Pathophysiology of communicating hydrocephalus

1. Conventional Theory Conventional Theory
VSVS
Continuous Medical Education, Department of Neurosurgery,
Hospital Kuala Lumpur
17 January 2007

2. Conventional Theory – Conventional Theory –
Bulk Flow Theory (Dandy) 1914Bulk Flow Theory (Dandy) 1914
CSF is produced in CSF is produced in
the choroid plexus the choroid plexus
and is transported by and is transported by
bulk flow to the bulk flow to the
arachnoid arachnoid
granulations at the granulations at the
venous sinuses, venous sinuses,
where it is absorbed where it is absorbed
by a valvular by a valvular
mechanism mechanism

3. The driving force of The driving force of
bulk flow is the CSF bulk flow is the CSF
pressure at the pressure at the
production site production site
being slightly in being slightly in
excess of the excess of the
pressure at the pressure at the
absorption site absorption site
An obstruction to the
CSF flow, inside or
outside the
ventricular system,
causes obstructive
and communicating
hydrocephalus,
respectively.
The CSF bulk flow
theory explains
hydrocephalus as
an imbalance
between CSF
formation and
absorption
Conventional Theory – Conventional Theory –
Bulk Flow Theory (Dandy) 1914Bulk Flow Theory (Dandy) 1914

4. Conventional Theory – Conventional Theory –
Bulk Flow TheoryBulk Flow Theory
The intracranial pressure is thought to be The intracranial pressure is thought to be
dependent on the balance between dependent on the balance between
production and absorption of CSF. production and absorption of CSF.
This indicates that patients with This indicates that patients with
hydrocephalus should have increased hydrocephalus should have increased
intracranial pressure. intracranial pressure.

5. Bulk Flow Theory??Bulk Flow Theory??
The ventricles should not dilate, if there is The ventricles should not dilate, if there is
a CSF blockage at the pacchionian a CSF blockage at the pacchionian
granulations granulations
This obstruction cannot cause a higher This obstruction cannot cause a higher
pressure in the ventricle than in the pressure in the ventricle than in the
subarachnoid space, but would instead subarachnoid space, but would instead
dilate the subarachnoid space dilate the subarachnoid space

6. Bulk Flow Theory??Bulk Flow Theory??
O Connel [O Connel [19431943] and Hakim [] and Hakim [19651965] described ] described
patients with the clinical syndrome of idiopathic patients with the clinical syndrome of idiopathic
normal-pressure hydrocephalus (NPH), normal-pressure hydrocephalus (NPH),
associated with communicating hydrocephalus associated with communicating hydrocephalus
and normal ventricular pressure and normal ventricular pressure
The ventricles should not dilate without an The ventricles should not dilate without an
increase of the CSF pressure, and the CSF increase of the CSF pressure, and the CSF
pressure in turn should increase at CSF outflow pressure in turn should increase at CSF outflow
obstructions. obstructions.
•O Connel JEA (1943) The vascular factor in intracranial pressure and the
maintenance of the CSF circulation. Brain 66:204–228
•Hakim S, Adams R (1965) The special clinical problems of symptomatic
hydrocephalus with normal cerebrospinal fluid pressure. J Neurol Sci 2:307–327

7. Bulk Flow Theory??Bulk Flow Theory??
The pacchionian granulations do not The pacchionian granulations do not
develop in children until the closure of the develop in children until the closure of the
fontanelsfontanels
No mechanical valves have been No mechanical valves have been
demonstrated anatomically in the demonstrated anatomically in the
pacchionian granulations pacchionian granulations
80–90% of radioactive isotope injected 80–90% of radioactive isotope injected
into the lumbar CSF is absorbed in the into the lumbar CSF is absorbed in the
spinal canalspinal canal

9. In 1943, O Connel for the first time In 1943, O Connel for the first time
correctly postulated that increased CSF correctly postulated that increased CSF
pulse pressure in the ventricles, without pulse pressure in the ventricles, without
increase of mean CSF pressure, could increase of mean CSF pressure, could
cause communicating hydrocephalus cause communicating hydrocephalus
Greitz [Greitz [19931993], using flow-sensitive ], using flow-sensitive
magnetic resonance imaging (MRI) and magnetic resonance imaging (MRI) and
radionuclide cisternography, rediscovered radionuclide cisternography, rediscovered
that the brain capillaries absorb CSF that the brain capillaries absorb CSF
•Greitz D (1993) Cerebrospinal fluid circulation and associated intracranial
dynamics. A radiologic investigation using MR imaging and radionuclide
cisternography. Acta Radiol 34:1–23
•O Connel JEA (1943) The vascular factor in intracranial pressure and the
maintenance of the CSF circulation. Brain 66:204–228

