A 38-year-old right-handed Chinese Han man presented with complaints of difficulty in language expression with no past medical history and no family history of neurological disease. He reported a 12-day history of intermittent fever and headache after catching a cold. On admission, a neurological examination revealed unremarkable except for motor aphasia and neck stiffness. His mini mental score examination (MMSE) was 28/30 (lost 1 point in recall, and lost 1 point in retell). Brain magnetic resonance imaging (MRI) showed extensive cortical edema in left cerebral hemisphere ( Figures 1A-C ). Electroencephalogram (EEG) showed diffuse sharp-slow wave activity in left frontal and temporal lobes ( Supplementary Figure 1 ). Complete blood cell count revealed leukocytosis (11.21 * 109/L). Routine biochemical tests, antinuclear antibody and thyroid function testing were normal. Human immunodeficiency virus and rapid plasma reagin were negative. Workup for malignancies (peripheral blood tumor marker, chest and abdominal CT scans) was negative. Cerebrospinal fluid (CSF) analysis indicated an elevated opening pressure (380 mm H2O), pleocytosis (white blood cell count 396 * 106/L; 60% lymphocytes), an elevated protein level (1.417 g/L) and a normal glucose concentration. CSF Gram staining, ink staining as well as bacterial and fungal cultures were negative. Testing for infectious encephalitis was unremarkable (CSF PCR for H. influenzae, N. meningitidis, S. pneumoniae, M. tuberculosis, Cytomegalovirus, Enterovirus, Herpes simplex 1 and 2, Varicella zoster, Japanese Encephalitis virus, Epstein-Barr virus and Cryptococcus neoformans). He was empirically treated for presumptive viral meningoencephalitis with intravenous acyclovir, and mannitol was used for the reduction of intracranial pressure.
On the seventh day of admission, the patient developed multiple episodes of psychomotor agitation, and he had an episode of generalized tonic-clonic seizure, all four limbs becoming rigid along with up-rolling of the eyes, which lasted for about two minutes and then resolved. The following day he developed convulsive status epilepticus, and intravenous diazepam 10 mg was administered to terminate the seizure activity. Subsequently, oral oxcarbazepine (300 mg b.i.d.) was given and antiviral treatment with intravenous acyclovir continued. Lumbar puncture was performed again, and the repeated CSF test still indicated leukocytosis (203 * 106/L) and a high protein level (1.132 g/L). Meanwhile, CSF and serum testings for MOG antibody and autoimmune encephalitis panel (antibodies against IgLON5, DPPX, GlyR1, DRD2, mGluR5, NMDAR, AMPA1, AMPA2, LGI1, CASPR2, GABAB, mGluR1, GAD65, and Neurexin-3alpha) were conducted on a cell based assay (CBA). MOG antibodies were positive in the serum (1:32) and CSF (1:10) ( Figure 2A ). Autoimmune encephalitis panel revealed positivity for serum and CSF mGluR5 antibody (both 1:10) as well as positivity for CSF NMDAR antibody (1:10) ( Figure 2B ). He was diagnosed with an overlapping syndrome of MOG antibody-associated cortical encephalitis and NMDAR, mGluR5 antibody autoimmune encephalitis. He was treated with intravenous methylprednisolone (1000 mg/day for 3 days, 500 mg/day for 3 days, 250 mg/day for 3 days, and 120 mg/day for 3 days) and immunoglobulin (400 mg/kg/day for 5 days), leading to the resolution of seizures and psychomotor agitation. Repeat brain MRI indicated alleviated cortical swelling ( Figures 1D-F ). Subsequently, the patient was discharged, and he received a gradual tapering dose of oral prednisone (60 mg/day followed by tapering by 5 mg every two weeks) and mycophenolate mofetil (1000 mg/day). Follow-up continued for 6 months, and the patient recovered his language expression ability and no further relapse was recorded. The repeated MMSE was 30/30. The follow-up EEG was normal and brain MRI revealed no obvious abnormalities ( Figures 1G-I ). In addition, repeated CSF analysis revealed normal cell count and protein. Reexamination of MOG antibody and autoimmune encephalitis panel indicated negativity for serum and CSF mGluR5 and NMDAR antibodies as well as CSF MOG antibody, and that serum MOG antibody titer decreased to 1:10 ( Figure 2C ). The patient also underwent tumor screening including tumor marker screening, chest CT scan and abdominal ultrasound. No tumor has been detected so far. The clinical manifestations, important results of examinations, relevant diagnosis and interventions of the patient have been summarized in  Figure 3 .