Altered Functional Network in Infants With Profound Bilateral Congenital Sensorineural Hearing Loss: A Graph Theory Analysis

Functional magnetic resonance imaging (fMRI) studies have suggested that there is a functional reorganization of brain areas in patients with sensorineural hearing loss (SNHL). Recently, graph theory analysis has brought a new understanding of the functional connectome and topological features in central neural system diseases. However, little is known about the functional network topology changes in SNHL patients, especially in infants. In this study, 34 infants with profound bilateral congenital SNHL and 28 infants with normal hearing aged 11–36 months were recruited. No difference was found in small-world parameters and network efficiency parameters. Differences in global and nodal topologic organization, hub distribution, and whole-brain functional connectivity were explored using graph theory analysis. Both normal-hearing infants and SNHL infants exhibited small-world topology. Furthermore, the SNHL group showed a decreased nodal degree in the bilateral thalamus. Six hubs in the SNHL group and seven hubs in the normal-hearing group were identified. The left middle temporal gyrus was a hub only in the SNHL group, while the right parahippocampal gyrus and bilateral temporal pole were hubs only in the normal-hearing group. Functional connectivity between auditory regions and motor regions, between auditory regions and default-mode-network (DMN) regions, and within DMN regions was found to be decreased in the SNHL group. These results indicate a functional reorganization of brain functional networks as a result of hearing loss. This study provides evidence that functional reorganization occurs in the early stage of life in infants with profound bilateral congenital SNHL from the perspective of complex networks.

Brief Postnatal Visual Deprivation Triggers Long-Lasting Interactive Structural and Functional Reorganization of the Human Cortex

Patients treated for bilateral congenital cataracts provide a unique model to test the role of early visual input in shaping the development of the human cortex. Previous studies showed that brief early visual deprivation triggers long-lasting changes in the human visual cortex. However, it remains unknown if such changes interact with the development of other parts of the cortex. With high-resolution structural and resting-state fMRI images, we found changes in cortical thickness within, but not limited to, the visual cortex in adult patients, who experienced transient visual deprivation early in life as a result of congenital cataracts. Importantly, the covariation of cortical thickness across regions was also altered in the patients. The areas with altered cortical thickness in patients also showed differences in functional connectivity between patients and normally sighted controls. Together, the current findings suggest an impact of early visual deprivation on the interactive development of the human cortex.

Para-Sports can Promote Functional Reorganization in the Ipsilateral Primary Motor Cortex of Lower Limbs Amputee

Background. Drastic functional reorganization was observed in the ipsilateral primary motor cortex (M1) of a Paralympic long jumper with a unilateral below-knee amputation in our previous study. However, it remains unclear whether long-term para-sports are associated with ipsilateral M1 reorganization since only 1 athlete with amputation was investigated. Objective. This study aimed to investigate the relationship between the long-term para-sports and ipsilateral M1 reorganization after lower limb amputation. Methods. Lower limb rhythmic muscle contraction tasks with functional magnetic resonance imaging and T1-weighted structural imaging were performed in 30 lower limb amputees with different para-sports experiences in the chronic phase. Results. Brain activity in the ipsilateral primary motor and somatosensory areas (SM1) as well as the contralateral dorsolateral prefrontal cortex, SM1, and inferior temporal gyrus showed a positive correlation with the years of routine para-sports participation (sports years) during contraction of the amputated knee. Indeed, twelve of the 30 participants who exhibited significant ipsilateral M1 activation during amputated knee contraction had a relatively longer history of para-sports participation. No significant correlation was found in the structural analysis. Conclusions. Long-term para-sports could lead to extensive reorganization at the brain network level, not only bilateral M1 reorganization but also reorganization of the frontal lobe and visual pathways. These results suggest that the interaction of injury-induced and use-dependent cortical plasticity might bring about drastic reorganization in lower limb amputees.

Dynamic Interplay between Lower-Grade Glioma Instability and Brain Metaplasticity: Proposal of an Original Model to Guide the Therapeutic Strategy

The behavior of lower-grade glioma (LGG) is changing over time, spontaneously, and in reaction to treatments. First, due to genomic instability and clonal expansion, although LGG progresses slowly during the early period of the disease, its growth velocity will accelerate when this tumor will transform to a higher grade of malignancy. Furthermore, its pattern of progression may change following therapy, e.g., by switching from a proliferative towards a more diffuse profile, in particular after surgical resection. In parallel to this plasticity of the neoplasm, the brain itself is constantly adapting to the tumor and possible treatment(s) thanks to reconfiguration within and between neural networks. Furthermore, the pattern of reallocation can also change, especially by switching from a perilesional to a contrahemispheric functional reorganization. Such a reorientation of mechanisms of cerebral reshaping, related to metaplasticity, consists of optimizing the efficiency of neural delocalization in order to allow functional compensation by adapting over time the profile of circuits redistribution to the behavioral modifications of the glioma. This interplay between LGG mutations and reactional connectomal instability leads to perpetual modulations in the glioma–neural equilibrium, both at ultrastructural and macroscopic levels, explaining the possible preservation of quality of life despite tumor progression. Here, an original model of these dynamic interactions across LGG plasticity and the brain metanetwork is proposed to guide a tailored step-by-step individualized therapeutic strategy over years. Integration of these new parameters, not yet considered in the current guidelines, might improve management of LGG patients.