Autoimmune Encephalitis

Other names
Types
Causes
Common symptoms
Diagnostic tests
Non-pharmacological Treatments (therapies & others)
Drug Treatments
Dietary “Molecular” Supplements
Immunity-booster / Regenerative / Stem-cell” Drugs
Surgeries
Preventions
When to See Doctors (red flags)
What to Eat and What to Avoid
Frequently Asked Questions

Autoimmune encephalitis is brain inflammation caused by the body’s own immune system attacking healthy brain cells by mistake. “Autoimmune” means your immune system is reacting against your own tissues. “Encephalitis” means inflammation of the brain. In AE, white blood cells and antibodies target proteins on brain cells. This attack changes how brain cells talk to each other. It can quickly lead to memory problems, confusion, seizures, unusual movements, behavior or mood changes, and trouble with sleep or thinking. AE often develops over days to a few weeks (subacute). Some forms are linked to specific antibodies against brain cell surface proteins (for example, the NMDA receptor, LGI1, CASPR2, GABA or AMPA receptors). Other forms are linked to “onconeural” antibodies that are often associated with a hidden tumor. Doctors diagnose AE using symptoms, spinal fluid tests, EEG, MRI, and antibody testing in blood and spinal fluid. Early treatment with immune-calming medicines is important because it improves recovery and reduces long-term disability. The Lancet+1

Autoimmune encephalitis is a group of brain diseases where your own immune system mistakenly attacks healthy brain tissue. This causes swelling (inflammation) of the brain and leads to problems with memory, thinking, mood, behavior, movement, sleep, and seizures. AE can develop over days to a few weeks (subacute). It can be triggered by antibodies that target brain cell proteins (such as NMDA, LGI1, CASPR2, GABA, AMPA) or by a cancer in the body that “wakes up” the immune system to attack the brain (paraneoplastic). Some people have all the clinical signs of AE but no detectable antibody; this is called “antibody-negative probable AE,” and it is still treatable if doctors are confident of the diagnosis. Early recognition and early treatment improve recovery and reduce disability. PubMed+2The Lancet+2

Other names

Autoimmune encephalitis (AE) – the umbrella term used most often.
Antibody-mediated encephalitis – highlights that antibodies are driving the illness.
Autoantibody encephalitis – same idea as above; stresses the role of autoantibodies.
Paraneoplastic limbic encephalitis – a classic tumor-related subtype that mainly affects memory centers of the brain (the limbic system). New England Journal of Medicine

Types

Anti-NMDA receptor (NMDAR) encephalitis – often causes behavior changes, psychosis, seizures, abnormal movements, and autonomic instability; can be linked to ovarian teratoma. A distinctive EEG pattern called “extreme delta brush” may appear. New England Journal of Medicine+1
LGI1 antibody encephalitis – typically in middle-aged/older adults; very brief jerks called faciobrachial dystonic seizures (FBDS), memory problems, and low sodium (hyponatremia) are common. PMC+1
CASPR2 antibody encephalitis – can cause limbic encephalitis, nerve irritability, sleep disturbance, or Morvan syndrome (agitation, sweating, muscle twitching, severe insomnia). JCN
GABA-B receptor encephalitis – often presents with severe seizures and can be linked to small-cell lung cancer. New England Journal of Medicine
GABA-A receptor encephalitis – seizures and multifocal MRI abnormalities; can be severe. New England Journal of Medicine
AMPA receptor encephalitis – memory loss and confusion, sometimes tumor-associated. New England Journal of Medicine
Glycine receptor (GlyR) encephalitis – stiffness, exaggerated startle, or brainstem symptoms. PMC
mGluR5 encephalitis – rare; can cause severe confusion and memory issues (sometimes called “Ophelia syndrome”). Hopkins Guides
DPPX antibody encephalitis – weight loss, diarrhea, tremor, and agitation are typical. PMC
IgLON5 disease – combines sleep disorder and movement/brainstem problems; a special overlap syndrome. PMC
D2 receptor encephalitis – mostly in children with movement disorders and psychiatric features. New England Journal of Medicine
Seronegative autoimmune encephalitis – clinical picture and tests fit AE, but no antibody is found; strict criteria are used to diagnose this carefully. The Lancet
Paraneoplastic limbic encephalitis with onconeural antibodies (e.g., Hu/ANNA-1, Yo/PCA-1, Ri, Ma2, CV2/CRMP5, amphiphysin, KLHL11) – usually tumor-driven immune responses; often more aggressive and may respond best when the tumor is treated. New England Journal of Medicine

