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Auditory N1, N2, and MMN to pure-tone and consonant–vowel stimuli in developmental dyslexia and benign rolandic epilepsy: A progressive insight into the underlying disruptive neurophysiology

dc.contributor.authorTomé, David
dc.contributor.authorPereira, Ilídio
dc.contributor.authorVieira, Maria Celeste
dc.contributor.authorSoares, Ana Paula
dc.contributor.authorBarbosa, Fernando
dc.date.accessioned2025-11-03T14:53:45Z
dc.date.available2025-11-03T14:53:45Z
dc.date.issued2025-06-25
dc.description.abstractBenign rolandic epilepsy or benign epilepsy in childhood with centrotemporal spikes (BECTS) and developmental dyslexia (DD) are two of the most studied disorders in childhood. Despite decades of research, the neurophysiological mechanisms underpinning these disorders are largely unknown. Here, we use auditory event-related potentials (AERPs) to shed light on these issues, since several authors have reported the existence of language and learning impairments. AERPs reflect the activation of different neuronal populations and are suggested to contribute to the evaluation of auditory discrimination (N1), attention allocation and phonological categorization (N2), and echoic memory (mismatch negativity (MMN]). This study aims to investigate and document AERP changes in a group of children with BECTS and another group with DD. AERPs were recorded to pure-tones and consonant–vowel (CV) stimuli in an auditory oddball paradigm in eight children with BECTS, seven with DD, and 11 gender- and age-matched controls. The results revealed perceptual deficits for pure-tone and CV stimuli (pre-attentional and auditory discrimination) in DD, related to N1 reduced amplitude (p< 0.05; Fz: 2.57 μV, Cz: 2.75 μV). The BECTS group revealed no significant results for N1; however, there was an increase in N2b latency. The findings in the DD group support the anchor-deficit hypothesis as an explanation for neurolinguistic deficits. The increased N2b latency in the BECTS group could be related to a potential lack of inhibitory mechanisms of pyramidal neurons, as justified by the process of epileptogenesis.por
dc.identifier.citationTomé, D., Pereira, I., Vieira, M. C., Soares, A. P., & Barbosa, F. (2025). Auditory N1, N2, and MMN to Pure-Tone and Consonant&ndash;Vowel Stimuli in Developmental Dyslexia and Benign Rolandic Epilepsy: A Progressive Insight Into the Underlying Disruptive Neurophysiology. Neuropsychiatric Disease and Treatment, 21, 1271–1286. https://doi.org/10.2147/NDT.S498193
dc.identifier.doi10.2147/NDT.S498193
dc.identifier.eissn1178-2021
dc.identifier.ismn1178-2021
dc.identifier.urihttp://hdl.handle.net/10400.22/30733
dc.language.isoeng
dc.peerreviewedyes
dc.publisherDovepress-Taylor&Francis
dc.relation2022.05618.PTDC
dc.relation.hasversionhttps://www.dovepress.com/auditory-n1-n2-and-mmn-to-pure-tone-and-consonantvowel-stimuli-in-deve-peer-reviewed-fulltext-article-NDT
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/
dc.subjectN1
dc.subjectN2b
dc.subjectAuditory processing
dc.subjectDevelopmental dyslexia
dc.subjectBECTS
dc.titleAuditory N1, N2, and MMN to pure-tone and consonant–vowel stimuli in developmental dyslexia and benign rolandic epilepsy: A progressive insight into the underlying disruptive neurophysiologypor
dc.typeresearch article
dspace.entity.typePublication
oaire.citation.endPage1286
oaire.citation.startPage1271
oaire.citation.titleNeuropsychiatric Disease and Treatment
oaire.citation.volume21
oaire.versionhttp://purl.org/coar/version/c_970fb48d4fbd8a85

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