Event related potentials during attention tasks in VLBW children with and without attention deficit disorder
S Potgieter1, J Vervisch, L Lagae
1Department of Paediatric Neurology, University Hospitals Gasthuisberg, 49 Herestreet, 3000, Leuven, Belgium. s.poltgieter@lzr.nl
Insights
Premature birth does not cause specific brain differences linked to attention deficit hyperactivity disorder (ADHD). Further research is needed to understand why premature children have higher ADHD rates.
Area of Science:
- Neuroscience
- Developmental Psychology
- Pediatrics
Background:
- Children born prematurely exhibit a higher incidence of attention deficit hyperactivity disorder (ADHD).
- Understanding the neurobiological underpinnings of ADHD in premature populations is crucial.
Purpose of the Study:
- To investigate potential brain dysfunctions in premature children that may contribute to the increased risk of ADHD.
- To compare electrophysiological responses between premature and full-term children with and without ADHD.
Main Methods:
- Utilized visual event-related potentials (ERPs) in a cohort of 41 children (VLBW and term-born, with/without ADHD), matched for IQ, age, and SES.
- Employed a visual oddball paradigm analyzing response times, error rates, and ERP components (N200, P300, P500).
Main Results:
- Children with ADHD, regardless of birth status, exhibited slower responses and increased commission/omission errors.
- ADHD was associated with altered N200 amplitude and topography, and reduced P500 amplitude over central leads.
- No significant differences in ERP latency, amplitude, or topography were observed between VLBW-ADHD and term-born ADHD groups.
Conclusions:
- Prematurity itself does not appear to induce specific attentional brain dysfunction or maturation delays.
- The higher incidence of ADHD in very low birth weight (VLBW) children likely stems from factors other than direct ERP-based processing deficits.
Objective:
Children born prematurely have a higher incidence of attention deficit disorder with or without hyperactivity. We have used visual event related potentials to study possible brain dysfunctions that could explain this higher incidence.
Methods:
Very low birth weight (VLBW) children with and without AD/HD and term born children with and without AD/HD, were matched for IQ, age and socio-economic status (n=41, mean age 104 months). A visual oddball paradigm, consisting of target and non-target stimuli, was used with analysis of response times, error scores, N200, P300 and a P500 component.
Results:
AD/HD children responded slower (F (1,38)=11.20, p<0.002); more varied (F (1,38)=21.77, p<0.000) and made more commission and omission errors (Kruskal-Wallis p<0.000). Non-target N200 was increased in amplitude (F (1.39)=4.01, p=0.05) with a wide anterior topography in children with AD/HD. The late positivity (P500) was decreased over central leads in children with AD/HD during the non-target stimuli (F (3,75)=3.00, p<0.036). No differences could be found in latency, amplitude or topography between VLBW children with AD/HD and term born children with AD/HD.
Conclusions:
Prematurity does not induce specific attentional brain dysfunction or maturation delays in stimulus processing during cognitive tasks. Other factors should be investigated to explain the higher incidence of AD/HD in VLBW children.
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