Acute and late changes in N-acetyl-aspartate following diffuse axonal injury in rats: An MRI spectroscopy and microdialysis study

N-acetyl-aspartate (NAA) measured by proton nuclear magnetic resonance spec troscopy (H-1-NMR) has been used as a marker of neuronal injury in many cer ebral pathologies. Therefore, we evaluate the roles of microdialysis vs. H- 1-NMR as techniques to assess NAA (NAA(d); NAA/Creatine ratio) in the livin g brain, and compare the results with whole brain NAA (NAA(w)) analyzed by HPLC after diffuse traumatic brain injury (TBI). Acute (4 h post-injury sur vival) and late (48 h survival) changes were studied in a sham-operated gro up (Sham, n = 4), and two injured groups (TBI/4h, n = 8; TBI/48h, n = 7). B aseline NAAd was 8.17 +/- 1 muM, and there was no significant difference be tween groups. There was only a small (twice of control), but transient incr ease in NAAd in the TBI/4 h group after trauma. Baseline NAA/Cr ratio was 1 .35 +/- 0.2, which did not change significantly between baseline, 1, 2, 3, 4 and 48 h or between groups after TBI. Whole brain NAA, (baseline 8.5 +/- 0.5 mmol kg(-1) wet weight) did not differ significantly between groups bef ore and after TBI. Diffuse TBI did not produce long-term changes in NAA, as sessed by three different methods. These results may indicate that NAA is n ot a sensitive marker of the severity of diffuse axonal damage. However, fu rther studies are needed to evaluate whether confounding factors such as mi crodialysis probe, voxel position and non-regional tissue homogenization mi ght have influenced our data.