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Health condition · Clinically reviewed

Autoimmune encephalitis, antibodies, immunotherapy and recovery.

Treatable brain inflammation driven by antibodies against neuronal proteins. Early recognition and immunotherapy change outcomes.

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Why trust this guide

  • 01

    Clinically reviewed

    Written by our editorial team and reviewed by a registered UK clinician before publication.

  • 02

    Sourced from guidance

    Checked against ABN, Encephalitis Society and peer-reviewed neurology sources you can see at the end.

  • 03

    Current for 2026

    Reflects modern UK practice including antibody panels, first-line immunotherapy and newer B-cell agents.

Key facts

Autoimmune encephalitis at a glance.

The essentials, in plain English: what it is, the main antibody groups and how it is treated in the UK today.

  • What it is

    Antibody-mediated brain inflammation where the immune system targets neuronal surface or intracellular antigens, producing subacute cognitive, psychiatric and seizure syndromes.

  • Most common form

    Anti-NMDA receptor encephalitis, especially in young women, with an ovarian teratoma association in around half of adult female cases.

  • Onset

    Subacute over days to weeks, usually within three months, and often preceded by a prodrome of headache, fever or flu-like illness.

  • Key investigations

    MRI brain, EEG, CSF analysis with paired serum and CSF autoantibody panels, and a tumour screen appropriate to age and sex.

  • First-line treatment

    High-dose intravenous methylprednisolone with IVIg or plasma exchange, plus tumour resection when a trigger is found.

  • Second-line therapy

    Rituximab and cyclophosphamide when response is partial, with newer agents such as inebilizumab, bortezomib and tocilizumab in refractory cases.

Why this guide matters

A treatable cause of encephalitis, often missed.

Autoimmune encephalitis can look like a primary psychiatric illness or a rapidly progressive dementia. Recognising the pattern is what unlocks treatment.

  • Antibody biology matters

    Surface antibodies (NMDAR, LGI1, CASPR2) respond well to immunotherapy; intracellular paraneoplastic antibodies point to underlying cancer.

  • Time is brain

    Every week of delay in immunotherapy worsens the long-term outcome; empirical treatment often starts before antibody results return.

  • Tumours change the plan

    Ovarian teratoma, small-cell lung, testicular and breast cancers can drive disease; resection is often part of the cure.

How the diagnosis is made

From first symptoms to a treatment plan.

The steps a UK neurology team will normally follow, in order, so you know what to expect and why.

  1. 01

    Assessing

    Clinical pattern recognition

    Subacute memory loss, new psychiatric symptoms, seizures, movement disorder, autonomic instability or reduced consciousness in someone previously well.

  2. 02

    Assessing

    MRI brain with contrast

    Looks for medial temporal T2 and FLAIR hyperintensity, cortical or subcortical inflammation, or a normal scan that does not exclude the diagnosis.

  3. 03

    Assessing

    EEG

    Detects focal or generalised slowing, epileptiform activity, and the extreme delta brush pattern that is highly suggestive of NMDAR encephalitis.

  4. 04

    Confirming

    CSF analysis

    Lumbar puncture for lymphocytic pleocytosis, elevated protein, oligoclonal bands and paired antibody testing.

  5. 05

    Confirming

    Autoantibody panel (serum + CSF)

    Cell-surface antibodies (NMDAR, LGI1, CASPR2, GABA-B, GABA-A, AMPA, DPPX, IgLON5, glycine receptor, mGluR5) and intracellular paraneoplastic antibodies (Hu, Yo, Ma2, CV2/CRMP5, amphiphysin).

  6. 06

    Preparing

    Tumour screen

    CT chest, abdomen and pelvis, whole-body FDG-PET, pelvic ultrasound in women and testicular ultrasound in men, guided by antibody profile.

  7. 07

    Preparing

    Multidisciplinary planning

    Neurology, neuropsychiatry, intensive care, oncology and rehabilitation align on immunotherapy, tumour management and long-term recovery.

Typical timeline: recognition and empirical immunotherapy within days, antibody confirmation over 1 to 3 weeks.

Symptoms

What autoimmune encephalitis looks like.

A subacute combination of cognitive, psychiatric, seizure, movement, autonomic and sleep symptoms in someone previously well.

  • Memory and cognitive change

    Rapidly progressive short-term memory loss, disorientation and executive dysfunction over days to weeks.

  • Psychiatric presentation

    New anxiety, psychosis, hallucinations, mania or catatonia, often the first sign in NMDAR encephalitis.

  • Seizures

    Focal, generalised or status epilepticus, including the faciobrachial dystonic seizures typical of LGI1 disease.

  • Movement disorder

    Orofacial dyskinesias, choreoathetosis, dystonia and neuromyotonia, prominent in NMDAR and CASPR2 syndromes.

  • Autonomic instability

    Blood pressure and heart rate swings, hyperthermia, hypoventilation and pupillary changes needing critical care.

  • Sleep disturbance

    Insomnia, REM sleep behaviour disorder and the distinctive parasomnia of IgLON5 disease.

  • Reduced consciousness

    Progressive drowsiness, mutism and coma, often after weeks of psychiatric or seizure symptoms.

  • Red flag - rapid neuropsychiatric decline

    Any subacute combination of psychiatric change, seizures and cognitive loss warrants urgent neurology admission.

Treatment

How autoimmune encephalitis is treated in the UK.

First-line steroids, IVIg or plasma exchange, second-line B-cell depletion, tumour resection and structured rehabilitation.

  • IV methylprednisolone

    High-dose corticosteroid pulse, typically 1 g daily for 3 to 5 days, as first-line immunosuppression alongside IVIg or plasma exchange.

