1

Proceedings of the 37
th
National & 4
th
International Conference on Fluid Mechanics and Fluid Power
December 16-18, 2010, IIT Madras, Chennai, India
FMFP2010


ANALYSIS OF BLAST INDUCED INTRACRANIAL PRESSURE
DYNAMICS IN CEREBROSPINAL FLUID LEADING TO
TRAUMATIC BRAIN IN1URY


Yashwanth B. L
Department of Mechanical
Engineering
ndian nstitute of Technology
Kanpur, ndia

A. Sarkar
Department of Physics
Jadavpur University
Kolkata, ndia

S. Sarkar
Department of Mechanical
Engineering
ndian nstitute of Technology
Kanpur, ndia
e-mail: subra@iitk.ac.in

ABSTRACT
A medical paradox was encountered by neurologists while treating soldiers who had survived explosions in
warIronts. There were evidences oI memory deIicits, speech problems and diIIiculties with decision-
making in these patients. The signiIicant observation was that most oI these patients had not suIIered a
direct head injury. Nevertheless scan reports suggested enlargement oI brain ventricles with minor
bleeding. Such conditions were termed as Blast Induced Traumatic Brain Injury (TBI). Certain studies
show the development oI stresses in various parts oI the brain due to explosions; none oI them directly
correlating the expansion oI Cerebrospinal Iluid (CSF) pathways and brain ventricles, which is believed to
be the indication oI TBI. This work primarily explores the role oI intracranial CSF pressure dynamics in
the genesis oI TBI; emphasis being on the evolution oI the unsteady pressure Iield within CSF pathways,
ventricular and the subarchnoid region with the brain parenchyma. The continuity and Navier-Stokes
equations are solved Ior the CSF Ilow under the inIluence oI blast. It has been observed that an unsteady
pressure response is developed in the CSF pathways. The pressure gradient between the ventricles and the
porous parenchyma is considerably high which is indicative oI the ventricular expansion. This intense
activity oI varying pressure gradient occurs within Iew milliseconds oI the blast application. Our work
qualitatively evaluates the CSF pressure instabilities at various instants oI time that may be related to the
cause oI expansion oI CSF pathways and ventricular spaces.

Keywords : TBI, CSF pathways, ventricular expansion, unsteady pressure, CFD


INTRODUCTION
It was observed by neurologists during the Balkan
war oI the 1990s |1| that soldiers who had
encountered blasts in the battleIield suIIered Irom
memory deIicits, dizziness, speech problems and
diIIiculties with decision-making with no obvious
brain injuries. A speciIic case has been reported,
where a 19 year old went to a grocery store and
couldn`t remember how to get back home. In such
cases, computed tomography and magnetic
resonance imaging scans indicate signs oI internal
damages. To be speciIic, these include the
enlargement oI brain ventricles (channels that carry
cerebrospinal Iluid) as well as evidences oI minor
bleeding. This kind oI trauma due to blast exposure
as mentioned in the abstract is called Blast Induced
571
Proceedings of the 37th National & 4th International Conference on Fluid Mechanics and Fluid Power
December 16-18, 2010, IIT Madras, Chennai, India.
FMFP10 - BN - 04

