• Patricia Pais-Roldán, Brian L Edlow, Yuanyuan Jiang, Johannes Stelzer, Ming Zou, and Xin Yu.
• High-Field Magnetic Resonance Department, Max Planck Institute for Biological Cybernetics, Tuebingen, 72076, Germany; Graduate Training Centre of Neuroscience, International Max Planck Research School, University of Tuebingen, Tuebingen, 72074, Germany.
• Neuroimage. 2019 Apr 1; 189: 615-630.

AbstractDespite the association between brainstem lesions and coma, a mechanistic understanding of coma pathogenesis and recovery is lacking. We developed a coma model in the rat mimicking human brainstem coma, which allowed multimodal analysis of a brainstem tegmentum lesion's effects on behavior, cortical electrophysiology, and global brain functional connectivity. After coma induction, we observed a transient period (∼1h) of unresponsiveness accompanied by cortical burst-suppression. Comatose rats then gradually regained behavioral responsiveness concurrent with emergence of delta/theta-predominant cortical rhythms in primary somatosensory cortex. During the acute stage of coma recovery (∼1-8h), longitudinal resting-state functional MRI revealed an increase in functional connectivity between subcortical arousal nuclei in the thalamus, basal forebrain, and basal ganglia and cortical regions implicated in awareness. This rat coma model provides an experimental platform to systematically study network-based mechanisms of coma pathogenesis and recovery, as well as to test targeted therapies aimed at promoting recovery of consciousness after coma.Copyright © 2019 Elsevier Inc. All rights reserved.

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