Different pain phenotypes are associated with anti-Caspr2 autoantibodies
Patrik Greguletz, Maria Plötz, Carolin Baade‐Büttner, Christian G. Bien, Katharina Eisenhut, Christian Geis, Robert Handreka, Jaqueline Klausewitz, Peter Körtvélyessy, Stjepana Kovac, Andrea Kraft, Jan Lewerenz, Michael P. Malter, Michael Nagel, Felix von Podewils, Harald Prüß, Anna Rada, Johanna Maria Helena Rau, Sebastian Rauer, Rosa Rößling, Thomas Seifert‐Held, Kai Siebenbrodt, Kurt‐Wolfram Sühs, Simone C. Tauber, Franziska Thaler, Judith Wagner, Jonathan Wickel, Frank Leypoldt, Heike L. Rittner, Claudia Sommer, Carmen Villmann, Kathrin Doppler, the GENERATE study group, Michael Adelmann, Luise Appeltshauser, Ilya Ayzenberg, Andreas van Baalen, Sebastian Baatz, Oliver Bähr, Bettina Balint, Sebastian Bauer, Annette Baumgärtner, Stefanie Becker, Sonka Benesch, Robert L. Berger, Birgit Berger, Martin Berghoff, Sascha Berning, Sarah Bernsen, Achim Berthele, Christian G. Bien, Corinna Bien, Andreas Binder, Stefan Bittner, Daniel Bittner, Franz Blaes, Astrid Blaschek, Amelie Bohn, Sergio Castro‐Gomez, Justina Dargvainiene, Timo Deba, Julia Maren Decker, Andre Dik, Juliane Dominik, Mona Dreesmann, Friedrich Ebinger, Lena Edelhoff, Laura Ehrhardt, Sven Ehrlich, Alexander Emmer, Dominique Endres, Marina Entscheva, Daniela Esser, Thorleif Etgen, Jürgen Faiss, Kim Kristin Falk, Walid Fazeli, Alexander Finke, Carsten Finke, Dirk Fitzner, Marina Flotats‐Bastardas, Mathias Fousse, Tobias Freilinger, Paul Friedemann, Manuel A. Friese, Marco Gallus, M. M. Gebhard, Anna Gorsler, Armin Grau, Oliver Grauer, Britta Greshake, Catharina C. Groß, Thomas Grüter, Aiden Haghikia, Niels Hansen, Jens Harmel, Antonia Harms, Yetzenia Dubraska Haro Alizo, Martin Häusler, Joachim Havla
Abstract
Autoantibodies against contactin-associated protein 2 (Caspr2) not only induce limbic autoimmune encephalitis but are also associated with pain conditions. Here, we analyzed clinical data on pain in a large cohort of patients included into the German Network for Research in Autoimmune Encephalitis. Out of 102 patients in our cohort, pain was a frequent symptom (36% of all patients), often severe (63.6% of the patients with pain) and/or even the major symptom (55.6% of the patients with pain). Pain phenotypes differed between patients. Cluster analysis revealed two major phenotypes including mostly distal-symmetric burning pain and widespread pain with myalgia and cramps. Almost all patients had IgG4 autoantibodies and some additional IgG1, 2, and/or 3 autoantibodies, but IgG subclasses, titers, and presence or absence of intrathecal synthesis were not associated with the occurrence of pain. However, certain pre-existing risk factors for chronic pain like diabetes mellitus, peripheral neuropathy, or preexisting chronic back pain tended to occur more frequently in patients with anti-Caspr2 autoantibodies and pain. Our data show that pain is a relevant symptom in patients with anti-Caspr2 autoantibodies and support the idea of decreased algesic thresholds leading to pain. Testing for anti-Caspr2 autoantibodies needs to be considered in patients with various pain phenotypes.