2
Traumatic Brain Injury (TBI). There are studies
that show the development oI stresses within the
brain structures due to a nearby explosion, which
may be a possible indication oI TBI. However, the
area oI research needs a lot more explorations to
enrich our understandings correlating the
interactions oI the blast wave and brain tissues,
enlargement oI ventricles via excitation oI
cerebrospinal Iluid (CSF).
The yearly incidence oI TBIs in the United
States has been estimated at 1.4 million people,
including 50000 deaths and 235000
hospitalizations |2, 3|. Military personnel and
civilians can also incur TBI as a consequence oI
explosive blasts, and in recent wars the incidence
oI such injuries has increased dramatically. This
increase can be attributed to the tactics oI
asymmetric warIare, where enemy combatants
detonate improvised explosive devices targeting
vehicles and exposed individuals. Recent statistics
Irom the conIlict in Iraq show that several thousand
United States soldiers have sustained TBI, 69 as
a result oI blasts |4, 5|. Injuries sustained Irom
blast exposure have been categorized into three
major components: primary, secondary, and tertiary
|6|. Primary blast injury is associated with direct
exposure oI the head and body to the blast wave. In
secondary blast injury, debris are accelerated into
the individual, while in tertiary injury the victim is
thrown into stationary objects by the blast. Both oI
the latter mechanisms are comparable to the
mechanical trauma that has been the subject oI
decades oI clinical, experimental, and
computational research. However, the role oI
primary blast exposure in the development oI TBI
remains less understood |7|. Primary blast may
induce linear and rotational cranial accelerations,
but the sharp wave Iront oI blast overpressure will
also trigger complex pressure wave motions,
transmitted by the skull into the high water (CSF)
content subarchnoid spaces and brain ventricles.
Multiple, oIten coexisting pathologies, can
underlie the consequences oI TBI, including easily
visualized damage Irom contusions and intra-
parenchymal or extra-axial hemorrhages. However,
at least one-third oI the deaths and poor outcomes
oI TBI are the result oI traumatic axonal injury
occurring at the microscopic level |8| that is
diIIicult to be clinically visualized. Most oIten
reIerred to as diIIuse axonal injury or DAI (severe
case oI TBI), this pathological Iinding actually
deIines a multiIocal process that can be widespread
throughout the white matter tracks and other areas
oI the brain.
The CSF is contained within and surrounds the
brain and spinal cord |9|. It suspends the brain
through its buoyancy Iorce and protects it Irom
impact on the cranial vault wall, acting as a
damper. CSF is produced in the choroid plexuses oI
the brain and is drained mainly through the
superior sagittal sinus. The steady Ilow oI CSF is
inIluenced by a periodically pulsating cardiac
cycle. Within the skull, the cerebrospinal Iluid is
contained in the ventricles and the subarchnoid
space. The ventricles are Iour cavities
interconnected by pathways. Figure 1 illustrates the
anatomy oI brain.
Recent studies on the subject modeled the
brain as a viscoelastic media simulating |2|
intracranial wave physics. The reason Ior TBI was
due to stretching oI the axonal Iibers (DAI) caused
by shear Iorces over a short span oI time (2ms).
However, in ReI. 10 it was stated that a signiIicant
translational and rotational acceleration over a span
oI 5-20 ms was the cause |10|. But none oI the
above studies directly correlates the reason behind
the expansion oI CSF pathways and brain
ventricles, which is believed to be the indication oI
TBI according to ReI. 1. No work has been done so
Iar to illustrate how exactly the pressure wave
propagates in CSF. The paramount Iunction oI CSF
is to act as a cushion against shocks and hence
protect it Irom trauma. Thus, an analysis is
extremely desired illustrating the pressure
dynamics oI CSF under inIluence oI shock wave
that may suggest the reason Ior expansion oI the
ventricles and subarchnoid space because oI
pressure augmentation within the CSF pathways,
which in a way correlates directly the pathological
Iindings in TBI.
The primary Iocus oI our work is to explore the
role oI intracranial CSF pressure dynamics in the
genesis oI traumatic brain injury Irom blast. Here,
emphasis is to evaluate qualitatively the unsteady
pressure Iield within CSF pathways, ventricular
and the subarchnoid region with the brain

3
parenchyma, which may draw an insight on this
complex intracranial phenomena and the actual
cause Ior the sudden ventricular expansion due to
the advent oI the blast wave.

METHOD
Our objective is to use the physics oI Iluid Ilow
to quantiIy the intracranial CSF dynamics. Thus,
the Iundamental conservation laws oI mass and
momentum, reIerred to as continuity and Navier-
Stokes equations, have been used to solve the CFS
Ilow under the inIluence oI blast. The governing
equations with appropriate boundary conditions in
the present case are solved by a commercial CFD
package Fluent 6.3 to visualize Ilow physics within
the CSF pathways. The solution methodology
invoked here uses the unsteady Simple algorithm
on unstructured grid, which is second order
accurate in space and time. The anatomy oI the
brain including CSF spaces was extracted Irom
digitization oI a human brain MRI |11| to deIine
the computational domain and boundaries. Our
work is limited to two-dimensional modeling. A
very careIul mesh generation has been done in
Gambit oI Fluent taking into account the intricacy
CSF Ilow path, ventricles and other parts oI the
brain anatomy. A total oI 67458 nodes with 57527
mixed quadrilateral and triangle cells and 27880
triangular cells were used (Fig. 1 Ior details).
DiIIerent assumptions are made to replicate CSF
Iluid and the brain structure that would be
discussed later.

