pathophysiology of communicating hydrocephalus

Conventional Theory Conventional Theory VSVS

Continuous Medical Education, Department of Neurosurgery, Hospital Kuala Lumpur

17 January 2007

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

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 An obstruction to the CSF flow, inside or CSF flow, inside or outside the outside the ventricular system, ventricular system, causes obstructive causes obstructive and communicating and communicating hydrocephalus, hydrocephalus, respectively. respectively.

The CSF bulk flow The CSF bulk flow theory explains theory explains hydrocephalus as hydrocephalus as an imbalance an imbalance between CSF between CSF formation and formation and absorption absorption

Conventional Theory – Conventional Theory – Bulk Flow Theory (Dandy) 1914Bulk Flow Theory (Dandy) 1914

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.

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

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

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

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

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

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

Communicating Hydrocephalus

Lack of CSF Accumulation in Subarachnoid Spaces

ConventionalConventional Pulsation ModelPulsation Model1. 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

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)


Temporal Horn Dilation

ConventionalConventional Pulsation ModelPulsation Model1. 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.

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


Pressure Gradient from the Subarachnoid Space to the Dural Venous Sinuses

ConventionalConventional Pulsation ModelPulsation Model1. 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)

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.


The Role of Choroid Plexus Pulsations

ConventionalConventional Pulsation ModelPulsation Model1. Distal occlusion of the CSF pathways

would cause symmetrical enlargement of the ventricles (Dandy, 1919)

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)

The resistive index is abnormal in communicating hydrocephalus.

It is defined asresistive 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

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

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

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.

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.

Elevated Intracranial PressureIn the pulsation model

1. Narrowing or reversal of the subarachnoid-venous pressure gradient causes malabsorption of CSF, which increases CSF pressure.

2. 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.

3. The loss of resonance, combined with autoregulated cerebral blood flow, causes increased pulse pressure in the cranium.

4. When the intracranial compliance diminishes, the model produces rhythmic waves of intracranial pressure.

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.

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.

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.

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


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.


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.

pathophysiology of communicating hydrocephalus

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