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EDUCATION EXHIBIT 1071

Virchow-Robin Spacesat MR Imaging1

Robert M. Kwee, MD ● Thomas C. Kwee, MD

Virchow-Robin (VR) spaces surround the walls of vessels as theycourse from the subarachnoid space through the brain parenchyma.Small VR spaces appear in all age groups. With advancing age, VRspaces are found with increasing frequency and larger apparent sizes.At visual analysis, the signal intensity of VR spaces is identical to thatof cerebrospinal fluid with all magnetic resonance imaging sequences.Dilated VR spaces typically occur in three characteristic locations:Type I VR spaces appear along the lenticulostriate arteries entering thebasal ganglia through the anterior perforated substance. Type II VRspaces are found along the paths of the perforating medullary arteriesas they enter the cortical gray matter over the high convexities and ex-tend into the white matter. Type III VR spaces appear in the midbrain.Occasionally, VR spaces have an atypical appearance. They may be-come very large, predominantly involve one hemisphere, assume bi-zarre configurations, and even cause mass effect. Knowledge of thesignal intensity characteristics and locations of VR spaces helps differ-entiate them from various pathologic conditions, including lacunar in-farctions, cystic periventricular leukomalacia, multiple sclerosis, cryp-tococcosis, mucopolysaccharidoses, cystic neoplasms, neurocysticerco-sis, arachnoid cysts, and neuroepithelial cysts.©RSNA, 2007

Abbreviations: CSF � cerebrospinal fluid, FLAIR � fluid-attenuated inversion recovery, GAG � glycosaminoglycan, MS � multiple sclerosis,VR � Virchow-Robin

RadioGraphics 2007; 27:1071–1086 ● Published online 10.1148/rg.274065722 ● Content Codes:

1From the Department of Radiology, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, the Netherlands. Received July 25,2006; revision requested October 24 and received November 30; accepted December 4. All authors have no financial relationships to disclose. Ad-dress correspondence to R.M.K. (e-mail: [email protected]).

©RSNA, 2007

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TEACHING POINTS

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IntroductionThe Virchow-Robin (VR) space is named afterRudolf Virchow (German pathologist, 1821–1902) (1) and Charles Philippe Robin (Frenchanatomist, 1821–1885) (2). VR spaces, orperivascular spaces, surround the walls of vesselsas they course from the subarachnoid spacethrough the brain parenchyma. VR spaces arecommonly seen at magnetic resonance (MR) im-aging and may sometimes be difficult to differen-tiate from pathologic conditions. Knowledge oftheir signal intensity characteristics and localiza-tion helps in this differentiation, which is impor-tant for correct patient management.

The purpose of this article is to provide an in-depth overview of the MR imaging features of VRspaces. Specific topics outlined are the micro-scopic anatomy of VR spaces, dilated VR spaces,prevalence, and normal and atypical appearanceof VR spaces. Subsequently, differential diagnos-tic considerations are discussed.

AnatomyVR spaces surround the walls of arteries, arte-rioles, veins, and venules as they course from thesubarachnoid space through the brain paren-chyma (Fig 1) (1–5). Electron microscopy andtracer studies have given insight into the locationof VR spaces and clarified that the subarachnoidspace does not communicate directly with the VRspaces (3–5).

Arteries in the cerebral cortex are coated by alayer of leptomeninges that is subtended from thepia mater; by this anatomic arrangement, the VRspaces of the intracortical arteries are in directcontinuity with the VR spaces around arteries inthe subarachnoid space (Fig 2). The lack of asimilar coating of leptomeningeal cells aroundveins in the cerebral cortex suggests that VRspaces around veins are in continuity with thesubpial space (4).

In contrast to arteries in the cerebral cortex,arteries in the basal ganglia are surrounded by notone but two distinct coats of leptomeninges, sepa-rated by a VR space that is continuous with theVR space around arteries in the subarachnoid

space. The inner layer of leptomeninges closelyinvests the adventitia of the vessel wall. The outerlayer abuts on the glia limitans of the underlyingbrain and is continuous with the pia mater on thesurface of the brain and the anterior perforatedsubstance. Veins in the basal ganglia have noouter layer of leptomeninges (similar to corticalveins), which suggests that their VR spaces arecontinuous with the subpial space (5).