Governing equations for CSF flow
CSF motion in the ventricles and the
subarchnoid space can be described by the mass
and momentum equations Ior an incompressible
Newtonian Iluid |13| as,

Conservation oI mass: 0 J =

(1)

Conservation oI momentum:

2
J
J J p J
t


+ = +

(2)
where, J

is the velocity vector, is the density oI

CSF and is its viscosity. The properties oI CSF
are close to water and are tabulated in Table I.
CSF flow through the brain tissues
Here, the brain tissue (parenchyma, brain stem
and cerebellum) is treated as a homogeneous
isotropic porous medium. The CSF is produced in
the choroid plexus Irom the blood and also Irom
the brain tissue Irom which it seeps through the
porous extracellular space towards the ventricles.
Two thirds oI the CSF production enters the
ventricles Irom the choroid arteries |14, 15|, one
third is generated diIIusely throughout the brain
parenchyma. Due to modeling complexity and in
order to simpliIy the case, we have neglected the
generation oI CSF in brain parenchyma and
considered only the production in choroid plexus.
The continuity equation oI CSF Ilow in the choroid
plexus has a source term (S) to account Ior new
CSF production as in Eq. 3.
The CSF Ilow though the extracellular space oI
the brain parenchyma is modeled by the continuity
and momentum equations Ior Ilow though porous
media. The momentum balances oI CSF seepage
are the Navier-Stokes equations augmented by an
additional term quantiIying Irictional interaction oI
CSF with the brain tissue. Equation (4), a
generalization oI the simpler Darcy`s law oI Ilow
through porous media |16, 17|, is used here. The
material properties oI the brain tissue are listed in
Table I.

Thus, CSF generation in the choroid plexus:
J S =

(3)

CSF Iluid seepage through the porous medium:
2 2
2
J
J J p J J J
t k



+ = + +

(4)

For realistic prediction, proper boundary
conditions are imposed with suitable assumptions.
To begin with, the pressure wave generated by an
explosive blast needs to be Iormulated keeping in
mind that the wave Iormed is a Iunction oI time
and distance Irom the blast location apart Irom
mass oI the detonation.


4
1. Sagittal Sinus
2. Subarchnoid Space
3. Brain Parenchyama
4. Lateral Ventricle
5. Choroid Plexus
6. Dura
7. Brain Stem
8. Cerebellum
9. Spinal Cord


5
3
4
2
1


















Fig.1 Computational domain, meshed geometry and boundaries.

Table-I. Properties used Ior CSF Iluid and brain tissue
Material Properties
1. Porosity oI tissue and sagital sinus(): 0.3
2. Permeability oI the tissue(): 710
-16
m
2

3. Source term at choroid plexus: 2.210
-10
kg/m
3
sec
4. Density oI CSF (): 998.2 kg/m
3

5. Viscosity oI CSF (): 0.0001003 kg/m-s
6. Inertia resistance oI tissue (): 10
4
m
-1



Table-II. Imposed boundary conditions (b.c)
Locations InIormation Marked in Fig. 1
Inlet pressure b.c Induced blast pressure as per the Eq.1-4. Boundary 1-2-3
Exit pressure b.c Atmospheric pressure Boundary 3-4-5
Spinal cord b.c Velocity induced by heart impulse as stated in
Eq. 9.
Boundary 5-1
Dura b.c No slip, uvw0 6
Choroid plexus b.c CSF generation, imposed a source term 5
Sagittal sinus b.c Distributed CSF sink 1
Porous Structures Brain Parenchyma, Cerebellum, Brain Stem,
Sagittal sinus
1, 3, 7, 8
Fluid Ilow CSF pathways 2, 4


