Prachi Mehndiratta, MD

Charidimou A, Hong YT, Jäger HR, Fox Z, Aigbirhio FI, Fryer TD, et al.White Matter Perivascular Spaces on Magnetic Resonance Imaging: Marker of Cerebrovascular Amyloid Burden? Stroke. 2015

White matter perivascular spaces are increasingly being recognized as markers of small vessel disease such as cerebral amyloid angiopathy (CAA). In recent times grading systems have been set up to quantify the number of perivascular spaces in the basal ganglia and centrum semiovale. The authors of this pilot study attempted to examine the association between the burden of overall centrum semiovale perivascular spaces (CSO-PVS) and deposition of amyloid as quantified by a PET scan. 

Non demented patients with intracerebral hemorrhage, graded as having probable cerebral amyloid angiopathy were included. Additionally healthy subjects with no cognitive complaints and normal mini mental exams were also enrolled. All subjects underwent a Pittsburgh Compound B (PiB) PET scan as well as a 3 Tesla MRI scan. MRI scans were reviewed independently and in a blinded fashion. Linear regression was used to quantify the relationship between the degree of amyloid deposition in the cortex and CSO-PVS grade.

A total of 31 patients (11 with amyloid angiopathy and 20 healthy subjects) were recruited. PiB retention was higher in patients with CAA vs. healthy patients (p = 0.0082). There was a linear increase in PiB distribution volume ratio (DVR) as the CSO-PCS score increased across the whole group however this association was not seen in patients with probable CAA only. PiB retention increased with age and was negatively associated with brain volume. There was no correlation observed between brain volume and CSO-PVS grade.

This study adds credence to the drainage hypothesis and suggests that impaired drainage by progressive amyloid deposition may lead to retrograde dilatation of the perivascular spaces however is plagued by several limitations – a) the number of subjects is very small, b) other small vessel disease risk factors are not accounted for and c) although the patients are clinically non demented/ healthy, they still may have pathological evidence for amyloid deposition/ Alzheimer’s disease pathology. The authors acknowledge these limitations and suggest that these are preliminary results. I agree with that assessment, and that this study needs replication in a larger cohort.