8 Dynamics of Cerebrospinal Fluid: From Theoretical Models to Clinical Applications
183
it provides a shock absorptive function for the brain and spinal cord, important in
trauma; (2) allows even distribution of pressure throughout the intracranial vault,
cancelling out pressure gradients and preventing brain shift or herniation; and (3)
allows washing out brain metabolites.
The second point explains why a very high ICP (>40 mmHg) can be tolerated
relatively asymptomatically in communicating hydrocephalus, for example, during
CSF infusion tests [13]. In contrast, when CSF pathways are obstructed, for
example, by diffuse cerebral oedema in TBI, marked clinical deterioration is seen at
ICP exceeding only 20 mmHg.
Absorption occurs in a pressure-dependent fashion via the arachnoid granulations
at the superior sagittal sinus (except for newborns), first mathematically described
by Davson [14]. This equation was recently validated in a population of patients suffering from idiopathic normal pressure hydrocephalus [15]. Alternative outflow of
CSF may occur by periventricular leakage into the brain parenchyma, as suggested
in NPH patients [16, 17]. CSF circulates not only in a constant way with a rate
equivalent to CSF production but also in pulsations. CSF pulsatile flow is observed
in the cerebral aqueduct (approximately 40 μL in stroke volume) and in the cervical
region of subarachnoid spaces (SAS) (approximately 500 μL stroke volume) [18].
For a half of the cardiac cycle, CSF flows down into the spinal SAS, and for the
other half, upward from it. The role of pulsatile CSF flow and pressure pulsations
is still unclear, but becomes more often studied in hydrocephalus and other diseases
manifesting with abnormal CSF dynamics [19–21]. Recently, Nedergaard et al. [22]
described an additional CSF rapid convective flow via the glymphatic system, a
highly organised brain-wide pathway, associating a paraarterial CSF influx route, an
intracellular transastrocytic path, and a paravenous ISF clearance route. Aquaporin
4 (AQP4) water channels, disposed on the vascular end feet of astrocytes, facilitate
fast exchanges between CSF and interstitial fluid (ISF), allowing a rapid clearance
of waste products related to high metabolic activity of neurons, which is not possible
with only the low CSF ‘classic’ bulkflow and the large tissue distances in most of
the brain regions and CSF spaces. This CSF flow through the brain is also discussed
in Bulat-Klarica-Oreškovi´ c hypothesis [23].
A specific pattern of CSF flow impairment should be distinguished from the
other situation: external hydrocephalus, which has been extensively described in
paediatric cases but very few in brain injured adult patients, refers to an extra-axial
CSF flow impairment with an enlargement of the subarachnoid spaces concomitant
to raised ICP [24] and CSF dynamics [25] alteration but not with ventriculomegaly.
Occurrence of traumatic or non-traumatic subarachnoid haemorrhage is probably
a significant cause of such condition. It should not be confused with ‘subdural
hygroma’, which is primarily caused by a vacuum effect on CSF precipitated by
atrophic brain sinking, without raised ICP [26]. Recently Nakae et al. describe
the same mechanism after a chemical meningitis with a patient improvement by
a ventriculo-peritoneal shunting [27]. In these two last references, the authors insist
on the difference between external hydrocephalus and hygroma (Fig. 8.1). Despite
several other publications [28–30] that describe this distinction, the concept of
external hydrocephalus is currently largely underknown and should be more spread
183
it provides a shock absorptive function for the brain and spinal cord, important in
trauma; (2) allows even distribution of pressure throughout the intracranial vault,
cancelling out pressure gradients and preventing brain shift or herniation; and (3)
allows washing out brain metabolites.
The second point explains why a very high ICP (>40 mmHg) can be tolerated
relatively asymptomatically in communicating hydrocephalus, for example, during
CSF infusion tests [13]. In contrast, when CSF pathways are obstructed, for
example, by diffuse cerebral oedema in TBI, marked clinical deterioration is seen at
ICP exceeding only 20 mmHg.
Absorption occurs in a pressure-dependent fashion via the arachnoid granulations
at the superior sagittal sinus (except for newborns), first mathematically described
by Davson [14]. This equation was recently validated in a population of patients suffering from idiopathic normal pressure hydrocephalus [15]. Alternative outflow of
CSF may occur by periventricular leakage into the brain parenchyma, as suggested
in NPH patients [16, 17]. CSF circulates not only in a constant way with a rate
equivalent to CSF production but also in pulsations. CSF pulsatile flow is observed
in the cerebral aqueduct (approximately 40 μL in stroke volume) and in the cervical
region of subarachnoid spaces (SAS) (approximately 500 μL stroke volume) [18].
For a half of the cardiac cycle, CSF flows down into the spinal SAS, and for the
other half, upward from it. The role of pulsatile CSF flow and pressure pulsations
is still unclear, but becomes more often studied in hydrocephalus and other diseases
manifesting with abnormal CSF dynamics [19–21]. Recently, Nedergaard et al. [22]
described an additional CSF rapid convective flow via the glymphatic system, a
highly organised brain-wide pathway, associating a paraarterial CSF influx route, an
intracellular transastrocytic path, and a paravenous ISF clearance route. Aquaporin
4 (AQP4) water channels, disposed on the vascular end feet of astrocytes, facilitate
fast exchanges between CSF and interstitial fluid (ISF), allowing a rapid clearance
of waste products related to high metabolic activity of neurons, which is not possible
with only the low CSF ‘classic’ bulkflow and the large tissue distances in most of
the brain regions and CSF spaces. This CSF flow through the brain is also discussed
in Bulat-Klarica-Oreškovi´ c hypothesis [23].
A specific pattern of CSF flow impairment should be distinguished from the
other situation: external hydrocephalus, which has been extensively described in
paediatric cases but very few in brain injured adult patients, refers to an extra-axial
CSF flow impairment with an enlargement of the subarachnoid spaces concomitant
to raised ICP [24] and CSF dynamics [25] alteration but not with ventriculomegaly.
Occurrence of traumatic or non-traumatic subarachnoid haemorrhage is probably
a significant cause of such condition. It should not be confused with ‘subdural
hygroma’, which is primarily caused by a vacuum effect on CSF precipitated by
atrophic brain sinking, without raised ICP [26]. Recently Nakae et al. describe
the same mechanism after a chemical meningitis with a patient improvement by
a ventriculo-peritoneal shunting [27]. In these two last references, the authors insist
on the difference between external hydrocephalus and hygroma (Fig. 8.1). Despite
several other publications [28–30] that describe this distinction, the concept of
external hydrocephalus is currently largely underknown and should be more spread