Diagnosis

1. Physical Diagnosis: The diagnosis of FAS and FASD should be made by a medical professional experienced with the disorder This is usually a medical geneticist, developmental pediatrician or neurologist or other interested physician. There is a differential diagnosis of conditions that look like FAS.

2. Neuropsychological Diagnosis: A psychologist and neuropsychologist needs to assess learning style and especially executive function, impulse control, memory and other frontal and prefrontal functions. Theses tests are not adequately covered in school psychological testing and many children may pass as able to function at school, when in fact they may have significant processing, memory and insight abnormalities in addition to ADHD. If this happens, the child may get blamed for not succeeding because disability is not recognized. Neuropsych testing should be undertaking after about age 5.

Management

A child with fetal alcohol syndrome, like children is recognizable has having special needs.

However for the majority of children exposed to brain damaging amounts of alcohol prenatally, there are no facial characteristics to draw attention to their needs.

“It is not the FACE that needs the services”


One of the most problematic issues is poly-drug exposure. Researchers have not found a group of women and their babies to enroll in these studies who use one and only one substance of abuse (the one exception may be tobacco use). Most also use at least tobacco and/ or alcohol. The studies published in the late 1980s and early 1990s most often did not address the issue of poly-drug exposure.

The issue of controlling for confounders becomes increasingly difficult when looking at outcomes beyond the newborn period. These longer term outcome studies are trying to relate behavioral and cognitive function of the exposed child to the in utero exposure. To do this, one must control for a long list of confounders including maternal mental health, maternal education level, socioeconomic status, whether the child was raised in a stable home without substance use, in a home with continuing substance abuse, in foster care, and the list can go on and on.

Especially when looking at outcomes such as attention deficit disorder and learning disabilities, it is important to know if the biologic parents had these diagnoses, yet there are only a few studies that have attempted to address this confounder. When one reads a study about outcome of the drug-exposed child, one should read carefully the methodology to assess how good the attempt was to control for confounders. As a blanket statement, studies published in the early 90s did not do a good job of addressing these confounders and resulted in overstatements about the effects of in utero exposure.

The Maternal Lifestyle Study and the Infant Development Environmental and Lifestyle Study

Because of the deficiencies in the research done in the early 90s, the major researchers in the area of outcome for drug-exposed newborns and children designed better and more comprehensive studies that addressed many of those deficiencies. The Maternal Lifestyle Study (MLS) and the Infant Development Environmental and Lifestyle Study (IDEAL) study are two multi-center longitudinal studies that are following cohorts of drug-exposed children. The MLS is a federal interagency collaborative effort and is the largest clinical prospective longitudinal study of acute neonatal events and long-term health and developmental outcomes associated with cocaine use during pregnancy. It was designed to address many of the methodological issues that limited the interpretability of prior studies, especially addressing the issues of polydrug use and the adequacy of the caregiving environment . Four institutions enrolled mothers and their infants between 1993 and 1995 and have been following them ever since. Those children are now entering adolescence and are continuing to be followed. The second study is the Infant Development Environmental and Lifestyle Study which again is a longitudinal prospective study, this time focusing on methamphetamine exposure. It follows many of the same methodologies of the MLS, in fact, it has some of the same lead investigators.

Next, a brief summary of the findings, when applicable, of the MLS and IDEAL study in regard to individual drugs.

Nicotine

The Maternal Lifestyle study did not look at nicotine effects, but one must never forget that tobacco smoking during pregnancy is the one of the leading causes of low birth weight in the United States. It is dose-related in that women can improve the birth weight of their babies by reducing the number of cigarettes they smoke each day. As for nicotine’s effect on the central nervous system, neonates born to mothers who smoke cigarettes have been shown to have neurobehavioral differences that begin shortly after birth. Importantly, maternal smoking while pregnant has emerged as a major risk factor in almost every epidemiologic study of SIDS. A review of nicotine outcome research published in the Journal of the American Academy of Child and Adolescent Psychiatry reported that in utero exposure to tobacco is associated with motor, sensory, and cognitive deficits in infants and toddlers. Findings in young children also seem to support a negative influence of in utero exposure to nicotine on behavior and cognitive function. There are many studies that have reported an increased rate of behavior disorders such as attention deficit disorder and conduct disorder among adolescents whose

Successful management is dependent upon making the right diagnosis. With a diagnosis, our percpetion of the child as having brain damage changes our expectations for the child. The characteristics that may enrage or frustrate before diagnosis are recognized as disability after.