Note: Doctors often organize AE by antibody target (cell-surface vs. intracellular) and by clinical syndrome (limbic encephalitis, diffuse encephalitis, brainstem/cerebellar forms). This helps guide testing and treatment. The Lancet

Causes

NMDA receptor autoantibodies (often post-infection or tumor-associated). New England Journal of Medicine
LGI1 autoantibodies (often in older adults; sometimes associated with hyponatremia). PMC
CASPR2 autoantibodies (limbic encephalitis or Morvan syndrome). JCN
GABA-B receptor autoantibodies (frequent severe seizures; small-cell lung cancer link). New England Journal of Medicine
GABA-A receptor autoantibodies (multifocal encephalitis with seizures). New England Journal of Medicine
AMPA receptor autoantibodies (memory/behavior change; tumor association possible). New England Journal of Medicine
GlyR autoantibodies (stiffness/startle; brainstem involvement). PMC
mGluR5 autoantibodies (rare; limbic features). Hopkins Guides
DPPX autoantibodies (GI symptoms plus agitation, tremor). PMC
IgLON5 antibodies (sleep disorder plus brainstem/movement issues). PMC
Onconeural antibodies (Hu, Yo, Ri, Ma2, CRMP5, amphiphysin, KLHL11) in paraneoplastic AE. New England Journal of Medicine
Ovarian teratoma (especially with NMDAR encephalitis). New England Journal of Medicine
Small-cell lung cancer (GABA-B; Hu). New England Journal of Medicine
Testicular germ-cell tumors (e.g., Ma2). New England Journal of Medicine
Thymoma (CASPR2). JCN
Recent viral infection (e.g., herpes simplex) acting as a trigger for downstream autoimmune encephalitis in some patients. JCN
Immune checkpoint inhibitor drugs (rarely, these cancer drugs trigger AE). JCN
Other autoimmune diseases (a personal or family history of autoimmunity can co-occur). BMJ Pain Medicine
Post-infectious immune response after a systemic infection (immune system becomes misdirected). JCN
Seronegative immune activation without detectable known antibodies but with a typical AE picture (diagnosed by clinical criteria and exclusion). The Lancet

Common symptoms

Short-term memory loss – trouble remembering recent events or conversations; a hallmark of limbic involvement. The Lancet
Confusion – feeling disoriented or unable to think clearly; often fluctuates during the day. The Lancet
Behavior or personality change – sudden irritability, disinhibition, or social withdrawal; families often notice first. New England Journal of Medicine
Psychiatric symptoms – anxiety, agitation, depression, paranoia, or hallucinations, especially in NMDAR encephalitis. New England Journal of Medicine
Seizures – brief staring spells, jerks, or convulsions; in LGI1, very short FBDS attacks can occur many times per day. PMC
Abnormal movements – mouth or facial grimacing, limb posturing, chorea, or catatonia-like movements. New England Journal of Medicine
Sleep disturbance – insomnia, REM behavior changes, or fragmented sleep; prominent in IgLON5 and Morvan syndromes. JCN
Speech problems – slowed or reduced speech, or difficulty finding words. BMJ Pain Medicine
Autonomic instability – changes in heart rate, blood pressure, or temperature control; common in severe NMDAR cases. New England Journal of Medicine
Movement-triggered jerks in one arm and face (FBDS) – brief, frequent jerks strongly suggest LGI1 encephalitis. ScienceDirect
Headache – due to brain inflammation or seizures. BMJ Pain Medicine
Sensitivity to light or sound – often during active inflammation. BMJ Pain Medicine
Weakness or coordination problems – unsteady walking or clumsiness if the cerebellum is involved. BMJ Pain Medicine
Low sodium (hyponatremia) symptoms – fatigue, confusion, or falls, especially with LGI1 encephalitis. ScienceDirect
Persistent fatigue and “brain fog” – slowed thinking and tiredness that can last even after treatment. JCN

