Giuseppe Barisano1, Samantha J. Ma2, Danny JJ. Wang2, Yonggang Shi2, Arthur Toga2, and Meng Law1,2
1Radiology, University of Southern California, Los Angeles, CA, United States, 2Stevens Institute of Neuroimaging and Informatics, University of Southern California, Los Angeles, CA, United States
Synopsis
The CSF microcirculation in
the brain is not well understood and the role of the perivascular spaces in the
clearance of metabolic waste products (including amyloid beta and tau) is still
debated. We hypothesize that the increased permeability of the BBB and the
resulting passage of blood products into the perivascular spaces may be
responsible for the obstruction of CSF-ISF flow. Using a novel T1-weighted 3D
Turbo spin-echo with variable flip angles at 3T and 7T, we are able to
demonstrate leakage of fibrin from the small lenticulostriate arteries into the
perivascular spaces.
Introduction
The CSF microcirculation in
the brain is not well understood and while there is controversy surrounding the
presence or lack of conventional lymphatics in the brain, high resolution and
ultrahigh field MRI (7T and above) is allowing visualization of the perivascular
spaces (PVS) and small lenticulostriate arteries (LSA) in humans. This
interaction between the LSAs and the PVSs may provide some insight into the passage
of metabolic waste products from the blood through the blood brain barrier
(BBB) and into the PVSs. The role of the PVSs in this clearance of metabolic
wastes is not known1,2. Pre-clinical
and some human studies have suggested the drainage of CSF and clearance of
metabolic wastes (including amyloid beta and tau) occurring via PVSs and also
the intramural peri-arterial drainage (IPAD) pathways3–5. We
hypothesize that with aging and brain inflammation, the leakiness and increased
permeability of the BBB allows for the passage of metabolic waste products (including
fibrin and other blood products) into the PVS. This can obstruct the CSF-ISF
(interstitial fluid) flow and PVSs, causing a “fibrin globe” resulting in dilatation
of the perivascular spaces6,7.Methods
We studied 15 subjects with
vascular risk factors from the Los Angeles Latino Eye Study (LALES) cohort. Young
and old healthy subjects were also used as controls. MRI scans were performed
on Siemens Prisma 3T and some subjects
also on the Siemens Terra 7T MRI scanner at the Center for Image
Acquisition, Institute of Neuroimaging and Informatics at University of
Southern California. We imaged the lenticulostriate arteries using a T1 high
resolution (isotropic 0.5mm) black blood TSE variable flip angle (VFA) sequence
and automated 3D vessel reconstruction algorithms8. 3D TSE T2 SPACE sequence was
used for the characterization of PVS surrounding the LSAs. 3D TOF MRA and SWI
were also performed. We analyzed the relationship between the 3D TOF MRA, T1
VFA TSE black blood, T2 TSE SPACE and the SWI sequence.Results and Discussion
In 4 of the subjects, we
found a globe like structure on the T1 VFA BB sequence. These “globes” are felt
to represent one of 3 pathologies.
- The first is a fibrin globe, thought to be due to the leakage of fibrin,
fibrinogen and other blood products through the BBB into the perivascular
spaces. This causes enlargement of the PVS seen in Figure 1 but is negative
on the TOF MRA for an aneurysm.
- The second is a true lenticulostriate
microaneurysm, so called Charcot Bouchard aneurysms, related to hypertension
and other vascular risk factors, which should then be visible on the TOF MRA.
- The third would be a pseudo-aneurysm with blood products in the media of
the LSA due to vessel wall lipohyalinosis.
Conclusions
Imaging of the cerebral microvasculature, CSF-ISF microcirculation and
perivascular spaces may provide insight into the clearance of metabolic waste
products such as amyloid beta in the brain. Using a novel VFA T1 BB sequence at
3T and 7T, we are able to demonstrate leakage of fibrin from the small LSAs
into the PVSs. This may be the mechanism leading to obstruction of CSF
clearance and dilatation of PVSs, very often described in neurodegenerative
diseases such as Alzheimer’s Disease9.Acknowledgements
This study was supported by the US National Institutes of Health grant UH2NS100614 and the National Institute of Biomedical Imaging and Bioengineering of the National Institutes of Health Award Number P41EB015922. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. #ML partially funded by NIH/NIA P50-AG05142, NIH P01AG052350, NIH P01AD06572.
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