10. Modern CSF physiologyModern CSF physiology
CSF is produced everywhere in the central CSF is produced everywhere in the central
nervous system nervous system
The absorption of CSF occurs in the capillaries The absorption of CSF occurs in the capillaries
of the central nervous systemof the central nervous system
The rapid transport of CSF in the subarachnoid The rapid transport of CSF in the subarachnoid
space occurs by space occurs by vascular pulsationsvascular pulsations causing causing
mixing of CSF mixing of CSF
The filtration and absorption of fluid in the brain The filtration and absorption of fluid in the brain
capillaries is governed by the Starling principle capillaries is governed by the Starling principle

11. In communicating hydrocephalus, the
ventricles communicate with the
subarachnoid space, and no significant
gradient should form.
If a pressure gradient did form, it would
favor expansion of the subarachnoid
spaces

12. Communicating Hydrocephalus
Lack of CSF Accumulation in Subarachnoid
Spaces
1. Ventricular expansion at the expense of
the subarachnoid space requires a
transmantle pressure gradient favoring
ventricular expansion. (pressure gradient
between the ventricular CSF and the
subarachnoid CSF)
1. If obstruction of the arachnoid villi did
cause accumulation of CSF, it should be in
the subarachnoid space adjacent to the
dural venous sinus.
2. Retrograde transmission of pressure to the
ventricles would not occur until the
subarachnoid space expanded and its
compliance was exceeded.
3. In communicating hydrocephalus, the
subarachnoid spaces are usually small
Pulsation ModelConventional

13. Communicating Hydrocephalus
Temporal Horn Dilation
1. Arterial pulsations in the choroid plexus
would not be of equal strength in all
regions of the plexus.
2. Dissipation of the pulsations occurs along
the course of the choroidal artery, and the
pulsations in the plexus near the arterial
pedicle would be stronger than the
pulsations in the plexus further from the
pedicle.
3. The arterial pedicle of the choroid plexus
of the lateral ventricle enters the ventricle
at the choroidal fissure of the temporal
horn.
4. The pulse pressure gradient between the
ventricles and the subarachnoid space
would be greatest in the temporal horn
1. Ventricular dilation, if it were to occur,
should begin distally in the ventricular
system, at the fourth ventricle, and
progress proximally to the lateral
ventricles.
2. The temporal horns are far from the site of
obstruction, and at the choroidal fissure.
3. Only the single layer of pia and ependyma
separates the temporal horn from the
subarachnoid space. A pressure gradient
originating from the subarachnoid space
should compress, not expand, the
temporal horns.
Pulsation ModelConventional

14. Communicating Hydrocephalus
Pressure Gradient from the Subarachnoid Space
to the Dural Venous Sinuses
1. The diminishment of the pressure gradient
across the arachnoid villi suggests that
venous hypertension, not mechanical
obstruction of the arachnoid villi, is the
cause of malabsorption of CSF.
2. The pulsation model simulates the actual
changes in the pressure gradient.
1. The CSF pressure normally exceeds the
sagittal sinus pressure by 2–14 cm H2O.
Obstruction of the arachnoid villi would
increase the resistance to CSF absorption
and should increase the pressure gradient
between the CSF and the sagittal sinus.
2. The actual pressure gradient across the
arachnoid villi is diminished or even
reversed (Shulman et al, 1964) (Olivero et
al, 1988)
Pulsation ModelConventional

15. Communicating Hydrocephalus
The Role of Choroid Plexus Pulsations
1. Ventricular enlargement was not the result
of increased intraventricular pressure from
accumulated CSF (Bering, 1962)
2. Choroid plexus pulsations which causes
elevated pulse pressure were necessary to
produce ventricular dilation in
hydrocephalus. (Bering, 1962)
3. Arterial pulsations in the choroid plexus
(choroidal artery) were necessary for
ventricular dilation. (Wilson and Bertan,
1967)
1. Distal occlusion of the CSF pathways
would cause symmetrical enlargement of
the ventricles (Dandy, 1919)
Pulsation ModelConventional

16. The resistive index is abnormal in communicating
hydrocephalus.
It is defined as
resistive index = peak systolic flow velocity – end diastolic flow velocity
peak systolic flow velocity
The resistive index is essentially a measure of the
pulsatility of the blood flow in the subarachnoid vessels.
It increases in hydrocephalus and often returns to normal
with treatment of hydrocephalus.
Elevation of the resistive index is evidence of increased
pulsatility of arterial blood flow in hydrocephalus.
Resistive Index and Hyperdynamic
Arterial Pulsations