Interstitial fluid within the brain parenchymadrains from the gray matter of the brain by diffu-sion through the extracellular spaces and by bulkflow along VR spaces. There is evidence fromtracer studies and from pathologic analysis of thehuman brain that VR spaces carry solutes fromthe brain and are, in effect, the lymphatic drain-age pathways of the brain (6).

Dilated VR SpacesDilatation of VR spaces was described by Durant-Fardel (7) in 1843. These dilatations are regularcavities that always contain a patent artery. Themechanisms underlying expanding VR spaces are

Figure 1. Photomicrograph (original magnification,�20; hematoxylin-eosin stain) of a coronal sectionthrough the anterior perforated substance shows twoarteries (straight arrows) with surrounding VR spaces(curved arrows).

1072 July-August 2007 RG f Volume 27 ● Number 4

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Teaching Point VR spaces surround the walls of arteries, arterioles, veins, and venules as they course from the subarachnoid space through the brain parenchyma (Fig 1) (1–5).

still unknown. Different theories have been postu-lated: segmental necrotizing angiitis of the arteriesor another unknown condition causing perme-ability of the arterial wall (8–10), expanding VRspaces resulting from disturbance of the drainageroute of interstitial fluid due to cerebrospinal fluid(CSF) circulation in the cistern (11,12), spiralelongation of blood vessels and brain atrophy re-sulting in an extensive network of tunnels filledwith extracellular water (9,13), gradual leaking ofthe interstitial fluid from the intracellular com-partment to the pial space around the metarteri-ole through the fenestrae in the brain parenchyma(14), and fibrosis and obstruction of VR spacesalong the length of arteries and consequent im-pedance of fluid flow (5).

PrevalenceSmall VR spaces (�2 mm) appear in all agegroups. With advancing age, VR spaces are foundwith increasing frequency and larger apparent size(�2 mm) (15). Some studies found a correlationbetween dilated VR spaces and neuropsychiatricdisorders (16–19), recent-onset multiple sclerosis(MS) (20), mild traumatic brain injury (21), anddiseases associated with microvascular abnormali-ties (22).

The prevalence of VR spaces at MR imaging isalso dependent on the applied technique. HeavierT2-weighted imaging results in better visualiza-tion of VR spaces (23). In addition, the use ofthinner sections will demonstrate more VR spacesas well (15,24). Also, high-field-strength MR im-aging is expected to have an increased clinicalimpact in the near future; the current magneticfield (�1.5 T) is likely to be switched to 3 or 4 T.The anticipated higher signal-to-noise ratio athigher magnetic field strengths may successfullyimprove spatial resolution and image contrast(25–27), leading to better visualization (and in-creased prevalence) of VR spaces on MR images.

Appearance at MR Imaging

Signal Intensity CharacteristicsVisually, the signal intensities of the VR spacesare identical to those of CSF with all pulse se-quences. However, when signal intensities aremeasured, the VR spaces prove to have signifi-cantly lower signal intensity than the CSF-con-taining structures within and around the brain

Figure 2. Drawing shows a cortical artery with a surrounding VR space crossing from the subarach-noid and subpial spaces through the brain parenchyma. The magnified view on the right shows the ana-tomic relationship between the artery, VR space, subpial space, and brain parenchyma.

RG f Volume 27 ● Number 4 Kwee and Kwee 1073

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Teaching Point Small VR spaces (<2 mm) appear in all age groups. With advancing age, VR spaces are found with increasing frequency and larger apparent size (>2 mm) (15).

Teaching Point Visually, the signal intensities of the VR spaces are identical to those of CSF with all pulse sequences.