5
Formulation of the blast wave
The Iormulation oI the blast wave Iollows Irom
the ReI. 12. A mathematical description oI the
pressure waveIorms that represent the typical
ranges and sizes oI explosives associated with brain
TBI can be accomplished by scaling Irom a
reIerence explosion and distance Irom the
explosion. The scaling equations are a system oI
empirically developed equations, tailored Ior
accuracy within speciIic ranges Irom the blast, as
well as the type oI blast (nuclear or conventional)
and are described in G.F. Kinney and K.J.
Graham`s book, Explosive Shocks in Air. The
equations that are critical to this research are
summarized in this section.
The Iirst step in determining appropriate
waveIorm is to determine a scaled distance (Z) that
relates the modeled (actual) distance to a reIerence
explosion:
1/ 3
(actual distance)
a
f
Z
W

= (5)

In this calculation, W, is the explosive yield, in
kilograms oI charge, oI the modeled explosive. The
parameter, f
a
, is considered the transmission Iactor.
Most explosions leading to TBI occur in near
proximity to the victim, and thereIore a
transmission Iactor oI f
a
1 is assumed Ior this
study.
The maximum overpressure, p
0
, against the
atmospheric pressure, p
a
, can then be calculated by:
2
2 2 2
808 1
4.5
1 1 1
0.0048 0.32 1.35
o a
Z
p p
Z Z Z
(
| |
( +
]
\ (

=
| | | | | |
+ + +
] ] ]
\ \ \
(6)
The two critical components oI the pressure
wave proIile that describe its potential to cause
injury to personnel, or damage to structures, are the
maximum overpressure and the duration oI the
positive phase. Together, these can be used to
estimate the energy impulse associated with the
blast. The impulse is deIined as the integral oI the
pressure-time curve (Fig. 2). The duration oI the
positive phase (t
a
) oI the pressure proIile is
estimated by:
10
1/ 3
3 6 2
980 1
0.54
1 1 1
0.02 0.74 6.9
a
Z
t W
Z Z Z
(
|
( +

' . (

=
( (
| | |
( ( + + +

' . ( ' . ( ' .

(7)
Thus, the actual waveIorm is approximated by the
Friedlander equation |12| as:
1
a
t
t
o
a
t
p p e
t


=


(8)
A typical pressure proIile oI a wave generated
by an explosive blast Iollowing Eqs. 5-8 is
illustrated in Fig 2. It illustrates an initial jump
discontinuity Irom ambient pressure to a maximum
overpressure, p
0
. This is Iollowed by a rapid decay
oI the positive overpressure back to the ambient
level within a Iew milliseconds. The inertia oI
motion oI expanded and displaced gas results in a
negative pressure phase that lasts approximately
three times as long as the positive phase, beIore
returning to ambient pressure. Further pressure
oscillations are possible, but are not typically
observed Ior blasts in air.









Fig.2 Typical pressure proIile Ior an
explosive blast in air.

A blast intensity oI around 10 bars assuming
20 reduction in the skull |ReI. 2| was imposed on
the anterior side oI the modeled geometry and the
blast conditions were equivalent to those predicted
Ior a location 2 to 3 m distant Irom a detonated
explosive device constructed Irom a 3 kg charge
according to the above equations.

Boundary Conditions
The boundary conditions Ior the CSF Ilow in
the cranium are summarized in Table II. The bulk

6
CSF production is implemented as source term at
the choroid plexus. The pulsatile Ilow oI CSF due
to the movement oI the spinal chord (heart pulse)
during systole is also accounted Ior and expressed
as
1
( ) sin cos
2 2 2
v t t t


( | | | |
=
| | (
\ \
(9)

The Irequency () oI the pulsatile motion is set
to 1 Hz approximating the normal cardiac cycle.
Most scientists believe that the majority oI
reabsorption oI the CSF is into the granulation oI
the sagittal sinuses. Accordingly, re-absorption oI
the Iluid takes place at the top oI the brain
geometry. In case oI a hydrocephalus patient, a
ventricular dilation due to increase in CSF pressure
is observed indicating that the pressure increase in
the subarchnoid space is not communicated to the
spinal canal. This will allow us to use a closed
boundary condition with a pulsatile motion Irom
spinal chord, which is actually the cause Ior CSF
motion. Since we have no idea oI what might be
the velocities oI the CSF aIter the blast impact, we
use a pressure inlet boundary condition as a blast
impulse with a certain reduction in blast intensity
as we have no dynamic model to judge the skull
deIormation and the pressure outlet as the normal
CSF pressure.

