http://www.pagepressjournals.org/index. ... /5398/4749
FACTORS INFLUENCING AQUEDUCTAL CEREBROSPINAL
FLUID MOTION IN HEALTHY INDIVIDUALS
C.B. Beggs,1 S.J. Shepherd,1 P. Cecconi,2 M.M. Lagana2
1Medical Biophysics Laboratory, University of Bradford,
Bradford, UK; 2Fondazione Don Carlo Gnocchi ONLUS, IRCCS
S. Maria Nascente, Milan, Italy
Background: Increased cerebrospinal fluid (CSF) pulsatility in
Aqueduct of Sylvius (AoS) has been associated with various neuropathologies.
However, the mechanisms driving the aqueductal CSF
(aCSF) pulse are poorly understood.
Objectives: To gain a deeper understanding the factors that influence
aCSF motion.
Methods: Twelve healthy young adults (aged 20 to 45 years) with no
known neurological disease were investigated using phase contrast
MRI. aCSF flow data, together with arterial, venous and CSF flow
data at the C2/C3 level, were collected for 32 points throughout the
Non-commercial use only
Invited Abstracts
[page 6] [Veins and Lymphatics 2015; 4:s1]
cardiac cycle (CC).
Intracranial fluid volumetric changes were computed
from these data to identify the factors that directly influence the
aCSF pulse.
Results: The aggregated flow rate signals for all subjects are shown
in Figure 1. Mean cervical CSF and aCSF stroke volumes were
801.8 (SD=501.2) and 17.6 (SD=19.3) μL/beat, respectively. Peak
negative aCSF flow (towards the fourth ventricle) occurred 14.1%
of CC after the arterial peak, while the positive aCSF peak flow
occurred after 77.9% of CC (Figure 1). The intracranial venous volume
increased by 626.6 μL over the CC, peaking at 64.0% of CC
after the arterial peak, while the corresponding change in aCSF volume
was 24.0 μL, peaking 71.3% of CC. There was a very strong
positive correlation between the intracranial venous blood volume
and the aCSF volume (r=0.966, P<0.001), as illustrated in Figure 2,
which shows the change in aCSF volume scaled to match the
change in intracranial venous volume.
Figure 1. Aggregated fluid flow rates.
Figure 2. Relative intracranial fluid volumes.
Conclusions: The motion of the CSF in the AoS appears to be strongly
influenced by changes in the intracranial venous volume. As the
intracranial CSF increases in volume during diastole it causes blood
to accumulate in the cortical veins.1,2 As the volume of the cortical
veins increases, so the volume of the sub-arachnoid space reduces,
with the result that CSF is forced up the AoS towards the lateral ventricles.
Only when the stored venous blood is voided from the cranium,
does CSF flow in the other direction occur in the AoS.
Disclosures: The authors have nothing to disclose.
References
1. Luce JM, Huseby JS, Kirk W, Butler J. A Starling resistor regulates cerebral
venous outflow in dogs. J Appl Physiol Respir Environ Exerc
Physiol 1982;53:1496-503.
2. Vignes JR, Dagain A, Guérin J, Liguoro D. A hypothesis of cerebral
venous system regulation based on a study of the junction between the
cortical bridging veins and the superior sagittal sinus. Laboratory investigation.
J Neurosurg 2007;107:1205-10.
Dr. Beggs abstract, too, from ISNVD.
It is good that he is finding things such as CSF pulsatility that are measureable. I feel like his approach is careful and consistent and that he is building the evidence. It was a good day for us when Dr. Beggs took an interest in CCSVI.
