Prenatal Alcohol Exposure

1. Prenatal Alcohol Exposure • Alcohol is a known teratogen. • Teratogens are substances that, when exposed to a developing fetus, impair normal development and cause birth defects in prenatal development. Teratogens can result in (Streissguth 1997): • death • malformations • growth deficiency • functioning deficits • Teratogens may have a dose-response effect, in that as the dose of the teratogen increases the deficits and impairments also increase.

2. Prenatal Alcohol Exposure • Alcohol has an interaction effect on development: alcohol interacts with the genes to produce impairments in offspring. • Not all children exposed to the same amount of alcohol will show similar deficits. Some children exposed to higher levels of alcohol may have less severe deficits than others exposed to lower levels or at different times during pregnancy. • In fact, the timing of the exposure during pregnancy, amount of alcohol consumed, other drug use, genetics of mother and children, stress, mothers ability to metabolize alcohol, and age of mother may all interact to produce various deficits. (Malbin, 2002)

3. PAE during the first trimester generally results in damage to physical structure and PAE during the third trimester typically affects growth or size of the fetus. The brain (CNS) develops throughout the entire pregnancy, and is affected by alcohol exposure at any time during pregnancy (Streissgith, 1997). Malbin (2002)

4. Fetal Alcohol Spectrum Disorder (FASD) • Prenatal alcohol exposure produces a range of effects including: • Fetal Alcohol Syndrome (FAS) • Fetal Alcohol Effect (FAE) • Fall under the new category of FASD • FASD refers to individuals who may have physical, mental, behavioral, and/or learning disabilities as a result of maternal alcohol consumption (Chudley et al., 2005).

5. Fetal Alcohol Syndrome (FAS) • FAS was first identified in 1973 by Jones & Smith, based on case observations in which clinicians noted a similar pattern of malformations among infants born to alcoholic mothers. • Similar effects of prenatal alcohol exposure were noted by Lemoine and Colleagues in France (1968).

6. FAS is characterized by: • growth deficiency in weight and or height • facial featuresthat may include short palpebral fissures (eye length), smooth philtrum (groove above upper lip), thin upper lip, flat midface, and short nose • damage to the CNSas indexed by microcephaly, cognitive deficits, learning problems, attentional difficulties, hyperactivity, and/or motor problems

7. From Streissguth and Little (1994).

8. Fetal Alcohol Effects (FAE) • FAEwas used to refer to children who did not have all the characteristics of FAS (usually absence of some or all facial features and/or lack of growth deficiency) but still had PAE and some CNS dysfunction (Clarren and Smith 1978). The Institute of Medicine (IOM) identified 3 classifications of Fetal Alcohol Effects: • Alcohol Related Neurodevelopmental Disorder (ARND): refers to individuals with alcohol exposure and CNS and neurobehavioral deficits. • Alcohol-Related Birth Defects (ARBD): refers to individuals with some congenital physical abnormalities as a result of alcohol exposure (heart, vision, hearing, skeletal problems). • Partial FAS: refers to individuals with some facial characteristics, and either growth or CNS deficits

9. FASD • Previously used diagnostic categories tended to focus on the presence or absence of facial dysmorphology. • With research we have learned that relatively few children prenatally exposed to alcohol have all of the physical features required to diagnose FAS. • The FAS facial features occur during a short period of vulnerability early in the first trimester (based on a mouse model) (Sulik et al., 1981). • The neurobehavioral consequences of prenatal alcohol exposure can occur with exposure throughout pregnancy.

10. From: Sulik K, Johnston M, Webb M. Fetal alcohol syndrome: embryogenesis in a mouse model. Science 1981;214:936-8.

11. FASD • Studies directly comparing the degree of neuropsychological impairments in those with and without the physical features of FAS yield no meaningful differences • The neuropsychological deficits associated with prenatal alcohol exposure appear to be independent of the physical characteristics of FAS. • The spectrum approach to terminology is advantageous over previous categorical approaches, because diagnosis of an FASD focuses more on CNS deficits as these are of greater functional significance than the physical features.

13. FASD • The incidence of FASD is estimated to range from 3-10 /1000 births. • FASD is one of the most common known cause of mental retardation. • Lifetime cost of FASD is estimated to be $1.5 - 2 million per person. • A recent Canadian study estimates annual costs of FASD at $344,208,000 for care of those less than 21 years of age.

14. Diagnosis of an FASD Chudley et al. recommend evaluating: • Growth • Facial Features • Neurobehavioral Functioning • Alcohol exposure • Physical features are not required for a diagnosis of an FASD.

