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130
L. J. D. Sebastian et al.
13.2.3 Pathology andClinical Aspects
Cerebral AVMs are vascular lesions composed of abnormal
tangles of blood vessels with pathologic shunting from arterial to venous side without an intervening normal capillary
bed (Fig.13.1).
The nidal vessels are indeterminate and indistinguishable
from arteries or veins. Macroscopically, they range from
well-differentiated arteries and veins to highly malformed,
hyalinized, poorly differentiated vessels with thick and thin
walls. Microscopically, most of these nidal vessels have only
a single endothelial layer like capillaries but unlike capillaries are hugely dilated.
The most common modes of clinical presentation of intracranial AVMs are, in the order, spontaneous intracranial
hemorrhage, seizures, and headaches not associated with
hemorrhage. Focal neurological decits and other symptoms
like tinnitus and trigeminal neuralgia are some of the less
common presenting symptoms. Most of these clinical symptoms can be correlated with specic angio-architectural features of the underlying AVM.
13.2.4 Classication
Valvanis and Yasargil developed a classication based on
the location of the nidus [6]. They classied brain AVMs
into two main groups, i.e., convexity AVMs with supra and
infratentorial subgroups and in deep central AVMs with
supra and infratentorial subgroups. These supercial
AVMs are sub-classied into sulcal, gyral, and mixed
sulco-gyral types based on their relation with adjacent sul-
AVM
Superficial
Sulcal
Gyral
Deep
Sub-arachanold
Parenchymal
cus, gyrus, and subcortical white matter. Deep brain AVMs
are also further subclassied into subarachnoid AVMs,
parenchymal AVMs, plexal or intraventricular AVMs, and
mixed deep AVMs. Classication of AVM is detailed in
Table13.1.
Lasjaunias included the role of feeding pedicles and
draining veins in addition to the location in the classication of AVM.Supercial AVMs like sulcal and gyral AVMs
were supplied by pial arteries in the subpial spaces and
drained into supercial cortical veins, whereas deeper
AVMs were supplied by the perforator/choroidal arteries
and drained into the deep venous system. Most of the individual lesions, however, involve more than one compartment. For example, rare cortical lesions were supplied
exclusively by cortical arteries and drained into supercial
cortical veins.
13.2.5 Angioarchitecture ofAVM
Structurally, an AVM consists of four main components: the
nidus, feeding arteries, draining veins, and the adjacent or
intervening brain parenchyma. DSA is the gold standard tool
to analyze the rst three components.
Nidus is derived from a Latin word meaning nest. Other
synonyms used could be the epicenter, nucleus, or focus of
the AVM.The nidus represents the area of the entire AVM
angioarchitecture between readily identiable distal segments of feeding arteries and draining veins [1]. It is the
source of all hemodynamic changes observed up and downstream of the AVM and is composed of multiple coiled and
intercommunicating vascular channels that empty into thinwalled tortuous veins. Angiographically, the nidus may consist of a plexiform network of vascular channels, large
arteriovenous stulae, or a mix of both plexiform and stulous parts (Fig.13.2).
The nidus of a cerebral AVM, especially that of a larger
one, can be composed of many compartments. A compartment is dened as an intranidal vascular unit characterized
by its own feeding arteries, AV shunting, and a draining vein.
The compartments of AVM are not rigid, well-dened vascular units but are rather hemodynamic units that may
intercommunicate.
Intranidal vascular cavities are weak components of an
AVM architecture and are represented by arterial aneurysms,
arterial pseudoaneursyms (post bleed), intranidal aneurysms,
venous pseudoaneurysm (post bleed), and venous intranidal
ectasias. These cavities are prone to rupture and hence should
be targeted during embolization.
Sulco-gyral
Fig. 13.1 Classication of AVM
Plexal/Ventricular
Feeding Arteries We have to determine the feeding artery
relationship to the nidus and look for any high-ow angiopathic changes. Depending on the anatomical location of
13 Interventions inIntracranial andSpinal Arteriovenous Malformations
Table 13.1 Classication of AVM
Cortical/Pial arteries Perforators Choroidal arteries Deep venous system Supercial venous sys
Cortical Sulcal
Corticosubcortical
Cortico-ventricular Sulco-gyral + + +
Deep seated +(insular and
Choroid plexus
Cortico-callosal +
AV M
Gyral +
− −
+
cerebellar)
− − −
− − +−
+
+ + +
−
−
−
+ + +
+
131
+
+
+
+−
+−
a
Fig. 13.2 Microcatheter runs show various combination in the nidus (a) Cork-screw type (b) Mixed cork-screw and linear vessels (c) linear frail
vessesls
b
c
Arterial high ow angiopathic changes include arterial
enlargements/ectasias, arterial stenosis, aneurysms, and
watershed transfer. High-ow stulas show arterial ow
aneurysms, which are directly seen on the arteries supplying
the nidus or distant from the nidus. High-pressure ow can
induce endothelial/smooth muscle hypertrophy resulting in
arterial stenosis. The watershed transfer is induced by the
perinidal brain parenchyma, which receives sub-optimal
blood ow.
