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ADHD May Stem from Slower Brain Network Connectivity

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The brains of children and adolescents with attention deficit hyperactivity disorder (ADHD) are slower to develop some key connections, according to a study published in the Proceedings of the National Academy of Sciences.

Slower brain connectivity developments may be the root of ADHD, according to a study from the University of Michigan.

The brains of children and adolescents with attention deficit hyperactivity disorder (ADHD) are slower to develop some key connections, according to a study published in the Proceedings of the National Academy of Sciences.

Researchers from the University of Michigan Medical School’s Department of Psychiatry examined 275 children and teens aged 7-21 years with ADHD to test if their brain connections develop slower than 481 of the non-ADHD counterparts. Each participant was scanned with function magnetic resonance imaging (fMRI) scanners to show brain activity during resting and conversational states.

The researchers used connectomics, the study of the web of connections in the brain, to observe nearly 400,000 connections in the cortex. The researchers noted slower development of connections in ADHD patients in the internally-focused network called the default mode network (DMN) and 2 networks that process externally-focused tasks, called task-positive networks (TPNs). The slower developments were seen in 2 specific areas of the brain: the frontoparietal and the anterior insula in the ventral attention networks. The researchers believe these connectivity lags could explain why people with ADHD are easily distracted.

“We and others are interested in understanding the neural mechanisms of ADHD in hopes that we can contribute to better diagnosis and treatment,” said lead author Chandra Sripada, MD, PhD, in a university press release. “But without the database of fMRI images, and the spirit of collaboration that allowed them to be compiled and shared, we would never have reached this point.”

The current body of research suggests ADHD stems from altered DMN-TPN interactions, which this study supports. The connections within these networks and between the 2 likely contribute to ADHD.

“The results of this study set the stage for the next phase of this research, which is to examine individual components of the networks that have the maturational lag,” Sripada concluded. “This study provides a coarse-grained understanding, and now we want to examine this phenomenon in a more fine-grained way that might lead us to a true biological marker, or neuromarker, for ADHD.”

Sripada mentioned that no such neuromarker exists for ADHD, let alone any psychiatric disorder. Sripada further suggested the over-maturation of these and other networks may be the cause of schizophrenia; other connectivity problems may be the cause of conditions such as depression, anxiety, bipolar disorder and others.

The investigators hope that these new findings can help doctors better diagnose ADHD in patients, and use brain scans to do so more effectively. In the future, they hope treatment responses can also be tracked this way. The research also contributes to the way doctors and the public think about ADHD: some children and teens are said to “grow out” of the disorder, while it plagues others their entire lives. By tracking the progression of ADHD, researchers can discover the truth.

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