Contrasting Emotion Processing and Response Inhibition Deficits in ADHD and Bipolar Disorder
MetadataShow full item record
Attention-deficit hyperactivity disorder (ADHD) and bipolar disorder (BD) are prevalent in the population, highly comorbid, and have similar clinical features that complicate diagnoses despite rather distinct diagnostic criteria. Executive functioning deficits in ADHD are similar to those reported in BD but lack the specificity to distinguish between these groups. Emotion processing similarly affects both ADHD and BD and, by combining these processes on a single task, we may increase sensitivity to differences between these populations in a way that may better categorize each disorder. Therefore, we compared performance on a cognitively demanding, affective oculomotor task. Adults, aged 18-62, with ADHD (n=22), BD (n=20), and healthy Controls (n=21) performed an interleaved pro- and antisaccade task (look toward versus looking away from a visual target, respectively). Task irrelevant emotional faces (fear, happy, sad, neutral) were presented on a subset of trials either before or with the target. We observed a group by task interaction (F(2,58)=3.849,p=.027,ηp2=.117) where the ADHD group made more direction errors (looked in the wrong direction) than Controls in the antisaccade condition (p=.027). A three way interaction between image, task, and group (Fig.6; F(8, 58)=2.607,p=.013,ηp2=.082) revealed that presentation of negatively valenced, fear (p=.044) and sad (p=.053), and ambiguous, neutral (p=.003), emotional faces increased saccadic reaction time in BD. In summary, the antisaccade task in general differentiated ADHD from Controls and simultaneous emotion processing further impaired processing speed in BD only. These findings suggest that response inhibition-emotion processing interactions differ between BD and ADHD and reinforce that emotion processing deficits are fundamental in BD and may be attention-driven in ADHD. We propose that response inhibition is critical in both processing systems, but this inhibitory signal is selectively slowed down by concurrent emotion processing dysfunction in BD. We refer to a hypothetical framework integrating these systems and suggest potential loci of dysfunction, the amygdala and orbitofrontal cortex, that may result in the emotional modulation of oculomotor behaviour we have observed here. The differences in how these processing systems interact in ADHD and BD may better characterize each disorder and suggests that refinement of an emotional antisaccade task may be clinically useful.