The present work investigated the use of 2D cine PC-MRI as a means of assessment of ICC/ICP dynamic in young healthy subjects in a situation of elevated IAP/ITP modeled by VM. In this study, we demonstrate that elevated IAP/ITP causes ICC/ICP changes during VM, which can be revealed using 2D cine PC-MRI. Larger CSAIJV indicated an elevation of back pressure of IJV. Compared with baseline, smaller AVD indicates a decreased ICC or increased ICP, while larger TTP indicates a decreased ICC or increased ICP. These indices have a potential use in non-invasive ICC/ICP monitoring in patients with elevated IAP/ITP.
Interpretation the results
It had been universally recognized that the VM is a model of IAP and ITP elevation. In the present study, the dilation of IJV is and indicator of CVP elevation, which is caused by the increased IAP and ITP. Although most of the indices changed during VM, the PI was the candidate for measurement ICP in most previous studies. Despite AVD and TTP were reported only in very few studies, these two indices played a powerful role reflecting the VM induced ICC/ICP changes in the present study. Here, the interpretation of the changes of these indices will be discussed.
Interpretation of the decreased PI
PI describes the pulsatility of blood flow waveform. Evidence suggests that either increased or decreased PI are harmful to the brain. During straining (VM phase Ⅱ), central venous pressure (CVP) increased, cardiac output (CO) decreased and blood flow of middle cerebral artery dropped significantly. Our result demonstrate the Fmax dropped more than Fmean, while the Fmin remained constant, so the PI decreased. Dropped Fmean indicated dropped cerebral perfusion pressure (CPP), that is consistent with previous study. However, although PI is commonly considered an indicator of CPP as opposed to ICP, there exists a complex relationship between PI and multiple hemodynamic variables including CPP, arterial pressure pulse amplitude, cerebrovascular resistance (CVR), arterial compliance, and heart rate. Under normal conditions, PI is predicted to increase linearly with ICP[23, 24]. While in a recent study, ICP estimated using PI method (ICP=a×PI + b) of five in eight individuals were reported a trend of decrement during VM state. Their results are consistent with the present study. A recent study also reported that increased ICP attenuates the pulsatility of cerebral venous outflow.
Theoretically, venous outflow is a passive component, the intracranial pulse wave is predominately determined by the arterial wave. Under conditions of the cardiac insufficiency and CVP increased, which is prevalent in critical ill patient and also in VM, venous pressure influences the intracranial wave more[27, 28]. During VM, the increased CVP impedes venous outflow, which in turn lead to an increment of cerebral blood volume and a “stiffer” brain. both the “stiffer” brain and the insufficiency cardiac function led to the CBF decrement and in particular the maximum blood flow. Thus, the pulsating component of the ICA and the IJV decreased.
Interpretation of the shortened AVD
Monroe-Kellie doctrine states that, the volumetric interplay between intracranial components (arterial blood, brain, venous blood and CSF) maintains ICP homeostasis. In a cardiac circle, heart contraction induces a pulsatile artery blood entering the closed cranial cavity, which causes brain remolding and a transient perturbation of ICP homeostasis[30, 31]. The arterial expansion must be compensated by venting CSF into the spinal canal and venous outflow[1, 32]. A minimal time delay between arterial inflow and venous outflow from the cranial cavity has constantly been observed in previous studies[32-36],which was measured as AVD.
Pulse wave velocity (PWV) or the time the pulse wave takes to travel the length of the artery was used to reflecting the compliance of the arterial tree [38, 39]. PWV has been considered the gold standard for measuring arterial stiffness[38, 40, 41], higher PWV was independently associated with greater target organ damage. Similarly, ICC can be estimated by measuring the PWV that traverses the intracranial space. In a certain distance, AVD, the time the pulse wave takes to travel from the arterial to the venous side of the cerebral circulation, is the reciprocal of PWV. AVD gauged from ICA to IJV at the skull base is a reflection of the compliance of the intracranial space, which includes arteries, subarachnoid space, brain parenchyma and veins. Smaller AVD have been reported in patients with normal pressure hydrocephalus (NPH), late-onset idiopathic aqueductal stenosis (LIAS) and Multiple sclerosis (MS) . What’s more, larger AVD have been reported in patients with NPH after a CSF drainage than pre-drainage.
There were few studies devoted to AVD measuring can be referred. In a study, AVD measured at the level of intervertebral disc of cervical-2 to cervical-3 using the same method, a smaller AVD (72±24 ms, representing 8±2% of the CC duration vs. 106 ) were reported in 18 (9 female, 9female) healthy young volunteers. In another study, a larger AVD (17%±7% of the CC) in 19 (3 female, 16 female) healthy young volunteers were reported. This difference might be contributed to the different temporal resolution we used (32 frames per CC vs. 60 frames per CC we used). More accurate measure was expected by adopting a higher temporal resolution. In several other studies, AVD was measured as the time delay between the center of arterial pulse and the center of venous pulse, and the AVD was measured at much higher plane than the present study, so the results can’t be compared directly[37, 43].
Under the VM state, forced expiration against a closed glottis increased IAP and ITP, damping IJV outflow and venting CSF upwards motion into the cranial cavity , in turn, leading to an immediate stiffening of the brain and a rise of ICP (or a decrease of ICC). Shear waves propagate more quickly through a stiffer material. Smaller AVD during VM than NB reflects the ICC decline during VM.
Interpretation of the prolonged TTP
A recent study using invasive monitoring methods simultaneously recorded ICP and CBF waveform in non-human primate, reported that a higher ICP led to a broadening and rightward shift of the ICP and CBF pulse wave, although the strength of this effect differed between subjects. In patients with NPH underwent CSF drainage, the arterial pulse became thinner, and peaked earlier than pre-drainage. These results are consistent with the prolonged TTP during VM reported in our work. The TTP reflects the resistance of blood flow. Elevated IAP/ITP caused a decreased ICC and increased ICP, and in turn, the increment resistance of arterial perfusion, this has been reported in both animal model of IAH  and in man during VM. In the present study, the smaller CSAICA and decreased Fmean also implied a restrictive effect of sympathetic activity during VM, which also led to an increase of vascular resistance.