Objective: To characterize movement disorder phenotypes in neuronal antibody–mediated autoimmune encephalitis (AE) and assess associations with specific antibody subtypes.

Background: Neuronal antibody–mediated AE is a major cause of subacute neuropsychiatric syndromes in pediatric and adult populations. Although, movement disorders are common manifestations in antibody encephalitis, they are inconsistently reported in the literature. The relationship between specific antibodies and movement disorder patterns has not been systematically explored.

Method: A systematic search of MEDLINE and PubMed was conducted on December 6, 2025 without date restrictions. Observational studies reporting pediatric or adult patients with laboratory-confirmed neuronal cell-surface or synaptic antibodies were included. Studies lacking antibody confirmation, involving intracellular/paraneoplastic antibodies alone, or without extractable data were excluded. Screening was performed independently by two reviewers with disagreements resolved by consensus. Data extraction and risk-of-bias assessment using the Joanna Briggs Institute checklist were conducted. Of 588 records identified, 106 duplicates were removed and 482 screened. After full-text review of 142 studies, 21 were excluded, leaving 121 included studies.

Results: One hundred cases were analyzed across eight antibody subgroups. Anti-NMDAR encephalitis (n=53) showed a predominantly hyperkinetic profile with dystonia (62%), orofacial dyskinesia (58%), chorea (42%), and catatonia/akinesia (21%). Anti-IgLON5 disease (n=19) was heterogeneous, with dystonia and parkinsonism (42% each), ataxia (37%), and bulbar and oculomotor involvement (47% each). Anti-LGI1 encephalitis (n=8) featured facio-brachial dystonic seizures (75%). Anti-GlyR/PERM (n=10) showed brainstem-spinal myoclonus (90%), rigidity/spasms (80%), and hyperekplexia (30%). Smaller subgroups included anti-CASPR2 (n=3) with myoclonus, anti-DPPX (n=2) with tremor and autonomic dysfunction, anti-mGluR (n=2) with myoclonus and ataxia, and anti-AMPAR (n=1) with parkinsonism.

Conclusion: Distinct movement disorder phenotypes were observed across antibody subgroups: orofacial dyskinesia/catatonia in anti-NMDAR, sleep-movement and oculomotor abnormalities in anti-IgLON5, and facio-brachial paroxysms in anti-LGI1. Recognizing these patterns may guide targeted antibody testing and expedite AE diagnosis.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/movement-disorder-phenotypes-in-neuronal-antibody-mediated-autoimmune-encephalitis/