Doctor of Philosophy
Department of Psychology
Bannon, Shelley, Executive function deficits in obsessive-compulsive disorder: episode or trait markers, Doctor of Philosophy thesis, Department of Psychology, University of Wollongong, 2003. https://ro.uow.edu.au/theses/1660
There is considerable research to suggest that a neurobiological deficit might underpin obsessive-compulsive symptoms or be responsible for Obsessive-Compulsive Disorder (OCD). Deficits in executive functions are commonly reported in OCD and are believed to be mediated by the frontal lobes, the broad site of this neurobiological deficit. This thesis comprised of five studies that collectively attempt to address several key questions that required clarification within the executive function literature of OCD. Study 1 assessed executive functions of inhibition, set shifting, working memory, planning, and verbal fluency in OCD subjects (n = 20) compared to a clinical control group of Panic Disorder (PD, n = 20). OCD subjects exhibited deficits in all areas except planning and verbal fluency, in comparison to the PD group. Study 2 recruited an additional sample of Remitted OCD subjects (n = 20), and compared their performance to the original Symptomatic OCD group (n = 20) and PD control group (n = 20). It was found that executive function deficits were specific to OCD, and that symptom status did not affect the profile of these deficits. Study 3 adopted a longitudinal design and retested a sub-sample (n = 10) of Symptomatic OCD subjects that evidenced symptom remission. The stability of these deficits, even after remission, was confirmed in this study. In order to further clarify the nature of executive function deficits, particularly the role of inhibition and facilitation abnormalities in OCD, Study 4 assessed Symptomatic OCD (n = 20), Remitted OCD (n = 11), PD control (n = 20) and normal control subjects (n = 20), in a paradigm that separately studied inhibition and facilitation processes. It was found that OCD subjects displayed both excessive facilitation to primed responses and impaired inhibition to suppressed responses, in comparison to both control groups. Again, these deficits were unaffected by symptom status (i.e. symptomatic or remitted), and together the findings were consistent with the notion that executive function deficits were trait markers of OCD, rather than episode markers. In order to examine the effects of overactive cognitive schemas on facilitatory and inhibitory processes, Study 5 assessed Symptomatic OCD (n = 20), Remitted OCD (n = 11), PD (n = 20) and normal control subjects (n = 20) using the same paradigms, but with personally threatening words. The findings indicated that overactive cognitive schemas, provoked by threat-related stimuli, exaggerated the inhibition deficit in Symptomatic OCD subjects, and interfered with normal inhibition processes in PD subjects. However, overactive cognitive schemata did not affect inhibition in non-anxious groups (i.e. Remitted OCD and normal control subjects). It was argued that this thesis provided evidence that: i) OCD individuals suffer executive function deficits, which are stable through the course of the disorder, and ii) overactive cognitive schemata is implicated in the maintenance and remission of OCD symptomatology, by serving to augment pre-existing inhibitory deficits. The theoretical and clinical implications of these findings are discussed.