Developmental alterations in brain network asymmetry in 3- to 9-month infants with congenital sensorineural hearing loss
Year: 2025
Type: article
Study design: Observational Study
Abstract: Auditory exposure plays crucial roles in shaping healthy brain development and generating lateralization of functional network organization. However, little is known about whether and how an initial lack of auditory exposure in early infancy may disrupt development of functional network lateralization. We addressed this issue by recruiting 55 infants with congenital sensorineural hearing loss (SNHL) and 60 typically developing (TD) controls. Resting-state fNIRS imaging data were acquired to construct hemispheric cerebral networks, and graph theory was applied to quantify the topological characteristics of hemispheric networks. The infants with SNHL exhibited efficient small-world characteristic within each hemispheric network, however, the lateralization of functional network efficiency was substantially disrupted. Compared with TD infants with significantly increased network efficiency lateralized toward left hemisphere with age, the SNHL infants did not exhibit the emergence and development of such cerebral lateralization. Furthermore, the increased leftward asymmetry in nodal efficiency with age was found in TD but not in SNHL infants. Interestingly, the degree of hearing loss had no correlation with lateralization strength in the SNHL group. These results suggest that SNHL infants exhibited disrupted development of cortical lateralization in functional network organization, and highlight the importance of auditory stimulation-promoted multisensory functional integration in early infancy.
Source: Science Advances
Authors: Guangfang Liu, Xin Zhou, Zhenyan Hu, Yidi Liu, Endi Huo, Heather Bortfeld, Qi Dong, Chunhui Chen, Haihong Liu, Haijing Niu
Language: English
Subfield: Cognitive Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $4,500
Awards: G2193529120, G7418900372
OpenAlex ID: W4415221119
