# Predictive value of foetal superior temporal sulcus asymmetry for neonatal speech discrimination

**Authors:** Sophie Mandl, Patric Kienast, Gregor Kasprian, Florian Ph S Fischmeister, Anna Weiskopf, Estella Ringelmann, Johannes Tischer, Michael Weber, Apeksha Hadole, Rainer Seidl, Lisa Bartha-Doering

PMC · DOI: 10.1093/braincomms/fcag048 · Brain Communications · 2026-02-13

## TL;DR

The study shows that less rightward asymmetry in a fetus's brain structure is linked to reduced right hemisphere activation during speech discrimination in newborns.

## Contribution

The study provides new insights into how prenatal brain asymmetry predicts early postnatal language processing.

## Key findings

- Children with leftward STS asymmetry showed less right hemisphere activation during speech discrimination.
- Less rightward asymmetry in the fetal STS was associated with reduced differentiation between speech types in the right hemisphere.
- The findings suggest earlier left temporal lobe development correlates with reduced right hemisphere involvement in speech processing.

## Abstract

While some anatomical brain asymmetries are seen across primates, the earlier appearance and larger depth of the right superior temporal sulcus (STS) is specific to human foetuses. Interestingly, the degree of STS asymmetry varies between foetuses, and it has been shown that this interindividual variability is related to the functional lateralization of the language network in school-aged children. It remains unclear, however, whether it is also indicative of language localization and functioning shortly after birth. In the present longitudinal study, we prospectively examined the predictive value of foetal STS asymmetry for neonates’ language lateralization and neural speech discrimination. We measured the STS depths and volumes in neurotypical foetuses (N = 35) using foetal MRI. After birth, we investigated the neonates’ haemodynamic response to forward and backward speech using functional near-infrared spectroscopy. We hypothesized that less rightward asymmetry of the STS depths in the foetal brain is related to increased left language lateralization and to a greater haemodynamic difference between speech conditions in the left hemisphere in neonates. While the foetuses demonstrated an overall rightward asymmetry of the STS depths and volumes, the degree of asymmetry varied between individuals. After birth, the group activated left frontal and right temporal regions during the speech discrimination paradigm. Again, there was variability in the degree of neural activation in response to speech. Importantly, we found that children with a foetal STS depth asymmetry towards the left hemisphere activated their right hemisphere less for forward speech (r = −0.58, P = 0.002) and differentiated less between forward and backward speech in their right hemisphere (r = −0.48, P = 0.014). Contrary to our initial hypothesis, the results suggest that an earlier structural development of the left temporal lobe goes along with reduced involvement of the right hemisphere, rather than an increased involvement of the left hemisphere, during neural speech discrimination. Given that rightward asymmetry of language-related brain areas has been associated with weaker language abilities, the present study provides important preliminary data regarding the neural underpinnings of language development during the prenatal and early postnatal period.

Mandl et al. report that less rightward asymmetry of the foetal superior temporal sulcus depths is associated with reduced activation in the right hemisphere during neonatal speech discrimination. Given that rightward asymmetry of language-related brain areas has been associated with weaker language abilities, this study provides important information regarding the neural underpinnings of early language development.

Graphical Abstract

## Full-text entities

- **Genes:** STS (steroid sulfatase) [NCBI Gene 412] {aka ARSC, ARSC1, ASC, ES, SSDD, XLI}, KIAA0319 (KIAA0319) [NCBI Gene 9856] {aka DYLX2, DYX2, NMIG}, FOXP2 (forkhead box P2) [NCBI Gene 93986] {aka CAGH44, SPCH1, TNRC10}
- **Diseases:** brain asymmetry (MESH:D005146), neurodevelopmental disorders (MESH:D002658), delayed language processing (MESH:D007805), neurobehavioral disorders (MESH:D019954), language deficits (MESH:D007806), autism spectrum disorder (MESH:D000067877), dyslexia (MESH:D004410), schizophrenia (MESH:D012559), psychiatric diseases (MESH:D001523)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12946156/full.md

## References

56 references — full list in the complete paper: https://tomesphere.com/paper/PMC12946156/full.md

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Source: https://tomesphere.com/paper/PMC12946156