October 14 Highlights

Abstract

Takahashi et al. found autoantibodies against the NMDA-type GluR epsilon2 in patients with chronic epilepsia partialis continua, including patients with proven or clinically suspected Rasmussen’s encephalitis, with an acute encephalitis or encephalopathy, and with nonprogressive epilepsia partialis continua. Antibodies were predominantly against cytoplasmic (C-terminal) epitopes but antibody profiles did not show consistent changes during the course of disease. The data suggest that cytotoxic T-cell-mediated neuronal damage occurs in these conditions. see page 891 Commentary by Robert A. Gross, MD, PhD Researchers seeking the basis for Rasmussen’s encephalitis (RE) were galvanized by a report1 of excitatory antibodies to the glutamate receptor GluR3, and the successful treatment of a patient with plasma exchange. Was excessive excitation the cause of the debilitating seizures and would immunotherapy therefore be effective?2 The evidence for an autoimmune basis of RE is sound—involving both B- and T-cell-mediated processes—but was tempered by reports that some patients were seronegative for gluR3 antibodies.3,4⇓ The root cause, the identity of the antigens against which antibodies reacted, and whether they were causative of pharmacoresistant seizures …