ArticlePeerJ2026
Investigation of brain connectivity alteration in the non-severe traumatic brain injury: an emotional condition study.
Article in PeerJ, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Traumatic brain injury (TBI) frequently results in persistent emotional and cognitive dysfunction, yet the neural mechanisms underlying these deficits remain incompletely understood. This study examined the impact of non-severe TBI (nTBI) on emotional processing, with a focus on brain activation, functional connectivity, effective connectivity, and their relationship to cognitive performance. Methods: Twenty right-handed male nTBI participants (mean age: 30.70 ± 11.78 years) and 20 age-matched healthy male controls (mean age: 27.85 ± 7.73 years) underwent functional magnetic resonance imaging (fMRI) while viewing emotional images from the International Affective Picture System (IAPS). Brain activation was analyzed using Statistical Parametric Mapping (SPM12). Functional connectivity was assessed with seed-based analysis (medial visual network, mVN) using the CONN toolbox. Effective connectivity was evaluated using dynamic causal modeling (DCM) and parametric empirical Bayes (PEB). Neuropsychological assessments covering memory, intelligence, and executive function were included to characterize general cognitive function within the cohort, with exploratory analyses examining relationships with connectivity measures. Results: Compared to controls, the nTBI group exhibited reduced activation in the calcarine cortex and lingual gyrus during emotional processing. Functional connectivity analysis showed decreased mVN connectivity with the frontal pole and dorsal anterior cingulate cortex (dACC), with increased mVN-ACC and mVN-supramarginal gyrus connectivity specifically during negative emotion processing. Effective connectivity analysis revealed altered directional influences within visual-limbic-cognitive control networks, including altered mVN-to-dACC and right amygdala-to-dACC connectivity patterns, as well as valence-specific modulation of self-inhibition. Exploratory analyses suggested potential correlations between connectivity alterations and cognitive performance, though these relationships varied across domains and should be interpreted cautiously. Conclusions: Non-severe TBI disrupts emotional network function by altering both functional and effective connectivity, particularly in visual, limbic, and cognitive control regions. These alterations may contribute to emotional dysregulation following injury. Findings support the relevance of brain connectivity-based markers in understanding post-TBI emotional processing and highlight potential targets for intervention. Interpretations should be made cautiously, given the study limitations, including the use of static visual stimuli and a homogenous male sample.
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