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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3609_Библиотеки_им_академика_М_И_Перельмана
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ac
b
Fig. 30.4 The images on the left hand side (a) show a sagittal section
passing through the Central Sulcus of the Insula (open arrow) on the top
image and through the Central Sulcus of Rolando (closed arrow) in the
bottom image (b). It can be seen that these are continuous anatomically
and divide the telencephalon into an anterior part and a posterior part.
The entire anterior part is referred to as the “Epistriatal Zone” and the
Zone” as it is in relation with the Hippocampal formation.
Each of these, i.e. the Epistriatal Zone and the Epihippocampal
Zone, contains eight histogenetic units. Each of these histogenetic units, while being completely different from each
other in terms of development, genetic markers, and protein
expression, is remarkably similar in terms of their overall
shape, orientation, and blood supply.
Each histogenetic unit has a stem of white matter, originating from the periventricular area, which divides into two
or more as it reaches the subpial location. This is capped by
its grey matter, and this entire construct is referred to as a
gyral unit (Fig.30.5). Gyri are much more than 16in each
hemisphere; however the white matter stems in each hemisphere are only 16, and these divide and subdivide to produce sub-gyri, which interdigitate to produce the Neopallial
gyral formation.
These “gyral units” are pyramidal in shape, with the
pointed apex towards the ventricle and the broad base
towards the pial surface. Eight of them interdigitate with
each other in the Epistriatal and Epihippocampal Zones, thus
producing the entire construct of the Neopallium.
As already mentioned, brain AVMs are predominantly
found in the Neopallium. Thus in order to understand the
angio-architecture, one needs to have a detailed understand-
entire posterior part is referred to as the “Epihippocampal Zone”. Each
of these contains eight histogenetic units. The image on the right (c) is
a cone beam CT angiography with the Central Sulcus approximately
superimposed, showing the striates (stars) related to the anterior and the
choroidals (arrowheads) related to the posterior
ing of the normal angio-architecture of a Neopallial Gyral
Unit. This will dene the “regional” Angio-architecture of
the lesion. Once that is identied, the second step will be to
elaborate the Angio-architectural, intralesional variations.
Arterial System: TheNeopallial,
Leptomeningeal Angio-architecture
The entire Neopallium is covered by a network of blood vessels originating from the branches of anterior, middle, and
posterior cerebral arteries. Middle cerebral contribution is
dominant on the convexity, anterior cerebral contribution is
predominant on the medial surface, and the posterior cerebral completes the network on the inferior surface. Since the
majority of the Neopallium is represented on the convexity,
it is reasonable to understand the pial leptomeningeal Angioarchitecture based on the middle cerebral artery as a prototype (Fig.30.6).
A leptomeningeal branch enters and dips into a Sulcus,
where it is called the “descending sulcal” segment. This
artery reaches the depths of the Sulcus, up to the fundus,
before taking a 180° turn and travelling up the opposite lip of
the Sulcus, referred to as the ascending sulcal segment. Upon
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Fig. 30.5 T1-weighted
sagittal and coronal sections.
Conceptualization of the
white matter stems (black
circles) superimposed over
the white matter showing the
branching white matter stems
being capped by the grey
matter to form the
interdigitating gyral structure
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ab c
Fig. 30.6 The upper left-hand side image (a) shows the pial surface
(grey solid line) as well as the grey-white junction (grey dotted line).
The second image in the top panel on the right-hand side (b) shows the
arterial system superimposed. It shows the descending (1) and ascending (2) Sulcal segments as well as the transverse gyral segment (3)
reaching the pial surface, this arterial twig continues its journey towards the next Sulcus, across the crown of the gyrus.
Here it is important to note that arteries in the Neopallium
cross transversely over the crown of the gyrus. This pattern
continues repeatedly over all the gyri thus creating a network
of vessels. This network is the main structure that supplies
the grey and white matter of the individual gyri via the nextorder branches that will be discussed below.
