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In addition to the presence of neural antibodies, clinical features suggestive of autoimmune
epilepsy include:

     Acute to subacute onset, with seizures occurring every three months or less
     Multiple types of seizures or faciobrachial dystonic seizures
     Resistance to anti-seizure medication
     Personal or family history of autoimmunity
     History of recent or past neoplasia
     Viral prodrome
     Evidence of CNS inflammation.

When autoimmune epilepsy is suspected on clinical grounds, CSF evaluation and
comprehensive screening for neural autoantibodies are indicated. If autoimmune epilepsy is
suspected, a trial of immunotherapy – intravenous steroids or intravenous immunoglobulin,
(IVIg) – is justifiable in the absence of other treatment options and may serve as additional
evidence for an autoimmune aetiology when a favourable seizure response is observed18,19.

Questions remaining unanswered include the natural history of autoimmune epilepsy, the
selection criteria for patients with epilepsy most likely to benefit from an autoimmune
evaluation, the timing for immunotherapy trial, and optimal duration of long-term
immunotherapy maintenance.

Epilepsy after cerebral infection

The risk of epilepsy after viral encephalitis has been estimated to be 1025%, and 310%
after bacterial meningitis, particularly if a fixed neurological deficit has been acquired20.
Uncomplicated viral meningitis has not been associated with an increased risk of seizures.

References

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2. JENNETT, B. Epilepsy after Non-Missile Head Injuries. Heinemann, London, 1975.
3. CAVENESS WF, MEIROWSKY AM, RISH BL et al. The nature of post-traumatic epilepsy. J Neurosurg

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13. LANCASTER E, LAI M, PENG X et al. Antibodies to the GABA(B) receptor in limbic encephalitis with seizures:

       case series and characterisation of the antigen. Lancet Neurol 2010;9(1):67-76.
14. LAI M, HUGHES EG, PENG X et al. AMPA receptor antibodies in limbic encephalitis alter synaptic receptor

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