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

Abstract

Background and objectiveTo 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. MethodsThe 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. ResultsControls’ 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±2.2cm3, was not significantly different than the non-BMS's 4.1±5.4cm3 (p>0.08) and T2-hyperintense loads: 6.0±5.7cm3 and 8.7±7.8cm3, were also not different (p>0.1). ConclusionsWBNAA 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.