Table 1.
Clinical entities | Age of the clinical entity | Role of inflammation | Part of immune response involved | Established Mechanisms | Hypothesis |
---|---|---|---|---|---|
Febrile seizures | Only in infants and children | Probable role on ictogenesis |
Cytokines Mostly IL1β |
No | IL1β from blood decreases seizure threshold |
Fever triggering of seizures in epilepsy patients | Mostly children | Probable role on ictogenesis | Unknown | No |
Contribution of proinflammatory cytokines Role of hyperthermia cannot be excluded |
Acute encephalopathy with inflammation‐mediated status epilepticus | Mostly children |
Role on cerebral injury Probable role on epileptogenesis |
Cytokines Mostly IL1β |
No | Inflammation increases cell injury related to initial status epilepticus |
Infectious encephalitis | Children and Adults |
Role on seizures at acute phase Probable role on epileptogenesis following the acute episode |
Cytokines Microglia/Marcophages |
No |
Cytokines Microglia/Macrophages Virus‐induced brain injury |
Autoimmune encephalitis |
Mostly Adults Also in children |
Role on ictogenesis |
Adaptative immunity Production of autoantibody Anti‐NMDA Anti‐VGKC |
No |
Auto‐Antibody Maybe proinflammatory cytokines also contribute to seizure occurrence Anti‐NMDA antibodies induce NMDA‐R internalization causing a decrease in inhibitory synapse density onto excitatory hippocampal neurons |
Rasmussen encephalitis |
Mostly children | Role on ictogenesis |
Activated microglial cells and proinflammatory mediators, and are infiltrated by lymphocytes presence of autoantibodies |
No |
Microglia Proinflammatory cytokines might contribute to seizure occurrence |
Epileptogenesis following febrile status epilepticus | Only in infants and children | Possible role on epileptogenesis |
Cytokines Mostly IL1 β |
No |
Precipitating initial injury increased by inflammation lead to epileptogenesis Prolonged brain inflammation following the initial episode contributes to epileptogenesis |
Focal epilepsy | Children and Aduts | Role on ictogenesis | Cytokines | No |
‐ Inflammation in the structural brain abnormalities facilitate seizure occurrence ‐ Possible role in refractoriness |