(28), a finding consistent with the fact that theVR spaces represent entrapments of interstitialfluid. This difference in signal intensity can alsobe explained by partial volume effects, since a VRspace with accompanying vessel is smaller thanthe contemporary volume of a voxel on MR im-

ages. VR spaces show no restricted diffusion ondiffusion-weighted images because they are com-municating compartments. T1-weighted imageswith substantial flow sensitivity may show highsignal intensity due to inflow effects, therebyhelping confirm that one is indeed dealing withVR spaces (29). VR spaces do not enhance withcontrast material. In patients with small to mod-erate dilatations of the VR spaces (2–5 mm), the

Figure 3. Bilateral type I VR spaces in a 6-year-old boy. (a) Axial proton-density–weighted image (repetition time msec/echo time msec � 2375/100) shows hyperintense ar-eas (arrows) in the anterior perforated substance on both sides. (b) Axial fluid-attenuatedinversion-recovery (FLAIR) image (6606/100) obtained at the same level shows that theseareas have CSF-like content (arrows). The signal intensity of the surrounding brain paren-chyma is normal. (c, d) Diffusion-weighted image (2574/81; b factor � 1000 sec/mm2) (c)and corresponding apparent diffusion coefficient map (d) show no restricted diffusion inthese areas (arrows).


surrounding brain parenchyma generally has nor-mal signal intensity (30,31).

Locations and MorphologyDilated VR spaces typically occur in three charac-teristic locations. The first type (type I) is fre-quently seen on MR images and appears alongthe lenticulostriate arteries entering the basal gan-glia through the anterior perforated substance(Figs 3, 4) (15,32). Here, the tortuous lenticulo-

striate arteries change direction from a lateral to adorsomedial path and are grouped closely to-gether. A proximal VR space, containing severalvessels, is the resulting physiologic finding (33).

The second type (type II) can be found alongthe path of the perforating medullary arteries asthey enter the cortical gray matter over the highconvexities and extend into the white matter (Figs5, 6) (15,32).

Figure 5. Type II VR spaces in a 73-year-old woman. (a) Axial proton-density–weightedimage (2376/100) shows multiple hyperintense foci in the centrum semiovale in both hemi-spheres. (b) On an axial FLAIR image (6614/100) obtained at the same level, the VR spacesare seen as hypointense dots without any surrounding high signal intensity. Note the twosmall lesions with a hypointense center and a hyperintense rim (arrows) in the left hemi-sphere; these lesions are not VR spaces but old lacunar infarctions.

Figure 4. Bilateral type I VR spaces in a53-year-old woman. Coronal T1-weightedimage (500/30) shows symmetrical hypoin-tense areas (arrows) in the anterior perfo-rated substance.


TeachingPoint

Teaching Point Dilated VR spaces typically occur in three characteristic locations.

The third type (type III) appears in the mid-brain. In the lower midbrain, VR spaces at thepontomesencephalic junction surround the pen-etrating branches of the collicular and accessorycollicular arteries (Figs 7, 8). They are mainlylocated between the cerebral peduncles in theaxial plane and correspond to the level of the ten-torial margin as seen in coronal sections. In theupper midbrain, where the VR spaces are visibleat the mesencephalodiencephalic junction, theyappear along the posterior (interpeduncular)thalamoperforating artery or the paramedian mes-encephalothalamic artery and short and long cir-

cumferential arteries originating from the upperbasilar artery or proximal posterior cerebral artery(23,34,35).

VR spaces are mostly seen as well-defined oval,rounded, or tubular structures, depending on theplane in which they are intersected. They havesmooth margins, commonly appear bilaterally,and usually measure 5 mm or less (32).

Atypical VR SpacesIt is reported that clusters of type II enlarged VRspaces may predominantly involve one hemi-sphere (36). There are even reports that describethe solely unilateral appearance of enlarged VRspaces in the high convexity (37,38).

Figure 6. Type IIdilated VR spaces ina 6-year-old boy.(a) Axial T2-weighted image(2620/100) showslinear to punctatehyperintense areasaround the occipitalhorns, especially onthe left side (arrow).(b) FLAIR image(7572/100) obtainedat the same levelshows no abnormalsignal intensity (ar-row), in accordancewith the fact thatthese areas are trueVR spaces.