Medication may be appropriate for many individuals, but the mainstay of management is about understanding the particular child, and modifying the environment so that he or she can succeed, and then learn. Trial and dose modification depending on symptoms takes time and patience/

Interpretation of Behaviors

Because of the patchy nature of the brain damage in ARND, some behaviors are typical and others are appropriate for much younger children. A helpful way to think of this is presented by Diane Malbin:

For an 18 year old:

SKILL EQUIVALENT DEVELOPMENTAL AGE (years)

Expressive Language 20

Comprehension 6

Money, time concepts 8

Emotional maturity 6

Physical maturity 18

Reading ability 16

Social skills 7

Living skills 11

A care provider or teacher must be alert to the potential range of abilities and it requires great skill to manage the behaviors in a single individual. Helpful management words are: SHOW me – they can parrot back words but may not understand the words.

Helpful concepts for care providers to reframe management include:

• Structure, structure, structure

• “Stretched toddlers”

• “10 second people in a 2 second world”

• They can talk the talk - can they really walk the walk?

These children are NOT competent adults at age 18, and if they are not provided structure and support as long as is necessary – often lifelong, they will fail, and will often end up in the criminal justice system where they deteriorate fast. FASD is a killing condition if we don’t provide adequate lifelong support.

Resources

Local Resources:

• www.utahfetalalcohol.org - has many references both local and national as well as local information and contacts. They also have a facebook page: Utah FASD Coalition

• Lynn Tanner, RN, 801 776-0054 [email protected]

At a Glance“ALARMS” or “ALARMMERS” helps us think about the behaviors

AdaptationMotorLearningExecutive functionADHDRegulation of stateReasoning (IQ)Speech/languageMemory Clarren et all 2005


The Utah Division of Substance Abuse reported for 2009 that 6300 women

were admitted to public substance abuse treatment programs (Figure 1). On admission to the program, they are asked what their primary substance of abuse is. Methamphetamine was the most common, followed by alcohol. Of particular interest is that opiate addiction (which includes heroin and other opiates like oxycodone), is a significant problem. 357 (5.7%) of these women entering treatment were pregnant, indicating that their newborn has been exposed to these substances. What are the consequences of this exposure? This article will briefly review the medical literature about prenatal drug exposure and outcomes for the children.

Why is there specific concern about exposure to substances of abuse during gestation?

There is biologic plausibility that adverse events are happening to the fetal brain when exposed to these substances that exert their effects through the central nervous system. All substances of abuse work in the brain by changing the levels of naturally-occurring neurotransmitters, the chemicals that are an essential part of how nerve cells communicate. In the developing fetal brain, animal research has shown that neurotransmitters are not only there to move messages from one neuron to the next, but they also serve as trophic or growth factors in brain development. These molecules are capable of inducing and sustaining the growth and differentiation of nerve cells in the brain. If the neurotransmitters necessary for normal brain development are disrupted or altered by maternal substance use, structural changes may occur in the fetal brain that may have subsequent effects on later brain function and behavior. This is one major concern regarding in utero exposure. Another major concern about prenatal exposure is that the use of drugs that work on the central nervous system can alter the hormonal balance in the growing fetal brain. Barry Lester and colleagues at Brown University have hypothesized that substance abuse during pregnancy acts as an intrauterine stressor that can alter the expression of genes that are important to placental function. This, then, can lead to changes in the levels of important nervous system hormones in the fetal brain. They hypothesize that these changes could lead to enduring developmental and behavioral alterations in children with prenatal drug exposure.

What do the outcome studies say about prenatal exposure?

In order to know whether or not these hypothesized changes in fetal brain structure after in utero exposure to a particular substance of abuse manifest themselves as problems as the child grows up, outcome studies must be performed. When reviewing the published outcome studies, it is important to understand the difficulties of this type of research. The challenge is to relate the outcome measure of interest, for example, abnormal newborn behavior, to the variable of interest, say, in utero cocaine exposure while controlling for all the other variables that also may influence newborn behavior.

Assessing the effects of prenatal exposure to substances of abuse: What does current research tell us?Karen F. Buchi, MD, Professor, Chief, Division of General PediatricsDepartment of Pediatrics, University of Utah

• Pat Smith, [email protected]

• Susan Lewin, MD, Division of Medical Genetics U of Utah for diagnosis and management consultation and educational presentations. [email protected]. For appointments call Central Scheduling: 801 213-3599 or if urgent contact Heather 801 587-7563

• Support Group in Davis County: 2nd Thursday of the month - every other month and runs September through May as follows: September, November, January, March, May Time: 6:00 p.m. - 7:30 p.m., Davis Family Advocate Program 836 S. State Street Clearfield, Utah 84015. Contact Lynn Tanner (contact above)for more information.

There are many websites, including these official national sites:

• SAMHSA FASD Center for Excellence: fasdcenter.samhsa.gov

• Centers for Disease Control and Prevention FAS Prevention Team: www.cdc.gov/ncbddd/fas

• National Institute on Alcohol Abuse and Alcoholism (NIAAA): www.niaaa.nih.gov

• National Organization on Fetal Alcohol Syndrome (NOFAS): www.nofas.org

• National Clearinghouse for Alcohol and Drug Information: www.ncadi.samhsa.gov

Final notes

Due to the broad range of expression of ARND, if a provider is suspicious that a person has ARND but cannot confirm it, it is be worth treating the child as if this were the correct diagnosis, because management is then geared to the whole child who has permanent organic brain damage, and is more likely to be successful. This does not mean that other diagnoses or co-ocurring diagnoses should be forgotten.