Small, 200-micron penetrating branches originate from
this leptomeningeal network and pierce the grey matter to
enter the white matter of the gyrus. These usually originate
from the mid-transverse gyral segment, from the mid ascending or descending sulcal segment and also from the fundal
segment of the leptomeningeal artery. The small twigs might
going over the crown of the gyrus. The third image (c) shows the nal
supplying the grey and white matter to various extents, and by extension supplying the AVMs located in the telencephalon
be very small and supply only a couple of cortical grey matter layers, or they might be very long and supply up to the
periventricular deep white matter.
The “Deep” Supply toNeopallial AVMs
As elucidated earlier, the “phylogenetic boundary” between
the Neopallium and the rest of the brain lies at an imaginary
line joining the three primordial sulci. This has important
implications for the vascular territories of the arterial systems. All the brain areas lying “outside” this circle is supplied by the leptomeningeal angio-arcade made up of vessels
from the middle cerebral, anterior cerebral, and posterior
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cerebral arteries. All the brain areas lying “inside” this phylogenetic circle derive the blood supply from the striate system or the choroidal system, depending on whether they lie
in the Epistriatal Zone or in the Epihippocampal Zone. The
internal watershed lies at the phylogenetic boundary. This
automatically tells us that if a Neopallial AVM crosses the
boundary zone, the deep supply to the AVM will come from
the striate or from the choroidal system. If the Neopallial
AVM is located in the Epistriatal Zone, i.e. anterior to the
Central Sulcus, the deep supply will mandatorily come from
the striate system. As for a Neopallial AVM located in the
Epihippocampal Zone, the deep supply, if it transgresses the
phylogenetic boundary, will come from the choroidal
system.
Venous Drainage oftheNeopallium
There are signicant differences between the arterial and
venous systems of the Neopallium. Unlike the arterial system, the venous system has many more built-in redundancies
that make it more complex and also more forgiving
(Fig.30.7).
A Neopallial Gyral Unit has two marginal veins on either
side in the sulci that demarcate the gyrus. These Marginal
Sulcal Draining Veins are formed by the union of many
smaller veins and venules from the substance of the gyrus.
As far as the sharing of the drainage of the gyrus between the
supercial leptomeningeal and the deep venous systems are
concerned, it is not as straightforward as the arterial system.
The phylogenetic boundary is not respected here, like in the
arterial distribution.
A small portion of the Neopallium drains into the supercial venous system. The remainder of the Neopallium that is
outside the phylogenetic boundary, as well as the entire brain
parenchyma within the phylogenetic circle, drains into the
deep venous system.
Therefore, apart from the very small, sulcal types of
AVMs, all the Neopallial AVMs of reasonable size will have
a dual venous drainage into both the supercial and deep
venous systems. This does not correlate with the phylogenetic boundary and needs to be kept in mind while planning
the curative embolization of brain AVMs.
Since brain AVMs are located in the Neopallium predominantly, the regional Angio-architecture of the lesion will be
based on the Angio-architectural characteristics of the
Neopallium elaborated above. Broadly speaking, these are of
two distinct subtypes:
1. A situation in which the AVM is located in the subpial
location, covered by a thin glial limiting membrane,
where a leptomeningeal artery is seen to end, haemodynamically, in the lesion. These are referred to as “Sulcal”
AVMs.
2. A second situation, where the AVM is located within the
Neopallium, in the subcortical white matter, covered by
the grey matter all around it. In this situation, the feeding
arteries are the 200 micron twigs mentioned earlier that
pass through the cortex and then either supply the AVM
exclusively or supply both the AVM and the brain parenchyma. These are referred to as “gyral” AVMs.
Very often during a clinical case, it becomes difcult to
compartmentalize a particular AVM into a strict sense, and
most often the lesion will demonstrate a mixed Angioarchitecture that shows some properties of each subtype
(Figs.30.8 and 30.9).
