Prenatal Alcohol Exposure

1. Prenatal Alcohol Exposure • Alcohol is a know 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. 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.

11. 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.

12. Neurobehavioral Assessment • Hard and soft neurological signs • Brain structure (MRI, 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

13. 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.

14. 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

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

16. Cognitive Functions (Kodituwakku, 2007) Language: some mixed effects but generally 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.

17. 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.

18. 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

19. Atypical Brain Development (Kodituwakku, 2007) • Decrease in white matter and increase in gray matter Abnormalities in: • Frontal lobe • Corpus Callosum • Basal Ganglia • Cerebellum

20. FASD • The incidence of FASD is estimated to range from 3-10 /1000 births. • FASD is one of the most common known causes 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.