Disturbances of Cerebral Metabolism of Aspartate, Glutamate, and N-Acetylaspartate after Traumatic Brain Injury According to 1H Magnetic Resonance Spectroscopy

Abstract

Cerebral concentrations of N-acetylaspartate, aspartate, and glutamate were determined for the first time simultaneously in patients with severe traumatic brain injury in the remote period using J-modulated editing of ¹H magnetic resonance spectra in vivo. It has been shown that the N-acetylaspartate and aspartate concentrations in the frontal lobes of the brain were significantly reduced (by 65 and 61%, respectively) with a constant concentration of glutamate in the remote period after severe brain injury. Our findings indicate that a decrease in the N-acetylaspartate concentration in the delayed period after brain injury is caused by a decrease in the concentration of aspartate, a precursor of the synthesis of N-acetylaspartate. The decrease in the aspartate level with a constant level of glutamate is a consequence of the dysfunction of one of the most important metabolism regulation systems, namely, the malate–aspartate shuttle.