Diagnostic tests

A) Physical examination (bedside assessment)

Neurologic exam – the doctor checks memory, attention, orientation, reflexes, strength, coordination, and gait. In AE, the exam often shows memory deficits, attention problems, abnormal movements, or focal neurologic signs. This helps confirm brain dysfunction and guides urgent testing. The Lancet
Mental status and behavior observation – clinicians look for agitation, psychosis, catatonia, or personality change. These features, when they start subacutely with neurologic signs, point toward AE rather than a primary psychiatric illness. The Lancet
Autonomic check – heart rate, blood pressure, temperature, and sweating patterns. Autonomic instability supports severe forms such as anti-NMDAR encephalitis. New England Journal of Medicine
Tumor search on exam – palpation and focused exams (for example, testicular exam in men) to look for signs that suggest an underlying tumor that could be provoking a paraneoplastic AE. This is part of comprehensive evaluation. New England Journal of Medicine

B) Manual cognitive and functional tests

MoCA (Montreal Cognitive Assessment) – a simple paper test of memory, attention, and executive function. AE often lowers scores, especially for short-term memory. It is useful to track improvement with treatment. BMJ Pain Medicine
MMSE (Mini-Mental State Examination) – another bedside cognitive screening tool. A drop in orientation, recall, and attention supports encephalitic involvement. BMJ Pain Medicine
Seizure diaries / FBDS counts – for LGI1, counting brief arm-face jerks helps doctors recognize FBDS and start prompt immunotherapy even before antibodies return. Early recognition prevents progression to full limbic encephalitis. ScienceDirect
Functional status scales – simple scales (e.g., modified Rankin Scale) track daily function and recovery over time after treatment. This helps guide rehab and follow-up. JCN

C) Laboratory and pathological tests

Lumbar puncture (spinal tap) with CSF analysis – doctors look for inflammatory changes (white cells, protein, oligoclonal bands) and send CSF antibody panels. CSF is often more sensitive than serum for many AE antibodies (especially NMDAR). Combined CSF+serum testing reduces false results. The Lancet+1
Serum (blood) neuronal antibody panel – looks for antibodies such as NMDAR, LGI1, CASPR2, GABA-A/B, AMPAR, DPPX, GlyR, IgLON5, and others. A positive, clinically matching antibody supports the diagnosis and may suggest a tumor screen for paraneoplastic forms. North West London Pathology
Cancer work-up blood tests – basic labs (CBC, electrolytes), tumor markers when indicated, and hyponatremia checks (common in LGI1). These tests support the whole picture and help with treatment safety. ScienceDirect
Autoimmune panel – other antibodies (ANA, thyroid antibodies) can co-exist and help identify a broader autoimmune tendency. Results do not diagnose AE by themselves but add useful context. BMJ Pain Medicine

D) Electrodiagnostic tests

EEG (electroencephalogram) – measures brain waves. In AE, EEG often shows diffuse slowing or seizure activity. In anti-NMDAR encephalitis, a special pattern called “extreme delta brush” may appear: slow delta waves with fast beta “brushes” on top. Finding this pattern supports the diagnosis, tracks severity, and sometimes predicts longer illness. PMC+1
Continuous EEG monitoring – used in severe cases to detect frequent or subtle seizures and guide treatment in the ICU. This helps prevent complications like status epilepticus. Critical Care Toronto
Evoked potentials (when needed) – specialized tests of brain response to stimuli can support central nervous system dysfunction if MRI is normal, but they are secondary tools compared with EEG and MRI. BMJ Pain Medicine

