ADHD and Development Lab
July 20, 2015
Aside from surviving the unbearable humidity, this past week was rather typical. I had only one lab visit this week as one of the participants had to reschedule. The rest of the week was spent doing original entry from recent lab visits, except from the recent appointment of double entry, which is essentially our way of making sure the data is ready for analysis. Double entry is the process where we make sure the data is reliable and free of administrative or scoring errors. After we scrutinize original entry files, we reenter all the data with their corrections. It’s more exciting than it sounds because it means were making progress!
Of course, that makes me think about the end of my internship that is fast approaching. With only four more weeks to go, we have made great strides on our project and I can say I continue to learn more and more about ADHD and my interests in clinical psychology in each passing day.
On Tuesday, Dr. Nikolas and I explored Sagvolden’s dynamic developmental behavioral theory of attention-deficit/hyperactivity disorder (ADHD) as discussed in his 2005 paper. Sagvolden’s theory is profoundly different than the cognitive neuroscience theories that I have wrote about in previous blog entries in that this theory is rooted in behavioral neuroscience, drawing heavily from behavior analysis. Other theories tend to focus on the developmentally abnormal neurocognitive, affective, or temperamental components of ADHD. Central to Sagvolden’s dynamic developmental behavioral theory is the notion that, with much owed to contemporary behavioral analysis, the clinical presentation of ADHD is the result of altered reinforcement of developmentally appropriate behavior and deficient extinction of previously reinforced behavior. If you have studied behaviorist approaches, Sagvolden’s behavioral theory should sound very familiar to you.
Expounded upon in Firgure 1, Sagvolden and colleagues cite hypofunctionality within the mesocortical, mesolimbic, and nigrostriatal dopamine systems as the underlying neurobiological cause. Sagvolden and colleagues consider the interaction of genetics, hyposensitivity to reinforcement, and exposure to environmental pollutants and stimulant drugs to be what causes the hypofunctionality within these dopaminergic systems. Because ADHD is a neurobehavioral disorder, as it has been conceived in Sagvolden’s theory, the behavioral symptoms of hyperactivity, impulsivity, response inhibition, response variability, deficits in sustained attention, and delay aversion commonly noticed thus arise from this system-wide hypofunctionality inherent in the brain. Hypofuncationality within the mesocortical dopamine system leads to dysregulated attentional control and behavioral organization, while hypofunctionality in the mesolimbic system begets deficiencies in delay of reinforcement and extinction. Hypofunctioning nigrostriatal circuitry is involved in poorer planning of behavioral output and habit learning. Figure 2 describes these hypofunctioning dopamine systems as more or less separable loops (though in actuality these are similar systems that often influence one another – I’ll save my criticisms for later).
In addition, the theory also supports what Sagvolden and colleagues call “Reinforcement/Extinction Disorder (RED)”, essentially a renaming of the hyperactivity-impulsivity subtype of ADHD. Consistent with the dynamic developmental behavioral theory, the symptoms observed within this sub-type are explained by poor reinforcement of adaptive behavior and inadequate extinction of previously reinforced behavior.
A criticism of Sagvolden’s behavioral theory is that it neglects to explain essentially every other aspect of the clinical presentation of ADHD beside the behavioral presentations, most importantly the top-down cognitive processes often involved in response inhibition, sustained attention, and delay aversion. Moreover, while the theory explores the involvement of dopamine systems, it fails to incorporate other implicated neurotransmitters (e.g. serotonin, epinephrine, norepinephrine, choline, etc.) interactions between neural systems, and top-down regulation of behavioral processes. In addition, it entirely ignores the deficits in emotional self-regulation often seen in ADHD. Though Sagvolden’s theory does expound upon the behavioral presentation of ADHD and provides a neuroscience-based explanation for those behaviors, it is simply too narrow to describe the neurocognitive, affective, and temperamental components and further research on the disorder.
Next week I hope to share a few empirical studies relevant to ADHD. Stay tuned!
Sagvolden, T., Johansen, E. B., Aase, H., & Russell, V. (2005). A dynamic developmental theory of attention-deficit/hyperactivity disorder (ADHD) predominantly hyperactive/impulsive and combined sub-types. Behavioral and Brain Sciences, 28(3), 397-419. doi: 10.1017/S0140525X05000075
Andrew is a Psychology and Philosophy major from Milwaukee, Wisconsin.