Abstract

Objective: Of the many sequelae of prenatal alcohol exposure (PAE), alterations in the developing brain and the resulting neurobehavioral deficits are among the most devastating. While effects occur on a continuum, research on the effects of PAE on language has been mixed. This case study will describe specific verbal deficits associated with PAE, and present a poly-etiologic hypothesis for the observed profile. Finally, treatment recommendations for educators and parents of alcohol-exposed youth will be discussed. Method: The client is a 7-year-old boy with moderate PAE and a history of severe neglect for the first five years of life. Client presented with symptoms including academic difficulties, confabulation in speech, ambiguous handedness, and poor peer relationships. Client underwent comprehensive neuropsychological evaluation that included measures of intellectual functioning, academic achievement, memory, phonological processing, executive functioning, and behavior. Results: Assessment revealed borderline intellectual ability, profound language impairment, impaired academic skills and verbal memory, intact visuospatial and executive skills, and variable behavioral functioning with significant discrepancies noted between teacher and parent ratings. Transcortical Sensory Aphasia, Agenesis of the Corpus Callosum, and hippocampal and amygdalar atrophy are all probable contributors to his cognitive impairments. Conclusion(s): The observed profile is a product of multiple areas of neurological injury caused by moderate PAE, a deprived early learning environment, and severe neglect in early childhood. The current case illustrates the importance of defining the multiple pathways through which PAE and early childhood experiences affect the developing brain.