Table 1.

Summary of Brain Metabolites in TBI

Metabolite	Chemical shift (ppm)	Comment
Lipid	0.9–1.5	Not usually visible in MRS unless released by pathological process such as trauma (Ashwal et al., 1997).
Lactate (Lac)	1.3	End product of anaerobic glycolysis. Indicator of hypoxia and impairment of perfusion (Ross et al., 1998).
N-acetyl-aspartate (NAA)	2.0	Synthesized in neurons. Marker of neuronal viability. Reduced with brain injury (Moffett et al., 2007).
Glutamate/Glutamine (Glx)	2.2–2.5	Glutamate is the primary excitatory neurotransmitter in the brain. Glutamine is found in astrocytes. Glx may be predictive of outcome after severe TBI and associated with immunoexcitotoxicity or secondary dysfunction (Shutter et al., 2004).
Choline (Cho)	3.2	Membrane marker. Elevated in cases of high membrane turnover. May indicate diffuse axonal injury (Andrew A. Maudsley et al., 2017) or continued repair at chronic time points in combination with normalized NAA levels (Babikian et al., 2018).
Creatine (Cr)	3.0	Found in metabolic active tissues, used in energy storage and transfer. Used as an internal standard for other metabolites (e.g. NAA/Cr, Cho/Cr). May be altered by TBI (Yeo et al., 2011).
Myo-inositol (mI)	3.5	Astrocyte marker and osmolyte. Involved in the metabolism of phosphatidyl inositol (a membrane phospholipid) - expected to increase after TBI due to membrane damage (Kierans et al., 2014). May also be a glial marker.