Cysts that Deceive: Tumefactive Virchow–Robin Spaces

Abstract

Tumefactive Virchow–Robin spaces (TVRS) are rare, enlarged perivascular spaces that can mimic neoplastic, vascular, or infectious brain lesions on imaging. These spaces are commonly found along the paths of penetrating arteries and typically measure less than 5 mm. However, when enlarged, they may produce a mass effect, cause hydrocephalus, or mimic cystic tumors. We report a case of a 48-year-old female presenting with mild, recurrent headaches whose magnetic resonance imaging (MRI) revealed multiple cystic lesions in the right frontoparietal lobe and anterior parafalcine region. The lesions followed cerebrospinal fluid (CSF) intensity on all sequences, without enhancement or diffusion restriction. No surrounding edema was noted. Thin-section susceptibility-weighted imaging (SWI) images were reviewed and showed no venous compression or vascular paucity. The imaging appearance and location were characteristic of TVRS. Recognizing this entity is crucial to prevent unnecessary biopsies. Differentiation from other cystic lesions—such as cystic neoplasms, cryptococcal infections, neurocysticercosis, or mucopolysaccharidosis—is essential and relies on specific imaging features. To our knowledge, this is the first reported case of tumefactive Virchow–Robin spaces causing mass effect on the ventricle along with overlying regional parenchymal atrophy, a combination not previously documented. This case highlights the importance of familiarity with the imaging spectrum of TVRS and its integration with radiology to make an accurate diagnosis.

Keywords

tumefactive Virchow–Robin spaces - cystic brain lesions - infections

Introduction

Virchow–Robin spaces (VRS) are pial-lined, interstitial, fluid-filled spaces that accompany penetrating arteries as they enter the brain parenchyma. Typically measuring less than 2 mm, these are incidental findings on brain imaging.[1] When abnormally dilated, these spaces are termed tumefactive Virchow–Robin spaces (TVRS); they can mimic lesions and may produce a mass effect or hydrocephalus.[2] Accurate identification is essential to avoid misdiagnosis and unnecessary intervention. We report a case of TVRS in a middle-aged female, emphasizing the importance of recognizing this rare entity and differentiating it from cystic brain lesions, supported by imaging characteristics and clinical correlation.

Case Report

A 48-year-old female presented with non-localized, mild headache over 6 months, without associated neurological deficits, fever, or seizures. There was no history of trauma, infection, or chronic illness. Routine laboratory investigations were within normal limits. Magnetic resonance imaging (MRI) of the brain showed multiple, well-defined, non-enhancing cystic lesions in the right frontoparietal lobe and left parafalcine region. These lesions appeared hypointense on T1-weighted images, hyperintense on T2-weighted and fluid-attenuated inversion recovery (FLAIR) sequences, and followed cerebrospinal fluid (CSF) signal intensity across all sequences. There was minimal mass effect on the right lateral ventricle. The cystic lesions were more prominent on the right side compared with the left. Mild right lobar atrophy is noted. No surrounding edema, contrast enhancement, or diffusion restriction was noted. Thin-section SWI images showed no venous compression or vascular paucity ([Figs. 1] [2] [3] [4]).

Fig. 1 Collated axial T2-weighted imaging (T2WI), axial diffusion-weighted imaging (DWI), the apparent diffusion coefficient (ADC), and postcontrast T1-weighted imaging are shown. This axial T2WI confirms multiple sharply circumscribed, bright (hyperintense), cerebrospinal fluid (CSF)-signal cystic lesions within the white matter. Some lesions demonstrate a “cluster” configuration, aligning along penetrating vessels. The signal is identical to CSF on T2 and shows no surrounding edema. The second image panel (DWI, b = 1,000 s/mm²) and the third panel (ADC map) demonstrate numerous well-defined, round lesions in the subcortical and deep white matter. These lesions are hyperintense on DWI with corresponding elevated signal on the ADC, indicating facilitated diffusion—consistent with cerebrospinal fluid-like fluid. The fourth image, axial postcontrast T1-weighted imaging does not reveal significant intra or perilesional enhancement.

Fig. 2 Collated sagittal T2-weighted imaging (T2WI) with follow-up T2 is shown. Sagittal T2WI provides excellent anatomic orientation, delineating linear “tubular” CSF-signal spaces along the course of perforating medullary arteries. These tumefactive Virchow–Robin spaces appear well-marginated, without contrast enhancement, mass effect, or perilesional hyperintensity. The findings are grossly unchanged compared with imaging done 2 years earlier.

