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Research ArticleBrain

Inflammatory CNS Demyelination: Histopathologic Correlation with In Vivo Quantitative Proton MR Spectroscopy

Andreas Bitsch, Harald Bruhn, Vassilios Vougioukas, Argyris Stringaris, Hans Lassmann, Jens Frahm and Wolfgang Brück
American Journal of Neuroradiology October 1999, 20 (9) 1619-1627;
Andreas Bitsch
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Harald Bruhn
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Vassilios Vougioukas
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Argyris Stringaris
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Hans Lassmann
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Jens Frahm
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Wolfgang Brück
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    fig 1.

    Bielschowsky's silver impregnation shows axonal density in the normal periplaque white matter (patient 1) (A), a reduction by 45% (patient 3) (B), and a reduction by 75% (patient 1) (C) within the plaques (magnification for all, ×166). Prominent protoplasmic gliosis with large astrocytes (D) is seen by immunocytochemistry for GFAP (patient 1). Numerous GFAP-positive cell processes (E) indicate fibrillary gliosis (patient 3). Immunocytochemistry for MOG (F) shows an early active demyelinating lesion (patient 2). Macrophages carry MOG-positive degradation products in their cytoplasm. Dense macrophage infiltrate (G) is seen in the same lesion as shown in F (immunocytochemistry for Ki-MlP)

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    fig 2.

    T1-weighted gradient-echo MR images (3D fast low-angle shot, 4-mm partitions, 15/6 TR/TE, 20° flip angle) of patient 1 indicating VOIs selected for MRS.

    A, Transverse section with VOIs centered at the left parieto-occipital lesion (20 × 20 × 20 mm3) and in a contralateral control region (16 × 30 × 16 mm3).

    B, Sagittal section with a smaller VOI (16 × 16 × 16 mm3) encompassing the same lesion (note small defect in the skull and corresponding biopsy canal),

    C, Coronal section depicting an ipsilateral VOI (20 × 20 × 20 mm3) in left frontoparietal cortex unsuspicious at MR imaging.

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    fig 3.

    Localized proton MR spectra (stimulated-echo acquisition mode, 3000/20/30 [TR/TE/TM]) of patient 1 from locations indicated in figure 2. Left occipitoparietal lesion (top) image using a 4-mL VOI and (second row) 8-mL VOI, an ipsilateral 8-mL VOI in unsuspicious left frontoparietal cortex (third row), and contralateral control (bottom). Major resonances are due to N-acetylaspartate (NAA), creatine and phosphocreatine (Cr), choline-containing compounds (Cho), myo-inositol (Ins), and lactate (Lac). Spectra are normalized for comparison

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    Table 1:

    Synopsis of clinical and diagnostic findings

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    Table 2:

    Lesion histopathology and corresponding proton MRS-detected metabolic alterations. Absolute metabolite levels (mM;shL VOI) derived from proton MR spectra (STEAM, TR;shTE;shTM = 3000;sh20;sh30 ms) of biopsied lesions of patients ;ns1 to ;ns3

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American Journal of Neuroradiology
Vol. 20, Issue 9
1 Oct 1999
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Cite this article
Andreas Bitsch, Harald Bruhn, Vassilios Vougioukas, Argyris Stringaris, Hans Lassmann, Jens Frahm, Wolfgang Brück
Inflammatory CNS Demyelination: Histopathologic Correlation with In Vivo Quantitative Proton MR Spectroscopy
American Journal of Neuroradiology Oct 1999, 20 (9) 1619-1627;

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Inflammatory CNS Demyelination: Histopathologic Correlation with In Vivo Quantitative Proton MR Spectroscopy
Andreas Bitsch, Harald Bruhn, Vassilios Vougioukas, Argyris Stringaris, Hans Lassmann, Jens Frahm, Wolfgang Brück
American Journal of Neuroradiology Oct 1999, 20 (9) 1619-1627;
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