Anterior cingulate cortex alterations in children and adolescents with Attention Deficit and Hyperactivity Disorder:

Tonia Salem1, Hayat Harati1, Marwa Summaka1

  • 1Faculty of Medical Sciences, Neuroscience Research Center, Lebanese University, Beirut, Lebanon.

Insights

Children and adolescents with Attention-Deficit/Hyperactivity Disorder (ADHD) show consistent brain differences. The anterior cingulate cortex (ACC) exhibits structural changes and functional disruptions impacting inhibitory control and connectivity.

Area of Science:

  • Neuroscience
  • Developmental Psychology
  • Child Psychiatry

Background:

  • Attention-Deficit/Hyperactivity Disorder (ADHD) is a prevalent neurodevelopmental disorder.
  • ADHD is characterized by persistent inattention and hyperactivity-impulsivity.
  • The anterior cingulate cortex (ACC) plays a crucial role in executive functions and emotional regulation.

Purpose of the Study:

  • To systematically review structural and functional alterations of the ACC in pediatric ADHD.
  • To synthesize neuroimaging findings in children and adolescents with ADHD.
  • To identify a coherent neurobiological pattern associated with ADHD in youth.

Main Methods:

  • Systematic review adhering to the PICO framework.
  • Inclusion of studies on individuals under 18 years with ADHD.
  • Neuroimaging modalities (MRI, fMRI, EEG) assessing the ACC compared to typically developing controls.

Main Results:

  • Structural MRI revealed reduced gray matter volume, cortical thinning, and atypical sulcal morphology in the ACC.
  • Functional MRI indicated diminished ACC activation during inhibitory control tasks and altered resting-state connectivity.
  • EEG studies showed attenuated N2/P3 amplitudes and disrupted theta oscillations.

Conclusions:

  • Pediatric ADHD is associated with a distinct neurobiological profile involving the ACC.
  • Structural changes include reduced volume, thinning, and atypical folding of the ACC.
  • Functional dysregulation encompasses abnormal activation, disrupted connectivity, and altered electrophysiological responses in the ACC.
Abstract