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1、会计学1第1页/共18页n定义n由于遗传缺损引起线粒体代谢缺陷,导致ATP合成障碍,能量产生不足而出现的一组多系统疾病。n分类第2页/共18页第3页/共18页n神经元过度兴奋、神经元脆弱、毛细血管通透性增加和充血第4页/共18页第5页/共18页第6页/共18页第7页/共18页1.2660.8261.172 0.765第8页/共18页1.0820.8310.851第9页/共18页第10页/共18页第11页/共18页nFig. 1 MRI exams were realized at admission (D0), at 15 days (D15) of evolution, and for co

2、ntrol 6 (M6) and 12 months later. Conventional FLAIR and DWI data arenrepresented in Fig. 1. FLAIR and DWI sequences are represented at two levels; the first 2 left columns corresponding to a view at the temporal level, and the 2 right columnsnto the occipital level. Rows represent successively MRI

3、exams realized at D0, D15, and M6 (MRIs at M12 were not represented as they were similar to images obtained 6nmonths earlier).nAt admission, recent left temporal lesion appeared with a hyper intensity on FLAIR sequence (1a), and ADCs were heterogeneous; elevated in anterior localization, andndiminis

4、hed in posterior region (1b). There were no signal abnormalities on FLAIR or DWI views in the occipital regions (2a and 2b).nAt D15, bilateral occipital FLAIR hyperintensities appeared (2c). ADCs increased in these regions (2d), and became homogeneously elevated in the left temporal lesionn(1d).nAt

5、M6, FLAIR hyperintensities diminished in the temporal lesion, replaced with gliosis (1e), and disappeared in the occipital region (2e). Lesion regression was more markednin those regions of the temporal lobe in which ADCs were previously the most elevated (white arrow). FLAIR abnormalities disappear

6、ed completely in occipital regions (2e),nand ADCs reached normal values (2f).第12页/共18页na mild energy failure resulting in moderate cellular dysfunction, responsible for vasogenic edema (high ADCs)na severe energy failure resulting in an irreversible cellular failure, with cytotoxic edema (low ADCs).第13页/共18页第14页/共18页第1

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