Fig. 13.3 Cerebral AVMs
arteries in relation to the brain parenchyma, they are divided
into pial, dural, perforating arteries; choroidal arteries; and
retrograde collaterals. Hemodynamically, they are also classied into dominant and supplementary, while geometrically
they are divided into direct/terminal feeders, pseudoterminal, and indirect/transit/en passage feeders based on their
supply to AVM and brain parenchyma (Fig.13.3, 13.4, 13.5,
13.6 and 13.7) [6].
Draining Veins
One should attempt to identify and classify
all the draining veins of an AVM.Those with only one or two
draining veins have a higher propensity to bleed.
Hemodynamically, they are classied into main and accessory veins. Anatomically, the draining veins are classied
into those connecting to the supercial cortical venous system or deep venous system. In general, supercial AVMs
(sulcal or cortical) drain into cortical veins, while deep brain
AVMs drain into sub-ependymal veins. Angiographic evidence of unexpected venous drainage should represent a secondary event. For example, any sulcal AVM draining into the
deep venous system indicates that the supercial cortical
vein(s) draining it have likely thrombosed.
132
L. J. D. Sebastian et al.
Venous reux can be into the cortical veins or deep venous
system (Fig. 13.8). Deep venous reux is associated with
higher bleeding risk. While cortical venous reux itself is not
associated with increased bleeding risk, it can interfere with
normal parenchymal drainage and can be a cause of
symptoms.
Venous high-ow angiopathy changes include venous stenosis, venous ectasias, and venous pouches or varices.
Venous stenosis without pouches is a high risk factor for
bleeding.
Hemorrhagic Risk One of the primary goals of analysis of
angioarchitecture of an AVM is assessing the risk of rupture.
Table13.2 summarizes the angiographic features indicating
a high risk for rupture (bleed) of an AVM.
13.2.6 Imaging inCerebral AVMs
Cerebral AVMs being complex conditions, every imaging
modality cross-sectional imaging (CT and MRI) as well as
DSA are exploited to the maximum to extract information
that is useful for management in a given patient. Yet, DSA
remains the gold standard for analyzing angioarchitectural
features described earlier.
Fig. 13.4 Right ICA run showing right choroidal AVM with direct
feeder from pericallosal artery (straight arrow) and indirect feeder from
Anterior choroidal artery (double ended arrow)
Fig. 13.5 (a) Right ICA run
shows splenial AVM with
feeder from pericallosal
artery. (b) Right vertebral run
showing retrograde pial-pial
collaterals between distal
branches of PCA and splenial
artery
a
CT Scan
• Non-contrast CT is usually the rst imaging to detect
intracranial bleeding in patients presenting acutely. It can
b
13 Interventions inIntracranial andSpinal Arteriovenous Malformations
Fig. 13.6 Pre-nidal and
intranidal aneurysms in left
posterior temporal AVM in
left vertebral run
Fig. 13.7 Law parietal AVM
case with major supply from
left MCA; Right ICA AP and
lateral runs showing
watershed transfer with
peri-nidal angiogenesis
between left ACA-MCA
teritorry (straight arrow)
133
a
Fig. 13.8 (a) Left vertebral run showing cerebellar AVM; (b) Capillary phase showing venous reux into posterior fossa veins; (c) Venous phase
shows parenchymal congestion in posterior fossa
b
c
134
L. J. D. Sebastian et al.
Table 13.2 The angiographic features indicating a high risk for rupture (bleed) of an AVM
1. Nidus
a. Size: < 2cm
b. Location: Deep > supercial
c. Nidal type: Fistulous > plexiform
d. Nidal aneurysms
2. Arterial side
a. Arterial aneurysms
3. Venous side
a. Single draining vein
b. Enlarged draining veins
c. Venous stenosis (without pouches)
d. Deep venous reux
e. Venous pseudoaneurysms
also show calcications in the nidus, venous sacs, or in
parenchyma.
