Degree Name

Doctor of Philosophy


University of Wollongong. Dept. of Psychology


Research, diagnosis and intervention in ADHD has been plagued by problems of definitionof the disorder, vagueness surrounding constructs held to be central to the disorder such as'attention deficit' and 'sustained attention', and limitations of diagnostic instruments loosely linked to such constructs (Douglas, 1980; Schachar, 1991; Corkum & Siegel, 1993).

Literature is reviewed which demonstrates the need, in both research and clinical work ADHD, for comprehensive theories of attentional dysfunction in these children as well asfor objective research and diagnostic instruments which are clearly grounded in such theories. To address these issues, a review is conducted of promising models of ADHD dysfunction followed by recent understanding of attentional processes based on two parallel visual systems known as the magnocellular (or transient) and parvocellular (sustained) systems (Breitmeyer, 1994). Recently, the implications of these systems to attention have been explored along with their potential application to attention disorders (Williams, Lettell,Reinoso & Greve, 1994). It is argued that an abnormality of the transient system may be involved in ADHD dysfunction and a tentative model is proposed which links the transient system to matching processes in the hippo campus, the dorsal attention system, and to regulation of sensory and motor processes in the frontal regions of the brain.

It is then argued that a paradigm capable of exploring the hypothesis of transient abnormality in ADHD is that used extensively to date in research into specific reading disability and more recently in schizophrenia research, namely visual masking. Visual masking, and particularly paradigms such as metacontrast, can be interpreted in terms of interaction between M and P pathways and therefore can be used to examine the hypothesisthat an M cell/transient system abnormality contributes to ADHD dysfunction. The current research therefore sought to explore, using visual masking paradigms, evidence for such anabnormality and incorporate findings into a model of ADHD dysfunction which is more inclusive than those reviewed.

Experiment 1 sought to investigate preliminary evidence for an abnormal visual masking function in ADHD children. A sample of children aged between 9 and 11 years with a diagnosis of ADHD were matched for age, sex and IQ with two comparison samples of children, one meeting criteria for learning disability (LD) but not ADHD and the other, a normal control sample. The experiment showed evidence for abnormal visual masking in both clinical groups. Experiment 2, using the same samples and a metacontrast paradigm, sought to examine more specifically the possible involvement of abnormal transient channel activity in ADHD children. The study indicated an abnormality in relative response speed but not magnitude of transient channels in ADHD children, with evidence for abnormally fast transient channel responses in these children.

In Experiment 3, the same metacontrast procedure was used to examine transient/sustained channel interaction in an ADHD sample when 'on' versus 'off stimulant medication. Stimulants appeared to normalise the response speed of transient channels in ADHD subjects. Results from the three experiments tended to confirm the model of ADHD dysfunction proposed from an integration of the literature and the model was then further elaborated. The capacity of the model for explaining characteristic symptoms of ADHD was then discussed. Finally, the potential of visual masking and other paradigms reflecting transient/sustained functioning for researching ADHD and for diagnostic purposes was noted.