Fig. 30.7 The angio-architecture of a gyral unit superimposed over a
gyrus as seen on MR.Arteries in red and veins in blue. Unlike arteries,
veins do not cross over the gyrus. Instead they are seen in the sulci and
are referred to as the Marginal Gyral Veins (open arrowheads). Many of
these coalesce to form a cortical vein (closed arrowhead) that empties
into a venous sinus
Nidus
In the available literature on brain AVMs, the description of
the “nidus” is nebulous at best. Any part of the Angioarchitecture apart from the named arterial twig(s) is clubbed
together as the “nidus”. It has been well established now that
the AVM nidus is mainly a venous structure. These are based
on histopathological as well as immunological ndings and
are in concurrence with the material that has accumulated
over the years from the interventional literature. Beyond this,
there is not much information, especially invivo.
Over the last decade, the authors of this chapter have
developed techniques that allow us to study the angioarchitectural characteristics of the nidus in vivo with the
information obtained during routine clinical work of curative
embolization sessions of brain AVMs. Just a small introduction to in vivo catheter cone beam CT angiography
(CCBCTA) is mentioned here for reference.
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Fig. 30.8 An example of a
microcatheter angiogram of a
Sulcal type of AVM.The
microcatheter is seen crossing
over the crown of the gyrus
(closed arrow) and is then
seen entering the AVM nidus
from the descending sulcal
segment (open arrow), with
no supply to any surrounding
structures
Fig. 30.9 An example of a
microcatheter angiogram of a
gyral type of AVM.The
microcatheter is seen in the
ascending sulcal segment
(arrow) just before crossing
over the crown of the gyrus
(arrowhead). From the
midpoint of the transverse
gyral segment on the crown of
the gyrus, a medullary branch
(open arrowhead) can be seen
entering deep into the white
matter of the gyrus and
supplying the AVM.The
transverse gyral segment
continues over to the next
histogenetic unit
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Catheter cone beam CT angiography (CCBCTA) is a technique performed in the interventional suite during catheter
angiography. This study can be done on any current generation
at-panel angiography system. The study is done with an
effective detector size of 20x20 cm, at magnication. A 0.5k
by 0.5k matrix is used for the raw image acquisition. The rotation speed is 10° per second, and the total coverage arc should
be at least 200° around the patient. Therefore, the total rotation
time will be about 25s, which includes the true rotation time
of 20s as well as a 5-s delay between the beginning of contrast
injection and the beginning of image acquisition. The images
are acquired under apnoea induced by the anaesthesiologist to
avoid any motion-related artefacts. The contrast agent used is
a diluted mixture of 25% contrast (Omnipaque 300, GE
Healthcare, USA) with normal saline, injected by a pressure
injector, at 200 PSI pressure at a rate of 3mL/s for 20s.
With this technique, a very high-resolution image dataset
is acquired that shows us the entire nidus preprocedure. The
same study is repeated after embolization is complete, and
this time the acquisition allows us to make a 3D model of the
cast of embolic material that has been lled inside the
AVM.The cast of the AVM nidus is a wonderful surrogate of
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the angio-architecture of the nidus per se. Combining the
information obtained from many such studies, an interesting
three-dimensional structure of the nidus has evolved
(Figs.30.10 and 30.11).
ab
ef
By superimposing many such images, we have come to
realize that the AVM “nidus” is a very complex structure
consisting of at least three zones, and the morphological
characteristics of the three zones are very different from each
other (Fig.30.12).
g
h
ab
ef
Fig. 30.10 Sequential 0.2mm sections through the AVM as seen on
catheter cone beam CT angiographic exploration. The uppermost panel,
consisting of images A through H, shows the native images as obtained
during the exploration. Thereafter, each of the components, i.e. arteries,
g
veins, and the nidus, has been colour coded. Arteries in red, veins in
blue, and the nidus in pink. The bottom panel shows a composite
impression of the entire AVM structure
h
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a
e
a
bcd
f
g
bcd
h
ef
Fig. 30.10 (continued)
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h
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R. Kumar et al.
