Default mode network connectivity and social dysfunction in children with Attention Deficit/Hyperactivity Disorder

• Ahmed Ameen Fateh ^[1] ; Wenxian Huang ^[1] ; Muhammad Hassan ^[1] ; Yijiang Zhuang ^[1] ; Jieqiong Lin ^[1] ; Yi Luo ^[1] ; Binrang Yang ^[1] ; Hongwu Zeng ^[1]
  1. [1] Shenzhen Children’s Hospital, Shenzhen, China
• Localización: International journal of clinical and health psychology, ISSN 1697-2600, Vol. 23, Nº. 4, 2023, págs. 151-160
• Idioma: inglés
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• Resumen

  • Objective Attention Deficit/Hyperactivity Disorder (ADHD) negatively affects social functioning; however, its neurological underpinnings remain unclear. Altered Default Mode Network (DMN) connectivity may contribute to social dysfunction in ADHD. We investigated whether DMN's dynamic functional connectivity (dFC) alterations were associated with social dysfunction in individuals with ADHD.

    Methods Resting-state fMRI was used to examine DMN subsystems (dorsal medial prefrontal cortex (dMPFC), medial temporal lobe (MTL)) and the midline core in 40 male ADHD patients (7-10 years) and 45 healthy controls (HCs). Connectivity correlations with symptoms and demographic data were assessed. Group-based analyses compared rsFC between groups with two-sample t-tests and post-hoc analyses.

    Results Social dysfunction in ADHD patients was related to reduced DMN connectivity, specifically in the MTL subsystem and the midline core. ADHD patients showed decreased dFC between parahippocampal cortex (PHC) and left superior frontal gyrus, and between ventral medial prefrontal cortex (vMPFC) and right middle frontal gyrus compared to HCs (MTL subsystem). Additionally, decreased dFC between posterior cingulate cortex (PCC), anterior medial prefrontal cortex (aMPFC), and right angular gyrus (midline core) was observed in ADHD patients relative to HCs. No abnormal connectivity was found within the dMPFC.

    Conclusion Preliminary findings suggest that DMN connectional abnormalities may contribute to social dysfunction in ADHD, providing insights into the disorder's neurobiology and pathophysiology.