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Cisternostomy Introducing the concept of CSF shift edema

Cisternotomia para tratamento cirrgico do edema cerebral, por

acumulao de LCR

Margarita Beltran & Iype Cherian

College of Medical Sciences, Bharatpur, Nepal

Corresponding author Iype Cherian; Email ID - drrajucherian@gmail.com

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16

Abstract
Brain edema after severe head injury plays an important role in the outcome, and overall survival of injured
patients, and it is one of the main targets in the therapeutic approach in the clinical practice. The
physiopathology of traumatic brain swelling is complex and not yet totally understood, but until now it is
supposed to be mainly vasogenic and cytotoxic, in origin. However, based on new understandings of the
hemodynamic of cerebrospinal fluid (CSF), an additional mechanism of brain swelling is proposed in this paper.
In our opinion, an increase of pressure in the subarachnoid space, secondary to traumatic subarachnoid
hemorrhage, would result in a shift of CSF from the cisterns into the brain parenchyma, through the paravascular spaces, following a pressure gradient, and resulting in an increase of the water content of the brain.
This mechanism of brain swelling has been described for the first time in this paper and would be termed as
CSF Shift edema. This CSF-shift, driven by pressure gradient, would lead in addition, to an increase of
pressure inside the para-vascular spaces and in the interstitium of the brain, disturbing the functions of the paravascular system with implications in the development of secondary brain injury. Cisternostomy, an innovative
technique in the handling of traumatic brain injury, would directly reverse the direction of the CSF Shift, what
would explain the fast decrease of brain swelling right after the procedure. In addition, this technique would
reduce the pressure in the para-vascular spaces and interstitium leading to a recovery of the functionality of the
para-vascular system, which would result in a decrease of secondary brain damage. The proposed mechanism
would explain the advantage of this technique in terms of morbidity and mortality, compared to decompressive
hemicraniectomy.

Keywords: head trauma, decompressive hemicraniectomy, cisternostomy, brain edema, CSF

shift edema, paravascular pathway

Resumo
O edema cerebral aps traumatismo craniano grave desempenha um papel importante no resultado final e
sobrevivncia global dos pacientes afetados, e um dos principais alvos na abordagem teraputica na prtica
clnica. A fisiopatologia do edema cerebral traumtico complexa e ainda no totalmente compreendida, mas
at agora supe-se ser principalmente vasognico e citotxico, na sua origem. No entanto, com base nos novos
entendimentos da hemodinmica do lquido cefalorraquidiano (LCR), proposto neste trabalho um mecanismo
adicional de edema cerebral. Na nossa opinio, um aumento de presso no espao subaracnide, secundria a
hemorragia subaracnide traumtica, resultaria numa mudana do LCR a partir das cisternas para o parnquima
cerebral, atravs dos espaos para-vasculares, na sequncia de um gradiente de presso, resultando num
aumento do contedo de gua do crebro. Este mecanismo de edema cerebral foi descrito pela primeira vez
neste trabalho e poderia ser denominado como "LCR-shift". Este "LCR-shift", impulsionado por um gradiente
de presso, conduzido pelo gradiente de presso, levaria a um aumento de presso no interior dos
espaos perivasculares e no interstcio do crebro, perturbando as funes do sistema para-vascular com
implicaes no desenvolvimento de leso cerebral secundria. A cisternotomia, uma tcnica inovadora no
tratamento da leso cerebral traumtica, iria reverter directamente a direco do "LCR-shift", o que poderia
explicar a diminuio rpida do edema cerebral logo aps o procedimento. Alm disso, esta tcnica iria reduzir
a presso nos espaos paravascular e interstcio que conduziria a uma recuperao da funcionalidade do sistema
para-vascular, o que iria resultar numa diminuio dos danos cerebrais secundrio. O mecanismo proposto
poderia explicar a vantagem desta tcnica em termos de morbidade e mortalidade, em comparao com a
hemicraniectomia descompressiva.

Palavras-Chave: traumatismo craniano, hemicraniectomia descompressiva, cisternostomia,

edema cerebral, edema LCR-shift, via paravascular

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Introduction

Traumatic brain injury (TBI) is a

vasogenic and cytotoxic edema have been

life threatening condition in which the

implicated in the pathophysiology of brain

development of secondary cerebral edema

swelling

is one of the most critical factors in

secondary to disruption of the bloodbrain

patients morbidity and mortality.

barrier (BB), and cellular swelling due to a

Excessive

accumulation

of

after

severe

head

injury,

leakage of intracellular osmolytes into the

interstitial fluid is detrimental to brain

extracellular

space,

respectively

function in a bilateral direction because

(Unterberg et al., 2004), (Stephens et al.,

this excessive accumulation of fluid

2015).

increases the diffusion distance for oxygen

additional source of brain swelling may be

and other nutrients from the vessels,

implicated in the pathophysiology of post-

compromising cellular metabolism, and

traumatic edema, as discussed above.

