To analyze the clinical feature, diagnosis, and treatment of voltage-gated potassium channel complex (VGKC) antibodies-associated encephalitis. Methods: We retrospectively analyzed the clinical data of 7 patients with VGKC antibodies-associated encephalitis. Results: Patients showed no prodromal symptoms prior to onset. There were 6 cases with seizure, 3 cases with psychiatric symptoms, and 2 cases with cognitive decline. There were 4 cases with sleep disorder, 1 case with palpitation or hyperhidrosis, 3 cases with hyponatremia, and 1 case with face, shoulder, and arm dystonia. There were 4 patients that were positive for cerebrospinal fluid (CSF) leucine-rich glioma-inactivated protein 1 (LGI-1) antibodies; among these, 2 patients were also positive for serum LGI-1 antibodies. One patient was positive for serum LGI-1 antibodies; 1 patient was positive for CSF and serum contactin-associated protein 2 (Caspr2) antibodies; 1 patient was positive for serum Caspr2 antibodies. Brain magnetic resonance imaging scans exhibited abnormalities mainly in the temporal lobe, hippocampus, and basal ganglia with or without high-intensity T2 and FLAIR sequence signals. Electroencephalographs showed abnormality in 3 patients. No tumor was detected by screening. Gamma globulin, methylprednisolone, or a combination of both were used as treatment. After a 3-month follow up, 6 patients showed improvement and 1 patient relapsed and abandoned treatment. Conclusion: Onset of VGKC antibodies-associated encephalitis is characterized by seizure. LGI-1 encephalitis is characterized by hyponatremia and sleep disorder. Caspr2 encephalitis is characterized by autonomic dysfunction. Brain MRI is unable to distinguish between encephalitis types. Electroencephalographs show no characteristic changes. Detection of CSF and serum autoimmune antibodies is conducive to confirming diagnosis. Early immunotherapy is effective in most cases, and relapse occurs in few cases.