Virchow-Robin Spaces - Function

Function

One of the most basic roles of the VRS is the regulation of CNS fluid movement and drainage. Virchow-Robin spaces ultimately drain fluid from neuronal cell bodies in the CNS to the cervical lymph nodes. In particular, the “tide hypothesis” suggests that the cardiac contraction creates and maintains pressure waves to modulate the flow to and from the subarachnoid space and VRS. By acting as a sort of sponge, the VRS are essential for signal transmission and maintenance of extracellular fluid (ECF).

Another role of the VRS is as an integral part of the blood–brain barrier (BBB). While the BBB is often described as the tight junctions between the endothelial cells, this is an oversimplification that neglects the intricate role that perivascular spaces take in separating the venous blood from the parenchyma of the brain. Oftentimes, cell debris and foreign particles, which are impermeable to the BBB will get through the endothelial cells, only to be phagocytosed in the VR spaces. This holds true for many T and B cells, as well as monocytes, giving this small fluid filled space an important immunological role.

VR spaces also play an important role in immunoregulation. VR spaces not only contain interstitial and cerebrospinal fluid, but they also have a constant flux of macrophages, which is regulated by blood-borne mononuclear cells, but do not pass the basement membrane of the glia limitans. Similarly, as part of its role in signal transmission, perivascular spaces contain vasoactive neuropeptides (VNs), which, aside from regulating blood pressure and heart rate, have an integral role in controlling microglia. VNs serve to prevent inflammation by activating the enzyme adenylate cyclase which then produces cAMP. The production of cAMP aids in the modulation of auto-reactive T cells by regulatory T cells. . VRS is a susceptible space for VN compromise and when VN function is reduced in the VRS, immune response is adversely affected and the potential for degradation increases. When inflammation by T cells begins, astrocytes begin to undergo apoptosis, due to their CD95 receptor, to open up the glia limitans and let T cells into the parenchyma of the brain. Because this process is aided by the perivascular macrophages, these tend to accumulate during neuroinflammation and cause dilation of the VRS.