Multiple Factors Involved in the Pathogenesis of White Matter Lesions.
Multiple Factors Involved in the Pathogenesis of White Matter Lesions.
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DOI：
10.1155/2017/9372050
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发表时间：
2017
影响因子：
--
通讯作者：
Fan Y
中科院分区：
文献类型：
--
作者：
Lin J;Wang D;Lan L;Fan Y
白质病变(WMLs)，又称脑白质疏松(LA)或白质高信号(WMHs)，主要表现为T2加权或液体衰减反转恢复(FLAIR)图像上的高信号。随着人口老龄化和影像技术的发展，白斑淋巴瘤的发病率和诊断率呈逐年上升的趋势。WML不是一个良性的过程。它们在临床上表现为认知能力下降和随后发展为痴呆症。尽管WML很重要，但其发病机制仍不清楚。本文从解剖学、脑血流自动调节、静脉胶原化、血脑屏障破坏及遗传因素等方面对白质瘤发病机制的研究进展作一综述。特别是，将WMLs归因于继发于静脉胶原化和脑血流自动调节紊乱的慢性缺血似乎是合理的。随着基因技术的发展，遗传因素在WMLs发病机制中的作用逐渐受到重视。
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.