Facial emotion processing in children with fetal alcohol spectrum disorders: A test of the emotion specificity hypothesis

FACIAL EMOTION PROCESSING IN CHILDREN WITH FETAL ALCOHOL SPECTRUM DISORDERS: A TEST OF THE EMOTION SPECIFICITY HYPOTHESIS Erin Lynn Way, Ph.D. George Mason University, 2010 Dissertation Director: Johannes Rojahn, Ph.D. Prenatal alcohol exposure is the leading non-genetic, biological cause of birth defects and other anomalies. Perhaps as many as 1 in 100 children born in the United States each year have been exposed to alcohol during prenatal development and meet the criteria for a Fetal Alcohol Spectrum Disorder (FASD) diagnosis (May & Gossage, 2001; Schonfeld et al., 2006; Wattendorf & Muenke, 2005). There is abundant evidence of deficits in social functioning as a result of prenatal alcohol exposure (Coggins et al., 2003; Kodituwakku, May et al., 2001; McGee et al., 2009; Thomas et al., 1998). Many other atypically developing populations with demonstrated social deficits also have emotion-specific impairments in facial recognition that are more pronounced than would be expected based on the overall cognitive functioning of these individuals (i.e. emotion specificity hypothesis; Rojahn et al., 1995). The documented social impairment in children with prenatal alcohol exposure indicates these individuals also have emotionspecific facial recognition impairments. This study tested the emotion specificity hypothesis in a group of children with FASD and compared the facial emotion processing abilities of these children with reports of their adaptive social behavior. Twenty-five children with a FASD diagnosis, 14 children with Down syndrome, and 23 typically developing children matched on mental age participated in this study. Four facial processing tasks (2 emotion processing and 2 control tasks) were administered to all participants. Both labeling and matching formats were included in the emotion and control tasks. Although not expected, the children with FASD had similar performance to the typically developing children on all facial processing tasks, which failed to support the emotion specificity hypothesis in this population. As predicted, the children with Down syndrome showed poorer performance than the children with FASD and the typically developing children across all facial processing tasks. These tasks failed to reveal performance differences between children with FASD and typically developing children; however, facial emotion processing deficits may still exist within the FASD population. Future studies should consider modifying task demands to more accurately reflect natural face processing situations and include children with a FASD diagnosis from less enriched environments and with documented intellectual delays. Chapter I. Fetal Alcohol Spectrum Disorders Prenatal alcohol exposure is responsible for more birth defects, developmental disabilities, and intellectual deficiencies than any other non-genetic, biological cause; yet Fetal Alcohol Syndrome (FAS), first identified by Jones and colleagues in 1973, is completely preventable (National Center on Birth Defects and Developmental Disabilities National Task Force on Fetal Alcohol Effect [NCBDDD], 2004; National Institute on Alcohol Abuse and Alcoholism [NIAAA], 2000; Caley, Kramer, & Robinson, 2005; O’Leary, 2004; Streissguth, Aase, Clarren, Randels, LaDue & Smith, 1991). The costs associated with FAS makes the fact that it is completely preventable even more significant. In 1992, the National Institute on Drug Abuse estimated the lifetime cost of caring for an individual with FAS to be $1.5 million (Caley et al., 2005). In 1998, the 10 Special Report to the U.S. Congress on Alcohol and Health noted FAS costs the United States $2.8 billion (Caley, et al., 2005). The teratogenic effects of alcohol include interfering with the growth, progression, and functioning of nerve cells during fetal development (Caley et al., 2005; NCBDDD, 2004; O’Leary, 2004). Specifically, prenatal alcohol exposure causes dysmorphia by hampering cell growth and survival, promoting the creation of free radicals that damage the cells, changing the way chemical signals pass through cells, and influencing gene expression (NCBDDD, 2004). There is also a direct link between the