Neuroimaging of Dilated Perivascular Spaces: From Benign and Pathologic Causes to Mimics

Abstract

Perivascular spaces (PVSs), also known as Virchow-Robin spaces, are pial-lined, fluid-filled structures found in characteristic locations throughout the brain. They can become abnormally enlarged or dilated and in rare cases can cause hydrocephalus. Dilated PVSs can pose a diagnostic dilemma for radiologists because of their varied appearance, sometimes mimicking more serious entities such as cystic neoplasms, including dysembryoplastic neuroepithelial tumor and multinodular and vacuolating neuronal tumor, or cystic infections including toxoplasmosis and neurocysticercosis. In addition, various pathologic processes, including cryptococcosis and chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids, can spread into the brain via PVSs, resulting in characteristic magnetic resonance imaging appearances. This review aims to describe the key imaging characteristics of normal and dilated PVSs, as well as cystic mimics and pathologic processes that directly involve PVSs.

Keywords: Neuroradiology; Virchow-Robin spaces; perivascular spaces.

Fig 1.

Characteristic locations of PVSs seen on T2 MR images. Type I: basal ganglia along the course of lenticulostriate arteries (A). Type II: subcortical white matter in the high convexities (B). Type III: midbrain at the pontomesencephalic junction (C).

Fig 2.

Dilated PVSs in the right greater than left basal ganglia. The PVSs are isointense to CSF on T1 (A), T1 postcontrast (B), T2 (C), and FLAIR (D) axial MR images.

Fig 3.

Sample-dilated PVSs in the superior right cerebral hemisphere subcortical white matter. The PVSs are isointense to CSF on T1 (A), T1 postcontrast (B), T2 (C), and FLAIR (D) axial MR images.

Fig 4.

Dilated PVSs in cerebellum. The PVSs are isointense to CSF on T1 (A), T1 postcontrast (B), T2 (C), and FLAIR (D) axial MR images.

Fig 5.

Dilated anterior temporal PVS. The perivascular space is isointense to CSF on T1 (A) and T1 postcontrast (B) MR images, but there is some mild associated T2/FLAIR signal abnormality (C, D), which is atypical for dilated PVS.

Fig 6.

Additional sample-dilated anterior temporal PVSs. The PVSs are isointense to CSF on all sequences and do not exhibit contrast enhancement (C), but there is some mild associated T2/FLAIR signal abnormality (A, B, D, E), which is atypical for dilated a PVS.

Fig 7.

Patient with multiple prominent basal ganglia PVSs. The multiple PVSs are consistent with the described “etat crible” pattern as seen on axial T1 (A), T2 (B), and FLAIR (C) MR images.

Fig 8.

Giant/tumefactive PVSs. Multiple dilated cystic foci seen in the pons and midbrain extending into the right thalamus with CSF signal intensity consistent with a giant/tumefactive PVS as seen on axial and sagittal T1 (A, B), axial T1 postcontrast (C), and axial FLAIR (D) MR images.

Fig 9.

Giant/tumefactive PVSs in the left medial frontal lobe. The PVSs are isointense to CSF on T1 (A), T1-post contrast (B), T2 (C), and FLAIR (D) axial MR images.

Fig 10.

Minimally dilated PVS causing hydrocephalus. Small dilated PVSs in the midbrain (left more than right) and pons seen on axial and sagittal T1 (A, B), axial T2 (C), axial and coronal T1 postcontrast (D, E), and axial FLAIR (F) MR images. The PVSs are isointense to CSF on all sequences. The lateral and third ventricles are dilated, consistent with compensated, obstructive hydrocephalus.

Fig 11.

Left basal ganglia lacunar infarct. Four-millimeter ovoid lesion in the anterior left putamen with CSF signal centrally as seen on axial T1 (A), T2 (B), and FLAIR MR images. There is a surrounding rim of T2/FLAIR hyperintensity (B, C), typical of a chronic lacunar infarct.

Fig 12.

Dysembryoplastic neuroepithelial tumor (DNET) mimicking dilated PVS. There are numerous small- to medium-sized cystic lesions with “bubbly appearance” involving the amygdala, anterior hippocampus, and anterior parahippocampal gyrus are seen on (A) axial T1 (B) and axial T2 images. There is a larger area of surrounding expansile FLAIR signal abnormality (C) extending through the left posterior hippocampus, mid-fusiform gyrus, and temporal periventricular white matter along the inferolateral temporal horn. Faint peripheral enhancement around one of cystic components in the left parahippocampal gyrus on axial and coronal T1 postcontrast images (D, E).

Fig 13.

Multinodular and vacuolating neuronal tumor mimicking prominent PVS. There is a cluster of well-delineated, variable sized FLAIR/T2 hyperintense cysts (C, D) within the left frontal subcortical white matter, without obvious mass effect, or postcontrast enhancement on the T1 precontrast and T1 postcontrast MR images (A, B).

Fig 14.

Intra-axial neuroglial cyst. CSF-filled lesion centered in the left frontal white matter without associated enhancement (A, B) or abnormal T2/FLAIR signal (C, D).

Fig 15.

Case of neurotoxoplasmosis. Axial T1 pre- and postcontrast (A, B), T2 (C), FLAIR (D), and GRE (E) MR images. In the right basal ganglia, there are tiny cystic foci with surrounding intrinsic T1 shortening (A), T2/FLAIR hyperintensity (C, D), abnormal enhancement (B), and mild susceptibility (E).

Fig 16.

CNS cryptococcosis directly involving the PVS in a patient with human immunodeficiency virus. There is enhancement along the PVSs in the right greater than left basal ganglia seen on T1 postcontrast axial (A) and sagittal images (B).

Fig 17.

Sample case of intravascular neurosarcoidosis involving the PVSs. Axial T1 (A), axial and coronal T1 postcontrast (B, C), and axial T2/FLAIR images (D, E). There are innumerable punctate T2/FLAIR hyperintense enhancing nodules in the centrum semiovale, corona radiata, basal ganglia, brainstem, and visualized upper cervical spine bilaterally, which largely appear near the deep penetrating vessels along PVSs.

Fig 18.

Sample case of intravascular CNS lymphoma involving PVSs, seen on axial T1 (A), axial and coronal T1 postcontrast (B, C), and axial T2/FLAIR images (D, E). There is linear, predominantly perivascular enhancement extending from the right thalamus and basal ganglia into the corona radiata, frontal, parietal, and temporal lobes with associated T2/FLAIR signal abnormality.

Fig 19.

Chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS) involving the PVSs. Diffuse leptomeningeal enhancement in the midbrain, pons, and medulla is seen on T1 postcontrast images (B, C) with foci of T2/FLAIR prolongation (A).

Fig 20.

Sample case of mucopolysaccharidosis involving the PVSs reproduced from Mohan et al with permission. There are multiple bilateral cystic lesions (isointense to CSF on T1; A) in the subcortical white matter with associated surrounding T2/FLAIR hyperintensity (B, C).