Combined 1H and 31P spectroscopy provides new insights into the pathobiochemistry of brain damage in multiple sclerosis

• DOI: 10.1002/nbm.1621
• Publication Date: 2010-12-13T05:09:54Z
• Authors: Elke Hattingen; Jörg Magerkurth; Ulrich Pilatus; Annemarie Hübers; Mathias Wahl; Ulf Ziemann
• Keywords: Adult; Male; Magnetic Resonance Spectroscopy; Multiple Sclerosis; Brain; Phosphorus Isotopes; Middle Aged; Glycerylphosphorylcholine; 03 medical and health sciences; 0302 clinical medicine; Case-Control Studies; Humans; Female; Protons; Inositol

Abstract1H MRSI has evolved as an important tool to study the onset and progression of brain damage in multiple sclerosis. Abnormal increases in total creatine, total choline and myoinositol have been noted in multiple sclerosis. However, the pathobiochemical mechanisms related to these changes are still largely unclear. The combination of 1H MRSI and 1H‐decoupled 31P MRSI can specify to what extent phosphorylated components of total creatine and total choline contribute to this increase. Combined 1H and 31P MRSI data were obtained at 3 T in 22 patients with multiple sclerosis and in 23 healthy controls, and aligned with structural MRI to allow for correction for partial volume effects caused by cerebrospinal fluid and lesion load. A significant increase in total creatine was found in multiple sclerosis, and this was attributed to equal changes in the phosphorylated and unphosphorylated components. The concentrations of the putative glial markers total creatine and myoinositol in lesion‐free 1H MRSI voxels correlated with the global lesion load. We conclude that changes in total creatine are not related to altered energy metabolism, but rather indicate gliosis. Together with the increase in myoinositol, total creatine can be considered as a biomarker for disease severity. A significant total choline increase was mainly a result of choline components not visible by 31P MRS. The origin of this residual choline fraction remains to be investigated. Copyright © 2010 John Wiley & Sons, Ltd.