Molecular Structure and Target Recognition:

• Targets NMDA receptor components, especially GluN1 subunit
• Predominantly IgG class antibodies (IgG1 and IgG3)
• Leads to receptor crosslinking and internalization
• Reduces synaptic NMDAR density

Pathophysiological Mechanisms - Receptor Interaction:

• Affects NMDA receptor through multiple pathways
• Causes direct effects: receptor internalization and decreased density
• Results in synaptic changes
• Reduces glutamatergic transmission
• Impairs long-term potentiation

Neurological Impact:

• Disrupts neurotransmitter signaling
• Alters neural network function
• Compromises synaptic plasticity
• Triggers neuroinflammatory responses

Clinical Manifestations - Anti-NMDAR Encephalitis:

• Early symptoms include psychiatric and behavioral changes
• Progressive symptoms include seizures and movement disorders
• Associated with conditions like:
• Ovarian teratomas
• Autoimmune disorders
• Viral infections
• Paraneoplastic syndromes

Diagnostic Approaches:

• Laboratory Testing:
• CSF analysis
• Serum testing
• Inflammatory markers
• Imaging Studies:
• MRI brain imaging
• PET scanning
• EEG monitoring

Treatment Strategies and Prognosis:

• First-line treatments:
• Immunotherapy
• Tumor removal when applicable
• Second-line treatments:
• Rituximab
• Cyclophosphamide
• Other immunosuppressants
• Regular monitoring of:
• Clinical improvement
• Antibody levels
• Cognitive function
• Neurological status
• Generally favorable prognosis with early intervention
• Recovery may take months to years