• More importantly, NCCT is done as a baseline before
embolization. Immediately after the embolization CT
scan is repeated, which should be carefully studied for
any bleed (perinidal, subarachnoid, or intraventricular) to
ag any procedure-related complications.
• Additionally, post-procedure CT demonstrates the disposition of embolic material also. Some centers use CT
angiography to study the location and architecture of an
AVM.
MRI
• MRI is invaluable to precisely localize brain AVM and
therefore aid in its classication.
• It depicts parenchymal changes secondary to the AVM
like hemorrhage, gliosis, mass effect, and
hydrocephalus.
• It also shows hemosiderin deposition, reminiscent of previous bleed, in the parenchyma and within the nidus as
well.
• Advanced imaging tools like DTI and functional MRI can
also be used in treatment planning and follow-up.
• MRI is a good adjuvant (to DSA) tool for short- and longterm follow-up of patients with brain AVMs.
• Arterial spin labeling (ASL) detects arterial transit artifacts in the veins (due to fast-owing blood), which is
mainly useful post-treatment to look for any residual/
recurrent AVM [7, 8].
Table 13.3 Spetzler martin classication
AVM characteristics Points
Size of AVM
<3cm 1
3–6cm 2
>6cm 3
Location of AVM
Non-eloquent 0
Eloquent 1
Venous drainage of AVM
Supercial 0
Deep 1
• The architectural analysis is complete with the superselective microcatheter angiography, which is described
in a later section.
13.2.7 Grading ofCerebral AVMs
Spetzler Martin classication system is the most commonly
used grading system (Table13.3). It is mainly designed to predict the surgical outcomes [9]. The total score (ranging from 1
to 5) helps guide the decision-making process regarding the
treatment approach, balancing the risks of surgery against the
potential benets. Higher scores indicate a higher risk of neurological decits from surgery, inuencing the consideration
of alternative treatments or careful weighing of intervention
risks. Surgery is favored in low grades like grades I, II, and III.
Over the years various other grading systems, such as the
Supplementary Grading System, Lawton’s Modication of
AVM Grading System, and the Buffalo Grading System, have
been developed to assess arteriovenous malformations
(AVMs) [10, 11]. These systems offer nuanced criteria for pre-
dicting treatment outcomes, surgical risks, and technical complexities associated with endovascular interventions. Buffalo
grading system is an endovascular grading scale taking into
account the number, diameter, and eloquent location of those
arterial pedicles. Each system serves to guide clinicians in
treatment planning and decision-making for AVM patients
though extensive clinical validations are lacking for them.
13.2.8 Treatment ofBrain AVMs
DSA
• DSA is the gold standard for the analysis of the angioarchitectural features of an AVM and therefore planning its
treatment strategies.
• Additional imaging techniques provided by most of the
modern angiographic suites like cone beam CT angiography and 3D rotational angiography help understand the
AVM architecture better.
13.2.8.1 Indications andGoals
All ruptured intracranial AVMs require treatment to prevent
recurrent hemorrhage and attendant morbidity and mortality.
However, the selection of unruptured AVMs for treatment is
not that straightforward. The ARUBA trial showed a threefold increase in morbidity and mortality in the multimodality
interventional arm compared to the medical arm [12]. The
SIVM study also corroborated these ndings [13].
13 Interventions inIntracranial andSpinal Arteriovenous Malformations
135
The target of any kind of treatment of cerebral AVMs is the
nidus, or more precisely, the complete elimination of the
same. However, this may not be feasible in all types of AVM
architecture. Hence, the aggressiveness of treatment pursued
in a given patient has to be tempered by a sense of clinical
pragmatism, which takes into consideration the specic
angio-architectural features in the individual, the severity of
his/her clinical symptoms, modality-based expertise available
in the treating center (microsurgery, endovascular embolization, radiosurgical obliteration), and the risks involved in the
treatment itself. Accordingly, the therapeutic goal in a given
individual may be curative or partial treatment directed to
high-risk areas or palliation aimed at alleviating symptoms
rather than a cure. Conservative or only symptomatic medical
treatment is also an appropriate option in some patients.
13.2.8.2 Endovascular Treatment
(Embolization) ofBrain AVMs
The following sections begin with the dening current role
of endovascular treatment (EVT) in the management of brain
AVMs followed by a brief on the advances in the devices and
a
b
technology and then by a detailed description of embolic
agents. The last sections dwell on the technical aspects of
embolization with liquid embolic agents. The terms EVT
and embolization are used interchangeably in the text.
