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

Amy May Lin Quek1,2, Orna O’Toole3 1Department of Medicine, National University Hospital, National University Health System, Singapore 119228, Singapore. 2Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228, Singapore. 3Department of Neurology, Mercy University Hospital, Grenville Place, Cork, Ireland. 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.