ACR Codes: 1.1
The Virchow-Robin spaces (VRS) are perivascular extensions of the pia mater that accompany the arteries entering and the veins emerging from the cerebral cortex. These spaces have been observed for well over a century and for much of this time they were thought to be in direct continuity with the subarachnoid space. Investigations have shown that these spaces are in fact extensions of the subpial compartment rather than the subarachnoid space. A thin layer of pia mater separates the extracellular fluid in the VRS from the CSF in the subarachnoid space, although tracer substances injected into the cerebral ventricles, and from there distributed to the subarachnoid space, have demonstrated a remarkably rapid penetration into the VRS.
The VRS are lined by a pial-glial layer peripherally, while the outer surfaces of the blood vessels lie centrally; they extend around the vascular tree as far as the capillaries. The physiological and pathological significance of these spaces are as follows:
Drainage of CSF: the ultimate drainage of CSF for the most part is into the blood via the arachnoid villi; however, there is a subsidiary and from the immunological point of view a potentially important route of drainage into the lymphatic channels of the head and neck. CSF reaches the cervical lymphatics possibly by way of leptomeningeal sheaths accompanying cranial and spinal nerves and through communications between perivascular spaces and lymphatic channels in the walls of major cerebral arteries.
The VRS could be considered as an immunological space: in the resting state the VRS contains resident perivascular macrophages that are capable of mounting an immunological response to foreign antigens that find their way to the brain, CSF, or extracellular fluid. In the reactive state these spaces become engorged with immune reactive cells (e.g., macrophages, lymphocytes and plasma cells).
Neoplastic and inflammatory meningeal processses may involve the brain via penetration of the VRS; Mirfakhraee et al have reported three cases of documented sarcoid meningoencephalitis using such a pathway of spread.
CT scan and especially MRI may elegantly demonstrate these spaces. Relatively small perivascular spaces are seen in patients of all ages; however, they tend to increase in size and frequency with advancing age. Although only usually 2 or 3 mm in diameter, they occasionally become quite large (5 to 20 mm) and may give the appearance of a lacunar infarct or brain cyst on MRI or CT studies. These spaces conform to the course of the penetrating arteries, and may be observed in the following locations:
Along the path of the lenticulostriate arteries as they enter the basal ganglia through the anterior perforated substance. These spaces are most commonly noted on axial MRI studies in the inferior putamenal region, adjacent to the lateral aspect of the anterior commissure. If the putamen is divided roughly into thirds from inferior to superior, the foci in the inferior one-third almost invariably prove to be normal VRS around branches of the lenticulostriate arteries. However, in the upper two-thirds, the cavities in actual brain specimens are usually lacunar infarcts. The relationship of these spaces to the lenticulostriate arteries is best appreciared on sagittal and coronal MR images.
The periventricular and supraventricular white matter.
Lateral mesencephalon and external capsule.
These spaces are not normally observed in the pons and thalamus. Benhaiem-Sigaux et al have reported a pathologically proven case of expanding cerebellar perivascular spaces associated with Binswanger's subcortical arteriosclerotic encephalopathy.
Regardless of the region of the brain involved, these space have three characteristic findings: (1) isointensity to CSF on all pulse sequences, (2) location along the path of penetrating arteries, and (3) a smooth ovoid shape on axial imaging (some larger Virchow-Robin spaces may demonstrate a subtle mass effect). Therefore, multiplanar imaging, combined with different pulse sequences might raise the diagnostic confidence, in doubtful cases of VRS.
Poirier et al proposed a neuropathologic classification of cerebral lacunae. Although the term 'lacunae' was used in a more general sense to encompass both destructive and nondestructive processes by these authors, some other groups believe that the term 'lacunae' should be reserved to the areas of tissue loss or damage caused by infarction. The classification is as follows: type 1 lacunae are old, small cerebral infarcts, type 2 lacunae are old, small hemorrhages, and type 3 lacunae are caused by dilatation of the perivascular spaces. Type 3 lacunae are also divided into four varieties on the basis of their number and volume. Type 3a lacunae are numerous and very small cavities, type 3b lacunae have the same size, location and number as the type 1 lacunae, type 3c lacunae correspond to single large perivascular dilatations, and type 3d lacunae present as space-occupying lesions. Type 3b lacunae, "lacunes de dŠ¹sintŠ¹gration", were first described by Marie, who claimed that they were due to perivascular dilatation destroying the adjacent brain by a specific process he named "vaginalite destructive". Type 3d or expanding lacunae may compress and thin the adjacent parenchyma without destroying tissue and they may cause reactive changes such as astrocytic gliosis, spongiosis, swollen oligodendroglia, and myelin loss with edema. The presence of mass effect and adjacent brain damage associated with some VRS, may suggest that these spaces may have clinical significance rather than representing merely an incidental finding.
Expanding VRS may result in symptoms if located in areas of critical functional significance; a patient with obstructive hydrocephalus secondary to compression of the cerebral aqueduct has been reported (neuropathological examination of a paramedian mesencephalic artery in this patient revealed severe lesions of segmental necrotizinbg angiitis of unknown etiology). Cunha Bastos et al have reported a case of a late-onset temporal lobe epilepsy in a patient demonstrating dilatation of the hippocampal sulcus by an enlarged VRS (although an anatomic variant with persistence of a large hippocampal sulcus should also be considered).
The pathophysiology of large perivascular spaces still remains to be elucidated. Several mechanisms such as increased CSF pulsations, an ex vacuo phenomenon, vascular ectasia, or an abnormality of arterial wall permeability may be related to their formation. Large Virchow-Robin spaces are positively correlated with age, atrophy, hypertension, dementia, and white matter lesions.
Reference(s): 1) Cunha Bastos A, et al. Late-onset temporal lobe epilepsy and dilatation of the hippocampal sulcus by an enlarged Virchow-Robin space. Neurology. 1998; 50(3):784-7.
2) Ogawa T, et al. Unusual Widening of Virchow-Robin Spaces: MR Appearance. AJNR Am J Neuroradiol. 1995;16:1238-42.
3) Esiri MM, et al. Immunological and neuropathological significance of the Virchow-Robin space. J Neurol Sci. 1990;100(1,2):3-8.
4) Jungreis CA, et al. Normal Perivascular Spaces Mimicking Lacunar Infarction: MR Imaging. Radiology. 1988;169(1):101-4.
5) Benhaiem-Sigaux N, et al. Expanding Cerebellar Lacunes Due To Dilatation Of the Perivascular Space Associated With Binswanger's Arteriosclerotic Encephalopathy. Stroke. 1987;18(6):1087-92.
6) Mirfakhraee M, et al. Virchow-Robin Space: A Path Of Spread In Neurosarcoidosis. Radiology. 1986;158(3):715-20. p