However, in our opinion, an

this would also limit the diffusional

Discussion

removal of potentially toxic byproducts

(Scallan et al., 2010).
Occurring

within

To understand the mechanisms that

the

closed

underlie postraumatic brain edema and

confines of the skull and meninges, overall

how cisternostomy may help, we would

brain swelling leads to raised intracranial

first need to review some new concepts

pressure, decrease of brains compliance

about the dynamics of fluid in the central

and cessation of the brain blood supply.

nervous system (CNS).

Therefore, the degree and extent of edema

Ventricular,

subarachnoid,

determines the clinical outcome of the

perivascular, and interstitial compartments

patient (Marmarou et al., 2007). Both,

constitute

METHODOLOGICAL

continuum,

or

fluid

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functional unit (Brodbelt et al. 2003),

connected

through

(Bulat & Klarica 2011). The cerebro spinal

spaces

fluid (CSF) in the subarachnoid space and

pathophysiology).

the

(Figure

1.

18

para-vascular
Schema

of

the interstitial fluid (ISF) are particularly

Figure 1 This schematic diagram shows the connection between brain interstitial fluid (in
yellow) and the cistern (in blue) through the para vascular spaces around the perforating
arteries (in red).

These are the spaces between the end

interstitium

and

called

glympathic

feet of the perivascular astrocytes and the

system(Iliff et al. 2012, 2013), (Xie et al.

vessel wall (Thrane et al. 2013), extending

2014),(Yang et al. 2013).

all the way along penetrating arterioles to

According to

the

capillaries and along veins (Iliff et al.

exchange,

2012).

These para-vascular spaces have

(AQP4), the main water channel in the

recently been described as a system to

brain (Iliff et al. 2012), (Papadopoulos &

clear interstitial waste from the brain

Verkman 2013)

METHODOLOGICAL

mediated

by

authors, fluid
aquaporin

(Nakada 2014) takes

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19

place between ISF and para-vascular

depends on the patency of para-vascular

spaces clearing solutes with outflow of

spaces and depends on the hydrostatic and

solutes mainly in the para-venular side

osmotic pressures between ISF, the para-

(Iliff et al. 2012). Arterial pulsation seems

vascular channels and the vascular system.

to play an important role in the flux of

The exchanges of fluid and waste take

fluid along this para-vascular pathway

place through AQP4, which allows very

(Iliff et al. 2013).

fast bidirectional flow in response to

Reabsorption of CSF is no longer

believed to occur through Pacchionnian

pressure and osmotic gradients, (Agre

2006).

granulations. Nowadays, it is believed that

In the setting of severe head trauma,

in physiological conditions, reabsorption

subarachnoid hemorrhage (SAH) is almost

of CSF and ISF occurs mainly across the

always associated (Cherian et al., 2016).

vessels of the brain, particularly across the

In our opinion, this arterial bleeding into

walls

and

the cisterns would lead to a rise of the

postcapillary venules (Bulat et al., 2008;

pressure in the subarachnoid compartment.

Bulat & Klarica, 2011) depending on

In the case of an aneurysm rupture, this

hydrostatic pressure and osmotic forces

bleeding

(Orekovi & Klarica, 2010), (Marakovi

intracranial pressure soon becomes equal

et al., 2010), (Chikly & Quaghebeur,

to that of the MAP. However, the capillary

2013),

(AQP4)

bleeding in trauma occurs at a relatively

(Papadopoulos & Verkman, 2007), in the

lower pressure and may continue on for a

perivascular astrocytic endfeet (Mathiisen

longer time, as long as the ICP is not equal

et al., 2010).

to the mean arterial pressure. This would

of

also

venous

capillaries

controlled

by

stops

immediately

as

the

To sum up, both reabsorption of

provoke a shift of CSF from the cisterns

excess water and waste from the ISF

into the para-vascular spaces and from

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20

there to the ISF, driven by pressure

mechanism of posttraumatic edema and

gradient and perhaps mediated by AQP4.

would call it CSF-shift edema, (Figure

We

2).

propose this as an additional

Figure 2. CSF shift Edema The subarachnoid hemorrhage in trauma raises the pressure
in the cisterns, however the intracerebral pressure remains lower than the cisternal
compartment. This results in a shift of CSF driven by the pressure gradient, through
the Virchow Robin spaces into the brain. This mechanism of edema has been termed
as CSF shift edema.

The increase in pressure originated in

the

subarachnoid

space

be

physically compressed (Unterberg et al.,

transmitted to the rest of the fluid unit:

2004). The blockage of function of the

para-vascular spaces and interstitial fluid.

paravascular spaces would lead to a

As a consequence of the increase of

decrease in the absorption of fluid from the

pressure in the interstitial fluid a functional

ISF by the capillaries and to a decrease of

blockage of the para-vascular system

clearance of mediators that are released

(glympathic system) may take place

from the injured cells, following traumatic

because the transmural pressure gradient

brain

between capillaries and interstitial fluid is

neurotrasminers (glutamate), lactate or free

METHODOLOGICAL

would

reduced and capillaries and veins are

injury,

including

excitotoxic

CISTERNOSTOMY

21

oxygen radicals (Unterberg et al., 2004).

less than the pressure in the subarachnoid

Those mediators enhance vasogenic and/or

compartment [(around 60mmHg which is

cytotoxic brain edema perpetuating the

the pressure in the small arteries in the

accumulation of fluid in the brain, as well

subarachnoid

as

and

source of the subarachnoid bleeding)]. It

inflammation that may lead to microglia

means that even if the intracranial pressure

activation, apoptotic and necrotic cell

is released by decompressive craniectomy,

death

2007),

the functional blockage of the para-

therefore

vascular system would persist to a

excitotoxic

(Werner

(Unterberg

et

cell

damage

&

Engelhard,

al.,

2004),

increasing secondary brain damage.

