8 Dynamics of Cerebrospinal Fluid: From Theoretical Models to Clinical Applications
193
between the pulse amplitude [A] and the mean intracranial pressure [P]) is derived
by linear correlation between 30 consecutive, time-averaged data points of pulse
amplitude of ICP (AMP) and mean ICP acquired within a 10-s-wide time window.
RAP describes the degree of correlation between AMP and mean ICP over short
periods of time (5 min). Theoretically, the RAP coefficient indicates the relationship
between ICP and changes in intracerebral volume – the ‘pressure-volume’ curve.
E and PVI describe how fast pressure rises per unit of volume addition in an
exponential region of the curve. RAP coefficient close to 0 indicates a lack of
coupling between the changes in AMP and the mean ICP. This denotes a good
pressure-volume compensatory reserve at low ICP, i.e. the ‘working point’ is still
below exponential region of the curve. When the pressure-volume curve starts to
increase exponentially, AMP covaries directly with ICP and consequently RAP rises
to +1. This indicates a low compensatory reserve [45, 61].
8.7 Pulsatile Flow of CSF: Phase-Contrast MRI Perspective
Previous sections described theory and clinical applications of the methods, which
may be implemented using CSF volume-pressure tests or continuous monitoring
of ICP. However, CSF flows in pulsatile manner. These pulsations can be detected
using phase-contrast MRI [62–66].
8.8 Pulsatile CSF Flow-Basic Models
Pulsatile movement of CSF is a consequence of pulsatile inflow and outflow of
cerebral blood. Therefore, the introductory modelling considerations start from the
dynamics of CBF.
Value of ICP directly results from the circulation of cerebral blood, CSF,
compliance of the cranio-spinal system, and conditions for venous blood outflow
[31, 67]. Mean CBF is around 700 mL/min in adult, but arterial inflow is not constant
during the cardiac cycle (systolic peak flow is around 1000 mL/min and diastolic
around 550 mL/min) [63]. Compared to arterial flow, cerebral venous outflow is
delayed with lower peak flow amplitude (around 800 mL/min) and a time profile
of flow shape less pulsatile [63]. The difference in time profile between arterial
and venous flows results in a net change in intracranial blood volume during a
cardiac cycle. The blood volume expansion during one cycle is of order of few
millilitres [64].
CSF moves into the spinal canal during systole and returns to the cranial
compartment during diastole (Fig. 8.7) [63, 64, 68–70].
The volume (‘stroke volume’) of intracranial CSF displaced during one cardiac
cycle is around 450 mL [63, 66]. Ventricular CSF contributes only in a small part
(around 10%) of cerebrospinal volume exchange [63, 66, 71].
193
between the pulse amplitude [A] and the mean intracranial pressure [P]) is derived
by linear correlation between 30 consecutive, time-averaged data points of pulse
amplitude of ICP (AMP) and mean ICP acquired within a 10-s-wide time window.
RAP describes the degree of correlation between AMP and mean ICP over short
periods of time (5 min). Theoretically, the RAP coefficient indicates the relationship
between ICP and changes in intracerebral volume – the ‘pressure-volume’ curve.
E and PVI describe how fast pressure rises per unit of volume addition in an
exponential region of the curve. RAP coefficient close to 0 indicates a lack of
coupling between the changes in AMP and the mean ICP. This denotes a good
pressure-volume compensatory reserve at low ICP, i.e. the ‘working point’ is still
below exponential region of the curve. When the pressure-volume curve starts to
increase exponentially, AMP covaries directly with ICP and consequently RAP rises
to +1. This indicates a low compensatory reserve [45, 61].
8.7 Pulsatile Flow of CSF: Phase-Contrast MRI Perspective
Previous sections described theory and clinical applications of the methods, which
may be implemented using CSF volume-pressure tests or continuous monitoring
of ICP. However, CSF flows in pulsatile manner. These pulsations can be detected
using phase-contrast MRI [62–66].
8.8 Pulsatile CSF Flow-Basic Models
Pulsatile movement of CSF is a consequence of pulsatile inflow and outflow of
cerebral blood. Therefore, the introductory modelling considerations start from the
dynamics of CBF.
Value of ICP directly results from the circulation of cerebral blood, CSF,
compliance of the cranio-spinal system, and conditions for venous blood outflow
[31, 67]. Mean CBF is around 700 mL/min in adult, but arterial inflow is not constant
during the cardiac cycle (systolic peak flow is around 1000 mL/min and diastolic
around 550 mL/min) [63]. Compared to arterial flow, cerebral venous outflow is
delayed with lower peak flow amplitude (around 800 mL/min) and a time profile
of flow shape less pulsatile [63]. The difference in time profile between arterial
and venous flows results in a net change in intracranial blood volume during a
cardiac cycle. The blood volume expansion during one cycle is of order of few
millilitres [64].
CSF moves into the spinal canal during systole and returns to the cranial
compartment during diastole (Fig. 8.7) [63, 64, 68–70].
The volume (‘stroke volume’) of intracranial CSF displaced during one cardiac
cycle is around 450 mL [63, 66]. Ventricular CSF contributes only in a small part
(around 10%) of cerebrospinal volume exchange [63, 66, 71].