In vivo 1H magnetic resonance spectroscopy, T2-weighted and diffusion-weighted MRI during lithium-pilocarpine-induced status epilepticus in the rat

被引:49
作者
van Eijsden, P [1 ]
Notenboom, RGE
Wu, O
de Graan, PNE
van Nieuwenhuizen, O
Nicolay, K
Braun, KPJ
机构
[1] Univ Utrecht, Ctr Med, Rudolf Magnus Inst Neurosci, Dept Neurol & Neurosurg, Utrecht, Netherlands
[2] Univ Utrecht, Ctr Med, Rudolf Magnus Inst Neurosci, Dept Pharmacol & Anat, Utrecht, Netherlands
[3] Univ Utrecht, Ctr Med, Image Sci Inst, Dept Expt In Vivo NMR, Utrecht, Netherlands
[4] Eindhoven Univ Technol, Dept Biomed Engn, NL-5600 MB Eindhoven, Netherlands
关键词
status epilepticus; pilocarpine; rat; magnetic resonance; spectroscopy; diffusion;
D O I
10.1016/j.brainres.2004.09.025
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Temporal lobe epilepsy (TLE) is associated with febrile convulsions and childhood status epilepticus (SE). Since as the initial precipitating injury, triggering epileptogenesis, occurs during this SE, we aimed to examine the metabolic and morphological cerebral changes during the acute phase of experimental SE noninvasively. In the rat lithium-pilocarpine model of SE, we performed quantified T-2- and isotropic-diffusion-weighted (DW) magnetic resonance imaging (MRI) at 3 and 5 b of SE and acquired single-voxel H-1 MR spectra at 2,4 and 6 h of SE. T-2 was globally decreased, most pronounced in the amygdala (Am) and piriformic cortex (Pi), in which also a significant decrease in apparent diffusion coefficient (ADC) was found. In contrast, ADC values increased transiently in the hippocampus (HC) and thalamus (Th). MR spectra showed a decrease in N-acetylaspartate (NAA) and choline (Cho) and an increase of lactate in a hippocampal voxel. The T-2 decrease. attributed to raised deoxyhemoglobin, and the presence of lactate both indicate a mismatch between oxygen demand and delivery. The ADC decrease, indicative of excitotoxicity, confirms that the amygdala and piriformic cortex are particularly vulnerable to lithium-pilocarpine-induced seizures. The transient ADC increase in the thalamus may reflect the breakdown of the blood-brain barrier (BBB). which is shown to occur in this region at these time points. Neuronal damage and failure of energy-dependent formation of NAA are likely causes of an observed decrease in NAA, while the decrease in Cho is possibly due to depletion of the cholinergic, system. This study illustrates that relative hypoxia. excitotoxicity and concomitant neuronal damage associated with SE can be probed noninvasively with MR. These pathological phenomena are the first to contribute to the pathophysiology of spontaneous recurrent seizures in a later stage in this animal model. (C) 2004 Elsevier B.V. All rights reserved.
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页码:11 / 18
页数:8
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