Improvement in anti-N-methyl-d-aspartate receptor antibody-mediated temporal lobe epilepsy with amygdala enlargement without immunotherapy

Abstract

Focal neuroinflammation is considered one of the hypotheses for the cause of temporal lobe epilepsy (TLE) with amygdala enlargement (AE). Here, we report a case involving an adult female patient with TLE-AE characterized by late-onset seizures and cognitive impairment. Anti-N-methyl-d-aspartate receptor (NMDAR) antibodies were detected in her cerebrospinal fluid. However, administration of appropriate anti-seizure drugs (ASD), without immunotherapy, improved TLE-AE associated with NMDAR antibodies. In the present case, two clinically significant observations were made: 1) anti-NMDAR antibody-mediated autoimmune processes may be associated with TLE-AE, and 2) appropriate administration of ASD alone can improve clinical symptoms in mild cases of autoimmune epilepsy.

Clinical, cognitive and neuroanatomical associations of serum NMDAR autoantibodies in people at clinical high risk for psychosis

“…The combination of impaired cognitive function, severe affective psychopathology [46,51,54] and increased volume of limbic brain regions [55][56][57][58] bears some resemblance to (but is less severe than) the pattern of findings seen in the acute stages of many autoimmune encephalopathies. This suggests that NMDAR antibodies, and possibly other NSAbs, could play an analogous, but not necessarily identical, role in the pathophysiology of some patients who present with psychiatric symptoms [59].…”