Casimiro Carlos, Martins Joana, Nunes César, Parreira Tiago, Batista Sónia, Cordeiro Miguel, Matias Fernando, Rebelo Olinda, Freitas Pedro
Serviço de Imagiologia dos Hospitais da Universidade de Coimbra, Coimbra, Portugal.
Acta Med Port. 2012;25 Suppl 1:59-64. Epub 2012 Nov 2.
MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes) is a mitochondrial hereditary dysfunction in which the physiopathological mechanism of cerebral lesions is not totally understood as yet. Typically, these lesions are described as having normal to increased apparent diffusion coefficient (ADC), and this has been used to distinguish stroke-like lesions from ischemic lesions. Notwithstanding this, within the last few years, there have been reports of diffusion restriction in stroke-like episodes.
Analysis of the diffusion characteristics on serial magnetic resonance imaging (MRI) over a 16 month period, on a patient with MELAS and stroke-like lesions, to investigate the controversial changes of the ADC, reported in the last years. Evaluation of the proton spectroscopy changes in stroke-like lesions and apparently spared brain.
We performed four serial magnetic resonance imaging (MRI), including two stroke-like episodes, in a 28-year-old man with MELAS (mitochondrial DNA mutation A3243G). Qualitative analysis of the magnetic resonance images, including the single voxel spectroscopy and ADC maps, with analysis of evolution patterns of the last ones.
Both MRI that were performed during those episodes of stroke-like lesion revealed areas of diffusion restriction, coexisting areas of high ADC. During the chronic phase, there was a regression of those changes. Proton spectroscopy showed the presence of lactate and reduction of N-acetyl aspartate peak in stroke-like lesion and the presence of lactate in apparently spared brain.
All alterations that were recorded strengthen the view that cytotoxic oedema can occur in stroke-like lesions. Thus, their presence should not weaken the possibility of MELAS, especially if those lesions affect the temporal, parietal and/or occipital lobes, or if they predominantly involve the cortical gray matter, spanning vascular borders and if proton spectroscopy reveals lactate peak in the apparently spared brain.
线粒体脑肌病伴高乳酸血症和卒中样发作(MELAS)是一种线粒体遗传性功能障碍,其脑部病变的生理病理机制尚未完全明确。通常,这些病变的表观扩散系数(ADC)被描述为正常或升高,这一点已被用于区分卒中样病变和缺血性病变。尽管如此,在过去几年中,已有关于卒中样发作时扩散受限的报道。
对一名患有MELAS和卒中样病变的患者在16个月期间进行的系列磁共振成像(MRI)的扩散特征进行分析,以研究近年来报道的有争议的ADC变化。评估卒中样病变和看似未受影响的脑区的质子波谱变化。
我们对一名患有MELAS(线粒体DNA突变A3243G)的28岁男性进行了四次系列磁共振成像(MRI)检查,其中包括两次卒中样发作。对磁共振图像进行定性分析,包括单体素质子波谱和ADC图,并分析后者的演变模式。
在卒中样病变发作期间进行的两次MRI检查均显示出扩散受限区域以及ADC值高的共存区域。在慢性期,这些变化有所消退。质子波谱显示卒中样病变中有乳酸存在且N-乙酰天门冬氨酸峰降低,在看似未受影响的脑区也有乳酸存在。
所记录的所有改变均支持细胞毒性水肿可发生于卒中样病变的观点。因此,这些改变的存在不应削弱MELAS的可能性,尤其是当这些病变累及颞叶、顶叶和/或枕叶,或主要累及跨越血管边界的皮质灰质,且质子波谱显示在看似未受影响的脑区有乳酸峰时。