Role ofEVT
(i) Curative: It is possible to cure certain brain AVMs by
EVT alone (Fig.13.9). Many endovascular series report
AVMs with the following characteristics as suitable for
curative embolization: small/medium-sized, compact
nidus, supercial location, and accessible feeders [14].
Larger AVMs are generally not suitable for curative
embolization, though, with the advent of newer techniques, the proportion and size of curable AVMs
increasing.
(ii) Partial-targeted embolization: It means the elimination of
weaker architectural areas (e.g., aneurysms, stulas) alone
by embolization, especially in large ruptured AVMs, which
are otherwise difcult to cure by embolization alone.
(iii) Partial embolization—presurgical/ preradiosurgical: In
large AVMs, embolization is used to reduce the AVM
c
d
Fig. 13.9 (a & b) Left ICA angiogram shows compact nidus lling
from distal MCA branches; Sonic microcatheter was navigated and
20% glue was injected; (c) Control angiogram shows complete emboli-
e
f
zation of the nidus; (d) Post embo CT showing embolic material; (e, f)
Post embolisation angiogram and CT conrming the technical success
of the procedure
136
L. J. D. Sebastian et al.
a d
e
f
cb
g
Fig. 13.10 (a, b) MRI shows gliosis and bleed in left occipital lobe; (c,
d, e) Right vertebral artery run shows nidus with venous pseudoaneu-
rysm; 20% glue was injected into the pseudoaneurysm; (f & g) Control
size so that they can be treated later by surgery or radiosurgery/as an adjunct (Fig.13.10).
(iv) Palliative: In large and/or untreatable AVMs, EVT can
help to treat weak areas (e.g., nidal or feeding artery
aneurysms) or to alleviate symptoms by reducing ow
(e.g., neuralgia due to nerve compression by vessels).
Advances inEndovascular Devices andEmbolic
Agents
• Biplane angio-suite is the essential component of a neurointerventional department. All the modern angio-suites
provide 3D rotational angiography and cone beam CT
angiography, which are very useful in analyzing the AVM
architecture and planning embolization.
• Flow-guided microcatheters come in 1.2F and 1.5F and have
made superselective navigation easier. Distal access catheters also help in this cause, particularly in tortuous anatomy.
• Detachable tip microcatheters meant a quantum jump in
developing curative embolization techniques.
angiogram shows residual nidus with obliteration of the venous sac.
The residual nidus was sent to gamma knife therapy
• Liquid embolic agents are the mainstay of AVM treatment. Especially, the nonadhesive copolymer liquid
embolic agents have changed the paradigm of AVM
treatment.
Embolic Agents
Historically, particulate embolic agents, such as PVA particles, have been used in the endovascular treatment of brain
AVMs in the early years. Currently, they have been almost
completely replaced by liquid embolic agents (LEA). Coils
are sometimes used alone or as an adjuvant to LEA in the
embolization of high-ow stulous components and in some
special techniques such as the pressure cooker technique.
LEAs fall into two major groups:
1. Cyanoacrylates, or adhesive liquid embolics, also known
commonly as “glue.”
2. Copolymers, or non-adhesive liquid embolics; DMSO as
a solvent is common to all of them.
13 Interventions inIntracranial andSpinal Arteriovenous Malformations
137
Each of the above groups have distinct properties such
that the embolization techniques employing them also differ
from each other. Hence, a review of commonly available
LEAs and their properties is pertinent.
Cyanoacrylates (Glue)
• Various available cyanoacrylates are isobutyl
2- cyanoacrylate, n-butyl cyanoacrylate (nBCA), n-hexyl
cyanoacrylate (nHCA), and 2-octyl cyanoacrylate (OCA).
• Normally, cyanoacrylates contain monomeric molecules
while in liquid form. When exposed to blood or any ionic
solution, these molecules undergo a rapid exothermic
chain growth polymerization, resulting in an adhesive
material that occludes the blood vessel.
• Glue is mixed with iodized oil (Lipiodol, Guerbet,
Villepinte, France) before injection via a microcatheter
for two reasons: (i) to reduce the speed of polymerization
of glue which in pure form would instantly polymerize
and occlude the microcatheter; (ii) to give radioopacity to
glue which is otherwise radioluscent and not visible under
uoroscopy.
