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Association between subcortical nuclei volume changes and cognition in preschool-aged children with tetralogy of
Liang Hu1, Kede Wu1, Huijun Li2
1Department of Cardiothoracic Surgery, Children's Hospital of Nanjing Medical University, 72 Guangzhou Road, Nanjing, 210008, China.
Background:
Neurocognitive disorders frequently occur in patients with cyanotic congenital heart disease (CCHD) because of the hemodynamic abnormalities induced by preoperative cardiac structural changes. We aimed to evaluate subcortical nuclei volume changes and cognition in postoperative tetralogy of Fallot (TOF) children, and analyze their relationship with preoperative cardiac structural changes.
Methods:
This case-control study involved thirty-six children with repaired TOF and twenty-nine healthy controls (HCs). We utilized three-dimensional (3D) T1-weighted high-resolution structural images alongside the Wechsler Preschool and Primary Scale of Intelligence-Fourth Edition (WPPSI-IV) to evaluate the cognitive differences between the TOF and HC group.
Results:
We observed notable differences in subcortical nuclei volume between the TOF and HC group, specifically in the left amygdala nucleus (LAM, TOF: 1292.60 ± 155.57; HC: 1436.27 ± 140.62, p < 0.001), left thalamus proper nucleus (LTHA, TOF: 6771.54 ± 666.03; HC: 7435.36 ± 532.84, p < 0.001), and right thalamus proper nucleus (RTHA, TOF: 6514.61 ± 715.23; HC: 7162.94 ± 554.60, p < 0.001). Furthermore, a diminished integrity of LAM ( β:-19.828, 95% CI: -36.462, -3.193), which showed an inverse relationship with the size of the preoperative ventricular septal defect (VSD), correlated with lower working memory indices in children with TOF.
Conclusions:
Our findings indicate that subcortical nuclei structural injuries possibly potentially stemming from cardiac anatomical abnormalities, are associated with impaired working memory in preschool-aged children with TOF. The LAM in particular may serve as a potential biomarker for neurocognitive deficits in TOF, offering predictive value for future neurodevelopmental outcomes, and shedding light on the neurophysiological mechanisms of these cognitive impairments.