RESULTS AND DISCUSSION
A study is made to analyze the outcomes oI
CSF pressures inside the subarchnoid region and
ventricular spaces and hence to indicate the cause
behind their enlargement in TBI through CFD
simulation. Here, the geometry is restricted to a 2D
brain section as obtained in MRI. The meshed 2D
geometry was imported to Fluent version 6.3 and a
blast intensity oI around 10 bars was imposed on
the anterior side as stated. The unsteady pressure
dynamics within CFS pathways aIter the onset oI a
blast are presented in Fig. 3 (a-h). These illustrate
the cascading oI events within a Iew milliseconds
(ms), which are very thought, provoking and
indeed explain the pressure propagation through
CSF Iluid. The details are explained below.
Fig 3a shows the peak rise oI pressure in CSF
in the Irontal region oI the brain due to the onset oI
blast wave (near the inlet pressure boundary) aIter
a time interval oI 0.5 milliseconds (ms). This
abnormal increase in pressure would deIinitely
perturb the Ilow oI CSF Iluid and a sudden drop oI
CSF pressure is observed in the ventricular region.
As time progressed (t2 ms), there is not much
change in distribution oI pressure gradient,
however the magnitude oI intense pressure in the
Irontal region is reduced and the pressure in the
ventricular region is increased indicating that the
pressure is transmitted to the ventricular spaces,
Fig 3b.
At t3 ms, a considerable change is observed in
pressure variation with augmentation oI pressure
around the cerebellum depicting reIlection oI
pressure wave Irom the boundary oI the constricted
passage between the brain and spinal chord, Fig 3c.
The pressure wave propagates along the
subarchnoid spaces towards the rear part oI the
brain, where the magnitude is about 10
4
Pa and the
pressure diminution begins in the Irontal region. At
this instant, the pressure in the ventricles is also
increased and a large pressure gradient oI about 10
3

Pa exists between the ventricles and porous
parenchyma. This pressure diIIerence is much
greater than what was observed by HoII and Barber
|18| during their studies with Iour patients
suIIering Irom pressure hydrocephalus, where they
Iound that mean ventricular pressure was 260 Pa
higher than mean pressure in the subdural space.
Thus, this momentarily rise in intense pressure may
cause a signiIicant damage.
At t4 ms, the pressure is high in the
ventricular region and also in porous parenchyma
as compared to the subarchnoid spaces, Fig 3d.
Now, the pressure gradient between the ventricle
with parenchyma and the subarchnoid spaces may
cause a potential damage to the axons due to
stretching. Here, the dark blue region in the Irontal
part oI the brain indicates the advent oI negative
phase oI the blast wave causing the pressure in CSF
to reach a low value. The trend continues to persist
upto t 6.5 ms, Fig 3e. At t 20 ms, the pressure is
now traveling back Irom ventricular space towards
the Irontal region along the CSF pathways similar
to a reIlected wave motion, Fig 3I. This unsteady
phenomena, indicating augmentation oI pressure as
a Iunction oI space and time appears Iar more

7
serious causing distortion in diIIerent parts oI the
brain. The pressure slowly eases to normal CSF
pressure as time progresses, although even at t 30
ms, Fig 3g, a pressure accumulation occurs behind
the cerebellum. By around 38 ms the pressure in
the CSF pathways and other parts oI the brain is
almost stabilized, Fig 3h.








Fig. 3 Pressure contours at diIIerent instant oI time
depicting unsteady pressure dynamics within CFS
pathways due to exposure to a blast wave.