E) Imaging tests

Brain MRI with and without contrast – looks for T2/FLAIR changes, especially in the medial temporal lobes (limbic system), or more patchy spots in other regions. MRI can be normal early, so a normal scan does not rule out AE. The Lancet
FDG-PET/CT of the brain – shows areas with abnormal metabolism (hypometabolism or hypermetabolism) when MRI is normal or unclear. PET can support diagnosis and monitor response to treatment. JCN
Whole-body tumor screening – CT chest/abdomen/pelvis, pelvic ultrasound (to look for ovarian teratoma), testicular ultrasound in men, or whole-body FDG-PET/CT. The goal is to find a hidden tumor that may be triggering the immune attack so it can be treated. New England Journal of Medicine
Follow-up MRI/PET – repeated scans help track healing over months and guide rehab or treatment tapering. Improvements often lag behind clinical recovery. American Academy of Neurology
Sleep study (polysomnography) – in suspected IgLON5 disease or Morvan syndrome, sleep testing shows characteristic patterns that support that specific AE subtype. JCN

Non-pharmacological Treatments (therapies & others)

(Below are the first 10 in full detail to keep this answer readable. I can add the next 10 in the same style.)

1) Early, structured neuro-rehabilitation
Description (≈150 words): After the acute phase, many people have problems with memory, attention, speech, balance, and behavior. A personalized rehab plan starts in the hospital and continues at home or in a rehab center. It blends cognitive therapy, physical therapy, occupational therapy, and speech-language therapy. Sessions are short but frequent to prevent fatigue. Goals are clear and measurable (e.g., remember 3 items after 5 minutes; walk 30 meters safely). Family education is essential so routines at home support therapy (sleep schedule, gentle prompting, calendars, reminder cards). Rehab adapts to fluctuations, because AE recovery is not linear—good and bad days happen. Safety plans cover seizures and falls. Progress is reviewed every 2–4 weeks and the program is adjusted.
Purpose: Speed recovery of brain functions and independence.
Mechanism: Repetition and task-specific practice drive neuroplasticity—healthy circuits strengthen and take over. American Academy of Neurology

2) Seizure safety education and lifestyle counseling
Description: Many AE patients have seizures. Education covers rescue steps, when to call for help, avoiding triggers (sleep loss, alcohol, missed medicines), and home safety (showers not baths, avoid heights, cook on back burners). Driving and work/school return are planned with clinicians.
Purpose: Reduce risk of injury and complications from seizures.
Mechanism: Hazard control + adherence to antiseizure plans lowers seizure-related harm while the immune disease is treated. PubMed

3) Sleep optimization program
Description: Sleep is often poor due to inflammation, steroids, anxiety, or hospital routines. A simple program includes consistent bed/wake times, quiet/dark rooms, avoiding caffeine after noon, limiting screens for an hour before bed, and brief daytime light exposure. If needed, short-term melatonin is considered.
Purpose: Improve brain recovery, mood, and seizure threshold.
Mechanism: Restorative sleep reduces neuroinflammation and stabilizes neuronal networks. PubMed

4) Speech-language therapy (language + cognitive-communication)
Description: AE can cause mutism, slurred/rapid speech, word-finding issues, or social-communication problems. Therapy starts with simple tasks (naming, repeating, short phrases) and builds to conversation and comprehension. Family learn cueing and pacing.
Purpose: Restore functional communication and reduce frustration.
Mechanism: Repetitive, graded language tasks strengthen fronto-temporal language circuits. PubMed

5) Cognitive rehabilitation (memory/attention/executive function)
Description: Therapists use memory notebooks, spaced-retrieval, errorless learning, and attention training. Apps with reminders and checklists are introduced carefully (avoid overload).
Purpose: Improve day-to-day functioning and independence.
Mechanism: Compensatory strategies + drill-based practice promote neuroplastic changes and practical work-arounds. American Academy of Neurology

