The influence of neuropathology on brain inflammation in human and experimental temporal lobe epilepsy

J Neuroimmunol. 2014 Jun 15;271(1-2):36-42. doi: 10.1016/j.jneuroim.2014.03.016. Epub 2014 Mar 29.


It is unclear to what extent neuropathological changes contribute to brain inflammation observed in temporal lobe epilepsy (TLE). Here, we compared cytokine levels between histopathologically-confirmed sclerotic hippocampi and histopathologically-confirmed normal hippocampi from TLE patients. We analyzed a similar cytokine panel in the hippocampi of amygdala-kindled rats and we evaluated neuropathological changes by immunohistochemistry. In TLE patients, cytokine levels were not significantly different between sclerotic and non-sclerotic hippocampi. Though kindling resulted in increased astrocyte activation, cytokine levels and microglia activation were unchanged. These results suggest that the chronic epileptic state in TLE can also occur in the absence of intracerebral inflammation. Highlights.

Keywords: Cytokines; Hippocampal sclerosis; Inflammation; Temporal lobe epilepsy.

MeSH terms

  • Adult
  • Amygdala / physiology
  • Animals
  • CD11b Antigen / metabolism
  • Cytokines / metabolism*
  • Electric Stimulation / adverse effects
  • Encephalitis / etiology*
  • Encephalitis / pathology*
  • Epilepsy, Temporal Lobe / complications*
  • Epilepsy, Temporal Lobe / pathology*
  • Female
  • Fluorodeoxyglucose F18
  • Glial Fibrillary Acidic Protein / metabolism
  • Hippocampus / pathology*
  • Humans
  • Kindling, Neurologic / physiology
  • Male
  • Middle Aged
  • Positron-Emission Tomography
  • Rats
  • Rats, Sprague-Dawley


  • CD11b Antigen
  • Cytokines
  • Glial Fibrillary Acidic Protein
  • Fluorodeoxyglucose F18