| Abstract [eng] |
Up to a third of patients have drug-resistant epilepsy, some of whom are diagnosed with autoimmune epilepsy, which alters the course of further treatment and prognosis. Autoimmune epilepsy is characterized by epileptogenesis induced by cellular or humoral immunity. Half of the patients have specific autoantibodies in their cerebrospinal fluid or blood serum that are responsible for recurrent seizures, but the other half are likely to have undiscovered autoantibodies. Antibodies acting on the surface of the neuron are associated with inflammation of the central nervous system of humoral immunity and have a better response to treatment with intravenous immunoglobulins or steroids while antibodies against intracellular proteins of the neuron are associated with cytotoxic activity induced by cellular immunity and are therefore more resistant to immunological treatment and may require a broader spectrum of immunosuppression. Some antibodies are associated with cancer and paraneoplastic syndromes, in which case the primary treatment becomes no longer immunotherapy but the elimination of the cancer pathology. Clinical features can vary, usually with no pathognomic symptoms, and half of the patients may not have specific antibodies, so diagnosis is based on rejection of other etiologies and response to immunotherapy. Immunotherapy is used for both treatment and diagnosis based on a positive response. There is no clear line between acute symptomatic seizures caused by autoimmune encephalitis and autoimmune epilepsy, which often complicates further treatment of patients and confirmation of the final diagnosis. Standard antiepileptic drugs are not as effective as pathogenetic immunotherapy, but are used for adjuvant treatment and, in rare cases, themselves reduce the frequency of seizures. New guidelines for the diagnosis and treatment of autoimmune epilepsy are currently being developed, but until approved, clinical practice and case reports will need to be used in day-to-day practice. |
