PT  - JOURNAL ARTICLE
AU  - Gonen, O.
AU  - Oberndorfer, T.A.
AU  - Inglese, M.
AU  - Babb, J.S.
AU  - Herbert, J.
AU  - Grossman, R.I.
TI  - Reproducibility of Three Whole-Brain <em>N</em>-Acetylaspartate Decline Cohorts in Relapsing-Remitting Multiple Sclerosis
DP  - 2007 Feb 01
TA  - American Journal of Neuroradiology
PG  - 267--271
VI  - 28
IP  - 2
4099  - http://www.ajnr.org/content/28/2/267.short
4100  - http://www.ajnr.org/content/28/2/267.full
SO  - Am. J. Neuroradiol.2007 Feb 01; 28
AB  - BACKGROUND AND PURPOSE: The cross-sectional rate of whole-brain N-acetylaspartate (NAA, a neuronal cell marker) loss in clinically similar relapsing-remitting multiple sclerosis (RRMS) patients has recently been shown to fall into 3 distinct decline rate strata. Our goal was to test the reproducibility of this observation in a new cohort of RRMS patients.MATERIALS AND METHODS: Sixteen serial patients (12 women, 4 men, median age 38 [27–55] years) with clinically definite RRMS for an average of 5 (0.3–18) years’ disease duration and a mean Expanded Disability Status Score of 2.0 (0–6) were studied, once each. Their whole-brain NAA (WBNAA) amounts, obtained with proton MR spectroscopy, were divided by brain volumes (segmented from MR imaging) to yield concentrations suitable for cross-sectional comparisons.RESULTS: Three distinct strata of cross-sectional NAA decline rates were found: −0.031, −0.32, and −1.71 mmol/L/y when disease duration was estimated from confirmed diagnosis, or −0.057, −0.20, and −1.38 mmol/L/y when measured from the first clinical symptom. These rates and their corresponding fractions of the study population were indistinguishable from those reported previously in a different group of 49 clinically similar (mean Expanded Disability Status Score also 2.0) RRMS patients.CONCLUSION: Reproducing the previous cohort’s cross-sectional WBNAA decline characteristics in this new group of clinically similar RRMS patients indicates that 3 WBNAA loss strata may be a general attribute of MS. Consequently, WBNAA could serve as a surrogate marker for the global load of neuronal and axonal dysfunction and damage in this disease.