Distractibility in ADHD associated with reduced ability to modulate alpha band oscillations in attentional tasks

Evidence has been recently provided for a major role of alpha activity (8-14Hz)
brain response in the active suppression of irrelevant information during
attention performance. According to the *inhibition timing hypothesis*, alpha
band oscillations show a typical pattern of activity that is reflected by a
decrease in related frequency power in task relevant brain regions
contralateral to the attended side, together with a power decrease in task
irrelevant regions ipsilateral to the stimulus.
Children with ADHD have recently been reported to show a reduced ability to
modulate alpha oscillations during covert attention as compared to typically
developing children. This finding is consistent with the notion that alpha band
activity has a major role in top-down inhibitory processes which are crucial
for attentional selection, whose impairment is indeed a core feature of ADHD
symptomatology.
Analyses of structural connectivity in anatomical pathways associated with top
down control, in particular the Superior Longitudinal Fasciculus (SLF), have
shown a relationship between white matter tract volume and ability to modulate
alpha band synchronization during attention performance.
Since, to date, pharmacological intervention represents the most effective
treatment of ADHD, a better understanding of the effects of ADHD medication on
alpha band modulation during attention performance will likely provide
important insights to elucidate the neural bases underlying the symptoms of
ADHD.

Posner spatial cueing task will be used to investigate electrophysiological
differences in brain oscillatory lateralization during attentional shifts in
children with and without ADHD. We hypothesize that the observed difference in
the ability to modulate alpha activity between ADHD and controls is normalized
by stimulant medication (MPH). To this aim two separate conditions will be
considered for the ADHD group: Alpha oscillatory activity will be measured
on-medication (medication suspended 24 hours prior to the experiment and
standardized dosage of MPH administered) and off-medication (medication
suspended 24 hours before the beginning of the experiment and placebo
administered instead) within a double blind placebo control crossover design.
Moreover, we postulate that patterns of reduced white-matter connectivity and
brain volume, along structures typically associated with attention, correlate
with the reduced to modulate the specified brain oscillations in ADHD with
respect to TD children.
To investigate this hypothesis, in line with Marshall et al. (2015), MEG
recording of neural synchronization will be coupled with structural measures
reflecting white-matter tract connectivity and brain volume estimation
respectively with Diffusion Tensor Imaging (DTI) and Voxel Based Morphometry
(VBM) in both groups.

Alpha activity will be measured by means of MEG recording while children
performing a covert attention task.
For the ADHD group, measurements of oscillatory brain activity will be done in
two separate sessions: in both conditions participants will undergo a
medication washout of 24 hours ( withdrawal of medication) prior to the
experiment and subsequently administration of a standardized dosage of ADHD
medication or placebo will follow.
Alpha lateralization will be computed and compared between ADHD and controls
and between on and off medication in the former group.
MEG data will be coupled with structural measures of white-matter tract
connectivity (DTI) and striatal volume estimation (VBM).

Participation is not associated with any indications of risks. Burden is
minimized as much as possible. Participation is of great importance. Without
measurement in this specific target group, generalization of recently obtained
new insights in the nature of abnormalities related to ADHD, will not be
possible. Because the brain develops during childhood, the only way to be able
to draw reliable conclusions in this target group is by comparing results to
typically developing children of the same age. In addition, studying this
typically developing group will help us understand normal development.
Therefore, participation of both groups will be greatly valued. Once we are
able to draw reliable conclusions on the nature of differences between typical
development and development with ADHD, we will be able to implement these
findings in treatment. Clearly, understanding the mechanism underlying ADHD
will benefit treatment.