Figure 7. Type IIIVR space in a 25-year-old man. (a) Ax-ial proton-density–weighted image(2620/100) shows ahyperintense spot inthe brainstem (ar-row). (b) AxialFLAIR image (7292/120) obtained at thesame level shows thatthe spot has CSF-likecontent without ab-normal surroundingsignal intensity (ar-row). These findingsconfirm that the spotis a VR space.


Occasionally, VR spaces appear markedly en-larged, cause mass effect, and assume bizarre cys-tic configurations that may be misinterpreted asother pathologic processes, most often a cysticneoplasm. As most of these giant VR spaces bor-der a ventricle or subarachnoid space, reports ofsuch cases (39–41) have offered an extensive dif-ferential diagnosis that includes cystic neoplasms,parasitic cysts, cystic infarctions, nonneoplasticneuroepithelial cysts, and deposition disorderssuch as mucopolysaccharidosis. Salzman et al(42) presented a series of 37 patients with giant

VR spaces. These spaces most often appear asclusters of variably sized cysts and are most com-mon in the mesencephalothalamic region (Fig 9),in the territory of the paramedial mesencephalo-thalamic artery, and in the cerebral white matter.Giant VR spaces in the mesencephalothalamicregion may cause hydrocephalus by direct com-pression of the third ventricle or the sylvian aque-duct (Fig 9), requiring surgical intervention(8,11,42–47).

Figure 8. Type III VR spaces in a 68-year-old man. (a) Axial proton-density–weighted image (2382/100) showsmultiple punctate hyperintense areas in the brainstem (arrow). (b) Close-up T2-weighted image (4615/120) clearlyshows the fine punctate pattern. (c) Axial FLAIR image (6609/100) shows the CSF-like content of the dots (arrow).No surrounding high signal intensity is seen. The typical configuration and the fact that no high signal intensity isseen on the FLAIR image confirm that the dots are VR spaces.

Figure 9. Giant VR spaces in the mesencephalothalamic region in a 19-year-old man. (a, b) Axial (a) and sagit-tal (b) T2-weighted images (5970/120) show a multicystic lesion in the mesencephalothalamic region. The lesionextends from the left cerebral peduncle to the left thalamus. The content of the cysts is CSF-like. The adjacent brainparenchyma has normal signal intensity. No solid components are identified. (c) Axial gadolinium-enhanced T1-weighted image (478/18) shows no enhancement. The process has caused obstruction of the sylvian aqueduct, result-ing in hydrocephalus. The size of the lesion and the degree of hydrocephalus were unchanged compared with the ap-pearance on MR images obtained 2 years earlier.


TeachingPoint

Teaching Point Occasionally, VR spaces appear markedly enlarged, cause mass effect, and assume bizarre cystic configurations that may be misinterpreted as other pathologic processes, most often a cystic neoplasm.

In one-half of cases, giant VR spaces that occurin the white matter may have surrounding signalintensity abnormality on T2-weighted or FLAIRimages (42). This may be viewed as a worrisomefinding and in some cases has prompted the per-formance of tissue biopsy. However, the abnor-

mal signal intensity stems from reactive gliosissurrounding the enlarged VR spaces and is not anominous finding (47).

DifferentialDiagnostic Considerations

In this section, the top differential diagnoses ofdilated VR spaces are discussed. MR imagingcharacteristics of each disease entity are summa-

Figure 10. Chronic lacunar infarction of the pons in a 59-year-old man. (a) Axial proton-density–weighted image (2200/100) shows a hyperintense lesion in the pons (arrow).(b) Axial FLAIR image (6614/100) shows that the lesion has a hypointense center with ahyperintense rim (arrow), an appearance that reflects gliosis.

Figure 11. Acute and chronic lacunar infarctions in a 66-year-old man. (a) Axial proton-density–weighted image(2385/100) shows multiple high-signal-intensity lesions bilaterally in the basal ganglia, internal capsule, and thalamus(arrows). The signal intensity of the periventricular white matter is abnormally increased. (b) Axial FLAIR image(6608/100) shows multiple small high-signal-intensity lesions and hypointense lesions surrounded by hyperintenserims in the same region (arrows). (c) Apparent diffusion coefficient map shows a recent infarction in the posteriorlimb of the right internal capsule (arrow).


rized, and clues to differentiate them from normalVR spaces are given.

