Abstract

In this study, we have reported a correlation between structural brain changes and electroencephalography (EEG) in response to tactile stimulation in ten comatose patients after severe traumatic brain injury (TBI). Structural morphometry showed a decrease in whole-brain cortical thickness, cortical gray matter volume, and subcortical structures in ten comatose patients compared to fifteen healthy controls. The observed decrease in gray matter volume indicated brain atrophy in coma patients induced by TBI. In resting-state EEG, the power of slow-wave activity was significantly higher (2–6 Hz), and the power of alpha and beta rhythms was lower in coma patients than in controls. During tactile stimulation, coma patients’ theta rhythm power significantly decreased compared to that in the resting state. This decrease was not observed in the control group and correlated positively with better coma outcome and the volume of whole-brain gray matter, the right putamen, and the insula. It correlated negatively with the volume of damaged brain tissue. During tactile stimulation, an increase in beta rhythm power correlated with the thickness of patients’ somatosensory cortex. Our results showed that slow-wave desynchronization, as a nonspecific response to tactile stimulation, may serve as a sensitive index of coma outcome and morphometric changes after brain injury.

Highlights

  • The relationship between brain damage and neurological mechanisms supporting recovery after severe brain injury has remained largely unknown [1]

  • Our findings indicated that the cortical thickness, the volume of the cortex, and the volume of subcortical structures were lower comatose patients than in of healthy participants

  • Our findings indicated that theincortical thickness, the volume the cortex, and the volume of were data, lower which in comatose patients than severe in healthy participants

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Summary

Introduction

The relationship between brain damage and neurological mechanisms supporting recovery after severe brain injury has remained largely unknown [1]. The connection between behaviorally defined clinical entities and underlying brain damage has been poorly investigated. Brain Sci. 2020, 10, 720 patients’ hippocampus, fornix, and other structures decreased [5]. According to Crick and Koch’s (2003) consciousness framework, brain networks, including sensory, semantic, and motor neural chains, are necessary for consciousness processes [6]. These neural coalitions could be described as a subset of cortical structures, including sensorimotor areas, the prefrontal cortex, the posteromedial cingulate cortex, and the parietal regions, as well as the relevant thalamocortical loops, which are capable of integrating the supervision, limited capacity, and re-entry properties of conscious sensory processing [7]. Impairment of the networks, including the frontoparietal and thalamocortical networks and encompassing the polymodal associative cortices, impaired consciousness [8,9,10,11,12,13]

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