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    Anti-NMDA Receptor Encephalitis Medical Slides

    Generate publication-quality anti-nmda receptor encephalitis lecture slides in 30 seconds. AI-powered content structured for clinical education.

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    Why teach Anti-NMDA Receptor Encephalitis?

    Anti-NMDA receptor encephalitis is the most common autoimmune encephalitis, predominantly affecting young women (median age 21) and frequently associated with ovarian teratoma (50% of adult women). First described by Dalmau in 2007, it follows a characteristic clinical progression from psychiatric symptoms to movement disorders, seizures, autonomic instability, and decreased consciousness. Early aggressive immunotherapy and tumor removal are critical for favorable outcomes, with 80% of patients achieving good recovery.

    Sample Lecture Slides

    What AI generates for Anti-NMDA Receptor Encephalitis

    Enter “Anti-NMDA Receptor Encephalitis” and SlideCraft generates a complete lecture deck with slides like these.

    01Pathogenesis: Anti-GluN1 IgG Antibodies, NMDA Receptor Internalization, and Synaptic Dysfunction
    02Clinical Stages: Prodromal, Psychiatric, Movement Disorders/Seizures, Autonomic/Hypoventilation, and Recovery
    03Differential Diagnosis: Viral Encephalitis, Primary Psychiatric Disease, and Other Autoimmune Encephalitides
    04Diagnosis: CSF Antibody Testing, EEG (Extreme Delta Brush), and MRI (Often Normal Initially)
    05Tumor Screening: Pelvic Ultrasound/MRI for Ovarian Teratoma and Whole-Body CT/PET
    06Immunotherapy Protocol: First-Line (Steroids, IVIG, PLEX) and Second-Line (Rituximab, Cyclophosphamide)
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    Anti-NMDA Receptor Encephalitis Presentation FAQ

    How should the characteristic clinical progression be taught?

    Present the stereotyped phases: (1) viral-like prodrome (fever, headache), (2) psychiatric symptoms (psychosis, agitation, paranoia — often leading to initial psychiatric admission), (3) neurological deterioration (seizures, movement disorders — orofacial dyskinesias are characteristic, decreased consciousness), (4) autonomic instability and hypoventilation requiring ICU, (5) slow recovery over weeks to months. This sequential pattern is a key diagnostic clue — the evolution from "psychiatric" to "neurological" should trigger antibody testing.

    What EEG findings should be highlighted for teaching?

    Present the "extreme delta brush" pattern: continuous rhythmic delta activity (1-3 Hz) with superimposed beta frequency bursts riding on each delta wave, seen in 30% of cases and highly specific for anti-NMDA receptor encephalitis. Also show generalized slowing (most common EEG finding) and electrographic seizures. Emphasize that EEG monitoring is essential because subclinical seizures are common, and the extreme delta brush pattern can appear before CSF antibodies are resulted.

    How should the immunotherapy protocol be structured in teaching slides?

    Present a staged approach: tumor removal is the single most important intervention (if teratoma found). First-line immunotherapy: IV methylprednisolone 1g/day × 5 days + IVIG 0.4 g/kg/day × 5 days (or PLEX). Assess at 2 weeks — if no improvement, escalate to second-line: rituximab 375 mg/m² × 4 weekly doses + cyclophosphamide. Reference the Titulaer 2013 observational study showing 53% responded to first-line, 97% of second-line responders improved, and 12% relapse rate (reduced with second-line therapy).

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