15. Confirmation of Alcohol Exposure Challenges: Birth mother no longer available Unreliable self-report Forgetfulness Conflicting reports Biomarkers for PAE: Fatty Acid Ethyl Esters (FAEE) Found in meconium and hair of newborns Research studies find high rates of FAEE

16. Neurobehavioral Assessment • Hard and soft neurological signs • Brain structure (MRI, head circumference) • Cognition (IQ) • Communication (receptive and expressive) • Academic achievement • Memory • Executive functioning and abstract reasoning • Attention/hyperactivity • Adaptive behavior, social skills, social communication. Chudley et al., 2005

17. Behavioral Phenotype (Kodituwakku, 2007) • A characteristic pattern of motor, cognitive, linguistic, and social observations consistently associated with a biological disorder (O’Brien & Yule, 1995) • Causal connections between PAE and neurobehavioral effects are difficult to make because of the interaction of environmental and genetic factors.

18. Cognitive Functions (Kodituwakku, 2007) Intellectual ability: decreased IQ in children and adults with FASD. • Some dose-dependent effects • Deficits in both verbal and performance aspects Attention and speed of processing: • Significant deficits in sustained and focused attention. • Slower processing speed

19. Cognitive Functions (Kodituwakku, 2007) Executive Functioning (EF): higher-order cognitive processes involved in goal-oriented behavior. • The EF deficits in FASD have been documented on tests of cognitive flexibility, inhibition, planning and strategy use, concept formation, verbal reasoning, set-shifting, working memory, and fluency – all cognitive-based or ‘cool’ EF tests. • Also show deficits on ‘hot’ EF tests assessing emotion-related behaviors and decision making.

20. Cognitive Functions (Kodituwakku, 2007) Language: some mixed effects, but children with FASD generally have poorer language abilities. Visual Perception: most impaired on tasks that involve integration of information, planning, and visual-motor integration. Learning and Memory: slower at learning • Deficits on both visual and verbal memory tasks.

21. Cognitive Functions (Kodituwakku, 2007) Number Processing: although children with FASD have difficulties in many academic areas, math appears to be the most severely affected. Streissguth et al. (1994) conducted a large longitudinal study on children with PAE. • Out of many cognitive and academic tests, math was the most difficult and most highly correlated with PAE. • These math deficits were stable over time • Effects were generally dose-dependent • Math deficits in FASD are even lower than expected based on IQ scores.

22. Behavioral Dysfunction (Kodituwakku, 2007) Classroom Behaviors: distractible, inattentive, hyperactive, restless Adaptive Behavior: personal and social skills needed to live independently • Most deficits in social skills, interpersonal relationships • One study of adolescents and adults with FASD (mean age 17 years) found adaptive functioning skills to be at the level of a 7-year-old (Streissguth et al., 1991) Emotional Functioning: mental health disorders and emotional difficulties

23. Atypical Brain Development (Kodituwakku, 2007) • Decrease in white matter and overall brain size Abnormalities in: • Frontal lobe • Corpus Callosum • Basal Ganglia • Cerebellum • Diffusion Tensor Imaging

24. FASD and Risky Behaviors (Rasmussen & Wyper, 2007) Primary disabilities: those which directly result from the brain injuries of PAE and are evident in some form from birth. Intelligence, memory, attention Secondary Disabilities: result from primary disabilities and environmental interactions and are not evident from birth In theory they are preventable with better understanding of appropriate interventions

25. Secondary Disabilities Streissguth et al. (1996) conducted a longitudinal study on secondary disabilities in FASD. The Life History Interview (LHI), which measures common secondary disabilities, was administered to 415 individuals (6-51 years old) with FAS and FAE. The results were astounding: More than 90% of the sample had mental health problems 49% of the adolescents/adults and 39% of the children demonstrated inappropriate sexual behaviors

26. More than 60% of adolescents/adults and 14% of the children had disrupted school experience 60% of adolescents/adults and 14% of the children had been in trouble with the law 50% of the adolescents/adults had been confined (e.g. incarceration, inpatient mental health programs, or alcohol and drug treatment programs) 35% of the adolescents/adults had alcohol and drug problems. 67% had experienced physical or sexual abuse, or were victims of domestic violence 80% were not reared by their biological mother

27. Risk Factors Three risk factors were identified that were associated with higher rates of secondary disabilities: being diagnosed with FAE rather than FAS having an IQ above 70 higher scores on the Fetal Alcohol Behavior Scale which measures behaviors of fetal alcohol exposure Thus, having less severe physical effects (FAE instead of FAS) and a higher IQ were associated with a higher rate of secondary disabilities.

