Engelhorn T, Doerfler A, Weise J, Baehr M, Forsting M, Hufnagel A
Department of Neuroradiology, University of Essen, Germany.
AJNR Am J Neuroradiol. 2005 Jun-Jul;26(6):1563-70.
Persistent generalized status epilepticus (SE) is associated with alterations of cerebral perfusion (CP). Because perfusion-weighted MR imaging (PWI) allows noninvasive CP-determination, the aim of this study was to investigate CP alterations during acute experimental SE correlated with SE-induced neuronal cell loss.
The rat pilocarpine model was used to induce SE. Multilocal PWI was performed before (baseline) and 3, 15, 30, 60, and 120 minutes after onset of SE. Bolus-peak ratio (BPR) was calculated for the retrosplenial and piriform cortex, hippocampus, amygdala, and thalamus and compared with baseline. Neuronal cell loss was quantified at different time points after induction of SE by cresyle violet staining.
Immediately after SE onset (3 minutes), BPR temporarily increased to 102%-130% in all regions, with a maximum in the amygdala (129 +/- 16%) and hippocampus (130 +/- 21%). At 15, 30, and 60 minutes, BPR decreased continuously to 57%-76%. BPR values <55% in the parietal and/or temporal cortex resulted in death. In surviving animals, BPR recovered to 66%-79% and there was a good correlation between neuronal cell loss in specific brain regions at 2 weeks after SE onset and maximal decrease in BPR (r > 0.73).
PWI demonstrated a transient cerebral hyperperfusion immediately after SE onset, followed by a significant continuous decline to different perfusion levels. In our experimental setting, a decline of cortical BPR below 55% of baseline seems to be a prognostic threshold value associated with subsequent death. In surviving animals, there is good correlation between the maximal decrease in BPR in the acute phase of SE and late neuronal cell loss.
持续性全面性癫痫持续状态(SE)与脑灌注(CP)改变相关。由于灌注加权磁共振成像(PWI)可进行无创性CP测定,本研究旨在探讨急性实验性SE期间与SE诱导的神经元细胞丢失相关的CP改变。
采用大鼠匹鲁卡品模型诱导SE。在SE发作前(基线)以及发作后3、15、30、60和120分钟进行多部位PWI。计算脾后皮质、梨状皮质、海马、杏仁核和丘脑的团注峰值比(BPR),并与基线进行比较。通过甲酚紫染色在SE诱导后的不同时间点对神经元细胞丢失进行定量。
SE发作后即刻(3分钟),所有区域的BPR暂时增加至102% - 130%,杏仁核(129 ± 16%)和海马(130 ± 21%)达到最大值。在15、30和60分钟时,BPR持续下降至57% - 76%。顶叶和/或颞叶皮质的BPR值<55%会导致死亡。在存活的动物中,BPR恢复至66% - 79%,且SE发作后2周时特定脑区的神经元细胞丢失与BPR的最大下降之间存在良好的相关性(r > 0.73)。
PWI显示SE发作后即刻出现短暂性脑血流灌注过多,随后显著持续下降至不同灌注水平。在我们的实验环境中,皮质BPR下降至低于基线的55%似乎是与随后死亡相关的预后阈值。在存活的动物中,SE急性期BPR的最大下降与晚期神经元细胞丢失之间存在良好的相关性。