Abstract
ADHD is a common childhood disorder that has been classified into three subtypes (ADHDI,ADHD-H and ADHD-C) but may involve a spectrum of symptoms. Deficits in executivefunctions have been considered to be a major source of the disability associated with ADHD. Impairments in behavioural inhibition fundamental to executive functions have been hypothesized as the core of ADHD symptoms (Barkley, 1997b; Quay, 1997). This thesis tests whether ADHD deficits derive from dysfunction of Gray’s Behavioural Inhibition System (BIS). It does so by assessing the differences between ADHD-I, ADHD-C and control groups in their Goal Conflict Specific Rhythmicity (GCSR), a biomarker of BIS function(McNaughton, 2014; McNaughton, Swart, Neo, Bates, & Glue, 2013).
Two studies were undertaken, one in New Zealand (initial study) and one in Iran (main study). They demonstrated that ADHD-C showed GCSR activity, at the right frontal site F8, similar to that in control groups. However, ADHD-I showed less GCSR activity than controls – consistent with BIS dysfunction. ADHD-I symptoms such as low levels of attention and arousal could be due to BIS under activity. However, hyperactivity and impulsivity symptoms in ADHD-C cannot be explained by BIS dysfunction as there was no evidence of abnormal BIS activity for ADHD-C in any of the studies. Behavioural Approach System (BAS) over-activity may better explain ADHD-C symptoms by producing a stronger tendency to approach and act. Given that ADHD-I differs from ADHD-C it follows that ADHD as a whole cannot be seen as a single homogenous entity, although both ADHD-I and ADHD-C may share a common factor. The distribution of GCSR, and other measures for the three diagnostic groups overlapped fairly strongly – supporting the concept of a multidimensional spectrum for ADHD symptoms rather than categorical divisions.
ADHD-I and ADHD-C varied from the control to some extent in terms of the accuracy of responses and SSRTs. However, there was no difference between ADHD-I and ADHD-C regarding their behavioural outputs in the SST. Longer SSRTs for ADHD participants have been interpreted as action stopping problems that involve a different, anxiolytic insensitive, neural system from behavioural inhibition. This finding supports the idea of a common factor in ADHD-I and ADHD-C.
Overall, both ADHD-I and ADHD-C share action stopping problems reflected by SSRTs. BAS abnormality might produce some ADHD-C symptoms. BIS abnormality might produce some ADHD-I symptoms. This thesis shows that BIS deficiencies are not sufficient to account for all cases of ADHD as hypothesized by Quay (1997)