6) Physical therapy and graded aerobic activity
Description: Weakness, abnormal movements, and deconditioning are common. PT starts with range-of-motion, balance drills, then gradually adds walking/cycling. Intensity is increased slowly to avoid post-exertional fatigue.
Purpose: Regain mobility, prevent falls, and boost brain health.
Mechanism: Exercise improves cerebral blood flow, reduces inflammation, and supports synaptic plasticity. American Academy of Neurology

7) Occupational therapy (ADLs & environmental adaptations)
Description: OT focuses on dressing, bathing, cooking, and simple work/school tasks. The therapist recommends tools (shower chair, grab bars, pill organizers), sets up checklists, and trains energy-saving techniques.
Purpose: Restore safe daily living and reduce caregiver load.
Mechanism: Simplifying tasks + adaptive devices reduce cognitive load while skills recover. American Academy of Neurology

8) Behavioral support & caregiver coaching
Description: Irritability, psychosis-like symptoms, or apathy can be very stressful. Caregivers learn de-escalation, calm routines, and how to spot relapse signs early. Short scripts and visual schedules reduce confusion.
Purpose: Stabilize the home setting and prevent crises.
Mechanism: Structure and predictable cues help frontal-limbic circuits regain control. PubMed

9) Cancer screening and tumor management pathway (non-drug step)
Description: Because some AE is driven by tumors (for example, ovarian teratoma in anti-NMDA), everyone should receive age- and sex-appropriate tumor screening on diagnosis and periodically afterward based on risk. Coordination with gynecology, oncology, urology, or thoracic teams is planned from day one.
Purpose: Find and treat the trigger so the brain inflammation settles.
Mechanism: Removing or treating the tumor removes the immune stimulus that fuels AE. PubMed

10) School/work reintegration plan
Description: A gradual return with adjustments (shorter days, quiet space, extra time for tasks, seizure plans) is safer. Teachers/employers get a short medical letter explaining cognitive fatigue and memory issues.
Purpose: Maintain life roles while protecting recovery.
Mechanism: Reasonable accommodations reduce stress and cognitive overload, supporting sustained improvement. American Academy of Neurology

Drug Treatments

(Below are the first 10 in detail. I can continue with the next 10.)

1) High-dose corticosteroids (e.g., methylprednisolone)
Class: Glucocorticoid (immunosuppressant).
Dose/Time: Common acute regimen: methylprednisolone 1 g IV daily for 3–5 days, then oral taper as guided by the team.
Purpose: First-line therapy to quickly reduce brain inflammation.
Mechanism: Broad anti-inflammatory effect; reduces cytokines, lymphocyte activity, and blood-brain barrier inflammation.
Key side effects: High blood sugar, mood changes, insomnia, infection risk, stomach irritation; taper prevents adrenal issues. PubMed

2) Intravenous immunoglobulin (IVIG)
Class: Pooled IgG immunomodulator.
Dose/Time: Often 2 g/kg total over 3–5 days; sometimes repeated.
Purpose: First-line therapy when steroids are contraindicated or as part of combination therapy.
Mechanism: Neutralizes autoimmune antibodies and modulates immune signaling.
Side effects: Headache, clot risk, kidney strain (rare), aseptic meningitis (rare). Hydration helps. PubMed

3) Plasma exchange (PLEX) / immunoadsorption
Class: Apheresis procedure (not a pill).
Dose/Time: 5–7 exchanges over ~10–14 days.
Purpose: First-line option to rapidly remove pathogenic antibodies.
Mechanism: Physically clears circulating autoantibodies and immune complexes.
Side effects: Low blood pressure, line infections, bleeding risks; done in hospital. PubMed

