Tzoulis Charalampos, Bindoff Laurence A
Department of Neurology, Haukeland University Hospital, Bergen, Norway.
Stroke. 2009 Feb;40(2):e15-7. doi: 10.1161/STROKEAHA.108.523118. Epub 2008 Dec 18.
Most diffusion MRI studies of mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episode stroke-like lesions report high- or normal-apparent diffusion coefficient, and this has been used to differentiate stroke-like lesion from ischemic stroke. There are, however, 3 recent reports of restricted diffusion in the acute phase of the stroke-like lesions. The purpose of our study was to investigate this apparent paradox.
We performed 9 serial MRI covering 2 stroke-like episodes in a 36-year-old man with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episode caused by the common mitochondrial DNA mutation 3243A>G.
We found clear evidence of initial restricted diffusion in the stroke-like lesions, which gradually evolved to high-apparent diffusion coefficient as lesions aged. Evolution was, however, asynchronous with both high- and low-apparent diffusion coefficients temporally coexisting.
Our findings suggest that cytotoxic edema does occur early in the course of a stroke-like lesions and that its presence or, conversely, the absence of vasogenic edema, should not weaken the possibility of mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episode in favor of ischemic stroke.
大多数关于线粒体脑肌病伴乳酸酸中毒及卒中样发作（MELAS）卒中样病灶的扩散加权磁共振成像（MRI）研究报告显示表观扩散系数（ADC）较高或正常，这一点已被用于区分卒中样病灶与缺血性卒中。然而，最近有3篇报道称卒中样病灶急性期存在扩散受限。我们研究的目的是探究这一看似矛盾的现象。
我们对一名36岁患有线粒体脑肌病伴乳酸酸中毒及卒中样发作的男性患者进行了9次连续MRI检查，该患者由常见的线粒体DNA突变3243A>G引起。
我们发现卒中样病灶最初存在明显的扩散受限证据，随着病灶的发展，其逐渐演变为高表观扩散系数。然而，这种演变是不同步的，高表观扩散系数和低表观扩散系数在时间上同时存在。
我们的研究结果表明，细胞毒性水肿确实在卒中样病灶病程早期出现，其存在或相反地不存在血管源性水肿，不应削弱线粒体脑肌病伴乳酸酸中毒及卒中样发作的可能性，而支持缺血性卒中的诊断。
