Abstract #0509

Redundancy and resiliency of arousal mechanisms in traumatic coma patients

Marta Bianciardi¹, Saef Izzy², Bruce R Rosen¹, Lawrence L Wald¹, and Brian L Edlow³

¹Department of Radiology, A.A. Martinos Center for Biomedical Imaging, MGH and Harvard Medical School, Boston, MA, United States, ²Department of Neurology, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, United States, ³Department of Neurology, A. A. Martinos Center for Biomedical Imaging, MGH and Harvard Medical School, Boston, MA, United States

Traumatic brain injury to brainstem/thalamic/hypothalamic/basal-forebrain arousal nuclei is implicated in the pathogenesis of coma. However, due to difficulty in localizing these nuclei with conventional MRI, it is unknown which lesioned nuclei cause coma, and which are compatible with recovery of arousal/consciousness. We mapped our recently developed brainstem arousal-nuclei atlases and current thalamic/hypothalamic/basal-forebrain atlases to 3Tesla susceptibility-weighted-images in twelve acute traumatic-coma patients, who recovered full arousal/consciousness within six-months. We identified multiple combinations of injured brainstem/thalamic arousal-nuclei that cause acute coma, yet are compatible with a full recovery of arousal/consciousness. Thus, there is redundancy and resiliency of arousal mechanisms in traumatic coma.

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