• The ratio between the cyanoacrylate and iodized oil deter-
mines the concentration of the glue prepared. For exam-
ple, 20% glue preparation contains cyanoacrylate and
iodized oil in the ratio of 1:4. The concentration required
in a given case depends on several factors, such as the
position of the microcatheter, the diameter of the emboli-
zed vessel, and the velocity of blood ow. For example, a
high ow stula requires high concentration (>90%) glue.
• Micronized tantalum powder is mixed in highly concen-
trated glue preparations to add radio-opacity. It is also
useful to reduce the viscosity of the oil.
• To prevent polymerization within the microcatheter, the
latter is initially ushed with 5–10% dextrose solution.
The volume of dextrose solution injected is often 2–3
times that of the dead space of the microcatheter. When
the microcatheter is in a wedged position in the feeder
artery, the dextrose accumulating in the feeder distal to
the tip acts like an extension of the microcatheter till the
stulous point. This is especially helpful when a micro-
catheter cannot be negotiated close to the stula/nidus via
a thin feeder.
• Due to its rapid polymerization on contact with blood,
glue can be injected only for a short duration of time—
usually less than a minute—before the feeder vascular
pedicle gets occluded.
• Glue is adhesive to the microcatheter (hence the name
adhesive embolics). Hence, prolonged injection and/or
reux along the catheter tip can lead to entrapment of the
microcatheter. Forcible pulling of the microcatheter then
can cause the rupture of blood vessels with dire conse-
quences. Hence, entrapped microcatheters are often left in
situ by cutting them at groin (puncture site).
• Histoacryl, Glubran 2, Magic Glue, TruFill, and Fuaile
are the commercially available cyanoacrylates manufactured by different companies. Of these, Histoacryl is the
most widely used one and available in India. Magic glue
contains nHCA and has the least adhesive strength to the
microcatheter and hence allows prolonged glue
injection.
Copolymers
The currently available copolymers are onyx, PHIL, and
squid. Onyx is an EVOH copolymer with DMSO and
micronized tantalum. EVOH is the active substance that
solidies after DMSO dissipation. Micronized tantalum
gives radiopacity of the embolic agent. The onyx vial has to
be vigorously shaken just prior to its use to ensure homogeneous mixing of the tantalum particles. Onyx is available as
onyx 18, onyx 20, and onyx 34. The numbers indicate the
viscosity in centipoise.
Squid It has the same components as onyx—EVOH copo-
lymer, micronized tantalum powder, and DMSO.The main
difference between squid and onyx is the smaller grain size
in squid to enhance the radiopacity and improve visibility
during longer injection times. Squid is available in six different formulations: Squid 12, 12LD, 18, 18 LD, 34, 34LD
(numbers indicate viscosity in centipoise).
PHIL It consists of two copolymers (polylactide-co-
glycolide and polyhydroxyethylmethacrylate) as active compounds and triiodophenol (an iodine compound); the latter
for radiopacity. PHIL also uses DMSO as a solvent. A PHIL
package consists of two pre-lled syringes containing 1ml
of PHIL and another of DMSO.It is ready to use and doesn’t
have to be shaken. PHIL is available in four formulations:
PHIL LV, PHIL 25%, PHIL 30%, and PHIL 35%.
Unlike cyanoacrylates that are relatively hard in their
solid form, copolymers are more in a plastic state. All the
copolymers occlude vessels by precipitation like that of
hardening of lava ow in a volcano (from outside to inside).
The solidication results from the dissipation of DMSO.The
microcatheter is ushed with DMSO prior to the injection of
the co-polymer. DMSO can cause local toxic effects on the
embolized blood vessels, resulting in vasospasm, inammation of the vessel wall, and angionecrosis. DMSO also damages the synthetic material of the device, hence should be
used with DMSO-compatible microcatheters only. The
mechanism of precipitation takes a few minutes; hence, longer injections are advocated with a detachable tip microcatheter (most frequently used detachable tip microcatheters are
138
L. J. D. Sebastian et al.
apollo and Sonic). While reux is undesirable when using
glue, reux is a part of the embolization in copolymers.
Embolization Techniques
Specic endovascular strategies and techniques depend on
the choice of embolic agent(s). However, some general considerations are relevant here:
1. Access: A 6F femoral access is sufcient in most of the situations, However, multiple vascular accesses like bifemoral
along with radial may be needed when multiple simultaneous LEA injection is planned as in multiplug (described
later) technique. Femoral or neck venous access may also be
needed when venous side embolization is contemplated.
