ArticleScientific reports2017
Response inhibition in Attention deficit disorder and neurofibromatosis type 1 - clinically similar, neurophysiologically different.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- A Systematic Review of Functional Brain Imaging Studies in Neurofibromatosis 1.Neuropsychology review · 2026Review
- Current states in understanding oligodendroglia-mediated neurological issues in neurofibromatosis type 1 (NF1).Acta neuropathologica communications · 2025Review
- Developmental trajectories in infants and pre-school children with Neurofibromatosis 1.Molecular autism · 2024Article
- Review
- Aberrant oscillatory activity in neurofibromatosis type 1: an EEG study of resting state and working memory.Journal of neurodevelopmental disorders · 2023Article
- The interplay of resting and inhibitory control-related theta-band activity depends on age.Human brain mapping · 2021Article
- Intact Stimulus-Response Conflict Processing in ADHD-Multilevel Evidence and Theoretical Implications.Journal of clinical medicine · 2020Article
- Conflict processing in juvenile patients with neurofibromatosis type 1 (NF1) and healthy controls - Two pathways to success.NeuroImage. Clinical · 2017Article
- Neuronal Intra-Individual Variability Masks Response Selection Differences between ADHD Subtypes-A Need to Change Perspectives.Frontiers in human neuroscience · 2017Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There are large overlaps in cognitive deficits occurring in attention deficit disorder (ADD) and neurodevelopmental disorders like neurofibromatosis type 1 (NF1). This overlap is mostly based on clinical measures and not on in-depth analyses of neuronal mechanisms. However, the consideration of such neuronal underpinnings is crucial when aiming to integrate measures that can lead to a better understanding of the underlying mechanisms. Inhibitory control deficits, for example, are a hallmark in ADD, but it is unclear how far there are similar deficits in NF1. We thus compared adolescent ADD and NF1 patients to healthy controls in a Go/Nogo task using behavioural and neurophysiological measures. Clinical measures of ADD-symptoms were not different between ADD and NF1. Only patients with ADD showed increased Nogo errors and reductions in components reflecting response inhibition (i.e. Nogo-P3). Early perceptual processes (P1) were changed in ADD and NF1. Clinically, patients with ADD and NF1 thus show strong similarities. This is not the case in regard to underlying cognitive control processes. This shows that in-depth analyses of neurophysiological processes are needed to determine whether the overlap between ADD and NF1 is as strong as assumed and to develop appropriate treatment strategies.
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