As awareness of how childhood trauma affects neurodevelopment grows, questions arise about symptom complexity and how neurodevelopment is affected by other comorbid conditions. Youth exposed to toxic stress from early, severe and/or chronic maltreatment can show alterations in brain structure and connectivity that impact cognition, emotion regulation and stress reactivity (Teicher & Samson, 2016). However, neurodevelopment is also influenced by genetics and other types of adversity, including in utero exposure to substances. As child maltreatment co-occurs frequently with parental substance use and prenatal alcohol exposure, understanding the relationship between the two is important to differential diagnosis and treatment.
The neurobiological sequelae of fetal alcohol exposure appear in the Diagnostic and Statistical Manual (DSM-5, APA, 2013) under an unofficial new diagnosis termed neurobehavioral disorder associated with prenatal alcohol exposure (ND-PAE). The diagnosis requires a child to demonstrate neurocognitive, self-regulatory and executive function deficits after exposure to alcohol in utero. ND-PAE is considered a fetal alcohol spectrum disorder (FASD) in which a child may or may not exhibit phenotypic facial traits or somatic growth impairment.
Many of the impairments seen in children with FASDs are similar to those that have been found in traumatized youth. Brain imaging studies indicate that fetal alcohol exposure decreases the brain’s overall size, with alterations in the hippocampus, thalamus, caudate putamen, globus pallidus, basal ganglia, corpus callosum, caudate nucleus, prefrontal cortex, temporal and parietal lobes, and cerebellum. Disorganization of network connectivity and atypical activity can occur in the basal ganglia, cerebellum, insula, amygdala, and the temporal and parietal lobes (Mattson et al., 2019; Nardelli et al., 2011) Reduced connectivity and functioning of different brain areas impair learning as well as emotional and behavioral control. Children with FASDs tend to show inattention, overactivity, impaired cognition, emotional dysregulation, poor executive functioning and disordered social relationships. The teratogenic effect of alcohol also targets the developing fetus’s stress response system, potentiating reactions to traumatic stress.
Results of the few studies on children struggling with both trauma and FASDs indicate that when the two conditions co-occur, they conspire to increase symptomology (see Price et al., 2017, for a review). Henry et al. (2007) found the combined group obtained lower scores on intelligence, attention, memory and expressive language measures and were rated by parents and teachers as showing more oppositional, social, impulsive and inattentive symptoms. Koponen et al. (2009) found that trauma aggravated the social, emotional and neurocognitive problems of a sample of foster children who had been exposed in utero to alcohol. The pre-existing difficulties wrought by fetal alcohol exposure increase a child’s reactivity to trauma and decrease coping ability.
One of the prime differences between FASDs and trauma is that neurodevelopmental changes due to trauma are considered adaptations that help an organism survive a threatening environment, while alcohol is a teratogen that is globally toxic to the developing fetus. Prenatal alcohol exposure impacts the child earlier in development and its effects appear to be more severe, widespread and permanent. As a consequence, brain plasticity is more limited. Children suffering from the dual effects of trauma and FASDs are likely to be less resilient and responsive to treatment than children showing more normative development prior to experiencing trauma. Consequently, evidence-based treatments for trauma may benefit them but likely not sufficiently. Longer-term supports and interventions will be required (Murawski et al., 2015; Stirling & Zilberstein, 2021).
Because children exposed to alcohol in utero manifest behavioral symptoms similar to those seen in maltreated children, the disorder often goes unrecognized. In two different studies, over 80 percent of children qualifying for a fetal alcohol diagnosis had been previously misidentified (Chasnoff, 2015; May, 2018). In Koponen et al.’s (2009) study of foster children, researchers found that children with missed diagnoses of FASD exhibited more behavior problems than diagnosed children, likely because symptoms were misunderstood and appropriate interventions lacking. Effectively treating the intersection of trauma and ND-PAE depends upon recognizing their co-occurrence and considering their combined neurodevelopmental consequences.
About the Author
Karen Zilberstein, LICSW, is a clinical director for A Home Within and a psychotherapist who specializes in the treatment of youth who have experienced trauma and foster care. Her recent narrative nonfiction book, Parenting Under Pressure: Struggling to Raise children in an Unequal America, won two Indie Book Awards.
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