4) Rituximab
Class: Anti-CD20 monoclonal antibody (B-cell depletion).
Dose/Time: Common protocols: 375 mg/m² weekly ×4 or 1,000 mg IV day 1 and day 15; maintenance varies.
Purpose: Preferred second-line for cases not improving after first-line therapy (often assessed ~2 weeks after starting first-line). Also used to prevent relapses in some subtypes.
Mechanism: Depletes B cells that mature into antibody-producing cells.
Side effects: Infusion reactions, infections (screen for hepatitis B), rare PML; vaccine planning needed. American Academy of Neurology+1

5) Cyclophosphamide
Class: Alkylating immunosuppressant.
Dose/Time: Typical IV pulse 500–1,000 mg/m² monthly (varies).
Purpose: Second-line alternative or add-on when rituximab is unsuitable or inadequate.
Mechanism: Broad suppression of rapidly dividing immune cells.
Side effects: Low blood counts, infections, bladder irritation (use mesna/hydration), infertility risk with cumulative dosing. American Academy of Neurology

6) Mycophenolate mofetil (MMF)
Class: Antimetabolite immunosuppressant.
Dose/Time: Often 1–1.5 g twice daily for maintenance, adjusted by tolerability.
Purpose: Maintenance therapy to lower relapse risk after stabilization.
Mechanism: Inhibits lymphocyte purine synthesis, reducing antibody production.
Side effects: GI upset, leukopenia, infections; contraception advice required. PMC

7) Azathioprine
Class: Antimetabolite immunosuppressant.
Dose/Time: ~1.5–2.5 mg/kg/day (TPMT/NUDT15 activity guides safety).
Purpose: Maintenance alternative to MMF.
Mechanism: Inhibits DNA synthesis in lymphocytes.
Side effects: Bone-marrow suppression, liver toxicity, infections; check TPMT/NUDT15. PMC

8) Tocilizumab
Class: Interleukin-6 receptor blocker (biologic).
Dose/Time: 8 mg/kg IV monthly (max 800 mg) or SC per protocol.
Purpose: “Third-line” escalation for refractory disease after second-line therapy.
Mechanism: Dampens IL-6–driven plasma-cell and antibody activity.
Side effects: Infection risk, high lipids, liver enzyme rise; TB/hepatitis screening. PubMed

9) Bortezomib
Class: Proteasome inhibitor (targets plasma cells).
Dose/Time: Common protocol: 1.3 mg/m² SC or IV on days 1, 4, 8, 11 in 21-day cycles (specialist use).
Purpose: Refractory AE when antibodies persist despite rituximab/cyclophosphamide.
Mechanism: Depletes long-lived plasma cells that keep making pathogenic antibodies.
Side effects: Peripheral neuropathy, low blood counts, infection risk; specialist monitoring required. PMC+2SpringerOpen+2

10) Daratumumab
Class: Anti-CD38 monoclonal antibody (plasma-cell depletion).
Dose/Time: Specialist off-label schedules (e.g., weekly then spaced); hospital-based.
Purpose: Rescue therapy in highly refractory cases when other options fail.
Mechanism: Targets CD38-positive plasma cells producing autoantibodies.
Side effects: Infusion reactions, infections, cytopenias; expert centers only. PMC

(Other commonly used agents I can detail next: IVIG/PLEX combinations; tacrolimus or cyclosporine in select cases; antiseizure medications tailored to symptoms; antipsychotics very cautiously and short-term; sleep/anxiety agents short-term; DVT prophylaxis during immobility.) PubMed

Dietary “Molecular” Supplements

(Evidence in AE is limited; these are adjuncts for general brain health and recovery. Always clear with your neurologist to avoid drug interactions.)

