Related Experiment Video
Updated: Jul 29, 2025

A Simple Cell-based Immunofluorescence Assay to Detect Autoantibody Against the N-Methyl-D-Aspartate NMDA Receptor in Blood
Published on: January 9, 2018
Pediatric anti-NMDA-receptor autoimmune encephalitis in siblings: Developmental, Electrophysiologic, and Genetic
Albert Aboseif1, Karlo Toljan1, Ahmad Mahadeen2
1Department of Neurology, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA.
Insights
Early treatment of anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis in children is crucial. Delayed diagnosis and treatment of this autoimmune condition can lead to severe, long-term neurological disability.
Area of Science:
- Pediatric Neurology
- Neuroimmunology
- Autoimmune Diseases
Background:
- Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a significant cause of autoimmune encephalitis in children.
- This condition can result in severe, long-term neurological impairment if left untreated.
Background:
Anti-NMDAR encephalitis is a leading cause of autoimmune encephalitis in children. Untreated disease can lead to long-term neurological disability.
Case Report:
We present siblings with pediatric-onset anti-NMDAR encephalitis. One was treated early, while the other's diagnosis and treatment were delayed by several years. Developmental, electrophysiologic, and genetic implications are discussed.
Conclusion:
Anti-NMDAR encephalitis is a severely debilitating disease that often requires prompt initiation and early escalation in treatment. Delayed treatment may lead to irreversible neurological sequalae. Further studies exploring associations between timing and tier of treatment initiation and longitudinal outcomes are needed.
More Related Videos
10:19High-throughput Flow Cytometry Cell-based Assay to Detect Antibodies to N-Methyl-D-aspartate Receptor or Dopamine-2 Receptor in Human Serum
Published on: November 23, 2013
09:57Author Spotlight: Advancing Pediatric Epilepsy Surgery in Children Through Novel Biomarkers and Enhanced Localization
Published on: September 20, 2024