Axonal damage in the spinal cord of multiple sclerosis patients detected by magnetic resonance spectroscopy
Andrew M. Blamire, Sarah Cader, Martin Lee, Jackie Palace, Paul M. Matthews
Abstract
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Andrew M. Blamire, Sarah Cader, Martin Lee, Jackie Palace, Paul M. Matthews
Abstract
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Axonal damage is a major factor contributing to permanent disability in patients with multiple sclerosis (MS); it has been extensively investigated in the brain using magnetic resonance spectroscopy (MRS). In this study, MRS was used to investigate the degree of neuronal damage in the cervical spinal cord in MS. Spectra were acquired from spinal cord and brain in 11 patients with MS (expanded disability status score [EDSS], range 2.5-7.0) and 11 controls. Brain lesion volume and spinal cord cross-sectional area were measured. Concentration of the neuronal metabolite N-acetyl-aspartate ([NAA]) was reduced in the spinal cord in MS patients relative to controls (reduced by 32%, P < 0.05), indicating significant neuronal damage. Additionally, the spinal cord was significantly atrophied in MS patients (15%, P < 0.001). No significant reduction in brain [NAA] was seen in the MS group. There were no correlations between clinical measures and cord atrophy or brain lesion volume on MRI; however, spinal cord [NAA] correlated with the cerebellar subscore of the neurological assessment (P < 0.005), while brain [NAA] correlated with disease duration (P < 0.05). MRS demonstrated cellular damage within the cord over and above the tissue atrophy seen by MRI. Combining MRI and MRS may therefore give a more complete picture of neurodegeneration in the spinal cord.
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Axonal damage is a major factor contributing to permanent disability in patients with multiple sclerosis (MS); it has been extensively investigated in the brain using magnetic resonance spectroscopy (MRS). In this study, MRS was used to investigate the degree of neuronal damage in the cervical spinal cord in MS. Spectra were acquired from spinal cord and brain in 11 patients with MS (expanded disability status score [EDSS], range 2.5-7.0) and 11 controls. Brain lesion volume and spinal cord cross-sectional area were measured. Concentration of the neuronal metabolite N-acetyl-aspartate ([NAA]) was reduced in the spinal cord in MS patients relative to controls (reduced by 32%, P < 0.05), indicating significant neuronal damage. Additionally, the spinal cord was significantly atrophied in MS patients (15%, P < 0.001). No significant reduction in brain [NAA] was seen in the MS group. There were no correlations between clinical measures and cord atrophy or brain lesion volume on MRI; however, spinal cord [NAA] correlated with the cerebellar subscore of the neurological assessment (P < 0.005), while brain [NAA] correlated with disease duration (P < 0.05). MRS demonstrated cellular damage within the cord over and above the tissue atrophy seen by MRI. Combining MRI and MRS may therefore give a more complete picture of neurodegeneration in the spinal cord.
Key concepts: Spinal cord, Multiple sclerosis, Medicine, Magnetic resonance imaging, Atrophy, Central nervous system disease, Lesion, Cord