2. Guiding: A 6F guide catheter placed in the neck vessel is
generally adequate. Sometimes, coaxial system may be
needed in tortuous neck anatomy. A distal access catheter
can also be helpful in microcatheter navigation in difcult
anatomy.
3. Angioarchitecture analysis: A detailed study of the angioarchitecture using multiple superselective (microcatheter)
angiography is an invaluable essential step before proceeding with embolization (Fig.13.11). Such an analysis
should be directed toward clarifying the following points.
a. Number, size, and nature of arterial pedicles—whether
direct/indirect or terminal/enpassant. This is especially needed to choose a safe feeder for LEA
injection.
b. Nature of the nidus: whether plexiform or stulous
or mixed? Whether it is multicompartmental and if
so feeder(s) and draining vein(s) of each
compartment.
c. The presence and extent of inter-communication
between the compartments.
d. Identifying all the draining veins, any venopathic
changes and assessing the suitability for venous side
embolization.
e. Identifying weak or vulnerable areas in the arterial,
nidal, and venous sides and the feeder pedicle supplying the same.
4. For conducting the angioarchitecture study described
above, a microcatheter can be sequentially navigated into
all the possible feeders. Alternatively, multiple microcatheters can be navigated at the same time into multiple
pedicles. Bifemoral and radial accesses may be needed
for this purpose. Simultaneous angiograms via two or
more microcatheters can reveal even more functional and
anatomic information.
Fig. 13.11 (a) Right ICA
smart-mask showing splenial
AVM with major feeders from
pericallosal artery and
callosomarginal artery (b)
Microcatheter run through
calloso-marginal artery lling
antero-superior part of the
nidus draining into two
corical veins (in arrows); (c)
Run through pericallosal
artery lls the anterior inferior
part of the nidus draining into
large vein; (d) Dual
microcatheter run shows
lling of both the
compartments
a
b
c
d
13 Interventions inIntracranial andSpinal Arteriovenous Malformations
139
a
d
b
e
c
f
Fig. 13.12 (a) Right ICA angiogram shows callosal AVM supplied by
pericallosal artery; (b, c, & d) Marathon was navigated into distal pericallosal artery and two draining veins: inferior sagittal sinus and internal cerebral veins. 25% glue was injected; (e) Immediate control angio
Technical Aspects ofGlue Embolization
The techniques of glue embolization were introduced in
1980s and perfected over the years by eminent practitioners
like P. Lasjaunias, K. Terbrugge, A. Berenstein, and
A.Valavanis [1, 15, 16]. Initially, the role of glue was limited
to targeted and adjunct embolization. Later as experience
gained substantial proportion of AVMs, particularly SM<3
grade lesions could be cured by glue embolization alone. For
example, in the Zurich series of Valavanis comprising 644
patients of brain AVMs, 40% were cured by complete embolization with overall morbidity and mortality of 1.5% and
0.8%, respectively [1]. Glue is still considered a valuable
embolic agent in the treatment of AVMs by many physicians
across the world (Fig.13.12). The following discussion highlights the essential strategies/technical aspects of glue
embolization.
• Strict intranidal deposition of the embolic material is the
goal in the embolization of an AVM.Though applies for
any liquid embolic agent, this should be religiously followed when using glue, as excessive or premature venous
penetration can result in rupture of the unobliterated stu-
shows complete embolization with a few residual angiogenetic changes;
(f) Check DSA 1 month later shows no evidence of any vascular
malformation
lae. Obliterating a long segment of the feeding artery, on
the other hand, can lead to ischemic damage of normal
brain parenchyma.
• To achieve this goal, repeated super selective microcatheterizations of various feeder pedicles are needed. A
larger or multicompartmental nidus with multiple feeders
will require several sequential microcatheterizations to be
completely obliterated. This can be achieved in the same
or multiple sittings.
• An alternative technique in multicompartmental AVMs is
the simultaneous multi-microcatheterization technique,
which means navigation of two or microcatheters via as
many feeder pedicles at the same time. This may require
bilateral femoral or even an additional radial access.
• Flow-guided microcatheters of size 1.2F or 1.5F are generally used for superselective navigation. While using
microguidewires (0.07″/0.08″) for navigating microcatheters through small caliber feeding arteries, care should
be taken not to perforate them or the nidi.
• The microcatheter tip is positioned as distally as possible
in the feeding artery, that is, beyond all the normal
branches supplying the adjacent brain parenchyma and