High functioning autism and common coexisting conditions: An EEG investigation

Abstract

Autism spectrum disorder is a lifelong neurodevelopmental condition for which there is no known cure. The rate of psychiatric comorbidity (and comorbidity with other neurodevelopmental disorders) in autism is extremely high, which raises questions about the nature of the co-occurring symptoms. It is unclear whether these additional conditions are true comorbid conditions, or simply behaviour that is better conceptualised through the ASD diagnosis. The overall aim of the current thesis is to investigate the shared behavioural and neural basis of coexisting ADHD and anxiety in ASD. The studies in the current thesis consisted of an investigation of behavioural characteristics using profiling techniques (Total n = 83 (ADHD = 23; anxiety = 12; ASD = 25; controls = 23)), in addition to four experimental studies conducted during concurrent EEG recording. These tasks were: emotion processing (Total n = 74 (ADHD = 22; anxiety = 12; ASD = 20; control = 20)); lexical decision (Total n = 83 (ADHD = 21; anxiety = 12; ASD = 20; control = 20)); inhibitory control (Total n = 57 (ADHD = 16; anxiety = 9; ASD = 15; control = 17)) and a resting state recording (Total n = 46 (ADHD = 11; anxiety = 10; ASD = 13; control = 12)). The diagnostic categories listed above include those with a comorbid condition, the groups are split further with respect to comorbid condition (e.g., ASD pure, ASD and comorbid ADHD) in each study. Together, these experiments covered a spectrum of core difficulties evident in ASD: difficulties with social interactions; language; repetitive behaviour (inhibitory control) and aberrant brain growth. By examining difficulties with they occur alone in ASD versus together with ADHD or anxiety, we are able to build a profile of singular and co-occurring ASD. In the behavioural profiling study, using the wider diagnostic categories (e.g., ASD, ADHD and anxiety), results demonstrate that each group was able to be distinguished from one another, and from neurotypical controls, using the profiling measures. In individuals who present with both ASD and anxiety together, the symptoms of ASD are not significantly higher, but symptoms of anxiety do increase compared to those with ASD alone. This suggests that anxiety is a separate condition when it occurs together with ASD. When ASD and ADHD occur together, there were significantly higher ASD symptoms than in the ASD only group and significantly lower ADHD symptoms than the ADHD alone group (but not the ASD only group). This suggests that there might be some degree of symptom overlap when ASD and ADHD present as a comorbid condition. In the emotion processing task, there were no group differences in the latency or amplitude of the N170. There were, however, differences in the amplitude of the P250. Those with ASD and ADHD showed a differential profile in response to sad and neutral stimuli on the P250 from one another. Those with ASD had larger amplitudes toward mouth stimuli than eye stimuli, and those with ADHD had larger amplitudes toward eye stimuli than toward mouth stimuli. In addition, there was larger N170 amplitudes in the ASD pure group versus those with ASD and anxiety or ADHD. This suggests an additive effect. In the lexical decision task, overall, the results indicated larger P100 amplitudes in the right versus the left hemisphere (most strongly shown in control participants). When the ASD and ADHD present as a comorbid condition, the mean P100 latency for the comorbid group lay between the two means for the ASD and ADHD pure groups. This suggests an additive effect. In the inhibitory control study, the group level analysis did not show any differences between the experimental groups on the latency or amplitude of the N2 or P3 components. Upon closer inspection using regression analyses, smaller N2 and P3 amplitudes were associated with more severe symptoms of ADHD. Therefore, it is possible that inhibitory control deficits are associated with ADHD but not ASD or anxiety. In the resting state study, the results demonstrate patterns of decreased coherence in those with ASD, and patterns of increased coherence in ADHD and anxiety compared to neurotypical controls. The patterns of coherence established in the ASD pure group are no longer evident when comorbid conditions are included in the analyses. Thus, this suggests that the conditions are additive. Taken together, the studies in this thesis demonstrate that when ASD presents as a comorbid condition, ERPs adopt unique characteristics of each condition in its pure form. We argue that this is evidence for an additive effect which suggests that the conditions are indeed separate, rather than a misinterpretation (or increased severity) of ASD symptoms. This information is important to researchers when screening for comorbid conditions in ASD research, as underlying brain activity appears to be altered in each condition. This may significantly influence research findings. In addition, the results of the current study will also help to inform medical practitioners when administering a diagnosis and deciding on a plan to treat specific difficulties associated with comorbid ASD.