Neural correlates of late talking: A systematic review of electrophysiological and neuroimaging studies.

Clinical Snapshot

Key Findings

• P Value: Not reported at the review level

• Effect Size: Not reported; no pooled effect sizes calculated (narrative synthesis only)

• Primary Outcome: Neural correlates of late talking identified via EEG/ERP and MRI, including: increased frontal gamma power, reduced Mismatch Negativity (MMN), absent Phonological Mismatch Negativity (PMN), altered N400 (lexical-semantic processing); reduced gray matter in left temporal regions, atypical right-hemispheric lateralization, reduced cortical-subcortical activation, and altered white matter connectivity

• Nnt Or Sensitivity: Not applicable; no diagnostic accuracy or therapeutic outcome data synthesised. Neural markers described as having 'significant predictive value' for later language outcomes but no sensitivity, specificity, or AUC statistics are reported at the review level

• Confidence Interval: Not reported

Clinical Application

EEG/ERP is feasible in toddlers and is available in specialist paediatric neuroscience and research centres, though not in routine primary care or community speech-language pathology settings. Clinical MRI in this age group typically requires sedation or natural sleep protocols, limiting routine clinical application. The neural biomarkers identified remain research-grade and are not validated for individual-level clinical decision-making. In Australia, late talking is typically managed within the RACGP primary care framework, with referral to speech-language pathologists (SLPs) and, where indicated, developmental paediatricians. The NDIS provides funding pathways for children with confirmed developmental language disorder. Current Australian practice does not incorporate EEG or MRI biomarkers in the diagnostic or prognostic workup of late talkers. The TGA has not approved any neuromodulation device for paediatric language disorders. PBS does not list any pharmacological intervention for late talking. The authors' advocacy for neuromodulation is premature in the Australian regulatory and clinical context. ASHA and Speech Pathology Australia guidelines emphasise watchful waiting with targeted intervention for late talkers, a position not substantially altered by this review's findings. Children aged approximately 18–36 months presenting with expressive vocabulary delay without comorbid autism spectrum disorder, intellectual disability, hearing impairment, or neurological conditions. The findings are most relevant to children meeting established late talker criteria (e.g., fewer than 50 words or no two-word combinations by 24 months).

Abstract

BACKGROUND: Late talking (LT), a delay in expressive vocabulary in early childhood, affects a significant minority of toddlers and can be a precursor to persistent language and literacy impairments. While behavioral profiles are well-documented, a systematic synthesis of its underlying neurobiology is lacking. This systematic review aimed to identify, evaluate, and synthesize evidence from electrophysiological (EEG) and neuroimaging (MRI) studies on the neural correlates of late talking in children. METHODS: We conducted a systematic search of Scopus, Web of Science, and PubMed from inception to September 2025, following PRISMA guidelines. Studies investigating children formally identified as late talkers without comorbid neurological or global developmental conditions, using EEG/ERP or MRI modalities, were included. Risk of bias was assessed using the Joanna Briggs Institute (JBI) critical appraisal tool. RESULTS: Sixteen studies (8 EEG, 8 neuroimaging) comprising 231 LT children in EEG studies and 315 in neuroimaging studies were included. EEG studies revealed a neurodevelopmental cascade, beginning with atypical oscillatory activity (increased frontal gamma power) and deficits in auditory discrimination (reduced Mismatch Negativity), progressing to higher-order impairments in phonological (absent PMN) and lexical-semantic (altered N400) processing. Neuroimaging studies consistently identified structural and functional anomalies within a distributed perisylvian network, including reduced gray matter in left temporal regions, atypical right-hemispheric lateralization, reduced activation in cortical-subcortical circuits, and altered white matter connectivity. These neural markers demonstrated significant predictive value for later language outcomes. CONCLUSION: Late talking is a clear neurodevelopmental disorder with a cascading pattern of neural dysfunction. The identified neural signatures are not just findings but have strong clinical potential as biomarkers for early identification and prognosis. This evidence advocates for a shift to a precision medicine approach, opening the door to novel, neurobiologically-informed interventions like neuromodulation that target the underlying brain circuits.

References

1. 1.Mohammadi, M. R., Dadgar, H., Baloochi, S. A., & Khaleghi, A. (2026). Neural correlates of late talking: A systematic review of electrophysiological and neuroimaging studies. Progress in Neuro-Psychopharmacology & Biological Psychiatry. Advance online publication. https://doi.org/10.1016/j.pnpbp.2026.111719