Lacunar InfarctionsLacunar infarctions are small infarctions lying indeeper noncortical parts of the cerebrum andbrainstem. They are caused by occlusion of pen-etrating branches that arise from the middle cere-bral, posterior cerebral, and basilar arteries andless commonly from the anterior cerebral and ver-tebral arteries (48,49). Sites of predilection arethe basal ganglia, thalamus, internal and externalcapsule, ventral pons, and periventricular whitematter (Figs 10, 11) (48).

In the upper two-thirds of the anterior perfo-rated substance and basal ganglia, cavities inbrain specimens usually appear to be lacunar in-farctions. Large VR spaces found in the inferiorthird of the anterior perforated substance andbasal ganglia are invariably VR spaces aroundbranches of lenticulostriate arteries (type I VRspaces) (32).

Lacunar infarctions tend to be larger than VRspaces and often exceed 5 mm. However, no con-sistent cutoff value with high diagnostic accuracyhas been reported in the literature, to our knowl-edge. In contrast to VR spaces, lacunar infarc-tions are generally not symmetric (30,32,33,50).It is difficult to distinguish lacunar infarctionsfrom VR spaces by means of shape. However,wedge-shaped holes are more likely to be lacunarinfarctions (50).

Lacunar infarctions can be differentiated fromVR spaces by signal intensity characteristics. Anacute lacunar infarction (12 hours up to 7 days)appears as a small high-signal-intensity region onT2-weighted and FLAIR images and as a hypoin-tense area on T1-weighted images. High signalintensity is seen on diffusion-weighted imageswith corresponding low signal intensity on theapparent diffusion coefficient map (Fig 11). En-hancement is variable.

A chronic lacunar infarction is better definedand has high signal intensity on T2-weighted im-ages and low signal intensity on T1-weighted im-ages. On FLAIR images, a hyperintense lesion ora lesion with a hypointense center and a hyperin-tense rim reflecting gliosis is seen (Figs 10, 11).Diffusion-weighted images are normal. Enhance-ment may persist up to 8 weeks after the acuteevent (51).

Cystic Periventricular LeukomalaciaPeriventricular leukomalacia, usually seen in pre-mature infants, is a leukoencephalopathy result-ing from a pre- or perinatal hypoxic-ischemicevent. In the acute stage, white matter undergoesvascular congestion and coagulative necrosis.Cavitation then occurs within necrotic regions.End-stage periventricular leukomalacia has a typi-cal appearance at MR imaging (Fig 12): T2-weighted and FLAIR images show abnormally

Figure 12. Cystic periventricular leukomalacia in a 3-year-old boy with a history of perina-tal asphyxia who had delayed motor and mental development and epilepsy. (a) Axial proton-density–weighted image (2611/100) shows hyperintense lesions predominantly in the rightperitrigonal area (straight arrow) but also in the left peritrigonal area (curved arrow). Theselesions could be mistaken for type II VR spaces. (b) Coronal FLAIR image (11,000/140)shows gliosis around the cystic lesions (arrows), a characteristic finding in end-stage cysticperiventricular leukomalacia.


increased signal intensity in the periventricularwhite matter. There is marked loss of periven-tricular white matter, predominantly in the peri-atrial regions, and compensatory focal ventricularenlargement adjacent to regions of abnormalwhite matter signal intensity. The involvementtends to be symmetrical. Corpus callosal thinningcan be seen as a secondary manifestation. Thereis relative sparing of the overlying cortical mantle.In more severe cases, cavitated infarcts have re-placed the immediate periventricular white matter(52,53). These cystic components have surround-ing gliosis, easily depicted on FLAIR images,which distinguishes them from enlarged VRspaces (Fig 12).

