ADHD and Development Lab
July 1, 2015
This past week I divided my time between data collection, data scoring, and data entry. Since we are somewhat behind on data scoring and data entry of past visits, I spent most of my time focusing on that.
As I have come to do more and more data entry, I’ve come to notice a trend that many of our participants seem to be generally intelligent individuals, at least thus far. This is quite typical, and shouldn’t raise too much alarm at this stage of the project. This may be due to the fact many of our participants have received word about the study through the University’s listservs. Moreover, other participants have been involved in other studies that the Iowa ADHD Lab has conducted, so this may simply be the result of practice effects related to being administered similar measures garnering the same neuropsychological constructs. Regardless, intelligence tests probably are not some ADHD folks are unfamiliar with. Here’s to hoping this doesn’t severely bias our study.
During our weekly meeting on Tuesday, Dr. Nikolas and I discussed three research articles. Molly had me read her recently published article titled, Moderators of Neuropsychological Mechanism in Attention-Deficit/Hyperactivity Disorder (2014). She and her colleague Joel Nigg at the Oregon Health and Science University examined groups of youth with ADHD and their unaffected siblings to identify potential endophenotypes of ADHD as to further explore the underlying genetic contribution to ADHD psychopathology. Figure 1 describes their findings graphically. They found that unaffected siblings were statistically different from both controls and their ADHD siblings on measures of cognitive control, response inhibition, response variability, and temporal processing. ADHD-positive youth and their unaffected siblings shared ADHD symptoms, particularly in regard to deficits in executive dysfunction, response inhibition, working memory, and temporal processing. This indicates there must be a genetic contribution to the development of ADHD psychopathology.
Other articles we discussed were Sonuga-Barke, Bitsakou, and Thompson (2010), in which Sonuga-Barke introduced the seminal Dual-Pathway Model of ADHD, and Bush (2010), where the attention networks in ADHD were reviewed.
Sonuga-Barke’s Dual Pathway Model intends to explain the neuropsychological heterogeneity (i.e. differences in functioning) of ADHD, namely dorsal frontostriatal dysfunction within the prefrontal cortex lead to deficits in executive functioning and ventral frontostriatal dysfunction leading to hypoactive patterns of signaling resulting in deficits in reward circuitry. A third pathway, which involves the basal ganglia and cerebellum, attempts to explain deficits in temporal processing. In their study Sonuga-Barke, Bitsakou, and Thompson demonstrate that neuropsychological deficits in ADHD are heterogeneous, affecting some individuals to greater or lesser degrees within different domains of impairment. Figure 2 describes quite well what they found in their study of ADHD youth.
Bush (2010) discussed in his review the neurocognitive theories of ADHD and the corresponding brain regions that have been implicated in the neuropsychological deficits in ADHD, particularly as they relate to attention. Figure 3 diagrams these regions that have been believed to be involved in attention deficits in ADHD, namely the dorsolateral prefrontal cortex, ventrolateral prefrontal cortex, parietal cortex, striatum, and the reticular activating system (i.e. thalamus and brain stem). The dorsolateral PFC and the ventrolateral PFC have been implicated in vigilance (i.e. sustained attention and alertness), attention, planning, executive control, and working memory. The parietal cortex is involved in attention regulation and houses sensory convergence areas. The striatum is implicated in reward processing and decision-making. The reticular activating system mediates attentional processes and suppresses irrelevant stimuli. These regions are thought to be involved in ADHD as these regions collectively foster the host of executive functions that are clinically relevant to ADHD, including deficits in cognitive control, attentional regulation, response inhibition, working memory, and decision-making to name only a handful.
More on the science of ADHD next week!
G. Bush (2010). Attention-deficit/hyperactivity disorder and attention networks. Neuropsychopharmacology, 35(1), 278-300. doi: 10.1038/npp.2009.120
Nikolas, M. A. & Nigg, J. T. Moderators of neuropsychological mechanism in attention-deficit hyperactivity disorder. Journal of Abnormal Child Psychology, 43(2), 271-81. doi: 10.1007/s10802-014-9904-7
Sonuga-Barke, E., Bitsakou, P., & Thompson, M. (2010). Beyond the dual pathway model: Evidence for the dissociation of timing, inhibitory, and delay-related impairments in attention-deficit/hyperactivity disorder. Journal of the American Academy of Child & Adolescent Psychiatry, 49(4), 345-355. doi: 10.1016/j.jaac.2009.12.018
Andrew is a Psychology and Philosophy major from Milwaukee, Wisconsin.