Fig. 30.10 (continued)
Fig. 30.11 Sequential 0.2 mm sections through the AVM glue cast
post-embolization as seen on catheter cone beam CT angiographic
exploration. These are AP and lateral view images of the glue cast
showing the details of the nidus per se
As already mentioned, a brain AVM within a histogenetic
unit of the Neopallium can be visualized as a pyramidal
structure, with its base towards the convexity and the apex
towards the ventricle. This AVM nidus has three distinct
zones and many more different types of vessels within itself
that have very different fragility and morphology.
The outermost zone is arterial, and this zone contains the
ramifying, arborizing arterial twigs from the leptomeningeal
system that form a dense meshwork on the outer aspect of
the pyramid. This is the area where the arterial system meets
the venous system, and the arteriovenous shunts are created
at this point. Angio-architecturally, these are pretty straightforward. This is also the zone that is accessible to the interventionalist for catheterization when doing a trans-arterial
embolization.
The complexity of the nidus starts when one reaches the
intermediate zone of the AVM.This is a venous zone and,
also in case of Neopallial AVMs, is the area that holds the
“compartments” of the AVM. This is a zone made up of
venous structures. The various types of vascular channels
found in this zone are the spiral types, the loose vertical
loopy type, the loose vertical plexiform type, and the very
distinct subtype of channels located at right angles to the previous subtypes. This fourth type represents the intercompartmental connections, and it is the most delicate in
terms of fragility. Most of the intranidal aneurysms in our
material were on this subtype of the intermediate zone vessel. The innermost zone is the collector zone. All the compartmental draining veins converge at this level and exit as
the nidal draining vein. In the recent years, this zone has also
become a potential target for the treatment of brain AVMs by
the transvenous route.
a
b
c
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Fig. 30.12 A composite
image of the AVM nidus as
seen during both invitro and
invivo explorations. The
types of vascular structures
found within the nidus are
elaborated in the colour-coded
diagram on the left and in a
tabular form on the right
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Fig. 30.13 A composite
image of the AVM nidus types
as seen during both invitro
and invivo explorations. The
rarest subtype seems to be the
pure “stulous” type (a),
where an artery is seen
connecting directly to a vein.
These are high-ow lesions.
The most common type seems
to be a mixture of stulous
and plexiform (b), followed
by the pure plexiform types
(c)
Nidal Subtypes
1. Pure stulous—Like pial stulae. These are the rarest
subtype of brain AVMs.
Based on CCBCTA studies of the treated AVMs at our institute as well as microcatheter explorations of these AVMs, we
have been able to subclassify these into at least three differ-
2. Pure plexiform—Our belief was this would be the most
common subtype, but it happens to be the second most
common type, representing a third of cases.
ent groups (Fig.30.13).
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3. Mixed stulous and plexiform—More than half of the
cases embolized belong to this subgroup and is the most
common phenotype that is encountered during the embolization sessions.
It is easy to understand that these three subtypes of brain
AVMs represent completely different anatomical, angioarchitectural, and haemodynamic situations; a “one size ts
all” approach towards brain AVMs is more than likely to produce suboptimal results.
At the end of this discussion, the regional and lesional
anatomy, angio-architecture, and possible sites of intervention for the curative embolization are clear. One has to be
able to get into the outermost arterial zone of the nidus with
a microcatheter(s), deposit the embolic material within the
nidus, either one compartment at a time or progressively
through the inter-compartmental connections, and occlude
just a small part of the nidal exiting vein for complete and
lasting cure.
Historical Aspects ofAVM Embolization
Luessenhop and Spence performed the rst-ever endovascular embolization of an AVM [4]. Since then a signicant
progress has taken place in the endovascular techniques
and materials that has allowed higher cure rates with the
endovascular modality. The understanding of the angioarchitecture and the ow dynamics has improved remarkably over time, especially with the advent of newer and
superior imaging modalities, aiding in proper selection of
patients, modalities of treatment, and better outcomes.