Multiple SclerosisMS lesions may be located anywhere in the cen-tral nervous system. Lesions in the periventricularand juxtacortical white matter correspond to thelocation of type II VR spaces. In addition, indi-vidual MS plaques often appear as ovoid lesions,mimicking the shape of dilated VR spaces (Fig13). However, MS lesions are usually arrangedlike fingers pointing away from the walls of thelateral ventricles (Dawson fingers) and can easilybe distinguished from enlarged VR spaces by sig-nal intensity characteristics. In the acute stage,MS lesions are isointense or mildly hypointenseto brain parenchyma on T1-weighted images. Inthe chronic phase, they have a hypointense centerwith a mildly hyperintense rim on T1-weighted

images. T2-weighted and FLAIR images demon-strate hyperintense lesions. Both solid and ringenhancement may occur. Enhancement is depen-dent on the current degree of inflammation (54).

CryptococcosisCryptococcosis is an opportunistic fungal infec-tion caused by Cryptococcus neoformans, affectingthe central nervous system in human immunode-

Figure 13. Ovoid MS lesion of the centrum semiovale in a 49-year-old man. Axial proton-density–weighted (2624/100) (a) and FLAIR (7291/120) (b) images show a hyperintenselesion (arrow) in the right centrum semiovale. Other MS lesions were located behind the leftoccipital horn and in the basal ganglia and brainstem.

Figure 14. Cryptococcosis in a 58-year-oldwoman with headaches and fever who wasseropositive for human immunodeficiencyvirus. Parasagittal T2-weighted image (5963/120) shows multiple dilated VR spaces inthe region of the basal ganglia (arrowheads).C neoformans was cultured from the CSF.


ficiency virus–seropositive patients and in patientswith other immunocompromised states. Centralnervous system infection can be either meningealor parenchymal. Infection usually starts as menin-gitis, most pronounced at the base of the brain(55,56). The infection often provokes little in-flammatory reaction, owing to the host’s immu-nity and to the immunosuppressive effect of theorganism’s capsule (55–57). Infection of the me-ninges may spread to the adjacent brain throughthe subarachnoid space or along the ependymalsurface.

As the infection spreads along the VR spaces,they may become distended with mucoid, gelati-nous material that originates from the organism’scapsule (56). Therefore, cryptococcosis should beconsidered in the differential diagnosis in anyimmunocompromised patient with dilated VRspaces. Larger collections of organisms and gelati-nous capsular material in the VR spaces havebeen termed gelatinous pseudocysts (55,56).Mass lesions representing cryptococcomas mayoccur, particularly in the deep gray matter (55).

Imaging findings are primarily manifestationsof meningitis. Hydrocephalus often develops as aresult of the acute meningeal exudate and mayalso occur in the course of the infection becauseof meningeal adhesions. Punctate hyperintenseareas representing dilated VR spaces or crypto-coccomas are frequently seen in the basal ganglia,thalami, and midbrain on T2-weighted images(Fig 14) (55,56). On FLAIR images they are also

hyperintense, making it possible to differentiatethem from normal VR spaces. Contrast enhance-ment is uncommon (58). On diffusion-weightedimages, there may be restricted diffusion in someof the lesions due to the high viscosity of theircontents.

MucopolysaccharidosesThe mucopolysaccharidoses are inherited disor-ders of metabolism characterized by enzyme defi-ciency and inability to break down glycosamino-glycan (GAG), which results in the accumulationof toxic intracellular substrate. Clinical featuresare mental and motor retardation, macrocephaly,and musculoskeletal deformities. The urinaryGAG level is elevated. Brain atrophy and abnor-malities of the white matter may be present.

Typically, the VR spaces are dilated by accu-mulated GAG, which results in a cribriform ap-pearance of the white matter, corpus callosum,and basal ganglia on T1-weighted images. Oc-casionally, arachnoid cysts (due to meningealGAG deposition) are seen. On T2-weighted andFLAIR images, the dilated VR spaces are isoin-tense to CSF (Fig 15). However, the surroundingwhite matter may show increased signal intensity,representing gliosis, edema, or de- or dysmyelina-tion (Fig 15). The latter helps in differentiatingthem from normal VR spaces. In addition, MR

Figure 15. Hurler syndrome (mucopolysaccharidosis type I) in a 2-year-old boy with typi-cal external features of this syndrome. A classic Hurler mutation with severe �-l-iduronidasedeficiency was demonstrated. (a) Axial proton-density–weighted image (3835/150) showsdilated VR spaces in both hemispheres (arrowheads). (b) Coronal FLAIR image (6381/100)shows increased signal intensity in the surrounding brain parenchyma (arrows); this findingindicates that the spaces are not normally dilated VR spaces. There is also increased CSFspace frontally.


spectroscopy shows a broad peak around 3.7 ppm(higher than the chemical shift of myoinositol),considered to contain signals from accumulatedGAG (59–61).

