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Review
. 2005;15(4 Suppl):46S-57S.
doi: 10.1177/1051228405284200.

Magnetic resonance spectroscopy in the monitoring of multiple sclerosis

Ponnada A Narayana  1
Affiliations
Review

Magnetic resonance spectroscopy in the monitoring of multiple sclerosis

Ponnada A Narayana. J Neuroimaging. 2005.

Abstract

In addition to providing information on tissue structure, magnetic resonance (MR) technology offers the potential to investigate tissue metabolism and function. MR spectroscopy (MRS) offers a wealth of data on the biochemistry of a selected brain tissue volume, which represent potential surrogate markers for the pathology underlying multiple sclerosis (MS). In particular, the N-acetylaspartate peak in an MR spectrum is a putative marker of neuronal and axonal integrity, and the choline peak appears to reflect cell-membrane metabolism. On this basis, a diminished N-acetylaspartate peak is interpreted to represent neuronal/axonal dysfunction or loss, and an elevated choline peak represents heightened cell-membrane turnover, as seen in demyelination, remyelination, inflammation, or gliosis. Therefore, MRS may provide a unique tool to evaluate the severity of MS, establish a prognosis, follow disease evolution, understand its pathogenesis, and evaluate the efficacy of therapeutic interventions, which complements the information obtained from the various forms of assessment made by conventional MR imaging.

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Figures

Fig 1
Fig 1
Deficiencies of conventional magnetic resonance imaging as a means of monitoring multiple sclerosis (MS) are illustrated by a study of 34 patients with untreated primary-progressive MS in which subgroups defined by a T2-weighted lesion load (LL) lower (light gray) or higher (dark gray) than 3 cm3 showed no significant difference in central brain N-acetylaspartate (NAA)-creatine (Cr), the ratio of NAA to Cr, a magnetic resonance spectroscopy measure of axonal pathology (A). The subgroups also failed to differ in an index of brain atrophy (B). From Pelletier et al. J Neurol Neurosurg Psychiatry 2003;74:950-952. Adapted and reproduced with permission from the BMJ Publishing Group.
Fig 2
Fig 2
Magnetic resonance spectroscopy (MRS) spectrum of brain along with molecular assignment of resonances. The normal 1H-MRS spectrum is dominated by an N-acetylaspartate (NAA) resonance, flanked at the left by peaks for glutamate/glutamine (Glx), creatine (Cr)/phosphocreatine, choline (Cho)-containing phospholipids, and myo-inositol (mI) and at the right by peaks for lactate and free lipids. In multiple sclerosis, abnormal findings often include a decrease in the NAA peak (indicative of axonal pathology) and an increase in the Cho peak (indicative of demyelination). Adapted with permission from Lin et al. Efficacy of proton magnetic resonance spectroscopy in neurological diagnosis and neurotherapeutic decision making. NeuroRx® 2:197-214. Copyright © 2005, American Society for Experimental Neuro Therapeutics. All rights reserved.
Fig 3
Fig 3
Contrast-enhanced and T1-weighted axial turbo spin-echo images of a small, acute, contrast-enhancing lesion and a large corresponding hyperintense lesion in the periventricular white matter of a patient with multiple sclerosis (MS). The saturation slices and position of the 8-mL volume of interest are noted. The STEAM spectrum shows a reduced N-acetylaspartate level (NAA) and an elevated myo-inositol (mI) level. Cho = choline; Cr = creatine; Lac + MM = lactate + lipids + macromolecules. Reprinted with permission from Mader et al. Proton MR spectroscopy with metabolite-nulling reveals elevated macromolecules in acute multiple sclerosis. Brain 2001;124(Pt 5):953–961, by permission of Oxford University Press.
Fig 4
Fig 4
Magnetic resonance spectroscopy of a multiple sclerosis patient’s centrum semiovale exhibits temporary changes in normal-appearing white matter, including the reversal of a depression in N-acetylaspartate (NAA) level. The spectra shown were obtained on days 98 (A), 147 (B), 189 (C), and 259 (D) of a longitudinal study; the second and third in the series show a fall in the NAA peak (at 2.0 ppm), but the fourth spectrum documents a recovery. The second spectrum also shows temporary free-lipid features, toward the right side of the data. The neuroanatomical region subsequently developed a magnetic resonance imaging–defined lesion. Adapted from Narayana et al. Serial proton magnetic resonance spectroscopic imaging, contrast-enhanced magnetic resonance imaging, and quantitative lesion volumetry in multiple sclerosis. Ann Neurol 1998;43:56–71.Copyright ©1998 Wiley-Liss, Inc., A Wiley Company. Reproduced with permission ofJohn Wiley & Sons, Inc.
Fig 5
Fig 5
Magnetic resonance spectroscopy findings for a total of 66 T2-weighted lesions that had persisted for at least 6 months in one or another of 9 relapsing-remitting multiple sclerosis (MS) patients showed NAA levels to be lowest in T1-weighted hypointensities, or “black holes” (HYPO), while creatine (Cr) and choline (Cho) are higher in T1-weighted isointensities (ISO) and in normal-appearing white matter (NAWM) than in white matter of normal controls (NWM). In all instances, horizontal lines are medians, boxes show 25% to 75% values, vertical lines span ±95%, and asterisks show outliers. Adapted with permission from He et al. Relapsing-remitting multiple sclerosis: metabolic abnormality in nonenhancing lesions and normal-appearing white matter at MR imaging—initial experience. Radiology 2005;234:211–217.
Fig 6
Fig 6
Whole-brain levels of N-acetylaspartate (WBNAA) for 49 patients with relapsing-remitting multiple sclerosis (MS) are plotted against each patient’s duration of MS, beginning with the initial clinical episode. The data define distinct trends for patients with an insignificant rate of NAA decline (black circles), a decline calculated not to exceed 1.7 mmol/L/y (squares, with shaded squares indicating patients who received MS treatment at the time of the NAA measurement), or a rapid decline (triangles). Dashed lines show 95% confidence intervals. Adapted with permission from Gonen et al. Relapsing-remitting multiple sclerosis and whole-brain N-acetylaspartate measurement: evidence for different clinical cohorts—initial observations. Radiology 2002;225:261–268.
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