Expanding Virchow Robin space in the midbrain causing hydrocephalus

Findings

Figure 1: Noncontrast CT brain image demonstrate a cluster of round cyst-like lesions in the right thalamic region with associated dilated 3rd and frontal horns of the lateral ventricles. Note the cyst-like lesions follow CSF attenuation. No evidence of calcification is seen.
Figure 2, Figure 3, Figure 4: Sagittal T1 weighted non-contrast images and axial T2 weighted images demonstrate a cluster of round cyst-like lesions in the midbrain/right thalamic region with associated aqueductal compression and hydrocephalus. The cyst-like lesions follow CSF signal intensity on all pulse sequences.
Figure 5: Coronal FLAIR images demonstrate a cluster of round cyst-like lesions in the midbrain/right thalamic region with associated aqueductal compression and hydrocephalus. The cyst-like lesions follow CSF signal intensity and attenuate completely on FLAIR images.
Figure 6: Coronal T1 weighted postcontrast image demonstrates a cluster of round cyst-like lesions in the midbrain/right thalamic region with associated aqueductal compression and hydrocephalus. The cyst-like lesions follow CSF signal intensity on all pulse sequences. No calcification or enhancement is seen.


Diagnosis: Expanding Virchow Robin space in the midbrain causing hydrocephalus


Pestalozzi and later Virchow in 1851 and Robin in 1859 characterized the perivascular space of Virchow-Robin. This is a pial-lined interstitial fluid – filled structure that accompanies penetrating arteries but does not communicate directly with the subarachnoid space. They affect 25-30% of the pediatric population. Mean age of occurance of enlarged PVSs in adults is mid 4th decade with a slight male preponderance. They occur at all locations and at all ages and are usually discovered incidentally. They occasionally present with non-specific symptoms such as headaches.

Normal PVSs are commonly seen in the basal ganglia region whereas giant or tumefactive PVSs are seen in the midbrain. Other common locations include deep white matter, subinsular cortex and extreme capsule. Less common sites include the thalami, dentate nuclei, corpus callosum and cingulate gyrus. They almost never involve the cortex. PVSs are usually 5mms or less. Occasionally they may enlarge up to several cms and may cause focal mass effect or obstructive hydrocephalus.

Imaging findings include clusters of round /ovoid/linear/punctuate cyst-like lesions which follow CSF density/signal intensity on all pulse sequences. They suppress completely on FLAIR images and show no restricted diffusion on DWI. They neither calcify nor enhance.

Differential diagnosis includes cystic neoplasm, lacunar infarct and infectious (neurocysticercosis, hydatid cyst) or inflammatory cysts. Enlarging PVSs are "DO NOT TOUCH" lesions unless they cause obstructive hydrocephalus where the patient needs to be shunted.