Cystic NeoplasmsGiant dilatations of the VR spaces may causemass effect and assume bizarre configurationsthat may be misinterpreted as a cystic brain tu-mor (39–42). However, cystic brain tumors oftenhave solid components, may enhance with con-trast material, mostly show surrounding edema,and have contents that usually are not equal toCSF, as can be seen on FLAIR images (Fig 16).They generally exhibit low signal intensity on dif-fusion-weighted images with corresponding highapparent diffusion coefficient values (62–64).When the lesions in question occur in a character-istic location along the path of a penetratingvessel, follow CSF signal intensity with all se-quences, do not enhance with contrast material,and have normal adjacent brain parenchyma,their appearance is virtually always pathogno-monic of giant VR spaces (Fig 9) (42). Still, dif-ferentiation between giant VR spaces and cysticbrain tumors is sometimes difficult and follow-upMR imaging may be useful.

NeurocysticercosisCysticercosis is the most common parasitic infec-tion of the central nervous system, caused by thelarval stage of the pork tapeworm Taenia solium.Fluid-filled oval cysts with an internal scolex (cys-ticerci) may be located in the brain parenchyma(gray-white matter junction, but also in the basalganglia, cerebellum, and brainstem), subarach-noid space, ventricles, or spinal cord.

MR imaging findings of neurocysticercosis arevariable, depending on the stage of evolution ofthe infection. Lesions can be seen at differentstages in the same patient.

In the initial vesicular stage, a cystic lesion isisointense to CSF with all MR sequences, resem-bling an enlarged VR space. However, a discreteeccentric scolex (hyperintense to CSF) may beseen (Fig 17). In general, the lesions do not en-hance in this stage.

In the colloidal vesicular stage, the cyst ismildly hyperintense to CSF. Mild to marked sur-rounding edema may be seen. A thick cyst wallenhances, including the scolex.

In the granular nodular stage, a thickened re-tracted cyst wall is seen, which may have nodularor ring enhancement. Edema decreases.

In the nodular calcified stage, the lesion isshrunken and completely calcified, appearing hy-pointense with all MR sequences. Gradient-echo

Figure 16. Desmoplastic pilocytic astrocytoma of the right thalamus, cerebral peduncle, and brainstem in a 15-year-old girl. (a, b) Axial proton-density–weighted (2374/100) (a) and FLAIR (6614/100) (b) images show a largemass with solid (arrow) and cystic (arrowheads) components. (c) Axial gadolinium-enhanced T1-weighted image(598/18) shows inhomogeneous enhancement of the solid component (arrow) and rim enhancement of the cysticcomponents (arrowheads). Obstruction of the third ventricle has caused hydrocephalus.


sequences are very useful to demonstrate the cal-cified scolex (65–67).

Arachnoid CystsArachnoid cysts represent intra-arachnoid CSF–containing cysts that do not communicate withthe ventricular system. The most common supra-

tentorial locations for an arachnoid cyst are themiddle cranial fossa, the perisellar cisterns (Fig18), and the subarachnoid space over the con-vexities. On MR images, arachnoid cysts appearas well-defined nonenhancing masses that areisointense to CSF with all sequences, includingdiffusion-weighted imaging (68). They can bedifferentiated from enlarged VR spaces by theirtypical location.

