Autism spectrum disorder (ASD) tends to co-occur with epilepsy, but it remains unclear if ASD predisposes to epilepsy or vice versa. Using the National Survey of Children’s Health (2012), we assessed the relationship between ASD and epilepsy as disease co-occurrence, examined racial/ethnic variability therein and the risk markers. Compared to whites, blacks/African Americans were 54% less likely to be diagnosed with ASD, prevalence odds ratio (POR)=0.46, 95% CI, 0.34-0.63. In contrast, compared to whites, blacks/African Americans were 56% more likely to be diagnosed with epilepsy, POR=1.56, 95% CI, 1.24-1.96. Similarly, racial differences were observed in cooccurrence, with significant 20% higher risk among Blacks relative to Whites, POR=1.20, p<0.0001. Public insurance, poverty, maternal education, and intellectual disabilities were the two most potent predictors of ASDepilepsy co-occurrence. After controlling for age, sex, parental education, insurance coverage, federal poverty level, and intellectual disability, significant racial differences did not persist but Blacks were 74% less likely to report ASD & epilepsy co-occurrence relative to Whites, aPOR=0.26, p=0.23. In summary, racial disparities exist in ASD-epilepsy co-occurrence prevalence, which did not persist after controlling for potential confounders; while public insurance, maternal education, poverty and intellectual disabilities remain potent predictors of the co-occurrence. These findings suggestive of cautious optimism in assessing the causal direction in the co-occurrence of ASD and epilepsy among children.

Autism spectrum disorder (ASD) is a range of neurodevelopmental disorders characterized by the broad autism phenotype (BAP) which demonstrates impairments in communication, difficult in social interactions, and stereotyped patterns of behaviors, interests and activities. Although, this condition is largely misunderstood, recent epidemiological evidence suggests that by age 8, 1 out of 88 children will be diagnosed with ASD, with more diagnoses being reported each year. Нe pathophysiology of ASD has been difficult to identify due to the uncertainty surrounding its origins. Нe early overgrowth of higher cognitive brain regions in development is believed to contribute to an imbalance between excitatory-inhibitory networks, which is reflected by ASD phenotypes such as child agitation and stereotyped behaviors. Нese phenotypes underscore the frequent comorbidities of ASD with Fragile X syndrome, tuberous sclerosis, Tourette syndrome, attention deficLt disorder and epileptic seizure.