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. 2014 Dec 23;21(2):141–151. doi: 10.1111/cns.12371

Table 1.

Epilepsy syndromes and clinical conditions with possible role of inflammation

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