Endovascular embolization of cerebral AVMs has evolved
from a simple technique of blocking the feeding arteries of
an AVM to a highly sophisticated technique of selecting
and accessing the feeding arteries to reach and obliterate
the nidus of an AVM [1]. Materials for endovascular embolization have also evolved from polyvinyl alcohol (PVA)
particles to n-butyl cyanoacrylate (NBCA) glue to nonadhesive liquid embolic agents comprising ethylene vinyl
alcohol (EVOH) copolymers dissolved in dimethyl sulfoxide (DMSO) and micronized tantalum powder (Onyx,
Squid, or PHIL). Also there has been an enormous progress
in the eld of neurovascular access systems and devices
with the renement of ow- guided and combined ow- and
guidewire-directed microcatheters since the mid-1980s,
allowing for precise, safe, and super-selective access to
AVMs in any location. Due to all these factors, endovascular embolization of AVMs nowadays can achieve complete
cure in many cases without requiring additional treatment
modality.
Role ofEmbolization intheManagement
ofAVM
The application of endovascular embolization in the management of AVM has expanded due to the recent development in the eld of neurovascular intervention. Embolization
of an AVM is no longer considered a mere adjuvant treatment modality. Currently the indications of embolization in
the management of AVM include the following.
1. Presurgical Embolization
Endovascular embolization can be done to reduce the
size of a large AVM, thus making it amenable for microsurgery or radiosurgery. In these scenarios, embolization
must be done in the immediate preoperative period, and a
delay of several days can make the procedure useless
because of AVM regrowth [5].
2. Therapeutic Embolization
Endovascular embolization alone may completely
obliterate an AVM. Appropriate selection of patients
based on certain factors as described below is crucial for
the success of this procedure. With the advent of newer
imaging modalities, devices, and improved understanding of the AVM angio-architecture, nowadays, therapeutic embolization is being performed in more and more
number of AVM cases.
3. Palliative Embolization
Many a time, complete obliteration of an AVM is not
possible via any of the three treatment modalities. In such
cases, embolization to eliminate the vascular elements
responsible for focal neurological decits or to reduce the
risk of haemorrhage by targeting the weak areas of the
AVM angio-architecture can be done. However, it needs
to be emphasized that such palliative procedure is not
indicated for epilepsy or headache related to AVM
because these symptoms can be controlled with medical
management, and AVM-related seizures occur probably
due to reactive gliosis in the adjacent brain parenchyma,
which cannot be altered by embolization.
Embolization Agents
1. N-Butyl-Cyanoacrylate (NBCA) Glue
NBCA glues act as occlusive agent. They are available
in liquid form, and when they come into the contact of an
ionic medium like blood, they polymerize rapidly to
become solid. This polymerization can be slowed by
diluting NBCA with lipiodol. More dilution means slower
polymerization. Usually higher glue concentrations
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(around 50%) are required to embolize the high ow or
stulous type of AVMs, while lower concentrations
(around 30%) are required for the slow ow or plexiform
type of AVMs. A delay in the appearance of a vein by
selective angiography at two frames per second can be
equated to one volume of lipiodol for one volume of
NBCA per image [5]. For example, if a vein appears after
three images then three volumes of lipiodol per volume of
NBCA (or 25% glue concentration in other terms) will be
appropriate for the embolization of that AVM.However,
the selection of the most appropriate glue concentration
for AVM embolization depends highly on the operator’s
experience, and mixed type of AVMs may require
different glue concentrations for its different parts or
compartments. NBCA is radiolucent, while lipiodol is
radio-opaque. Hence, lipiodol helps in the visualization
of the mixture during endovascular procedure. Before
injecting glue, the microcatheter needs to be rinsed with a
5% dextrose solution to prevent the polymerization of
NBCA inside the microcatheter. Glue injection should be
carried out within a period of 10–15s to 1–2min, depending upon its concentration. Longer injection time will
cause NBCA to polymerize, and the microcatheter will
become stuck. This is a disadvantage of the glue. Another
disadvantage is that glue poorly penetrates to the adjacent
compartments of a multi-compartmental AVM, and each
compartment needs to be embolized separately. However,
glue penetrates very well towards the venous part of an
AVM, and thus there is a better chance of occlusion of the
venous connections with glue. Glue allows immediate
occlusion of a vascular rupture site which can be lifesaving in certain situations while performing endovascular
procedure. Another advantage of glue is that it can be
injected through thinner microcatheters allowing for successful embolization of AVMs in difcult locations like
deep-seated AVMs. Metacryloxysulpholane when mixed
with NBCA as a co-monomer lowers the polymerization
temperature and prolongs the polymerization time. This
mixture is marketed as Glubran2. N-hexyl cyanoacrylate,
marketed as Magic Glue, is another occlusive agent similar to NBCA glue, with lower adhesive strength that
allows for prolonged injections up to 1h [6].
