Patients were identified during initial routine screening of a cohort (C1) of 646 patients consecutively diagnosed with anti-NMDAR encephalitis, and from another cohort (C2) of 200 patients retrospectively re-screened. Seventy patients with isolated NMDAR-Ab served as controls.  

Concurrent antibodies were identified in 42 patients (4% from C1 and 7.5% from C2): 30 (71%) with glial-Ab, and 12 (29%) with NS-Ab. Glial-Ab included: MOG (57%), GFAP (33%), and AQP4 (10%). NS-Ab included: AMPAR (50%), GABAaR (42%), and GABAbR (8%). In 39 (95%) of 41 patients concurrent antibodies were detected in CSF and in 17 (41%) were undetectable in serum. On routine clinical-immunological studies the presence of MOG-Ab and AQP4-Ab were suggested by: previous episodes of encephalitis or demyelinating disorders (8, 27%), current clinical-radiological features (e.g., optic neuritis, white matter changes), or standard rat brain immunohistochemistry (e.g., AQP4-reactivity). GFAP-Ab did not associate with distinct clinical-radiological features. NS-Abs were suggested by: MRI findings (e.g., medial temporal lobe changes [AMPAR-Ab], or multifocal cortico-subcortical abnormalities [GABAaR-Ab]), uncommon co-morbidities (e.g., recent herpesvirus encephalitis), atypical tumors (e.g., breast cancer, neuroblastoma), or rat brain immunostaining. Patients with NS-Ab were less likely to have substantial recovery than those with glial-Ab (5/10 [50%] vs 17/19 [89%], p=0.03).