PERIVASCULAR SPACES IN THE BASAL GANGLIA OF THE HUMAN BRAIN - THEIR RELATIONSHIP TO LACUNES

There is evidence for lymphatic drainage of interstitial fluid from th e brain along perivascular spaces in a number of mammalian species. Ul trastructural studies suggest that there are similar drainage pathways in the human cerebral cortex. Perivascular spaces in the basal gangli a, however, differ from those in the cortex in that they dilate to for m lacunes and rarely accumulate beta-amyloid (amyloid angiopathy) in A lzheimer's disease; in the cortex, lacunes are rare but amyloid angiop athy is common. The aim of the present study is to compare the structu re of perivascular spaces in the basal ganglia and at the anterior per forated substance with perivascular spaces in the cerebral cortex. Eig ht postmortem brains from patients aged 23-80 years (mean 68 y) were e xamined by light microscopy, by scanning and transmission electron mic roscopy and by direct visualisation of etched paraffin blocks. The res ults show that arteries in the basal ganglia are surrounded by 2 disti nct coats of leptomeninges separated by a perivascular space which is continuous with the perivascular space around arteries in the subarach noid space. The inner layer of leptomeninges closely invests the adven titia of the vessel wall and the outer layer is continuous with the pi a mater on the surface of the brain at the anterior perforated substan ce. Veins in the basal ganglia have no outer layer of leptomeninges an d thus the perivascular space is continuous with the subpial space. Th e anatomy of the periarterial spaces in the basal ganglia differs sign ificantly from that in the cerebral cortex where there is only a singl e periarterial layer of leptomeninges. Differences in structure of per ivascular spaces around arteries may reflect relative efficiencies in the drainage of interstitial fluid from different sites in the brain. Furthermore, the structure of the perivascular spaces may contribute t o the relatively high frequency of lacunes in the basal ganglia, and t he low frequency of amyloid angiopathy at this site in Alzheimer's dis ease.