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Cognitive impairment in early multiple sclerosis: role of conventional and multimodal quantitative magnetic resonance imaging

Background: Conventional and contrast-enhanced magnetic resonance imaging (MRI) cannot fully explain the commonly observed cognitive impairment in multiple sclerosis (MS) patients. So far, little is known about the stage at which tissue abnormalities occur. Cognitive studies with quantitative MRI me...

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Bibliographic Details
Published in:Multiple sclerosis 2008-09, Vol.14, p.S211-S211
Main Authors: Matzke, M, Apel, A, Baum, K, Daehne, D, Deppe, R, Daume, L, Gottken, T, Hoffmann, F, Koehler, W, Kunkel, A, Prawdzik, G, Scheerschmidt, S, Schilling, H, Faiss, J H
Format: Article
Language:English
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Summary:Background: Conventional and contrast-enhanced magnetic resonance imaging (MRI) cannot fully explain the commonly observed cognitive impairment in multiple sclerosis (MS) patients. So far, little is known about the stage at which tissue abnormalities occur. Cognitive studies with quantitative MRI measurements in early MS revealed inconsistent results. Objective: To evaluate the relationship between cognitive deficits in early MS, conventional and multimodal quantitative MRI. Methods: MRI brain scans were acquired from 47 patients within 3 months of the first MS-related clinical event. All patients underwent a neuropsychological assessment and were allocated into groups according to their cognitive performance. T2-hyper-intense lesion volume (LV), T1 LV and gadolinium-enhancing LV measurements were performed. Magnetization transfer ratio (MTR) histogram analysis, mean diffusivity (MD) and fractional anisotropy (FA) quantities and histograms of the normal-appearing white matter (NAWM) and grey matter (GM) were calculated. Additionally, single-voxel proton magnetic resonance spectroscopy (MRS) of the corpus callosum was performed with measurements of relative concentrations of N-acetylaspartate (NAA), creatine (Cr) and calculation of the NAA/Cr ratio. Results: Around 47% of MS patients had cognitive impairment. In this group, we found a significantly reduced NAWM-MTR compared with cognitively unimpaired MS patients (p=0.03). This was substantiated by MRS that differentiated significantly NAA concentration in the corpus callosum in patients with mild compared with more severe cognitive impairment (p=0.04). Lesion quantification of T2 and T1 lesions did not significantly separate cognitively impaired from unimpaired patients. Conclusions: Cognitive deficits in patients after the first clinical attack are frequent and may be underestimated. While conventional MRI scan of the brain does not provide supportive evidence for cognitive impairment, MTR and MRS separated the cognitively impaired from the non-affected group early in the disease course. Our data depict the role of diffuse microscopic brain damage in the early stage of disease.
ISSN:1352-4585