2. Ethylene Vinyl Alcohol (EVOH) Copolymer
EVOH is a liquid agent held in suspension by dimethyl
sulfoxide (DMSO) solvent. This solution is made radioopaque by mixing with tantalum powder. The mixture is
marketed as Onyx and Squid. After injection into the vessel, DMSO diffuses slowly, and EVOH deposits in the
vascular lumen thereby occluding it. As this process is
much slower compared to polymerization of NBCA,
Onyx/Squid allows for longer injection time. This is the
main advantage of EVOH copolymer over NBCA glue.
However, EVOH copolymers cannot be injected through
any type of microcatheter as DMSO can damage the
walls of non-compatible microcatheters. Onyx/Squid
preferentially percolates into the arterial parts of an AVM
and frequently reuxes into the vascular lumen thereby
trapping the microcatheter. This situation can be catastrophic, and microcatheters with detachable tips are
required to minimize the risk of this complication while
using EVOH copolymers. Such microcatheters are not
easy to navigate through narrow vessels. Hence, Onyx/
Squid is not a good choice for the embolization of AVMs
in difcult location or in case of small-calibre arterial
feeders. NBCA glue has advantages in these situations.
Onyx is available in three different viscosities—Onyx 18
(6% EVOH), Onyx 20 (6.5% EVOH), and Onyx 34 (8%
EVOH). Onyx 18 has the lowest viscosity and is used
most commonly. Higher-viscosity Onyx formulations are
used for high-ow shunts and large feeders. Compared to
Onyx, Squid has better visibility owing to ner grains of
tantalum powder. Both Onyx and Squid vials need to be
shaken continuously for at least 20 min before use to
make the suspension homogeneous and to prevent precipitation of the agent in the microcatheter. PHIL is
another liquid embolic agent consisting of two copolymers (polylactide-co-glycolide and polyhydroxyethylmethacrylate) covalently bound to triiodophenol. DMSO
is used as a solvent for this compound. Unlike Onyx and
Squid, PHIL does not need to be shaken before use. PHIL
has higher embolic capacity than Onyx or Squid [6].
PHIL produces much fewer CT artefacts and no MRI
artefacts compared to Onyx and Squid.
3. Injectable Coils
Injectable coils or ow coils are platinum microcoils
with a diameter of 2.5mm. They are used for proximal
occlusion of a feeding artery in preoperative embolization, plugging the distal tip of a microcatheter to prevent
reux of EVOH copolymer or NBCA glue, and occlusion
of the venous ow of an AVM to prevent distal migration
of a liquid embolic agent during AVM embolization via
trans-arterial and transvenous routes.
4. Polyvinyl Alcohol (PVA) Particles
PVA particles are no longer used as their injection
requires larger-diameter microcatheters and vascular
occlusion by this agent is temporary. Recanalization rate
is around 43% with PVA particles. [7]
Techniques ofAVM Embolization
The ultimate goal of AVM embolization is complete obliteration of the nidus, which requires delivery of the embolization
material to the entire and all the compartments of an AVM,
right up to the draining veins. The deposition of the embolization material should be strictly intranidal, and the extrani-
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