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Hippocampal T 2 Signal Change during Amygdala Kindling Epileptogenesis
Author(s) -
Jupp Bianca,
Williams John P.,
Tesiram Yasvir A.,
Vosmansky Milosh,
O'Brien Terence J.
Publication year - 2006
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1167.2006.00368.x
Subject(s) - epileptogenesis , kindling , hippocampal formation , neuroscience , dentate gyrus , hippocampus , temporal lobe , amygdala , kindling model , epilepsy , psychology , magnetic resonance imaging , medicine , radiology
Summary: Purpose: The rat electrical amygdala kindling model is one of the most widely studied animal models of temporal lobe epilepsy (TLE); however, the processes underlying epileptogenesis in this model remain incompletely understood. Magnetic resonance imaging (MRI) is a powerful method to investigate epileptogenesis, allowing serial imaging of associated structural and functional changes in vivo. Here we report on the results of serial MRI acquisitions during epileptogenesis in this model. Methods: Serial T 2 ‐weighted MR images were acquired before, during, and after the induction of kindling, to investigate the development and progression of imaging abnormalities. Results: T 2 ‐weighted acquisitions demonstrated the development of regions of increased signal in the rostral ipsilateral regions of CA1 and dentate gyrus in kindled (five of seven) but not in control rats (p < 0.05). Quantification of the T 2 signal demonstrated a significant increase in kindled animals when compared with controls, 2 weeks after kindling ceased, in the ipsilateral hippocampus and the hippocampal sub regions of CA1 and the dentate gyrus (p < 0.05). No significant difference was observed in hippocampal volumes between kindled or control animals at any of the times. Conclusions: The results of this study validate a method for acquiring serial MRI during amygdala kindling and demonstrate the induction of T 2 signal abnormalities in focal regions of the hippocampus. These regions may be important sites for the neurobiologic changes that contribute to epileptogenesis in this model.