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April 2015; 2 (2) Clinical/Scientific NotesOpen Access

Complement-associated neuronal loss in a patient with CASPR2 antibody–associated encephalitis

Peter Körtvelyessy, Jan Bauer, Christian M. Stoppel, Wolfgang Brück, Ivonne Gerth, Stefan Vielhaber, Falk R. Wiedemann, Hans J. Heinze, Claudius Bartels, Christian G. Bien
First published February 12, 2015, DOI: https://doi.org/10.1212/NXI.0000000000000075
Peter Körtvelyessy
From the Department of Neurology (P.K., I.G., S.V., H.J.H., C.B.), University Clinic Magdeburg, Germany; Department of Neuroimmunology (J.B.), Center for Brain Research, Medical University of Vienna, Austria; Department of Psychiatry and Psychotherapy (C.M.S.), Charité University Hospital, Berlin, Germany; Department of Neuropathology (W.B.), University Medical Center Göttingen, Germany; Department of Neurology (F.R.W.), Median Clinic NRZ Magdeburg, Germany; and Epilepsy Center Bethel (C.G.B.), Krankenhaus Mara, Bielefeld, Germany.
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Jan Bauer
From the Department of Neurology (P.K., I.G., S.V., H.J.H., C.B.), University Clinic Magdeburg, Germany; Department of Neuroimmunology (J.B.), Center for Brain Research, Medical University of Vienna, Austria; Department of Psychiatry and Psychotherapy (C.M.S.), Charité University Hospital, Berlin, Germany; Department of Neuropathology (W.B.), University Medical Center Göttingen, Germany; Department of Neurology (F.R.W.), Median Clinic NRZ Magdeburg, Germany; and Epilepsy Center Bethel (C.G.B.), Krankenhaus Mara, Bielefeld, Germany.
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Christian M. Stoppel
From the Department of Neurology (P.K., I.G., S.V., H.J.H., C.B.), University Clinic Magdeburg, Germany; Department of Neuroimmunology (J.B.), Center for Brain Research, Medical University of Vienna, Austria; Department of Psychiatry and Psychotherapy (C.M.S.), Charité University Hospital, Berlin, Germany; Department of Neuropathology (W.B.), University Medical Center Göttingen, Germany; Department of Neurology (F.R.W.), Median Clinic NRZ Magdeburg, Germany; and Epilepsy Center Bethel (C.G.B.), Krankenhaus Mara, Bielefeld, Germany.
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Wolfgang Brück
From the Department of Neurology (P.K., I.G., S.V., H.J.H., C.B.), University Clinic Magdeburg, Germany; Department of Neuroimmunology (J.B.), Center for Brain Research, Medical University of Vienna, Austria; Department of Psychiatry and Psychotherapy (C.M.S.), Charité University Hospital, Berlin, Germany; Department of Neuropathology (W.B.), University Medical Center Göttingen, Germany; Department of Neurology (F.R.W.), Median Clinic NRZ Magdeburg, Germany; and Epilepsy Center Bethel (C.G.B.), Krankenhaus Mara, Bielefeld, Germany.
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Ivonne Gerth
From the Department of Neurology (P.K., I.G., S.V., H.J.H., C.B.), University Clinic Magdeburg, Germany; Department of Neuroimmunology (J.B.), Center for Brain Research, Medical University of Vienna, Austria; Department of Psychiatry and Psychotherapy (C.M.S.), Charité University Hospital, Berlin, Germany; Department of Neuropathology (W.B.), University Medical Center Göttingen, Germany; Department of Neurology (F.R.W.), Median Clinic NRZ Magdeburg, Germany; and Epilepsy Center Bethel (C.G.B.), Krankenhaus Mara, Bielefeld, Germany.
MA
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Stefan Vielhaber
From the Department of Neurology (P.K., I.G., S.V., H.J.H., C.B.), University Clinic Magdeburg, Germany; Department of Neuroimmunology (J.B.), Center for Brain Research, Medical University of Vienna, Austria; Department of Psychiatry and Psychotherapy (C.M.S.), Charité University Hospital, Berlin, Germany; Department of Neuropathology (W.B.), University Medical Center Göttingen, Germany; Department of Neurology (F.R.W.), Median Clinic NRZ Magdeburg, Germany; and Epilepsy Center Bethel (C.G.B.), Krankenhaus Mara, Bielefeld, Germany.
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Falk R. Wiedemann
From the Department of Neurology (P.K., I.G., S.V., H.J.H., C.B.), University Clinic Magdeburg, Germany; Department of Neuroimmunology (J.B.), Center for Brain Research, Medical University of Vienna, Austria; Department of Psychiatry and Psychotherapy (C.M.S.), Charité University Hospital, Berlin, Germany; Department of Neuropathology (W.B.), University Medical Center Göttingen, Germany; Department of Neurology (F.R.W.), Median Clinic NRZ Magdeburg, Germany; and Epilepsy Center Bethel (C.G.B.), Krankenhaus Mara, Bielefeld, Germany.
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Hans J. Heinze
From the Department of Neurology (P.K., I.G., S.V., H.J.H., C.B.), University Clinic Magdeburg, Germany; Department of Neuroimmunology (J.B.), Center for Brain Research, Medical University of Vienna, Austria; Department of Psychiatry and Psychotherapy (C.M.S.), Charité University Hospital, Berlin, Germany; Department of Neuropathology (W.B.), University Medical Center Göttingen, Germany; Department of Neurology (F.R.W.), Median Clinic NRZ Magdeburg, Germany; and Epilepsy Center Bethel (C.G.B.), Krankenhaus Mara, Bielefeld, Germany.
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Claudius Bartels
From the Department of Neurology (P.K., I.G., S.V., H.J.H., C.B.), University Clinic Magdeburg, Germany; Department of Neuroimmunology (J.B.), Center for Brain Research, Medical University of Vienna, Austria; Department of Psychiatry and Psychotherapy (C.M.S.), Charité University Hospital, Berlin, Germany; Department of Neuropathology (W.B.), University Medical Center Göttingen, Germany; Department of Neurology (F.R.W.), Median Clinic NRZ Magdeburg, Germany; and Epilepsy Center Bethel (C.G.B.), Krankenhaus Mara, Bielefeld, Germany.
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Christian G. Bien
From the Department of Neurology (P.K., I.G., S.V., H.J.H., C.B.), University Clinic Magdeburg, Germany; Department of Neuroimmunology (J.B.), Center for Brain Research, Medical University of Vienna, Austria; Department of Psychiatry and Psychotherapy (C.M.S.), Charité University Hospital, Berlin, Germany; Department of Neuropathology (W.B.), University Medical Center Göttingen, Germany; Department of Neurology (F.R.W.), Median Clinic NRZ Magdeburg, Germany; and Epilepsy Center Bethel (C.G.B.), Krankenhaus Mara, Bielefeld, Germany.
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Full PDF
Citation
Complement-associated neuronal loss in a patient with CASPR2 antibody–associated encephalitis
Peter Körtvelyessy, Jan Bauer, Christian M. Stoppel, Wolfgang Brück, Ivonne Gerth, Stefan Vielhaber, Falk R. Wiedemann, Hans J. Heinze, Claudius Bartels, Christian G. Bien
Neurol Neuroimmunol Neuroinflamm Apr 2015, 2 (2) e75; DOI: 10.1212/NXI.0000000000000075

