Fig 6 - uploaded by Licia Romagnoli
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CSF flow rate along the fourth ventricle (solid line) and the spinal SAS (dotted line) (color figure online)
Source publication
In this paper, we introduce a one-dimensional model for analyzing the cerebrospinal fluid dynamics within the fourth ventricle and the spinal subarachnoid space (SSAS). The model has been derived starting from an original model of Linninger et al. and from the detailed mathematical analysis of two different reformulations. We show the steps of the...
Contexts in source publication
Context 1
... of 2.5 · 10 −4 minutes, corresponding to 0.015 seconds. After time t = 1.5 the system evolves to reach its periodic physiological configuration which is reached at about t = 25 minutes. The numerical results presented in this section refer to the first 3 heartbeats after t = 25. A periodic sine wave has been imposed at z = 0 as pressure input. In Fig. 6 it is possible to observe that flow rate profile in fourth ventricle reaches values significantly greater than the one in spinal SAS. This is due to the fact that, as mentioned before, the CSF dynamics is not affected by the forcing function a(t) in SSAS. This behaviour is inherited by the CSF pressure (Fig. 7) in the intracranial ...
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... between the inner ventricles and the subarachnoid space is the driving force of the cerebral aqueduct flow rate. Due to the different forms of the ventricular and subarachnoidal pressures, the transmural pressure difference assumes both positive and negative values during an heartbeat leading to temporary inversion of the flow as illustrated in Fig. ...
Context 3
... of 2.5 · 10 −4 minutes, corresponding to 0.015 seconds. After time t = 1.5 the system evolves to reach its periodic physiological configuration which is reached at about t = 25 minutes. The numerical results presented in this section refer to the first 3 heartbeats after t = 25. A periodic sine wave has been imposed at z = 0 as pressure input. In Fig. 6 it is possible to observe that flow rate profile in fourth ventricle reaches values significantly greater than the one in spinal SAS. This is due to the fact that, as mentioned before, the CSF dynamics is not affected by the forcing function a(t) in SSAS. This behaviour is inherited by the CSF pressure (Fig. 7) in the intracranial ...
Context 4
... between the inner ventricles and the subarachnoid space is the driving force of the cerebral aqueduct flow rate. Due to the different forms of the ventricular and subarachnoidal pressures, the transmural pressure difference assumes both positive and negative values during an heartbeat leading to temporary inversion of the flow as illustrated in Fig. ...
Citations
... Within the SAS, the flow of CSF is not static nor steady but is subject to a complex pulsating motion that is in sync with the heartbeat (Donatelli D & Romagnoli L., 2020). Further complicating the flow of CSF is its movement within the spinal cord SAS, specifically below the level of S2 where CSF encounters spinal cord and dorsal and ventral nerve rootlets. ...
Beyond its neuroprotective role, CSF functions to rid the brain of toxic waste products through glymphatic clearance. Disturbances in the circulation of CSF and glymphatic exchange are common among those experiencing HCP syndrome, which often results from SAH. Normally, the secretion of CSF follows a two-step process, including filtration of plasma followed by the introduction of ions, bicarbonate, and water. Arachnoid granulations are the main site of CSF absorption, although there are other influencing factors that affect this process. The pathway through which CSF is through to flow is from its site of secretion, at the choroid plexus, to its site of absorption. However, the CSF flow dynamics are influenced by the cardiovascular system and interactions between CSF and CNS anatomy. One, two, and three-dimensional models are currently methods researchers use to predict and describe CSF flow, both under normal and pathological conditions. They are, however, not without their limitations. “Rest-of-body” models, which consider whole-body compartments, may be more effective for understanding the disruption to CSF flow due to hemorrhages and hydrocephalus. Specifically, SAH is thought to prevent CSF flow into the basal cistern and paravascular spaces. It is also more subject to backflow, caused by the presence of coagulation cascade products. In regard to the fluid dynamics of CSF, scar tissue, red blood cells, and protein content resulting from SAH may contribute to increased viscosity, decreased vessel diameter, and increased vessel resistance. Outside of its direct influence on CSF flow, SAH may result in one or both forms of hydrocephalus, including noncommunicating (obstructive) and communicating (nonobstructive) HCP. Imaging modalities such as PC-MRI, Time-SLIP, and CFD model, a mathematical model relying on PC-MRI data, are commonly used to better understand CSF flow. While PC-MRI utilizes phase shift data to ultimately determine CSF speed and flow, Time-SLIP compares signals generated by CSF to background signals to characterizes complex fluid dynamics. Currently, there are gaps in sufficient CSF flow models and imaging modalities. A prospective area of study includes generation of models that consider “rest-of-body” compartments and elements like arterial pulse waves, respiratory waves, posture, and jugular venous posture. Going forward, imaging modalities should work to focus more on patients in nature in order to appropriately assess how CSF flow is disrupted in SAH and HCP.