17. Windkessel Effect
Cerebral blood flow is the superposition of two
components: bulk flow and oscillating motion.
Blood flow in the large subarachnoid arteries is a
combination of the two kinds of flow, i.e. oscillating bulk
flow.
As flow continues through the arterial tree, the
oscillations are dissipated through the arterial walls into
the CSF and surrounding tissues so only the bulk flow
remains.
Capillary blood flow is nearly smooth.
The mechanism by which arterial pulsations are
progressively dissipated to render the capillary
circulation almost pulseless is called the windkessel
effect

18. Windkessel Effect
Intracranial blood vessels and CSF
spaces are arranged as parallel
pathways branching from a series flow.
Normal intracranial blood flow and CSF
dynamics can be represented by a
series-parallel array of blood vessels and
CSF spaces.
Normal pulsatile dynamics represents
resonance, in which intracranial CSF
pulsations are synchronous with arterial
pulsations.
The CSF dissipates pulsations from the
arterial blood entering the cranium, and
this mechanism appears to be necessary
for normal cerebral blood flow

19. Windkessel Effect
In normal patient, CSF pulsations
in the ventricles and the
subarachnoid space are normally
of equal amplitude; normally,
there is no transmantle pulse
pressure gradient.
When the windkessel mechanism
is effective, the arterial pulsations
are short-circuited through the
CSF to the veins; the capillary
blood flow is nearly smooth.

20. Windkessel Effect in
Communicating hydrocephalus
In communicating hydrocephalus,
increased impedance to pulsations in the
subarachnoid space increases the
pulsations in the blood flow to the
choroidal arteries and the choroid plexus
and increases the pulsations in the
ventricular CSF.
The amplitude of the pulsations of the
ventricular CSF exceeds the amplitude of
the pulsations in the subarachnoid CSF.
This causes a transmantle pulse
pressure gradient and ventricular
expansion at the expense of the
subarachnoid space.

21. Elevated Intracranial Pressure
In the pulsation model
Narrowing or reversal of the subarachnoid-venous
pressure gradient causes malabsorption of CSF, which
increases CSF pressure.
Breakdown of the windkessel mechanism causes the
delivery of stronger arterial pulse pressure to the
capillary circulation. The higher pressure in the
capillaries would lead to cerebral edema.
The loss of resonance, combined with autoregulated
cerebral blood flow, causes increased pulse pressure in
the cranium.
When the intracranial compliance diminishes, the model
produces rhythmic waves of intracranial pressure.

22. Malabsorption of CSF of
communicating hydrocephalus
In the pulsation model
The elevation of capillary and venous pulse
pressure that occurs as a result of the
redistribution of pulsations within the cranium
diminishes the hydrostatic gradient necessary
for CSF absorption throughout the cranium.
Malabsorption is not dependent on mechanical
obstruction of individual absorption sites.

23. Resistive Index of communicating
hydrocephalus
in the pulsation model
Resistive Index measures the pulsatility of the
blood flow in the subarachnoid vessels.
The resistive index increases substantially in
hydrocephalus and decreases with shunting
The rise is the result of the breakdown of the
windkessel mechanism, which normally filters
the pulsations out of the arterial blood.

24. Selective Compression of White
Matter and Sparing
of Gray Matter in the pulsation
model
In communicating hydrocephalus, ventricular expansion occurs
primarily at the expense of the white matter; the gray matter is less
attenuated
The breakdown of the windkessel mechanism that occurs in
communicating hydrocephalus causes increased pulse pressure in
the capillary blood flow as well as increased pulse pressure in the
ventricular CSF.
Because the gray matter has greater blood flow than the white
matter, the transependymal pulse pressure gradient would be
greater between the ventricular CSF and the white matter than
between the ventricular CSF and the gray matter. The white matter
would be compressed more than the gray matter.

25. ConclusionConclusion
The salient features of communicating
hydrocephalus are the result of the redistribution
of CSF pulsations in the cranium.
Redistribution of the vascular pulsations to the
capillary bed and the venous circulation raises
the venous pressure and causes malabsorption
of CSF.
Adequate dissipation of arterial pulsations in the
rigid cranium seems to be necessary for normal
cerebral blood flow

26. ConclusionConclusion
If the dissipation of pulsations is blocked in
one pathway, the pulsations will flow with
greater intensity through parallel
pathways. This differential flow through
adjacent pathways establishes pulse
pressure gradients, which tend to cause
expansion of the CSF spaces in which the
pulsations are excessively dissipated at
the expense of the CSF spaces in which
the pulsations are dampened.

27. ConclusionConclusion
In the pulsation model, hyperdynamic
ventricular CSF pulsations and narrowing
of the CSF venous pressure gradient are
the cause of ventricular dilation and
malabsorption of CSF in communicating
hydrocephalus.
Communicating hydrocephalus is a
disorder of intracranial pulsations.