Lin Jing, Wang Dilong, Lan Linfang, Fan Yuhua
Department of Neurology, Guangdong Key Laboratory for Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department, National Key Discipline, First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China.
Department of Medicine and Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong.
Biomed Res Int. 2017;2017:9372050. doi: 10.1155/2017/9372050. Epub 2017 Feb 21.
White matter lesions (WMLs), also known as leukoaraiosis (LA) or white matter hyperintensities (WMHs), are characterized mainly by hyperintensities on T2-weighted or fluid-attenuated inversion recovery (FLAIR) images. With the aging of the population and the development of imaging technology, the morbidity and diagnostic rates of WMLs are increasing annually. WMLs are not a benign process. They clinically manifest as cognitive decline and the subsequent development of dementia. Although WMLs are important, their pathogenesis is still unclear. This review elaborates on the advances in the understanding of the pathogenesis of WMLs, focusing on anatomy, cerebral blood flow autoregulation, venous collagenosis, blood brain barrier disruption, and genetic factors. In particular, the attribution of WMLs to chronic ischemia secondary to venous collagenosis and cerebral blood flow autoregulation disruption seems reasonable. With the development of gene technology, the effect of genetic factors on the pathogenesis of WMLs is gaining gradual attention.
白质病变（WMLs），也被称为脑白质疏松症（LA）或白质高信号（WMHs），主要特征是在T2加权或液体衰减反转恢复（FLAIR）图像上呈现高信号。随着人口老龄化和成像技术的发展，WMLs的发病率和诊断率逐年上升。WMLs并非良性病变。它们在临床上表现为认知功能下降以及随后发展为痴呆症。尽管WMLs很重要，但其发病机制仍不清楚。本综述阐述了对WMLs发病机制认识的进展，重点关注解剖学、脑血流自动调节、静脉胶原化、血脑屏障破坏和遗传因素。特别是，将WMLs归因于静脉胶原化和脑血流自动调节破坏继发的慢性缺血似乎是合理的。随着基因技术的发展，遗传因素对WMLs发病机制影响正逐渐受到关注。
