A new study in Translational Psychiatry suggests adults with ADHD exhibit stronger, longer-lasting patterns in brain activity than their neurotypical peers, with these patterns linked to the severity of ADHD symptoms across both groups. The researchers propose that ADHD symptoms may reflect individual differences in where each person’s brain operates on a spectrum between order and disorder.
ADHD is characterised by difficulties such as inattention, impulsivity and hyperactivity, but symptoms vary widely from person to person. While scientists have long studied brain activity in ADHD, less is known about how brain patterns relate to symptom severity across both diagnosed and non-diagnosed adults.
Central to the study is the framework of brain criticality, which describes shifts in activity between states that are too uncoordinated and states that are overly synchronized. The idea is that the brain functions best near the transition point between these states, balancing excitation and inhibition. Given ADHD has been linked to greater excitability, the researchers hypothesised that ADHD symptoms would reflect a tilt toward the overly synchronized side.
To test this, the team led by Hamed Haque of the University of Helsinki measured long-range temporal correlations—how fluctuations in brain rhythm strength at one moment relate to fluctuations seconds or minutes later. These correlations peak near the critical transition point and thus serve as an indirect marker of where the brain is operating.
The study involved 70 adults: 36 neurotypical participants (average age 34; 13 women) and 34 adults with a prior ADHD diagnosis (average age 37; 19 women). Participants underwent a resting-brain recording and two attention tasks while their brain activity was measured with magnetoencephalography. In one task they attempted to detect faint images; in the other they responded quickly to one stimulus while withholding a response to another.
Participants also completed questionnaires on ADHD symptoms and impulsivity. Three neurotypical participants scored above a screening threshold for ADHD and were excluded from group comparisons, though they were included in analyses linking brain activity to symptoms. Those with other psychiatric or neurological conditions were excluded, and individuals with ADHD stopped taking their medication 24 hours before testing.
Behaviorally, the two groups performed similarly on most aspects of the tasks. However, those with ADHD were more likely to respond when they should have held back, a pattern echoed in earlier work. The researchers found no group difference in reaction-time variability, which is often associated with ADHD; they suggest the task may not have been demanding enough to reveal differences, or scanner-related arousal may have affected both groups.
In the brain recordings, the ADHD group showed stronger long-range temporal correlations than the neurotypical group in slower alpha-band rhythms (8 to 13 Hz) during the detection task and in faster gamma-band rhythms (35 to 65 Hz) during the response task, with moderate effect sizes. These differences could not be explained by age or overall rhythm strength. The groups also differed in how their brain activity shifted from rest to task: the neurotypical group displayed a widespread decrease in alpha correlations during the detection task, a change that was weak in the ADHD group, while the ADHD group showed a robust rise in gamma correlations during the response task.
When examining symptom scores across all participants, the relationship with brain activity depended on frequency and task. In the gamma range, stronger long-range correlations accompanied higher symptom scores, most clearly during the response task. In the beta range (22 to 24 Hz), the pattern was curved: the strongest correlations appeared among participants with moderate symptom scores, while those with lower or higher scores showed weaker correlations.
The authors interpret these findings as reflecting differences in where each person’s brain sits within its operating range. Small increases in excitability might nudge a brain toward the critical point, where long-range correlations peak, whereas larger increases could push it past the point into overly synchronized activity, potentially explaining why more severe symptoms correlate with weaker beta correlations. The researchers also note that moderate ADHD traits might sometimes be beneficial, aligning with studies on hyperfocus and novelty-seeking. Importantly, no single brain pattern distinguished all ADHD from all non-ADHD participants; long-range correlations varied widely between individuals.
“Our study thus proposes a novel complex systems-level framework to explain the emergence of ADHD symptoms and their continuum across the population,” the authors stated.
While the study contributes to understanding the brain dynamics underlying ADHD symptoms, it is correlational and cannot establish causation. It also involved a modest sample size and excluded individuals with comorbid conditions, which may limit how broadly the findings apply. The researchers acknowledge that other mechanisms could explain the results, noting that long-range correlations can occur in systems not near a critical point, so the criticality interpretation remains indirect. Results also varied by task and frequency, and an earlier resting-state study found no differences in long-range temporal correlations in adults with ADHD. Additionally, participants with ADHD paused their medication for 24 hours before testing, which may not reflect their typical functioning.
The study, titled ADHD symptoms across the population are explained by individual variability in brain criticality, was authored by Hamed Haque, Jonni Hirvonen, Sheng H. Wang, Jaana Simola, Isabel Morales-Muñoz, Benjamin U. Cowley, J. Matias Palva and Satu Palva.
