Immunological perspectives of temporal lobe seizures

J Neuroimmunol. 2013 Oct 15;263(1-2):1-7. doi: 10.1016/j.jneuroim.2013.08.001. Epub 2013 Aug 13.


The temporal lobes are affected in many different neurological disorders, such as neurodegenerative diseases, viral and immunological encephalitides, and epilepsy. Both experimental and clinical evidence suggests a different inflammatory response to seizures in patients with temporal lobe epilepsy (TLE) in comparison to those with extra-TLE (XTLE). Proinflammatory cytokines and several autoantibodies have been shown to be associated with TLE compared to other epilepsy types suggesting the specific role and structure of the temporal lobe. Abundant experience suggests that activation of both innate and adaptive immunity is associated with epilepsy, particularly refractory focal epilepsy. Limbic encephalitis often triggers temporal lobe seizures, and a proportion of these disorders are immune-mediated. Histological evidence shows activation of specific inflammatory pathways in resected temporal lobes of epileptic patients, and certain epileptic disorders have shown increased incidence in patients with autoimmune diseases. Rapid activation of proinflammatory cytokines is observed after single seizures, but there is also evidence of chronic overproduction of cytokines and other inflammatory mediators in patients with TLE, suggesting a neuromodulatory role of inflammation in epilepsy. In this review we summarize current data on the presence and the role of immunological factors in temporal lobe seizures, and their possible involvement in epileptogenesis.

Keywords: Adaptive immunity; Antibody; Cytokine; Innate immunity; Neurodegeneration; Neuromodulation.

Publication types

  • Review

MeSH terms

  • Adaptive Immunity
  • Animals
  • Autoantibodies / biosynthesis
  • Epilepsy, Temporal Lobe / immunology*
  • Epilepsy, Temporal Lobe / metabolism
  • Humans
  • Immunity, Innate
  • Inflammation Mediators / physiology
  • Seizures / immunology*
  • Seizures / metabolism


  • Autoantibodies
  • Inflammation Mediators