In addition, the patency of paravascular

system

may also

(Shulman,

significant

level

and

underlying

mechanism

1965),

therefore
for

the

cytotoxic

an

edema persists as well as the impairment

important role in local control of brain

of absorption of interstitial fluid by the

temperature which appears to increase

capillaries and probably the lack of

after head injuries (Soukup et al., 2002).

buffering of temperature by CSF. It is

Decompressive

have

space

craniectomy

possible that as a part of the entire

decreases the intracranial pressure and

expansion of the intracranial volume all

therefore the pressure in the interstitium by

these pressures do come down, but this

increasing the volume, resulting in an

procedure does not address the root of the

expansion of the brain through the

problem,

craniectomy site. However, as the origin of

subarachnoid pressure and consequent

the high pressure in the fluid unit would be

intracerebral pressure.

in

the

subarachnoid

compartment,

which

is

Cisternostomy,

the

is

increase

in

surgical

particularly in the basal cisterns, the

procedure combining the principles of

pressure in the interstitial fluid cannot be

microvascular and skull base surgery, to

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CISTERNOSTOMY
open the basal cisterns of the subarachnoid

22

We hypothesize that interstitial

space to atmospheric pressure (Cherian &

fluid

Munakomi, 2013). This technique applied

postraumatic brain, exits along the para-

in selected cases of severe traumatic brain

vascular pathway, following a pressure

injuries

dramatically

gradient, after cisternostomy; moving fast

decrease the mortality and morbidity of

from the high pressure of the edematous

patients compared with decompressive

brain towards the lower atmospheric

hemicraniectomy (Cherian et al., 2013,

pressure of the opened basal cisterns

2016).

(Figure 3).

has

proved

to

(ISF),

accumulated

in

the

Figure 3. The surgical procedure of Cisternostomy utilizes skullbase technique to access and
open the cisterns. This results in reversal of the pressure gradient of the CSF shift edema
and the fluid shifts back into the cisterns. This also brings down the intracerebral pressure.
brain, an increase of the brain compliance
This mechanism would explain the
fact that immediately after the opening of
the cisterns a decrease of the tension of the

METHODOLOGICAL

and increase of cerebral pulsation are

observed (see the video below).

CISTERNOSTOMY
Neurosurgeons are familiar with

23

increasing the reabsorbing of ISF fluid by

this phenomenon in aneurysm and tumor

capillaries,

surgery where opening the brain provides

neurotoxic substances in the interstitium

an improvement in the compliance of the

and locally reducing brain heat, that would

brain. However, this had never been

help in the decrease of secondary damage

applied in trauma patients, as opening the

of post-traumatic brain.

cisterns in those cases is challenging and

The

allowing

proposed

to

removal

of

pathophysiology

commonly are in hands of juniors,

would explain the improvement of the

residents or consultants. Furthermore, the

evolution and clinical outcome in the short

movement of fluid from the injured brain

and long term of the patients treated with

towards

by

cisternostomy compared with those treated

cisternostomy, would wash out mediators

with decompressive craniectomy (Cherian

that are released from the injured cells,

et al., 2013, 2016). In our opinion,

following

cisternostomy address one of the possible

the

cisterns,

trauma

and

achieved

thus

reduce

secondary traumatic brain damage of the

roots

of

traumatic

brain

edema

by

brain.

reversing the edematous mechanism of

The decrease of pressure in the

csf-shif edema, allowing to a removal of

opened cisterns would be transmitted

neurotoxic substances in the interstitium

through the fluid unit to para-vascular

and recovering the functionality of the

spaces and interstitial level allowing a

para-vascular system.

recovery of the paravascular flow so

Conclusion

The shift of CSF from the cisterns

to the brain following a pressure gradient
or CSF-shift edema, could play an

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24

essential role in the pathophysiology of

immediate reduction of the brain swelling

brain swelling and in the development of

and probable alleviation of the underlying

secondary brain damage of the brain.

mechanism leading to secondary brain

By cisternostomy, the direction of

damage.

the CSF-shift is reversed resulting in a

Video Cisternostomy

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CISTERNOSTOMY
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How to cite this Article: Beltran, M., & Cherian, I.(2016). Cisternostomy Introducing the concept of CSF shift edema. International
METHODOLOGICAL
Journal
of Psychology and Neuroscience, 2(1), 15-29
Received: 13/04/2016; Revised: 18/04/2016; Accepted: 22/04/2016; Published online: 09/05/2016
ISBN 2183-5829