Although paraneoplastic neurologic syndromes have been known for over half a century, developments during the last decade have reshaped the field of autoimmune neurology. The discovery of over 15 new antibodies has expanded the clinical phenotypes associated with neurologic paraneoplastic diseases, increased therapeutic opportunities, and improved outcomes.1 Initially, paraneoplastic neurologic syndromes were mainly categorized as limbic encephalitis and cerebellar degeneration, without more varied or nuanced phenotypes. More recently, hyperkinetic movement disorders have been linked to some of the newly discovered antibodies, typically as part of an autoimmune encephalitis.2 Most frequently, chorea is reported in patients with LGI1 or CV2 antibodies, and a mixture of movement disorder phenotypes occur in patients with anti-NMDAR and anti-IgLON5 encephalitis (table).3,4

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