28. Protective Factors Streissguth et al identified 5 protective factors that resulted in lower rates of secondary disabilities: living in a good quality stable home environment infrequent changes in living arrangement not being exposed to violence receiving services for developmental disabilities being diagnosed before the age of 6

29. Delinquency and FASD Maladaptive behaviors: impulsivity, teasing/bullying, dishonesty (lying, cheating, stealing), avoiding school or work, destruction of property, physical aggression, and self-injury behaviors (LaDue et al, 1992). FASD linked to behavior problems and delinquency in adolescents (Carmichael Olson et al., 1997). Children with PAE have higher rates of delinquent behaviors than children with ADHD, including cruelty, bullying (48% of children), lying or cheating (90% of children), and stealing. 97% children with fetal alcohol exposure lacked guilt after misbehaving. Nash et al (2006)

30. Delinquency and FASD PAE is also associated with conduct behaviors and lower overall moral maturity (Schonfeld et al., 2005) Home environment related to delinquency in that youth living in biological or foster homes were more likely to engage in delinquent behaviors than youth living in adoptive homes. It is clear that individuals with FASD are particularly prone to delinquent behaviors; however some researchers suggest that this may be due to factors (e.g., family and individual characteristics) other than prenatal alcohol exposure (Lynch et al, 2003).

31. FASD and the Criminal Justice System Adolescents and adults with FASD are at particular risk for ending up in the criminal justice system. In Streissguth’s studies 60% of adolescents and adults with FASD had been in trouble with the law and 50% had been confined. A Canadian study found that 23% of youth remanded for a psychiatric inpatient assessment had an FASD (Fast et al., 1999). A recent Canadian report indicated that 10% of inmates had an FASD, which is 10 times higher than in the general population (Sandrers, 2007).

32. FASD and Psychopathology High rates of psychiatric disorders among children with PAE: 87% met criteria for a psychiatric disorder including mood disorders (61%), bipolar disorder (35%), major depressive disorder (26%) (O’Connor et al., 2002) PAE is linked to depressive symptoms among 6-year-old girls (O’Connor et al., 2001). In one study 97% of the alcohol-exposed children were diagnosed with an axis 1 disorder (Fryer et al., 2007) ADHD, depressive disorders, oppositional defiant disorder (ODD), conduct disorder (CD), phobias Adults with binge alcohol exposure have higher rates of many disorders including: somatoform, substance dependence/abuse, paranoid, passive-aggressive, antisocial, and personality disorders (Barr et al (2006)

33. FASD and Substance Abuse PAE is associated with alcohol problems in adolescents and adults (Baer et al. 2003) In one sample of adults with PAE, 25% had an alcohol disorder. (Alati et al., 2006) PAE is associated with the development of nicotine, alcohol and illicit drug dependence, even when biological parental alcohol abuse is controlled for. (Yates et al, 1998).

34. FASD and Suicidality Adolescents and adults with FASD are at risk for suicide and attempted suicide. O’Malley and Huggins (2005) carried out a pilot study of 11 individuals affected by FASD. Over half (6) of the participants reported attempted suicide, a rate that is drastically higher than the general Canadian population rate of 4.6%.

35. Factors Relating to Risky Behaviors in FASD The significant EF deficits in individuals with FASD likely contribute to high risk behaviors. Impairments in EF skills such as planning, cause-effect reasoning, learning from past mistakes, and the lack of social adaptability may be related to why youth with FASD are overrepresented in the justice system. The connection between poor executive functioning and juvenile delinquency has been well-documented in other populations. Adolescent/adult offenders are impaired on many tests of EF Inhibition appears to be one aspect of EF that is strongly related to delinquency and high risk behaviors.

36. Factors Relating to Risky Behaviors in FASD Poor decision making is linked to the frontal lobe Individuals with frontal lobe damage show similar risky and maladaptive behaviors as those with FASD. PAE has a negative effect on the frontal cortex, thus putting individuals with FASD at increased risk for engaging in problematic behaviors. Risk taking increases during adolescence because they are more sensation-seeking and reward-driven but have a prefrontal cortex that is still developing. In FASD, adolescence is a time of heightened vulnerability, as these individuals have even more of a gap between their brain/cognitive development and their behaviors.