Ian D Driver1, Fabrizio Fasano2, and Richard G Wise1
1CUBRIC, School of Psychology, Cardiff University, Cardiff, United Kingdom, 2Siemens Healthcare Ltd, Frimley, Caberley, United Kingdom
Synopsis
We
report the first measurement of venous flow pulsatility in cerebral veins with
sub-millimeter diameters using phase contrast MRI. This work exploits the
increased signal and finer spatial resolution available at 7 Tesla, over lower
field strengths. We suggest that the observed venous pulsatility is a passive
response to intracranial pressure changes caused by arterial pulsatility. These
measurements may be applied to pathology in which there is compromised venous
flow, extending such investigations to the smaller cerebral veins and offering
a better understanding of the temporal dynamics of cerebral venous flow.
Introduction
Pulsatility
in cerebral veins is thought to be a passive process, reacting to intracranial pressure
changes arising due to arterial pulsatility. This normal process may be
compromised in some pathologies, such as normal pressure hydrocephalus1.
Non-invasive measurements of venous pulsatility have the potential to provide
insight to such pathologies. Phase contrast MRI (pcMRI) is a powerful tool for
measuring blood velocity in cerebral blood vessels and venous pulsatility has
been observed previously2. However, so far, these studies of venous
pulsatility have been limited to large cerebral veins, such as the superior
sagittal sinus and jugular veins. Applying these measurements to smaller
cortical veins would allow subtler changes to be studied and a better
understanding to be gained of the functional consequences of venous pulsatility
at the tissue level. Our study makes use of the increased signal to image at finer
spatial resolution at 7 Tesla. We assess whether venous pulsatility can be
resolved in veins with sub-millimeter diameters.Methods
Image
acquisition: Six subjects (4 female/2 male; 26-38
years) participated in this study. Measurements were performed on a whole-body
7T research MR-system (Siemens Healthcare GmbH, Erlangen, Germany), with a
32-channel head receive/volume transmit coil. A T2*-weighted 3D
FLASH image (1mm isotropic, TR/TE = 23/11ms) was acquired for slice planning
and identification of cerebral veins (hypointense) and arteries (hyperintense).
Two sets of cardiac-gated pcMRI data (venc = 50cm/s through slice,
single slice, 3 averages per cardiac phase) were acquired over an acquisition
window 100ms shorter than the subject’s average cardiac period, approximately
40 phases of the cardiac cycle. Prospective cardiac gating was performed using
a photoplethysmogram placed on the subject’s finger. The first
pcMRI was positioned perpendicular to the superior sagittal sinus (1x1x40mm;
256mm FOV; TR/TE = 19.1/5ms). The second pcMRI was acquired at finer voxel
resolution (0.6x0.6x5mm; 192mm FOV; TR/TE = 19.3/5ms), positioned perpendicular
to a small medial-posterior cortical vein, draining into the superior sagittal
sinus, selected for being straight over the extent of the image volume.
Analysis: Cerebral blood vessels were segmented using the
magnitude of the pcMRI and their diameter was estimated manually. Each vessel
was categorized as superior sagittal sinus, vein or artery based on the T2*-weighted FLASH
image. Cardiac cycle resolved velocity time-courses were calculated
from the phase of the pcMRI.
Results
Cardiac
cycle time-locked pulsatility was observed in a range of veins, including at
least one sub-millimeter diameter vein in each subject. The cardiac cycle time-course
for an example 0.6 mm diameter vein is shown in Figure 1, as well as example images. Figure 2 shows the shape of the pulsatile time-course, comparing
small veins, the superior sagittal sinus and small arteries. The small vein
time-course is similar to that of the small arteries, whereas the sagittal
sinus time-course is delayed by approximately 50ms (p<0.05) with respect to
small arteries.Discussion
The
similar pulsatile time-courses between small veins and small arteries are
consistent with a passive mechanism causing venous pulsatility, due to venous
volumes decreasing in response to arterial volume increase and transient rise
in intracranial pressure. A delayed sagittal sinus time-course is consistent
with waves of pulsatile flow propagating downstream from the pulsatile small
veins. We used a simple method for segmenting blood vessels, based on
thresholding the magnitude of the pcMRI. We chose not to use more sophisticated
methods, which use the characteristic signal of pulsatility for segmentation3,
since these signals were the objective of our study and we did not want to bias
our results. Future work will incorporate these methods into our measurement.
Our measurements feature variability in delay across subjects due to the
anatomical distance between the finger photoplethysmogram and
the cerebral vasculature. Future work will assess whether using an
electrocardiogram for cardiac gating would provide a less variable delay than
the photoplethysmogram. Further, our technique may benefit from the increased
coverage available with a 3D acquisition, as demonstrated recently by Schuchardt
et al.4.Conclusion
We
report the first MRI-based observations of pulsatility in sub-millimeter
diameter cerebral veins. This approach makes use of the increased signal and
finer spatial resolution available at 7 Tesla.Acknowledgements
No acknowledgement found.References
1. Greitz D. Radiological assessment of
hydrocephalus: new theories and implications for therapy. Neurosurg Rev.
2004;27:145–65.
2. Stoquart-ElSankari S, Lehmann P, Villette
A, et al. A phase-contrast MRI study of
physiologic cerebral venous flow. J Cereb Blood Flow Metab. 2009;29:1208-1215.
3. Alperin N and Lee S. PUBS:
Pulsatility-based segmentation of lumens conducting non-steady flow. Magn Reson
Med. 2003;49(5):934-944.
4. Schuchardt
F, Schroeder L, Anastasopoulos C, et al.
In vivo analysis of physiological 3D blood flow of cerebral veins. Eur Radiol. 2015;25:2371–2380.