Attention-deficit/hyperactivity disorder in childhood epilepsy: a neuropsychological and functional imaging study
Nina Bechtel1, Maja Kobel, Iris-Katharina Penner
1Division of Neuropediatrics and Developmental Medicine, University Children's Hospital Basel, Basel, Switzerland. nina.bechtel@unibas.ch
Insights
Attention-deficit/hyperactivity disorder (ADHD) in children with epilepsy shares similar behavioral and neural mechanisms with developmental ADHD. Methylphenidate improved working memory performance in both ADHD groups, suggesting a common underlying pathophysiology.
Area of Science:
- Neuroscience
- Pediatrics
- Child Psychology
Background:
- Children with epilepsy have a higher risk of attention-deficit/hyperactivity disorder (ADHD), often accompanied by working memory deficits.
- The underlying mechanisms of working memory in epilepsy-related ADHD versus developmental ADHD are not fully understood.
- Methylphenidate's efficacy in epilepsy-related ADHD requires further investigation.
Purpose of the Study:
- To evaluate shared behavioral, pharmacoresponsive, and neurofunctional pathophysiology between epilepsy-related ADHD and developmental ADHD in boys.
- To compare working memory performance and brain activation patterns in boys with epilepsy-related ADHD, developmental ADHD, and healthy controls.
- To assess the impact of methylphenidate on working memory in boys with ADHD, with or without epilepsy.
Main Methods:
- Functional magnetic resonance imaging (fMRI) was used to record brain activation during working memory tasks (N-back).
- Seventeen boys with epilepsy/ADHD, 15 with developmental ADHD, and 15 healthy controls (aged 8-14) participated.
- Each participant was tested twice, once with methylphenidate and once without, in a counterbalanced order.
Main Results:
- Boys with both epilepsy-related ADHD and developmental ADHD exhibited similar deficits in working memory tasks with high cognitive load compared to controls.
- Methylphenidate intake improved performance on these tasks to near-normal levels in both ADHD groups.
- fMRI revealed similar reductions in working memory network activation in both ADHD groups compared to controls, with no significant change after methylphenidate.
Conclusions:
- Epilepsy-related ADHD and developmental ADHD show significant similarities on behavioral, pharmacoresponsive, and neural levels.
- These findings support the hypothesis of a common underlying neurobehavioral pathophysiology for ADHD, regardless of epilepsy comorbidity.
- The study highlights shared mechanisms in working memory deficits and treatment response in pediatric ADHD.
Purpose:
Children with epilepsy have a significant risk for attention-deficit/hyperactivity disorder (ADHD), which is often accompanied by deficits in working memory performance. However, it is not yet clear whether there are specific differences in the underlying mechanisms of working memory capability between children with epilepsy-related ADHD and those with developmental ADHD. There is evidence that methylphenidate can improve the behavioral difficulties in children with developmental ADHD. Whether this medication has the same effect on ADHD symptoms in patients with epilepsy is not yet well understood. The aim of the present study is, therefore, to evaluate whether boys with epilepsy-related ADHD and developmental ADHD share a common behavioral, pharmacoresponsive, and neurofunctional pathophysiology.
Methods:
Seventeen boys with diagnosed combined epilepsy/ADHD, 15 boys with developmental ADHD, and 15 healthy controls (aged 8-14 years) performed on working memory tasks (N-back) while brain activation was recorded using functional magnetic resonance imaging. Each patient was tested twice: once after the intake of methylphenidate and once without in a counterbalanced order.
Key Findings:
On a behavioral level, we show that boys with epilepsy-related ADHD as well as those with developmental ADHD performed similarly poorly on tasks with high cognitive load when compared to healthy controls, and that intake of methylphenidate improved performance almost to normal levels in both ADHD groups. On the functional level, both patient groups showed similar reductions of activation in all relevant parts of the functional network of working memory when compared to controls. Of interest, intake of methylphenidate did not significantly alter this activity pattern.
Significance:
Our data show strong similarities between epilepsy-related and developmental ADHD on the behavioral, pharmacoresponsive, and neural level, favoring the view that ADHD with and without epilepsy shares a common underlying neurobehavioral pathophysiology.
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