Researchers identify 3 novel etiological pathways underlying impairments in adolescent and adult ADHD

By Naveed Saleh, MD, MS, for MDLinx
Published June 13, 2018

Key Takeaways

Researchers have identified three partially separable pathways leading to cognitive-neurophysiological impairments in adolescents and young adults with persistent ADHD—or ADHD first diagnosed in childhood, as detailed in a recent study in the Journal of Attention Disorder.

These findings shed light on a multifactorial structure of ADHD cognitive and brain function impairments, and concur with proposed ADHD models positing that cognitive and brain dysfunction in ADHD could develop via multiple pathways.

“This multifactorial structure may explain the observed individual differences in cognitive profiles that exist among adolescents and adults with ADHD, who may display various degrees of impairments in different cognitive domains,” wrote first author Giorgia Michelini, PhD, MSc, King’s College London, London, UK, and coauthors.

The degree to which ADHD cognitive impairments in childhood demonstrate similar etiological structure and shared familial influences in adolescents and young adults has yet to be elucidated. Accordingly, Dr. Michelini and colleagues looked at the etiological structure underlying cognitive-neurophysiological processes in ADHD- and control-sibling pairs first examined as children.

The researchers used a multivariate approach involving brain activity (EEG), IQ, digit span forward (DSF) and digit span backward (DSB), and cognitive-performance and event-related potential (ERP) measures in 356 subjects from ADHD- and control-sibling pairs aged between 11 and 27 years.

The team identified the following three familial factors underlying the link between cognitive-neurophysiological impairments and persistent ADHD:

  1. Response speed and variability, and IQ
  2. Short-term and working memory
  3. Sustained attention, error processing, and to a lesser degree, response inhibition

“Familial influences on ADHD overlapped strongly with both the first and third factors, but only moderately with the memory (second) factor,” wrote the authors. “The same number of factors emerged for nonfamilial influences, with the only exception that IQ clustered with memory rather than RT [reaction time] measures.”

These etiological pathways could underlie dysfunctional brain networks, which correlate with impaired cognition and behavior in patients with persistent ADHD.

One potential limitation of this study is that sibling data permit only the analysis of familial and nonfamilial effects, and not genetic factors.

“A possible clinical implication of these findings,” wrote the researchers, “is that future efforts to implement new treatments for ADHD could consider including various intervention components, each targeting these different cognitive processes.”

This research was supported by Action Medical Research and the Peter Sowerby Charitable Foundation.

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