|Ph.D Student||Fisher Revital|
|Subject||Attention Deficit Hyperactivity Disorder(ADHD):|
A Single pathology?
|Department||Department of Medicine||Supervisors||PROFESSOR EMERITUS Hillel Pratt|
|CKINICAL PROFESSOR E Judith Aharon-Peretz|
|Full Thesis text - in Hebrew|
Attention-deficit/hyperactivity is a heterogeneous disorder that is classified into subtypes of inattentive and combined types. The symptoms of inattention are present in both subtypes, but the mechanisms underlying the behavioral symptoms in each subtype is unknown.
We compared the performance and recorded brain activity (ERP) of 14 adult ADHD - combined type and 14 adult ADHD - inattentive type with 14 controls. We used an auditory cued attention paradigm for assessing spatial attention, and auditory Go-NoGo paradigm to assess inhibitory mechanisms.
In the cued attention task the subjects responded to the location of targets that were either preceded by a spatial cue (valid = correct side; invalid = opposite side) or uncued. The Go-NoGo task required a button press (Go) to 80% of the tones, or inhibition of the response (NoGo) to 20% of the tones, depending on the tone's pitch.
Behavioral results revealed significantly more errors in the ADHD - combined type in the two tasks compared to control subjects.
In the cued attention task, Event-Related Potentials revealed negative slow potential (CNV) in all task conditions in the controls. This component, originates from the dorsolateral prefrontal cortex, and is related to preparation for target processing and response. It was absent in both ADHD subtypes in the "no cue" condition. Source current density estimation revealed that ADHD combined- type subjects showed hypoactivation in medial prefrontal cortex after cue presentation and hyperactivity in limbic areas (amygdala, uncus) after invalid target.
In the Go-NoGo paradigm, the results replicate earlier findings that ADHD combined-type subjects made significantly more commission errors on the NoGo trials, and showed smaller amplitudes, and longer latencies of ERPs components N2 and P3. These ERP components have been documented as being essential in inhibition and conflict monitoring tasks. Source current density estimation revealed hypoactivity in the right frontal dorsolateral cortex and in the posterior cingulate in the ADHD group.
Contrary to prevailing opinion, ADHD subjects also showed significantly enhanced response inhibition in the GO condition that manifested in more omission errors and significantly larger N2 amplitudes. We therefore suggest that the disorder is broader and involves disrupted regulation and not only reduced response inhibition and conflict monitoring.
The results suggest that both ADHD types share the same deficit in arousal attributed to the dorsolateral prefrontal cortex. ADHD-combined type has a larger deficit in both arousal and inhibitory control mechanisms that stems from dorsolateral orbital and anterior cingulate prefrontal circuits.