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November 2017; 4 (6) ArticleOpen Access

Improving the antibody-based evaluation of autoimmune encephalitis

Lindsey McCracken, Junxian Zhang, Maxwell Greene, Anne Crivaro, Joyce Gonzalez, Malek Kamoun, Eric Lancaster
First published October 11, 2017, DOI: https://doi.org/10.1212/NXI.0000000000000404
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  • Figure 1
    Figure 1 Flow of samples through the clinical and research laboratories

    All 731 samples referred to the Hospital of the University of Pennsylvania for antibody testing were examined using commercial testing kits and in our research laboratory as described in the methods section. CBA = cell-based assay; GABAB-R= γ-aminobutyric acid-B receptor; GAD65 = glutamic acid decarboxylase; IHC = immunohistochemistry; LGI1 = leucine-rich glioma-inactivated 1; NMDAR = NMDA receptor.

  • Figure 2
    Figure 2 Patterns of reactivity observed with rat-brain IHC

    Immunohistochemistry was performed with rat brain sections using human CSF. Whole brains (left) and higher power views of the hippocampus (right) are shown for control (A, B), anti-NMDAR encephalitis (C, D), anti-LGI1 encephalitis (E, F), anti-GABA-B encephalitis (G, H), and anti-GAD65 (I, J). The cases with reactivity on brain section IHC showed characteristic staining of the synaptic layers of the hippocampus. GABA= γ-aminobutyric acid; GAD65 = glutamic acid decarboxylase; IHC = immunohistochemistry; LGI1 = leucine-rich glioma-inactivated 1; NMDAR = NMDA receptor.

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