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    Figure Disease course and neuropathology of CASPR2 encephalitis

    (A) Summary of the most important changes during the disease course. Shown are consecutive cerebral fluid-attenuated inversion recovery (FLAIR) MRI scans in relation to therapeutic treatment, clinical symptoms, and CASPR2 titer. The swollen hippocampus (HC) and amygdala (AM) were resected in January 2013. Note the progressive global atrophy of the brain (from August 2012 to July 2013), which largely stopped in October 2013. The left HC, however, remained FLAIR intense in October 2013. (B) Changes in CASPR2 antibody (ab) titers in serum (dots) and CSF (squares) during the disease course. The graph shows a decline of the titers in serum and CSF after prolonged administration of cyclophosphamide and oral prednisolone (indicated by the gray bars on top). The star indicates the time point of the biopsy. (C–K) Neuropathology of the right hippocampus. (C) Double staining for CD3 and CD8 shows moderate numbers of T cells (CD8+ T cells are blue, CD3+CD8− [CD4+] T cells are brown). (D) CD68 staining shows moderately activated microglial cells. (E) Staining for CD20 shows the presence of B cells in a perivascular cuff. (F) Staining for CD138 shows the presence of some plasma cells. (G) Staining for immunoglobulins (Ig) reveals strong leakage into the parenchyma. Deposition of immunoglobulin on neuronal membranes is indicated by the arrowheads. The arrow in the upper corner points at a degenerating neuron with nuclear changes. The inset shows an additional degenerating neuron (arrow) with a condensed nucleus. (H) Staining for TUNEL (black) and MAP2 shows the absence of degenerating cells in the amygdala of this patient. (I) In the hippocampus, a single TUNEL-positive neuron is indicated by the arrowhead. The insets show an enlargement of this neuron (left side) and a second MAP2+ TUNEL+ neuron. (J, K) Staining for complement C9neo (end complex) reveals a neuron with minor deposition, depicted by arrows (J), and a neuron with major deposition (K). CP = cyclophosphamide; MP = methylprednisolone.

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