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Editorial
January 2017

Rethinking Outcomes in Leucine-Rich, Glioma-Inactivated 1 Protein Encephalitis: “Good” Isn't Good Enough

Author Affiliations
  • 1Charles F. and Joanne Knight Alzheimer’s Disease Research Center, Department of Neurology, Washington University School of Medicine, St Louis, Missouri
JAMA Neurol. 2017;74(1):19-21. doi:10.1001/jamaneurol.2016.4538

The past decade has heralded an unprecedented expansion in knowledge concerning autoimmune-mediated central nervous system diseases, particularly those associated with autoantibodies against neuronal surface antigens. Previously unknown diagnostic entities, including N-methyl-d-aspartate receptor encephalitis; leucine-rich, glioma-inactivated 1 (LGI1) protein encephalitis; and contactin-associated protein-like 2 antibody–associated encephalitis, are now routinely included in the differential diagnoses of patients presenting with abrupt changes in behavior and cognition. In turn, increased experience with autoantibody testing has broadened the spectrum of symptoms and signs associated with antibody-mediated diseases,1-4 facilitating the development of consensus criteria for the evaluation and stratification of patients with possible, probable, or definite autoimmune encephalitis.5

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