Small vessel disease (SVD) is a common instigator of dementia in the aging population. The hallmarks of SVD are enlargement of the perivascular spaces and white matter hyperintensities. The latter represents local fluid accumulation in white matter that either subsides or develops into lacunar infarcts. We here propose that failure of brain fluid transport—via the glymphatic system—plays a key role in initiation and progression of SVD. Our major case for this concept is that perivascular spaces are utilized as waterways for influx of cerebrospinal fluid. Stagnation of glymphatic transport may drive loss of brain fluid homeostasis leading to transient white matter edema, perivascular dilation, and ultimately demyelination. This review will discuss how glymphatic rodent studies of hypertension and diabetes have provided new insight into the pathogenesis of SVD.

小血管病 (SVD) 是老年人群痴呆的常见诱因。SVD 的标志是血管周围空间扩大和白质高信号。后者代表白质中的局部积液，其消退或发展为腔隙性梗塞。我们在此提出脑液转运失败——通过淋巴系统——在 SVD 的起始和进展中起关键作用。我们对这个概念的主要案例是血管周围空间被用作脑脊液流入的水道。淋巴运输的停滞可能会导致脑液稳态的丧失，导致短暂的白质水肿、血管周围扩张，并最终导致脱髓鞘。