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

Go Taniguchi, Hitomi Fuse, Yumiko Okamura, Harushi Mori, Shinsuke Kondo, Kiyoto Kasai, Yukitoshi Takahashi, Keiko Tanaka
Author Information
  1. Go Taniguchi: Department of Neuropsychiatry, The University of Tokyo Hospital, Japan.
  2. Hitomi Fuse: Department of Neuropsychiatry, The University of Tokyo Hospital, Japan.
  3. Yumiko Okamura: Department of Neuropsychiatry, The University of Tokyo Hospital, Japan.
  4. Harushi Mori: Department of Radiology, The University of Tokyo Hospital, Japan.
  5. Shinsuke Kondo: Department of Neuropsychiatry, The University of Tokyo Hospital, Japan.
  6. Kiyoto Kasai: Department of Neuropsychiatry, The University of Tokyo Hospital, Japan.
  7. Yukitoshi Takahashi: National epilepsy center, Shizuoka Institute of Epilepsy and Neurological Disorders, Japan.
  8. Keiko Tanaka: Department of cellular neurobiology, Brain research institute, Niigata University, Japan.

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--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.

Keywords

References

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