Please use this identifier to cite or link to this item: http://hdl.handle.net/2080/5836
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dc.contributor.authorD, Annuncy Vinoliya-
dc.date.accessioned2026-07-01T05:03:39Z-
dc.date.available2026-07-01T05:03:39Z-
dc.date.issued2026-06-
dc.identifier.citation45th International Linguistics Conference (TABU Dag), University of Groningen, Netherlands, 11-12 June 2026en_US
dc.identifier.urihttp://hdl.handle.net/2080/5836-
dc.descriptionCopyright belongs to the proceeding publisher.en_US
dc.description.abstractChildhood Apraxia of Speech (CAS) is a neurodevelopmental language disorder characterized by impaired planning and programming of speech movements, resulting in inconsistent phonological errors, deficient coarticulatory transitions, and disrupted prosody. Though historically classified as a motor speech disorder, converging evidence from cognitive linguistics, neuroimaging, and molecular genetics firmly repositions CAS within the broader domain of language disorders, with significant implications for neurolinguistic theory and clinical intervention. From a cognitive-linguistic standpoint, CAS extends beyond articulatory dysfunction. Affected children demonstrate morphosyntactic errors, phonological memory deficits, impaired prosodic encoding, and delayed metalinguistic and literacy development hallmarks of a systemic language disorder. Deficits in non-word repetition reflect breakdowns at the transcoding and phonological encoding interface, implicating the core systems of spoken language production rather than peripheral motor execution alone. Neuroimaging studies reveal structural and functional abnormalities across the classical language network, including reduced grey matter in the left inferior frontal gyrus, superior temporal gyrus, and supplementary motor area, alongside decreased fractional anisotropy in corticobulbar white matter tracts. Disrupted cerebellar-cortical connectivity further impairs the forward modeling mechanisms essential for phonological prediction and sensorimotor integration in speech. Genetically, over 17 genes have been implicated in CAS, including FOXP2, FOXP1, and CNTNAP2 all expressed within language-critical neural circuits and shared with broader developmental language disorder phenotypes. CAS is additionally documented as a secondary language phenotype across metabolic, epileptic, syndromic, and traumatic neurological conditions, underscoring its status as a core feature of neurolinguistic disruption rather than an isolated motoric anomaly. This review argues that a neurolinguistic framing of CAS advances both theoretical understanding and clinical practice, and calls for integrated linguistic, neurological, and genomic approaches in future research.en_US
dc.subjectChildhood Apraxia of Speech (CAS)en_US
dc.subjectNeural Substrateen_US
dc.subjectGenetic Etiologyen_US
dc.titleChildhood Apraxia of Speech as a Language Disorder: A Neurolinguistic Overviewen_US
dc.typePresentationen_US
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