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September 2018; 5 (5) ArticleOpen Access

GFAPα IgG-associated encephalitis upon daclizumab treatment of MS

Felix Luessi, Sinah Engel, Annette Spreer, Stefan Bittner, Frauke Zipp
First published July 13, 2018, DOI: https://doi.org/10.1212/NXI.0000000000000481
Felix Luessi
From the Department of Neurology and Focus Program Translational Neuroscience (FTN), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Germany.
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Sinah Engel
From the Department of Neurology and Focus Program Translational Neuroscience (FTN), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Germany.
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Annette Spreer
From the Department of Neurology and Focus Program Translational Neuroscience (FTN), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Germany.
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Stefan Bittner
From the Department of Neurology and Focus Program Translational Neuroscience (FTN), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Germany.
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Frauke Zipp
From the Department of Neurology and Focus Program Translational Neuroscience (FTN), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Germany.
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Citation
GFAPα IgG-associated encephalitis upon daclizumab treatment of MS
Felix Luessi, Sinah Engel, Annette Spreer, Stefan Bittner, Frauke Zipp
Neurol Neuroimmunol Neuroinflamm Sep 2018, 5 (5) e481; DOI: 10.1212/NXI.0000000000000481

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    Figure 1 MRI findings over time

    (A) Upper row: FLAIR axial images show progressive white matter lesions without contrast enhancement and distinct cerebral atrophy. Middle row: T1Gd-weighted images show no gadolinium enhancement. Lower row: T2-weighted sagittal images. A prominent radial pattern within T2-weighted axial pictures resembles a previously published patient with glial fibrillary acidic protein meningoencephalitis with a radial pattern of periventricular gadolinium enhancement. (B) T2-weighted sagittal images before daclizumab therapy and during encephalitic illness. T2-weighted axial image shows new focal gliosis at Th 3/4. FLAIR = fluid attenuated inversion recovery; Gd = gadolinium; Th = thoracic vertebra.

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    Figure 2 Overview of the patient's history and immunofluorescence pattern of patient CSF IgG

    (A) Disability assessed by the EDSS is displayed as a blue line. Clinical relapses and MRI activity (red arrows) are indicated. Duration of immunomodulatory treatments is depicted with lines of different colors on the top of the diagram. (B) Distribution of patient CSF IgG (green) in the rat hippocampus parenchyma is consistent with astrocytes (arrows). (C) Absence of specific patient serum IgG binding (diluted 1:100, green) in the brain parenchyma. (D) Antigen specificity of CSF IgG was further confirmed by glial fibrillary acidic protein α-transfected HEK293 cell-based assay CBA. (E) Absence of CSF IgG binding on control-transfected cells. Scale bars: 20 μm (B–E). DMF = dimethyl fumarate; EDSS = Expanded Disability Status Scale; IgG = immunoglobulin G; WBC = white blood cell.

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