Fig. 3 Axial fluid-attenuated inversion recovery (FLAIR). Coronal FLAIR image demonstrates multiple signal-void or low-signal lesions following cerebrospinal fluid intensity, dispersed within the centrum semiovale and peritrigonal white matter, indicating complete suppression. There is no surrounding T2/FLAIR hyperintense signal, thereby excluding demyelinating or inflammatory edema.

Fig. 4 Susceptibility-weighted imaging (SWI). Axial SWI demonstrates that the lesions have no signs of microhemorrhage, hemosiderin, or other susceptibility artifacts.

The findings were suggestive of TVRS. Given the typical imaging features and the absence of clinical signs of infection, malignancy, or hydrocephalus, a conservative management approach with CSF and regular follow-up was adopted. The patient remained asymptomatic over a 2-year follow-up period. Repeat MRI at that time showed no significant change in the size, number, or signal characteristics of the lesions, further supporting the benign nature of the findings ([Fig. 2]).

Discussion

VRS, first described by Rudolf Virchow and Charles Robin, are extensions of the subarachnoid space along penetrating arteries.[3] While they are commonly incidental and tiny, enlargement to a tumefactive form is rare and may present diagnostic challenges.[4] Enlarged VRS may occur in the basal ganglia, midbrain, and centrum semiovale. On MRI, they follow CSF signal intensity on all sequences, show no post-contrast enhancement, no restricted diffusion, and lack perilesional edema.[5] In contrast, differential diagnoses include cystic gliomas, cryptococcal infections, neurocysticercosis, and mucopolysaccharidosis-associated perivascular spaces, which often show additional findings, such as, enhancement, restricted diffusion, or clinical indicators.[6] TVRS are considered benign and require no intervention unless they are symptomatic due to hydrocephalus or mass effect.[7] In this case, the absence of neurological deficits justified conservative management. Atrophy enlarges the Virchow–Robin (VR) and ventricular spaces passively due to neuron and axon loss from aging, multiple sclerosis, dementia, vascular disease, or injury. Mass effect occurs when the VR spaces (or subdural collections) enlarge enough to compress nearby structures. Notably, this is the first reported case combining tumefactive Virchow–Robin spaces causing both ventricular mass effect and overlying parenchymal atrophy, a dual presentation not previously documented ([Fig. 5]), [Table 1]. The minimal perilesional FLAIR hyperintensity likely represents gliotic changes secondary to chronic parenchymal compression. SWI sequences showed no evidence of venous paucity or compression; however, early vascular etiology cannot be excluded.

Fig. 5 Illustration demonstrating the dual potential effects of prominent Virchow–Robin spaces. Asymmetrical cystic parenchymal changes are seen within the brain. On one side, marked volume loss is seen, consistent with cerebral atrophy, characterized by widened sulci and ex-vacuo dilatation of the ipsilateral ventricle. On the opposite side, the enlarged cystic spaces create local mass effect, with displacement of adjacent parenchyma and effacement of sulci, reflecting the spectrum of possible clinical impacts in patients.

Table 1 Imaging features of Virchow–Robin spaces

Feature	Tumefactive Virchow–Robin spaces
Location	Basal ganglia, midbrain, centrum semiovale
Signal (T1/T2/FLAIR)	Follows CSF on all sequences
Diffusion restriction	Absent
Contrast enhancement	None
Perilesional edema	None
Susceptibility (GRE/SWI)	No hemorrhage or calcification
Multiplicity	Frequently multiple, bilateral
Mass effect	Minimal or none

Abbreviations: FLAIR, fluid-attenuated inversion recovery; GRE, gradient echo; SWI, Susceptibility-weighted imaging.

Conclusion

TVRS are rare but benign entities that can mimic pathological brain lesions. Recognition of characteristic MRI findings, coupled with clinical correlation, is vital to avoid misdiagnosis and unwarranted invasive procedures. This case reinforces the importance of considering TVRS in the differential diagnosis of cystic brain lesions. This case highlights an uncommon presentation of TVRS, with concurrent ventricular compression and overlying regional parenchymal atrophy, thereby broadening the recognized imaging spectrum of this benign entity.

Conflict of Interest

None declared.

Acknowledgments

The author would like to acknowledge colleagues from the Department of Imaging, Jaslok Hospital and Research Centre, Mumbai, for their assistance with image acquisition and technical support. No additional contributions meeting authorship criteria were made.

Note

This manuscript was not presented.

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Publication History

Article published online:
10 February 2026