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Spectroscopic imaging of the pilocarpine model of human epilepsy suggests that early NAA reduction predicts epilepsy
Author(s) -
Gomes W.A.,
Lado F.A.,
de Lanerolle N.C.,
Takahashi K.,
Pan C.,
Hetherington H.P.
Publication year - 2007
Publication title -
magnetic resonance in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.696
H-Index - 225
eISSN - 1522-2594
pISSN - 0740-3194
DOI - 10.1002/mrm.21310
Subject(s) - epilepsy , pilocarpine , hippocampal formation , temporal lobe , voxel , magnetic resonance imaging , neuroscience , neuroimaging , medicine , nuclear medicine , chemistry , psychology , radiology
Reduced hippocampal N‐acetyl aspartate (NAA) is commonly observed in patients with advanced, chronic temporal lobe epilepsy (TLE). It is unclear, however, whether an NAA deficit is also present during the clinically quiescent latent period that characterizes early TLE. This question has important implications for the use of MR spectroscopic imaging (MRSI) in the early identification of patients at risk for TLE. To determine whether NAA is diminished during the latent period, we obtained high‐resolution 1 H spectroscopic imaging during the latent period of the rat pilocarpine model of human TLE. We used actively detuneable surface reception and volume transmission coils to enhance sensitivity and a semiautomated voxel shifting method to accurately position voxels within the hippocampi. During the latent period, 2 and 7 d following pilocarpine treatment, hippocampal NAA was significantly reduced by 27.5 ± 6.9% ( P < 0.001) and 17.3 ± 6.9% ( P < 0.001) at 2 and 7 d, respectively. Quantitative estimates of neuronal loss at 7 d (2.3 ± 7.7% reduction; P = 0.58, not significant) demonstrate that the NAA deficit is not due to neuron loss and therefore likely represents metabolic impairment of hippocampal neurons during the latent phase. Therefore, spectroscopic imaging provides an early marker for metabolic dysfunction in this model of TLE. Magn Reson Med 58:230–235, 2007. © 2007 Wiley‐Liss, Inc.