Despite the decline in fatal traumatic brain injury (TBI) incidence in recent years, TBI morbidity remains a public health challenge and is the leading cause of disability in the United States To combat these effects, new research is needed to identify mechanisms of injury that will lead to potential targets for therapeutic interventions that improve neurological outcome. One promising area of research is the cerebral metabolic dysfunction following TBI. Studies of post-traumatic cerebral metabolism have shown that cerebral metabolic rate of glucose (CMRglc) decreases for a period of days, weeks or months after injury with the duration and degree of hypometabolism correlating to level of consciousness and a strong predictor of long-term neurological outcome. However, specific changes in intermediary carbohydrate metabolic pathways have not yet been identified. In addition, the role of astrocyte metabolism in the post-injury metabolism has not been studied. This study uses in vivo 13C magnetic resonance spectroscopy (MRS) at 3 Tesla, a novel method in the clinical study of TBI, to non-invasively study the metabolic fate and flux of glucose (metabolized in both neurons and astrocytes) and acetate (metabolized in astrocytes) through metabolic pathways during the hypometabolic period. In addition, the investigators will study the association of decreased cerebral perfusion with changes in glucose and acetate metabolism following TBI, as changes in cerebral perfusion could profoundly affect cerebral metabolism by limiting substrate availability.