(PS7-C59) An Examination of Response Inhibition Deficits in the Context of “not Just Right” Experiences

Background: Response inhibition (RI), or the ability to suppress a pre-potent response during goal-driven behavior, has been examined as a potential cognitive deficit regarding impulsivity and has been previously linked to obsessive-compulsive (OC) symptoms. As OC symptoms are heterogenous, there must be consideration for which symptoms RI deficits may contribute to. RI deficits have been studied in those whose symptoms are motivated by harm avoidance (HA) and  “Not Just Right” experiences (NJREs). RI deficits were significantly greater in those with fear-related symptoms when measured in the context of fear-based contamination stimuli (Adams, 2015). There is less of a clear link with NJRE-based symptoms as the studies that exist used neutral stimuli to measure RI deficits. We aim to examine the utility of RI deficits measured by an NJRE-specific go/no-go task to predict NJRE symptom severity.

Methods: Data was collected from 114 individuals at a state university, ranging from 18 to 59 years old (M = 24.8 years; 73% White, 84% female). Participants were given questionnaires to assess severity of obsessive-compulsive symptoms (OCI-R), general impulsivity (BIS), difficulties with emotion regulation (DERS-SF), symptoms of anxiety, depression, and stress (DASS-21), and severity of NJREs (NJRE-QR, OCTCDQ-R2, PIC-NR10). Participants also completed two go/no-go tasks to measure RI, one with neutral stimuli (pictures of furniture and clothing), and another with NJRE-specific pictures (“just right” and “not just right” versions of the same picture).

Results: Our preliminary analyses showed that after controlling for relevant covariates, a hierarchical regression showed a trend for NJRE severity on the PIC-NR10 (β = -.28) to predict response inhibition deficits on the NJRE-specific go/no-go (commission error rate; R2 = .128, p = .057), but not on the neural go/no-go.
Conclusion: The findings of this study further delineate the importance of considering response inhibition in the exacerbation of OC symptoms. This study also examines the unique contributions of separate measures of NJRE severity. Our findings show that elevated NJRE severity contributes to poor response inhibition that is specifically linked to NJRE contexts, as compared to neural stimuli. This demonstrates the content specificity of the NJRE-relevant RI deficits. The next investigation will directly examine whether underlying NJRE will cause OCD symptoms through the exacerbation of RI deficits. As such, implications for treatment of OC symptoms and response inhibition deficits, as well as future directions, will be discussed.