Author Response: Clinical Significance of Anti-NMDAR Concurrent With Glial or Neuronal Surface Antibodies

We appreciate Dr. Lancaster's comments on our article.¹ Indeed, the co-occurrence of MOG- or aquaporin-4-(AQP4) antibodies with anti-NMDAR encephalitis was associated with symptoms of this encephalitis, accompanied by a history or MRI features of a demyelinating disease. However, the co-occurrence of anti-NMDAR encephalitis with other neuronal antibodies was associated with symptoms of this encephalitis and clinical or MRI features of the associated antibody—e.g., medial temporal lobe MRI changes with AMPAR-antibodies or cortical-subcortical FLAIR MRI abnormalities with GABAaR-antibodies. Patients with an additional neuronal surface antibody had a worse prognosis than those with isolated anti-NMDAR encephalitis or with a concurrent glial antibody. Our experience with GFAP-antibodies suggests that the syndrome-specificity of these antibodies is less clear. In our study, GFAP-antibodies did not confer any additional clinical or radiologic features to anti-NMDAR encephalitis. Moreover, the meningoencephalomyelitis with linear perivascular enhancement that has been considered characteristic of GFAP-antibodies can also occur without these antibodies.² If a patient with encephalitis and CSF NMDAR-antibodies develops a syndrome atypical for anti-NMDAR encephalitis, one should be concerned for (1) a potential laboratory error (e.g., the NMDAR-antibody test was falsely positive) or (2) that the syndrome represents a manifestation of 2 disorders with concurrent autoantibodies.