  • Intravenous immunoglobulin

    IVIg 2 g/kg over 2 to 5 days modulates the humoral immune response and is often paired with steroids.

  • Plasma exchange

    Removes circulating pathogenic antibodies, useful when antibodies are surface-directed and disease is severe.

  • Rituximab

    Anti-CD20 B-cell depletion as second-line therapy for partial or non-response, with sustained benefit in NMDAR and LGI1 disease.

  • Cyclophosphamide

    Broader immunosuppression reserved for aggressive or refractory disease, often combined with rituximab.

  • Tumour resection

    Removing an ovarian teratoma, small-cell lung cancer or other trigger tumour is critical to recovery and relapse prevention.

  • Newer targeted agents

    Inebilizumab (anti-CD19), bortezomib (plasma-cell depletion) and tocilizumab (anti-IL-6) for refractory cases in specialist centres.

  • Supportive and rehabilitative care

    ICU support, antiseizure medication, psychiatric input and structured neurorehabilitation shape long-term outcome.

What this guide is based on

The sources behind every claim on this page.

UK national guidance, specialist neurology consensus and peer-reviewed evidence, current at the time of last review.

Key references

Guidelines and consensus we relied on.

A quiet reminder

This guide is for information, not medical advice.

Your neurologist knows your history and can tell you which parts apply to you. If in doubt, get seen urgently.

  • Association of British Neurologists (ABN). Guidelines on autoimmune encephalitis.

  • Graus F et al. A clinical approach to diagnosis of autoimmune encephalitis. Lancet Neurology.

  • Titulaer MJ et al. Treatment and prognostic factors for long-term outcome in NMDAR encephalitis.

  • Encephalitis Society (UK). Patient information and support resources.

Red flags

When to escalate urgently.

Autoimmune encephalitis can deteriorate quickly. These are the situations that need immediate specialist care.

  • Status epilepticus

    Prolonged or recurrent seizures without recovery need immediate emergency management and ICU admission.

  • Central hypoventilation

    Autonomic failure with reduced respiratory drive is common in NMDAR encephalitis and mandates airway protection.

  • Severe autonomic instability

    Wide swings in blood pressure, heart rate or temperature can precipitate cardiac arrest and require critical care.

  • Progressive coma

    Falling GCS in someone with unexplained psychiatric or seizure onset should prompt urgent immunotherapy.

  • Hyponatraemia with LGI1

    Low sodium plus faciobrachial dystonic seizures is a classic LGI1 pattern that must not be missed.

  • Occult malignancy

    Paraneoplastic antibodies such as Hu, Yo or Ma2 signal underlying cancer that must be sought aggressively.

  • Relapse after initial recovery

    New neuropsychiatric symptoms months after treatment suggest relapse and need urgent specialist review.

  • Missed teratoma in young women

    NMDAR encephalitis without pelvic imaging risks missing an ovarian teratoma driving refractory disease.

  • Delayed immunotherapy

    Every week of delay worsens outcome; empirical treatment is often started before antibody results return.

Living with it

Recovery is real, and it takes time.

Four things that make the biggest difference during recovery: patience with the arc, structured rehabilitation, relapse awareness and community support.

A quiet reminder

You do not have to navigate this alone.

The UK Encephalitis Society provides helplines, peer support and family resources for people affected by autoimmune encephalitis.

  1. 01 Recovery

    Expect a long arc

    Cognitive and psychiatric recovery can take 12 to 24 months, with gradual gains rather than a sudden return to baseline.

  2. 02 Rehabilitation

    Neurorehab makes a difference

    Structured input from neuropsychology, occupational therapy, speech therapy and physiotherapy shapes long-term function.

  3. 03 Relapse watch

    Know your warning signs

    Learn your early symptoms with your clinician so any recurrence is caught and treated quickly.

  4. 04 Support

    The Encephalitis Society

    The UK charity offers helplines, peer support and family resources that many patients and carers find invaluable.

Frequently asked

Everything we get asked about autoimmune encephalitis.

Quick answers on antibody types, investigations, immunotherapy and recovery.

  • What is autoimmune encephalitis?

    Autoimmune encephalitis is brain inflammation caused by antibodies that target neuronal proteins. It produces a subacute mix of memory loss, psychiatric change, seizures, movement disorder and autonomic instability, and it is treatable when recognised early.

  • What is anti-NMDA receptor encephalitis?

    It is the most common form of autoimmune encephalitis, particularly in young women. Around half of adult female cases are associated with an ovarian teratoma. Presentation typically moves from psychiatric symptoms to dyskinesias, seizures, autonomic instability and reduced consciousness over weeks.

  • What are LGI1 and CASPR2 encephalitis?

    LGI1 encephalitis usually affects older adults and features faciobrachial dystonic seizures, limbic encephalitis and hyponatraemia. CASPR2 antibodies cause Morvan syndrome with neuromyotonia, insomnia, autonomic features and cognitive change.

  • What are paraneoplastic antibodies?

    These are intracellular antibodies such as Hu, Yo, Ma2, CV2/CRMP5 and amphiphysin that signal an underlying cancer, often small-cell lung, ovarian, testicular or breast. Finding and treating the tumour is essential to controlling the neurological disease.

  • How is autoimmune encephalitis treated?

    First-line treatment is high-dose IV methylprednisolone with IVIg or plasma exchange. Second-line agents include rituximab and cyclophosphamide. Tumour resection is critical when a trigger is identified, and newer agents such as inebilizumab, bortezomib and tocilizumab are used in refractory cases.

  • Can people recover fully?

    Many people do recover well, particularly when treatment starts early. Recovery is often gradual over 12 to 24 months and benefits from structured neurorehabilitation, psychiatric support and careful monitoring for relapse. The UK Encephalitis Society offers valuable support during this time.

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