1. The influence of neuropathology on brain inflammation in human and experimental temporal lobe epilepsy.
- Author
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Aalbers MW, Rijkers K, Majoie HJ, Dings JT, Schijns OE, Schipper S, De Baets MH, Kessels A, Vles JS, and Hoogland G
- Subjects
- Adult, Amygdala physiology, Animals, CD11b Antigen metabolism, Electric Stimulation adverse effects, Female, Fluorodeoxyglucose F18, Glial Fibrillary Acidic Protein metabolism, Humans, Kindling, Neurologic physiology, Male, Middle Aged, Positron-Emission Tomography, Rats, Rats, Sprague-Dawley, Cytokines metabolism, Encephalitis etiology, Encephalitis pathology, Epilepsy, Temporal Lobe complications, Epilepsy, Temporal Lobe pathology, Hippocampus pathology
- 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 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., (Copyright © 2014 Elsevier B.V. All rights reserved.)
- Published
- 2014
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