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

M.W. Aalbers, K. Rijkers, H.J.M. Majoie, J.T. Dings, O.E.M.G. Schijns, S. Schipper, M.H. de Baets, A. Kessels, J.S.H. Vles, G. Hoogland

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

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 nonsclerotic 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.
Original languageEnglish
Pages (from-to)36-42
JournalJournal of Neuroimmunology
Volume271
Issue number1-2
DOIs
Publication statusPublished - 1 Jan 2014

Cite this