Characterizing cortical signatures of inhibitory control - PROJECT SUMMARY
Attention deficit hyperactivity disorder (ADHD) is a multifaceted disorder that impacts 11% of American children
and persists into adulthood for roughly 1/3 of those diagnosed. The prevalence of ADHD surged by 42%
between 2003 and 2011, sparking concern about the reliance on subjective diagnoses and treatment with
stimulants. A comprehensive understanding of the neurophysiological basis of ADHD pathophysiology is a
promising way to accelerate the development of objective diagnostic tools and expansion of treatment options.
Current research suggests that disruption of the prefrontal-basal ganglia network that supports inhibitory
control is a key factor in the cognitive (i.e. inattentiveness) and motoric (i.e. hyperactivity) inhibitory deficits
associated with ADHD. This hypothesis is further supported by the relationship between ADHD and diminished
prefrontal beta frequency activity (13-30Hz)- a putative signature of network communication between nodes of
the inhibitory control system. Typical motor inhibition tasks used to study inhibitory control, such as the stop
signal task, require comparing trials in which subjects moved to trials in which they withheld movement (i.e.
comparing going to stopping) to identify neurological substrates of stopping. This comparison confounds
physiological processes involved in motoric inhibition and the cognitive control processes preceding motoric
inhibition. That is, activity underlying suppression of movement cannot be differentiated from that underlying
reaction to a sudden change in environmental demands. Given the potential for these mechanisms to
asymmetrically contribute to different facets of ADHD, the obfuscation of cognitive and motoric aspects of
inhibition is a significant barrier to progress.
To address this gap in knowledge, I developed a novel stop signal task that instructs participants to stop an on-
going movement under conditions in which the stop signal is expected (planned stop) and unexpected
(unplanned stop), providing an opportunity to isolate cognitive and motoric aspects of inhibition. Based on
previous research, my central hypothesis is that I will observe prefrontal beta increases on unplanned
stop trials in which subjects must react to a sudden change in environmental demands, reflecting
cognitive aspects of inhibition, and I will observe beta increases in sensorimotor areas (but not
prefrontal areas) on planned stop trials, reflecting suppression of physical movement. I will leverage my
novel task to test this hypothesis by (1) using scalp electroencephalography to dissociate electrophysiological
signatures associated with cognitive and motoric aspects of inhibition and (2) using intracranial
electroencephalography to identify precise anatomical substrates contributing to cognitive and motoric aspects
of inhibition. The information gained through this research will advance our understanding of the
neurophysiological underpinnings of inhibitory control and pave the way for the potential use of EEG to
diagnose ADHD and to monitor patient response to treatment regimens.