And from a couple of parents:

To Label or to Diagnose

“Most parents of children with FAS/pFAS already feel that their children are labeled,-- as lazy, non-compliant, mean or stupid…We’d prefer an accurate diagnosis that describes what is happening with our children. A diagnosis of FAS (or ARND) makes REAL that our children experience, and that we experience raising them. We aren’t excusing our children’s behavior or imagining the difficulties they experience. An accurate diagnosis can motivate others to learn more about our children and how to work with them. At the very least, it helped me understand my son better, and I was able to learn strategies that made me a more effective parent for him.” --Don Adams, 1999

“We must move from viewing the individual as failing if s/he does not do well in a program

to viewing the program as not providing what the individual needs in order to succeed.”

—Dubovsky, 2000

To provide for our children successfully it is important to remember:

• FASD is a permanent lifelong condition

• Organic brain damage never goes away

• Diagnosis is helpful, label is not

• Progress continues throughout life

• Scaffold of support should never be removed

Utah Division of Substance Abuse Annual Report 2009

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Figure 1.

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February 2011 Dedicated to research, clinical training, and education in chemical addiction

INSTITUTIONAL ADVISORY BOARD

Glen W. Hanson, Ph.D, D.D.S

Utah Addiction CenterUniversity of UtahHealth Sciences Center410 Chipeta Way, Suite 280Salt Lake City, Utah 84108

ContaCt Us

University of UtahHealth Sciences Center410 Chipeta Way, Suite 280Salt Lake City, Utah 84108

Phone: (801) 581-8216Fax: (801) 587-7858E-mail: [email protected]: http://uuhsc.utah.edu/uac/

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The Utah Addiction Center is based in the office of the University of Utah Senior Vice President for Health Sciences

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Volume 2 Issue 12

“Jonah’s mother was a heroin addict. Shortly after birth, it was obvious Jonah was in withdrawal. His jittery movements and crying persisted for the next 2 days and there was little anyone could do to console him. He scratched his face trying to get his hands to his mouth. His knees and elbows were rubbed raw from his agitated movement, and the muscles in his tiny legs were so stiff

that it was difficult to straighten his legs to diaper him” (Available: http://drugabuse.gov/consequences/prenatal/ ). This real-life account illustrates the disturbing impact of exposing a developing fetus to potent drugs of abuse during pregnancy. Most of the symptoms described above are due to the fact that the infant’s body is going through withdrawal from the effects of months of exposure to heroin. As difficult as it is to watch an innocent newborn suffer through this process, it is of some consolation to know that these withdrawal effects can be relieved with proper treatment and with time they will subside. However, effects of drugs of abuse during prenatal periods or exposure to these substances postnatally or even through adolescence can sometimes permanently affect a child’s development in dramatic or sometimes less obvious ways depending on the drug, the exposure pattern and environmental factors. Most people are aware that consumption of large quantities of alcohol through pregnancy frequently debilitates the offspring because expression of the resulting fetal alcohol syndrome (FAS) includes severe physical and emotional damage that compromises the intellectual, cognitive and motor functions of the afflicted child. Such damage can be evident during the pregnancy or immediately after birth. By comparison, the impact of other drugs of abuse is more difficult to identify and may be associated with subtle diminished capacity that doesn’t fully express until years after the drug exposure. For example, over the past two decades, particularly during the height of the cocaine epidemic in the United States, considerable scientific effort was focused on determining the adverse effects of this potent stimulant, especially in cocaine-exposed infants and toddlers. Early reports of severe damage in children exposed to crack cocaine lead to the stigmatizing label of so-called ‘crack babies.’ After conducting better controlled studies with improved elements of prospective designs, it was determined that exposure of these young children to cocaine per se was much

A. Lorris Betz, M.D., Ph.D.Louis H. Callister, J.D.Edward B. Clark, M.D.

M. David Rudd, PhD, ABPP Patrick Fleming, LSAC, MPARaymond Gesteland, Ph.D.

Jay Graves Ph.D.John R. Hoidal, M.D.

Glen W. Hanson Ph.D, D.D.S,Maureen Keefe, RN, Ph.D

Jannah Mather, Ph.D.Chris Ireland, Ph.D.

John McDonnell, Ph.D.Barbara N. Sullivan, Ph.D.

Ross VanVranken, ACSWKim Wirthlin, MPA

Drug Exposure and Development

» See Alcohol page 5

drug exposure & development

Documents

effects of drugs

drug exposure

withdrawal effects

exposure pattern

potent drugs of abuse

cocaineexposed infants

cocaine epidemic

cocaine lead