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. 2007 May;254(5):631-7.
doi: 10.1007/s00415-006-0415-5. Epub 2007 Apr 6.

N-acetylaspartic acid in cerebrospinal fluid of multiple sclerosis patients determined by gas-chromatography-mass spectrometry

Bas Jasperse  1 , Cornelis Jakobs, M Judith Eikelenboom, Christine D Dijkstra, Bernard M J Uitdehaag, Frederik Barkhof, Chris H Polman, Charlotte E Teunissen
Affiliations

N-acetylaspartic acid in cerebrospinal fluid of multiple sclerosis patients determined by gas-chromatography-mass spectrometry

Bas Jasperse et al. J Neurol. 2007 May.

Abstract

Background: Axonal degeneration is considered to play a major role in the development of clinical disability in multiple sclerosis (MS). N-AcetylAspartic Acid (NAA) is a neuron-specific marker constantly identified in MR-spectroscopy studies of the normal and MS brain. To our knowledge there are no studies available that evaluated NAA in cerebrospinal fluid (CSF) as a possible marker for disease severity.

Objective: To evaluate CSF concentrations of NAA in MS in relation to disease phenotype, clinical measures of disability and MRI markers of disease burden.

Methods: NAA concentrations were determined in CSF of 46 patients with MS (26 relapsing remitting (RRMS), 12 secondary progressive (SPMS) and 8 primary progressive (PPMS)). Prior to lumbar puncture, MS-patients underwent MRI and clinical examination, including the Expanded Disability Status Scale (EDSS) and the MS Functional Composite (MSFC). Additionally, CSF concentrations of NAA were determined in 12 patients with other neurological diseases (OND).

Results: Median CSF NAA concentration was 0.74 (IQR: 0.59-0.94) in RRMS , 0.54 (IQR: 0.35-0.73) in SPMS and 0.83 mumol/l (IQR: 0.56-1.03) in PPMS patients. SPMS patients had a significantly lower NAA concentration than RRMS patients. NAA concentrations correlated with EDSS (r = )0.37, p = 0.016), MSFC (r = 0.41, p = 0.010), normalised brain volume (r = 0.49, p = 0.001), T2 lesion load (r = )0.35, p = 0.021) and black hole lesion load (r = )0.47, p = 0.002). No differences were observed between OND (median: 0.57 IQR: 0.28-0.73) and MS patients.

Conclusion: CSF NAA concentration in MS patients is related to clinical performance and MRI measures of disease burden and may therefore be an important neuron specific marker of disease severity and possibly progression.

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Figures

Fig. 1
Fig. 1
Concentrations of NAA in MS-subtypes and other neurological diseases (OND). Boxes represent values from the 25th to the 75th percentiles, inner lines represent the median and whiskers show the minimum value. SP patients had a significantly lower NAA than RRMS patients (p = 0.015), as indicated by an asterisk(*)
Fig. 2
Fig. 2
Correlation between NAA concentrations in CSF and EDSS in MSpatients. The regression line was fitted for all MS patients (r = 0.37, p = 0.016). (squares: RRMS patients, triangles: SPMS patients, dots: PPMS patients)
Fig. 3
Fig. 3
Correlation between NAA concentrations in CSF and NBV in MSpatients. The regression line was fitted for all MS patients (r = 0.49, p = 0.001). (squares: RRMS patients, triangles: SPMS patients, dots: PPMS patients)
See this image and copyright information in PMC

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