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. 2023 Feb 13;23(3):67–82. doi: 10.1007/s11910-023-01250-w

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© The Author(s) 2023

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — MRI and antibody test findings in paraneoplastic disorders. Top row, axial MRI images demonstrate (left, T2 FLAIR) bilateral mesial temporal hyperintensities in a patient with ANNA-1-associated paraneoplastic limbic encephalitis (middle, T2 FLAIR) multifocal extra-limbic hyperintensities in a patient with GABA-A receptor (R) encephalitis, and (right, T1 post-gadolinium) spinal cord tractopathies in a patient with seronegative renal cell carcinoma-associated paraneoplastic myelopathy. Bottom row, indirect immunofluorescence assay using mouse brain tissue as substrate reveals a typical synaptic pattern of IgG staining of hippocampus (left) and cerebellum (right) produced by CSF from a patient with GABA-A-R encephalitis. GABA-A-R specificity was confirmed by GABA-A-R alpha 1 subunit specific cell-based assay (not shown). Top right image from reference 58 reproduced with permission from American Academy of Neurology