Global N-acetylaspartate concentration in benign and non-benign multiple sclerosis patients of long disease duration

To examine whether clinically benign multiple sclerosis patients (BMS) show similar losses of their global N-acetylaspartate (NAA) neuronal marker relative to more clinically disabled patients of similar disease duration.

The whole-brain NAA concentration (WBNAA) was acquired with whole-head non-localizing proton MR spectroscopy. Fractional brain parenchymal volume (fBPV), T2 and T1 lesion loads, were obtained from the MRI in: (i) 24 BMS patients: 23.1 ± 7.2 years disease duration, median Expanded Disability Status Scale (EDSS) score of 2.0 (range: 0-3); (ii) 26 non-benign MS patients (non-BMS), 24.5 ± 7.4 years disease duration, median EDSS of 4.0 (range: 3.5-6.5); (iii) 15 healthy controls.

Controls' 12.4 ± 2.3mM WBNAA was significantly higher than the BMS's and non-BMS's 10.5 ± 2.4 and 9.9 ± 2.1mM (both p<0.02), but the difference between the patients' groups was not (p>0.4). Likewise, the controls' 81.2 ± 4.5% fBPV exceeded the BMS and non-BMS's 77.0 ± 5.8% and 76.3 ± 8.6% (p<0.03), which were also not different from one another (p>0.7). BMS patients' T1-hypointense lesion load, 2.1 ± 2.2 cm(3), was not significantly different than the non-BMS's 4.1 ± 5.4 cm(3) (p>0.08) and T2-hyperintense loads: 6.0 ± 5.7 cm(3) and 8.7 ± 7.8 cm(3), were also not different (p>0.1).

WBNAA differentiates normal controls from MS patients but does not distinguish BMS from more disabled MS patients of similar disease duration. Nevertheless, all MS patients who remain RR for 15+ years suffered WBNAA loss similar to the average RR MS population at fourfold shorter disease duration suggesting relative global neuronal sparing or leveling-off of the neurodegeneration rate.