1) Vitamin D
Dose: Often 1,000–2,000 IU/day (check levels).
Function/Mechanism: Supports immune balance and bone health (important during steroids). Limited AE-specific data; general neuro-immune support. PubMed

2) Omega-3 fatty acids (EPA/DHA)
Dose: ~1–2 g/day combined EPA/DHA.
Function/Mechanism: Anti-inflammatory lipid mediators may modestly reduce neuroinflammation; evidence indirect. PubMed

3) Thiamine (Vitamin B1)
Dose: 50–100 mg/day (higher if deficiency risk).
Function/Mechanism: Supports energy metabolism in neurons; helpful if nutrition is poor or alcohol use present. PubMed

4) Magnesium
Dose: 200–400 mg elemental/day.
Function/Mechanism: May aid sleep, reduce muscle cramps, and support neuronal stability; avoid with significant kidney disease. PubMed

5) Melatonin
Dose: 2–5 mg at night, short-term.
Function/Mechanism: Resets sleep patterns disrupted by steroids and hospitalization; improves sleep quality. PubMed

(I can add five more—e.g., folate/B12 when deficient, zinc if low, probiotic during antibiotics, calcium during steroids, and cautious antioxidant use—if you’d like.) PubMed

Immunity-booster / Regenerative / Stem-cell” Drugs

Important note: there are no stem-cell or “immunity booster” drugs approved specifically for AE. A few therapies target immune cells more deeply and are used in refractory cases at expert centers. Below are research-context summaries

1) Bortezomib (plasma-cell depleting)
Dose: See above.
Function/Mechanism: Removes long-lived plasma cells that continue to make pathogenic antibodies when standard therapy fails. Evidence comes from case series and reviews in refractory AE (not first-line). PMC+1

2) Daratumumab (anti-CD38)
Dose: Specialist infusions.
Function/Mechanism: Depletes CD38-expressing plasma cells; used when B-cell depletion was not enough. Data are limited to small series/case reports in refractory AE. PMC

3) Tocilizumab (IL-6 blockade)
Dose: See above.
Function/Mechanism: Reduces IL-6–driven plasma-cell survival and antibody production; an escalation option after failure of second-line agents. PubMed

4) Autologous hematopoietic stem-cell transplantation (AHSCT)
Dose: Procedure, not a drug.
Function/Mechanism: “Resets” the immune system after high-dose chemotherapy. Only considered in exceptional, life-threatening autoimmune diseases; not standard for AE. Evidence is extremely limited; risks are substantial. PubMed

5) Tofacitinib (JAK inhibitor)
Dose: Specialist-directed, off-label in select refractory cases.
Function/Mechanism: Dampens cytokine signaling; reported in small refractory AE series. Infection risk requires close monitoring. PMC

6) Low-dose IL-2 (experimental immune modulation)
Dose: Research settings only.
Function/Mechanism: Aims to expand regulatory T cells and restore immune tolerance. Not established for AE; consider only in clinical trials. PubMed

Surgeries

1) Ovarian teratoma removal
Procedure: Laparoscopic or open surgery to remove the tumor.
Why: Strongly linked to anti-NMDA AE; removing it speeds and improves recovery and reduces relapses. PubMed

2) Testicular tumor surgery
Procedure: Orchiectomy for germ-cell tumor when present.
Why: Paraneoplastic trigger; removing tumor reduces the immune attack on the brain. PubMed

3) Lung cancer treatment (e.g., resection/oncology care)
Procedure: Cancer-specific surgery or oncologic therapy.
Why: Some paraneoplastic AE (e.g., anti-Hu, anti-GABA $_B$ ) is linked to small-cell lung cancer; treating the tumor is essential. PubMed

4) Thymoma resection
Procedure: Surgical removal of thymic tumor.
Why: Rarely associated with AE; tumor control can help immune stabilization. PubMed

5) Long-term feeding tube or tracheostomy (selected severe cases)
Procedure: PEG tube or airway support if prolonged swallowing or breathing failure.
Why: Safety and nutrition during prolonged ICU-level AE; used only when necessary and revisited as recovery occurs. PubMed

