ArticlemedRxiv : the preprint server for health sciences2025
Emotional Processing After Severe Traumatic Brain Injury: Insights from Functional MRI and Pupillometry.
Article in medRxiv : the preprint server for health sciences, 2025. 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
Objective: Emotional dysfunction is a common consequence of severe traumatic brain injury (TBI), yet the mechanisms underlying these symptoms remain poorly understood. This study investigated whether brain network and autonomic mechanisms involved in emotional processing are abnormal in TBI. Methods: We conducted a cross-sectional study of chronic severe TBI (n=26) and healthy control participants (n=15). We analysed functional MRI (fMRI) data to assess brain processing of emotionally salient music (joyful and fearful stimuli; n=15 TBI, n=15 controls), and resting-state fMRI (rsfMRI) to measure the functional connectivity of relevant intrinsic brain networks (limbic, salience, and default mode networks; n=16 TBI, n=15 controls). We additionally measured the pupillary light reflect (PLR) to assess parasympathetic and sympathetic function (n=14 TBI, n=11 controls). Results: Individuals with severe TBI did not demonstrate the left insula activation elicited by joyful versus fearful musical stimuli seen in healthy controls. rsfMRI revealed decreased connectivity between the salience network, caudate and hippocampus in severe TBI compared to controls. Exploratory analyses identified reduced connectivity between default mode (bilateral medial prefrontal cortex) and limbic (bilateral amygdala) nodes in TBI compared to controls. PLR measurements revealed blunted dark-adaptation responses in individuals with severe TBI compared to controls (F(1,24)=27.4, p<0.001). Interpretation: Individuals with chronic severe TBI show reduced insula activation during emotional stimuli processing, resting connectivity abnormalities in salience, limbic and default mode networks, and evidence of sympathetic dysfunction. Brain network and autonomic alterations may be potential neural mechanisms of post-TBI emotional dysregulation.
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