8
The evolution oI pressure history Irom Iew
points (marked as P1, P2, P3 and P4) shown in
Fig 4 is very revealing. The pressure variation at P1
is similar to the blast wave as expected since the
point lies near the inlet boundary. At P2, which is
behind the cerebellum, there is a sudden increase
Iollowed by a sharp drop oI pressure within 1 ms
and again the pressure increases to about 2 bar that
decays as time progresses. It is interesting to note
that the pressure at the rear part oI the brain is
substantial Ior a considerable time Irom 2.5 ms to
12 ms. This high pressure acting Ior a relatively
longer time has a potential to cause serious material
acceleration and associated injury, which has not
been shown earlier.
Pressure excitation at P3 and P4, the ventricular
space and the CSF passage below respectively,
Iollow the trend oI the blast wave but the
interesting part is that there exist high pressure
Iluctuations during the time t 10 ms to 25 ms.
The amplitude oI oscillations at least in Iew
instances shows very high values. There is a second
phase oI oscillations as seen at around 38 ms,
although the amplitude is low. These oscillations
would be associated with Ilow reversals and
perturb the CSF Ilow. Furthermore the ventricular
space is exposed to a large negative pressure Ior a
longer time t4ms to 12 ms (except Iew instances).
This Iigure also illustrates that although there are
signiIicant changes in pressure Iields and thus
induced stresses within a short interval oI time oI 6
ms aIter the advent oI blast, however there can be
excitation that may appear over a longer span oI
time even up to 30 ms.
The velocity Iields oI CSF Iluid are illustrated
by velocity contours and magniIied velocity
vectors at instants oI 3.5 ms and 95 ms aIter the
onset oI blast. At 3.5 ms the Ilow is directed
towards the ventricles, which is attributed to the
relatively negative pressure in the region and this
Ilow direction is opposite to the normal CSF Ilow.
AIter a considerable long interval oI time, almost
normal Iluid movements inside the subarchnoid
and ventricular region are established, although the
magnitudes in some portion are higher than the
normal conditions.
The present study explains that the pressure
wave can propagate through the CSF and may
develop an intense pressure in CSF pathways;
while some investigations did not consider CSF
separately rather they modeled the whole brain as
viscoelastic media |2| and showed how it
responded under a shock wave. Thus, there is a
need to model both the CSF and the brain
parenchyma separately and we believe that there
exist nonlinear interactions between the brain tissue
and CSF, which need to be resolved.

CONCLUSIONS
Analysis through CFD has been made to
indicate the pressure dynamics in CSF that may
lead to blast induced TBI. Previous studies made in
this direction concentrated on transmission oI
pressure pulse into the brain considering the
parenchyma region as a viscoelastic medium
neglecting the role oI CSF and did not discuss the
reason behind the expansion oI CSF space and
brain ventricles. Our main analysis is centered on
CSF examining its role in blast induced cases.
The momentum equations oI Iluid have been
solved with continuity and realistic boundary
conditions Ior the blast wave and the heart pulse
have been applied to the 2D brain geometry with
necessary material properties oI the brain. It has
been observed that an unsteady pressure response is
developed in the CSF pathways. The pressure
gradient between the ventricles and the porous
parenchyma is considerably high that indicates the
reason oI ventricular expansion. Instantaneous
pressure also becomes high in the subarchnoid and
backward region oI the brain. A pressure
oscillation is seen in the ventricular region that is
noteworthy. The intense activity oI this varying
pressure gradient occurs within 6ms oI the blast
application; however it is noted that even aIter
30ms the residuals pressure in some portion oI the
CSF pathways is considerable, which then
gradually reduces to normal CSF pressure as time
progresses.
In our opinion, this work provides a qualitative
evaluation oI CSF pressure that may be related to
the cause oI expansion oI CSF pathways and
ventricular spaces as cited in ReI 1 while observing
patients suIIering Irom TBI through CT scans.
However, the present model can be improved by
considering the grey material to be viscoelastic.

9































Fig. 4 Variation oI pressure Irom diIIerent points as marked in the CFS pathways.













a) Time3.5 ms (b) Time95 ms

Fig. 5 Velocity contours and vectors at two time intervals.

P
3

P
4

P
1

P
2

10 20 30 40 50 60
-2.0E+05
0.0E+00
2.0E+05
4.0E+05
6.0E+05
10 20 30 40 50 60
-30000.0
-20000.0
-10000.0
0.0
10000.0
20000.0
10 20 30 40 50 60
-50000.0
-40000.0
-30000.0
-20000.0
-10000.0
0.0
10000.0
20000.0
10 20 30 40 50 60
-2.0E+05
0.0E+00
2.0E+05
4.0E+05
6.0E+05

P
1
P
2

p (Pa)











P
3
P
4

p (Pa)






t (ms) t(ms)

10
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