Preventions

Seek urgent care for subacute confusion, behavior change, new seizures, or abnormal movements. Early treatment improves outcomes. PubMed
Follow tumor-screening plans if your AE type has cancer associations. PubMed
Vaccination planning with your neurologist before or between immunotherapies. PubMed
Infection prevention (hand hygiene, dental care) while on immunotherapy. PubMed
Medication adherence (immune and seizure medicines). Missed doses risk relapse or seizures. PubMed
Sleep, stress, and routine to stabilize brain recovery. PubMed
Healthy diet + bone protection (calcium/vitamin D if on steroids, per clinician). PubMed
Avoid alcohol and recreational drugs that lower seizure threshold or impair recovery. PubMed
Regular follow-up with neurology/rehab to catch relapses early. American Academy of Neurology
Personalized relapse action plan (who to call, what labs/infusions to consider). American Academy of Neurology

When to See Doctors (red flags)

Sudden or subacute confusion, memory loss, or major behavior change (days to weeks).
New seizures or repeated fainting spells.
Abnormal movements, extreme sleep changes, or speech problems.
Autonomic instability: fast heart rate, fluctuating blood pressure, breathing problems.
Worsening symptoms after initial improvement, or new symptoms during steroid taper.
Any sign of infection while on immunotherapy: fever, cough, burning urine, wounds. PubMed

What to Eat and What to Avoid

Eat: balanced meals with lean protein, vegetables, fruits, whole grains; adequate fluids; calcium/vitamin D sources (or supplements if prescribed) to protect bones during steroid therapy; potassium-rich foods if steroids raise blood pressure; fiber to prevent constipation from medicines.
Avoid/limit: alcohol; energy drinks; excessive sugar/salt (steroid side-effects); grapefruit if it interacts with your medicines; undercooked foods when immune-suppressed. Always check for drug–food interactions with your care team. PubMed

Frequently Asked Questions

1) Is AE curable?
Many people recover well, especially in antibody-defined AE, when treated early; some have long-term issues that improve with rehab. Relapses can happen but can be managed. PubMed

2) How is AE diagnosed?
By a combination of symptoms, MRI/EEG/CSF tests, and antibody studies. Doctors can start treatment based on strong clinical criteria even before antibodies return. PubMed

3) Are antibodies always found?
No. “Antibody-negative probable AE” is recognized when the overall picture fits and other causes are excluded. The Lancet

4) What’s first-line treatment?
High-dose steroids, IVIG, and/or plasma exchange. PubMed

5) What if first-line fails?
Second-line therapy with rituximab is preferred; cyclophosphamide is another option. American Academy of Neurology

6) Are there “third-line” options?
Yes—tocilizumab, bortezomib, and sometimes daratumumab in expert centers for refractory cases. PubMed+1

7) Do all AE types need cancer checks?
Screening is guided by the antibody type and risk; paraneoplastic forms require thorough tumor search and treatment. PubMed

8) How long does recovery take?
Months to years. Recovery is often step-wise and needs regular rehab and follow-up. American Academy of Neurology

9) Will I need seizure medicine long-term?
Sometimes. It depends on seizure control and EEG findings; your neurologist decides during follow-up. PubMed

10) Can I be vaccinated?
Usually yes, with timing coordinated around immunotherapies to optimize protection. PubMed

11) Is AE more common than viral encephalitis?
Some data suggest AE forms are at least as common or more common in certain settings—and importantly, they are treatable. PubMed

12) What predicts a good outcome?
Early diagnosis/treatment, tumor removal when present, and access to rehab. PubMed

13) Are psychiatric symptoms common?
Yes, especially in anti-NMDA AE; they are part of the disease and improve with immune treatment. NCBI

14) Can AE relapse?
Yes, but relapse risk can be reduced with appropriate maintenance therapy and monitoring. American Academy of Neurology

15) Where can clinicians find up-to-date guidance?
The 2016 diagnostic approach (Graus et al.), 2023–2024 updates, and consensus treatment recommendations (including pediatric NMDARE) are key references. American Academy of Neurology+3PubMed+3The Lancet+3

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