During the welcome and opening plenary session of the annual meeting of the American Professional Society of ADHD and Related Disorders (APSARD), 3 speakers gave an overview of different models of cognitive and neural processes that underlie the symptoms, impairments, and medication treatment models of attention-deficit/hyperactivity disorder (ADHD).
"ADHD and Cognition" was moderated by Philip Asherson, MBBS, MRCPsych, PhD, who began with his own talk called "ADHD and the Wandering Mind: A New Perspective on Inattention in ADHD."
According to Asherson, a professor of molecular psychiatry at King's College London, mind wandering (MW) is a core feature of the ADHD mental state because of a dysregulation of the default mode network (DMN) and salient network activity (ie, the brain’s reward network). The DMN is a distributed brain system normally deactivated during tasks requiring attention to the outside world.
Because different parts of a gene cause multiple outcomes, the effects on ADHD are difficult to sort out, so he focused on treatment effects.
“If I bring about a change in dopamine transmission, what change does that have on neural function? And how does that change cognition and behavior?” he posited.
MW, which is universal in 20% to 50% of the population, happens when the mind drifts away from what a person is supposed to be doing and focuses on internal thoughts and images unrelated to the primary task. MW can sometimes have beneficial results, such as sparking creativity. Other forms can be harmful, such as when the thoughts are spontaneous, uncontrolled, continuous, and distracting.
Two types of MW have been referred to as deliberate mind-wandering and spontaneous mind-wandering; they are believed to involve an imbalance of regulatory processes on internal controls.
The spontaneous, harmful type is thought to explain many of ADHD’s symptoms and impairments, reflecting dysfunctional connectivity between the brain's DMN and task positive networks.
The 12-item Mind Excessively Wandering Scale captures 3 points:
- thoughts constantly on-the-go
- thoughts flooding from one topic to another
- multiple thoughts at the same time.
Asherson raised the possibility that deficient regulation of DMN activity leads to spontaneous and excessive MW in ADHD.
Trevor Robbins, CBE, FRS, FMedSci, FBPsS, from the University of Cambridge, discussed the role of noradrenaline (NA) and dopamine (DA) and sustained attention on working memory and impulse control, in a talk called "The Translatiomal Neuropsychopharmacology of ADHD."
He highlighted the lack of detailed information on the mechanisms by which changes in catecholamine functioning lead to changes. He noted how a thorough understanding of stimulant drug therapy in terms of DA and NA across brain networks is lacking. He reviewed some neuroscience studies that suggest there may be different components to ADHD, depending on which system is disrupted in ADHD.
Anthony Grace, PhD, a professor of neuroscience at the University of Pittsburgh, discussed the "Tonic-Phase Dopamine Regulation of Limbic System Integration in the Pathophyophysiology and Treatment of ADHD."
He noted that stimulant drugs used for ADHD cause hyperactivity and confusion in normal subjects; in patients with ADHD, they focus attention and decrease activity levels. How the drugs are administered can also have different effects.
Grace described how dopamine system activity is characterized into 2 categories: the slowly changing homeostatic low-level tonic transmission and the rapid high-amplitude phase of transmission.
These 2 types of transmission interact to modulate dopamine system responsibility and reduce systems such as inattention and hyperactivity when used to treat ADHD.
Tonic dopamine modulates phasic amplitude in 2 directions, whereas phasic transmission is believed to represent the signaling events that increase attention to a stimulus.
At high doses, amphetamine will amplify phasic transmission by amplifying the impact of the rapid dompamine release by attenuation of synaptic uptake. This will cause a nonselective potentiation of dopamine transmission and nonselectively distribute orientation of attention throughout the target areas.
But at low doses orally, the slow increase in extracellular dopamine produced will lead to a presynaptic attenuation of response, while altering the proportion of dopamine neurons active will lead to increase focused response to stimuli. There can be a combined increase focusing of attention while limiting background activity.