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Clinical Atlas Prestige · Evidence-first

Psych MEQs / SAQsConsultation-liaison psychiatry

Psych MEQs / SAQs · Consultation-liaison psychiatry

Autoimmune encephalitis presenting as first-episode psychosis (MEQ)

FRANZCP-style MEQ on anti-NMDAR/autoimmune encephalitis red flags, work-up, immunotherapy, and psychiatry's role in FEP interface.

20 marks20 min
On this page & tools

Target exams

FRANZCPMRCPsychABPNMD-DNB

Target exams

FRANZCPMRCPsychABPNMD-DNB
Prompt
A 22-year-old university student is brought to ED after 12 days of progressive insomnia, persecutory delusions, and agitation following a brief flu-like illness. On day 3 of the psychiatry ward stay she becomes nearly mute with repetitive orofacial movements; temperature is 37.6 C; sodium is normal. IM olanzapine has been given twice with little benefit. MRI brain overnight is reported as normal. Staff ask you to 'just increase the antipsychotic' and consider depot. (i) List red flags and state the leading organic differential with key discriminators from primary FEP. (ii) Outline a complete investigation plan including what not to rely on alone. (iii) Describe first-line and second-line immunotherapy principles and the role of tumour search. (iv) Explain your approach to symptomatic psychotropics, capacity/legal principles, and communication with family. (20 marks)

Model answer

Reveal model answer

(i) Red flags and differential. Red flags: subacute (days–weeks) first psychosis after viral-like prodrome; explosive tempo; speech reduction/mutism; orofacial dyskinesias; limited response to antipsychotics; young woman. Leading diagnosis: anti-NMDAR autoimmune encephalitis / probable autoimmune psychosis pending confirmation. Discriminators from primary FEP: rapid multistage evolution, hard neurologic signs (speech, movement), normal MRI does not exclude AE, need for EEG/CSF/Abs and immunotherapy rather than antipsychotic escalation alone.[1][6][4]

(ii) Investigations. Urgent neurology co-management. EEG (encephalopathic slowing; extreme delta brush supportive if present). MRI already done — normal MRI does not stop the pathway. LP: cell count, protein, glucose, OCB, infection panel including HSV PCR as indicated; paired serum and CSF neuronal cell-based assays (NMDAR and broader panel as advised). Do not rely on serum-only commercial tests. Metabolic baseline, pregnancy test. Tumour search: pelvic ultrasound/MRI for ovarian teratoma. Apply Graus possible/probable AE and Pollak frameworks to document rationale.[2][5][4]

(iii) Immunotherapy and tumour. When probable AE criteria are met, start first-line immunotherapy without waiting indefinitely for serology: high-dose IV methylprednisolone (commonly about 1 g daily for 3–5 days per local protocol), IVIG (commonly total 2 g/kg over 2–5 days), and/or plasma exchange (often about 5 exchanges). If inadequate response: second-line rituximab and/or cyclophosphamide under specialist protocols. Parallel teratoma resection if found — disease-modifying. Titulaer: early treatment and tumour removal improve outcomes.[3][5][6]

(iv) Psychotropics, capacity, family. Stop the "depot-only" plan. Use benzodiazepines for catatonia/agitation; cautious lowest-effective antipsychotic only for safety as a bridge — not definitive therapy. Assess capacity for LP/immunotherapy; if lacking, use local least-restrictive legal framework for emergency investigation/treatment (do not invent foreign section numbers). Explain to family: treatable brain inflammation, need for CSF and possible immunotherapy, hope for recovery over months with early care, psychiatry remains involved for symptoms and aftercare.[4][3][5]

Common errors

  • Escalating depot antipsychotic as the main plan
  • Treating normal MRI as exclusion of anti-NMDAR disease
  • Serum-only antibody testing
  • Waiting weeks for results before any immunotherapy when probable AE is clear
  • Inventing Mental Health Act section numbers instead of stating principles
[1] [3] [5] [4]

Examiner notes

High-scoring scripts name Graus, Pollak, Titulaer, and teratoma, and keep psychiatry's role as recognition + bridge + partnership rather than solo neuroimmunology. [2][3][4]

References

  1. [1]Herken J, Prüss H Red Flags: Clinical Signs for Identifying Autoimmune Encephalitis in Psychiatric Patients Front Psychiatry, 2017.PMID 28261116
  2. [2]Graus F, Titulaer MJ, Balu R, et al. A clinical approach to diagnosis of autoimmune encephalitis Lancet Neurol, 2016.PMID 26906964
  3. [3]Titulaer MJ, McCracken L, Gabilondo I, et al. Treatment and prognostic factors for long-term outcome in patients with anti-NMDA receptor encephalitis: an observational cohort study Lancet Neurol, 2013.PMID 23290630
  4. [4]Pollak TA, Lennox BR, Müller S, et al. Autoimmune psychosis: an international consensus on an approach to the diagnosis and management of psychosis of suspected autoimmune origin Lancet Psychiatry, 2020.PMID 31669058
  5. [5]Abboud H, Probasco JC, Irani S, et al. Autoimmune encephalitis: proposed best practice recommendations for diagnosis and acute management J Neurol Neurosurg Psychiatry, 2021.PMID 33649022
  6. [6]Dalmau J, Gleichman AJ, Hughes EG, et al. Anti-NMDA-receptor encephalitis: case series and analysis of the effects of antibodies Lancet Neurol, 2008.PMID 18851928