Encephalitis associated with autoantibodies binding to γ-aminobutyric acid-A, γ-aminobutyric acid-B and glycine receptors: immunopathogenic mechanisms and clinical characteristics

Abstract

Recent, discoveries of neural antibodies have facilitated the diagnosis of immune-mediated, immunotherapy-responsive neurologic disorders. Antibodies that target inhibitory central nervous system receptors, such as γ-aminobutyric acid-B, γ-aminobutyric acid-A, and glycine receptors, disrupt inhibitory regulatory synaptic functions, and lead to neuronal hyperexcitability. The myriad of neurologic, manifestations associated with these antibodies includes seizures, encephalopathy, muscle rigidity and stiffness. This article provides a review of the immunopathogenic mechanisms and the clinical and therapeutic implications of autoimmune encephalitis associated with these antibodies that target inhibitory receptors.