Neuroepithelial CystsNeuroepithelial cysts are rare and benign lesions,mostly asymptomatic. Their etiology is controver-sial but developmental anomalies are likely. Le-sions are spherical to ovoid, measure up to severalcentimeters in size, and may have mass effect.They are lined with thin epithelium and have aCSF-like content. On the basis of pathologicstudies, neuroepithelial cysts are regarded asependymal in origin (69). Neuroepithelial cystsmay involve the lateral ventricles or fourth ven-tricle, with which they do not communicate (in-traventricular cysts). They can also be foundwithin the cerebral hemispheres, thalamus(Fig 19), midbrain, pons (Fig 20), and cerebellar

Figure 17. Parenchymal neurocysticercosisin the vesicular stage in a 17-year-old boy.Axial T1-weighted image (605/18) shows acystic lesion with an eccentrically locatedscolex (arrow), a finding pathognomonic ofneurocysticercosis.

Figure 18. Arachnoid cyst in the perisellarcistern area in a 16-year-old girl. Axial FLAIRimage (7292/120) shows a well-defined,round cyst with CSF-like content in the su-prasellar cistern (arrow).

Figure 19. Neuroepithelial cyst of the thala-mus in a 53-year-old woman with migraineheadaches. Axial FLAIR image (7291/120)shows a multiloculated cyst with CSF-likesignal intensity in the right thalamus (arrow).The adjacent brain parenchyma has normalsignal intensity. Note that this lesion couldalso be an enlarged VR space. A final diagno-sis can be made with certainty only afterpathologic study.


vermis and in the medial temporal lobe in or nearthe choroidal fissure (choroidal fissure cysts) (Fig21) (70,71).

MR imaging confirms the CSF-like signal be-havior of the cyst with all sequences and allowsexclusion of adjacent brain edema, soft-tissuemass, and gliosis in or around the cyst. There isno enhancement with contrast material (70,71).Differentiation between neuroepithelial cysts andenlarged VR spaces can be made with certaintyonly by pathologic study.

ConclusionsVR spaces surround the walls of the vessels asthey course from the subarachnoid space throughthe brain parenchyma. They can be seen on MRimages in all age groups. They may become mark-edly enlarged. Knowledge of their signal intensitycharacteristics and localization helps in differenti-ating them from different pathologic conditions.

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2. Robin C. Recherches sur quelques particularitesde la structure des capillaires de l’encephale.J Physiol Homme Anim 1859;2:537–548.

3. Hutchings M, Weller RO. Anatomical relation-ships of the pia mater to cerebral blood vessels inman. J Neurosurg 1986;65:316–325.

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Figure 20. Neuroepithelial cyst of the cerebral peduncle and pons in a 60-year-old womanwith epilepsy. Axial T1-weighted (30/13) (a) and coronal FLAIR (11,000/140) (b) imagesshow a cyst with CSF-like content in the left cerebral peduncle (arrow). The adjacent tissuehas normal signal intensity. The cyst has a diameter of 15.7 mm as measured on the coronalFLAIR image (b). This benign lesion probably represents a neuroepithelial cyst, although itcould also be a huge VR space.

Figure 21. Choroidal fissure cyst in a1-week-old boy. Axial T1-weighted spec-tral presaturation inversion-recovery image(5094/30) shows a medial temporal lobecyst with CSF-like content arising in thechoroidal fissure (arrow).


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RG Volume 27 • Volume 4 • July-August 2007

Virchow-Robin Spaces at MR Imaging Robert M. Kwee, MD, and Thomas C. Kwee, MD

Page 1072 VR spaces surround the walls of arteries, arterioles, veins, and venules as they course from the subarachnoid space through the brain parenchyma (Fig 1) (1–5). Page 1073 Small VR spaces (<2 mm) appear in all age groups. With advancing age, VR spaces are found with increasing frequency and larger apparent size (>2 mm) (15). Page 1073 Visually, the signal intensities of the VR spaces are identical to those of CSF with all pulse sequences. Page 1075 Dilated VR spaces typically occur in three characteristic locations. Page 1077 Occasionally, VR spaces appear markedly enlarged, cause mass effect, and assume bizarre cystic configurations that may be misinterpreted as other pathologic processes, most often a cystic neoplasm.

RadioGraphics 2007; 27:1071–1086 ● Published online 10.1148/rg.274065722 ● Content Codes:

Kwee and Kwee

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