Abstract
Phase contrast MRI (pcMRI) has been used to investigate flow pulsatility in cerebral arteries, larger cerebral veins, and the cerebrospinal fluid (CSF). Such measurements of intracranial pulsatility and compliance are beginning to inform understanding of the pathophysiology of conditions including normal pressure hydrocephalus, multiple sclerosis, and dementias. We demonstrate the presence of flow pulsatility in small cerebral cortical veins, for the first time using pcMRI at 7 T, with the aim of improving our understanding of the hemodynamics of this little-studied vascular compartment. A method for establishing where venous flow is pulsatile is introduced, revealing significant pulsatility in 116 out of 146 veins, across eight healthy participants, assessed in parietal and frontal regions. Distributions of pulsatility index (PI) and pulse waveform delay were characterized, indicating a small, but statistically significant (p < 0.05), delay of 59 ± 41 ms in cortical veins with respect to the superior sagittal sinus, but no differences between veins draining different arterial supply territories. Measurements of pulsatility in smaller cortical veins, a hitherto unstudied compartment closer to the capillary bed, could lead to a better understanding of intracranial compliance and cerebrovascular (patho)physiology.
Highlights
Pulsatility in cerebral veins is thought to be a passive process, a response to intracranial pressure changes arising due to arterial pressure pulsatility through the cardiac cycle (Greitz et al, 1992)
Reduced intracranial compliance has been observed in both normal pressure hydrocephalus and multiple sclerosis patients (Bateman et al, 2016)
3D (0.6 mm isotropic, 60 slices) T2∗weighted FLASH (T2∗w) and time of flight (TOF) images were acquired with the same center and orientation as the Phase contrast MRI (pcMRI) slice, for use in distinguishing veins from arteries
Summary
Pulsatility in cerebral veins is thought to be a passive process, a response to intracranial pressure changes arising due to arterial pressure pulsatility through the cardiac cycle (Greitz et al, 1992). This normal process may be altered in some pathologies, such as normal pressure hydrocephalus, dementias, including Alzheimer’s disease, and multiple sclerosis (Bateman, 2000; Greitz, 2004; Mitchell, 2008; Henry-Feugeas and Koskas, 2012; Beggs, 2013; Bateman et al, 2016; Rivera-Rivera et al, 2017). Intracranial compliance in this context refers to the capacity of the intracranial tissue to dissipate the arterial pulse wave, predominantly through CSF movements and in the cerebral vasculature
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