Abstracts

Rationale: Anxiety is the second most frequent psychiatric comorbidity in individuals with epilepsy. Genetics is increasingly being emphasized as the cause of epilepsy, but few studies have examined potential psychosocial impacts of this information. We examined predictors of anxiety in affected and unaffected individuals in families containing multiple individuals with epilepsy, with a particular focus on the possible impact of attribution of epilepsy to a genetic cause. Methods: Participants completed a survey that assessed the psychosocial impact of having a personal or family history of epilepsy, beliefs about epilepsy genetics, and interest in genetic testing. The survey targeted 929 adult members of 113 families containing multiple individuals with epilepsy (average 4 affected per family). Among 701 participants contacted (76%), 592 (85%) agreed to participate. Here we report results on 366 individuals (179 with epilepsy and 187 unaffected biologic relatives) with complete information on anxiety who completed the survey as of May 8, 2015.We used the Generalized Anxiety Disorder-7 scale to screen for current symptoms associated with a diagnosis of generalized anxiety disorder (GAD). We used three questions to assess participants’ attribution of epilepsy to a genetic cause: “How big a role has genetics had in causing the epilepsy in your family?,” “What do you think the chances are that you have a change or mutation in a gene that affects risk for epilepsy?,” and (in people with epilepsy), “How much do you think genetics or inheritance influenced your risk of developing epilepsy?” Results: Individuals with epilepsy were significantly more likely to screen positive for GAD than were their unaffected biologic relatives (13% vs 6%, p=0.03). Among individuals with epilepsy, prevalence of a positive screen for GAD was associated with the perceived role of genetics in causing epilepsy in the family (no/small role 8% vs. medium role 26% vs. big role 9%, p=0.008). This association persisted after controlling for potential confounders.  A positive screen was not associated with the other two genetic attribution questions.  The proportion who screened positive for GAD increased with total reported number of lifetime seizures (≤20 12% vs. 21-100 18% vs. >100 21%), although these differences were not significant. Among biologic relatives without epilepsy, the only significant predictor of a positive screen was age ( Conclusions: In this study of families with multiple individuals with epilepsy, the strongest predictor of a positive screen for GAD was the belief that genetics caused the epilepsy in the family. Individuals with epilepsy who believed genetics had a medium role in causing the epilepsy in their family may have a higher risk of GAD. Funding: This research was supported by R01 NS078419.