Clark J M, Marks M P, Adalsteinsson E, Spielman D M, Shuster D, Horoupian D, Albers G W
Stanford Stroke Center, Palo Alto, CA 94304-1705, USA.
Neurology. 1996 Jan;46(1):223-7. doi: 10.1212/wnl.46.1.223.
We describe the clinical, imaging, and pathologic findings in a patient with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). The patient experienced her first stroke-like episode at age forty-four. Brain MRI, obtained at symptom onset, at 3 weeks, and at 1 year, revealed migrating T2-weighted hyperintensities in the temporal/parietal and occipital cortices and later revealed atrophy. Abnormal cerebrovascular reserve was evident on xenon/CT four days after the first MRI. MR spectroscopy at 1 year revealed increased lactate in both the occipital and temporal lobes. Histologic sections demonstrated spongy degeneration of the cortex that was most prominent at the crests of the gyri. Electron microscopy of the blood vessels showed increased numbers of abnormal mitochondria within the vascular smooth muscle and in endothelial cells. We hypothesize that the stroke-like episodes in MELAS may be due to impaired autoregulation secondary to the impaired metabolic activity of mitochondria in the endothelial and smooth muscle cells of blood vessels.
我们描述了一名患有线粒体肌病、脑病、乳酸酸中毒和卒中样发作(MELAS)患者的临床、影像学和病理学表现。该患者在44岁时首次出现卒中样发作。在症状发作时、3周时和1年时进行的脑部MRI显示,颞叶/顶叶和枕叶皮质出现迁移性T2加权高信号,随后显示萎缩。首次MRI检查4天后的氙/CT显示脑血管储备异常。1年时的磁共振波谱显示枕叶和颞叶的乳酸均增加。组织学切片显示皮质海绵状变性,在脑回顶部最为明显。血管电子显微镜检查显示血管平滑肌和内皮细胞内异常线粒体数量增加。我们推测,MELAS中的卒中样发作可能是由于血管内皮和平滑肌细胞中线粒体代谢活动受损继发的自动调节功能受损所致。