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Q. Holay et al.
Asymptomatic ICAS
While symptomatic ICAS has been the subject of many studies, there are few data about asymptomatic ICAS.
Recent studies have suggested that asymptomatic ICAS
is associated with a low risk of stroke, <1% over 10years
[53–55]. Based on these results, several authors have suggested that no additional management strategy or follow-up
is required routinely for this commonly identied pathology [55].
Forthcoming Improvements inPTAS
Despite the publication of three randomized controlled trials,
there are still major gray areas in the management of symptomatic ICAS (optimal timing of intervention, DAPT, endovascular strategy, etc.).
Regarding the available evidence, PTAS is not recommended as a treatment of rst choice in symptomatic ICAS
[6, 7, 9, 10, 32]. The three RCTs have shown that PTAS is
associated with an increased risk of 30-day stroke and death
events compared to medical treatment alone [6, 7, 9].
Moreover, the more recent CASSISS trial has shown that the
risk of recurrent stroke was not signicantly different
between the two groups during the 3-year follow-up [9]. This
data implies that even if the periprocedural risk in the stenting group could be reduced to as low as the 30-day rate in the
medical therapy alone group, stenting still may not provide a
long-term benet over medical therapy [51].
Thus PTAS use remains for patients with ICAS and recurrent stroke despite optimal medical treatment [11]. However,
the optimal strategy in these patients has yet to be dened.
Most studies have used the Wingspan stent systems [6, 9,
12]. Although this stent has advantages over balloon-
expandable stents due to its relative ease of delivery, the
effectiveness of the self-expanding stent in restoring lumen
diameter and preventing restenosis has been debated [40].
Furthermore, new drug-eluting stent [40, 56] (DES; NOVA®
(Sinomed) and Maurora® (Alain Biotechnology) Sirolimus
Eluting Stent System) and balloon catheter (AcoArt-Litos®
(Acotec) drug-eluting balloon catheter) have been introduced to the market (summarized in Table28.4).
The recently published NOVA trial has compared drugeluting stent (DES) with bare-metal stent (BMS) [40]. This
trial has suggested that DES could reduce the risks of instent restenosis. However, ischemic stroke recurrences or
deaths were similar at 1year [40]. The randomized ACOART
trial [57] is currently investigating the safety and efcacy of
new drug-coated balloons (DCB) with paclitaxel compared
to the Apollo balloon-mounted stent system. Theoretically,
the use of DCB, in addition to rapidly restoring normal arterial caliber, may allow the delivery of a high local dose of
Table 28.4 List and characteristics of new drug-eluting stent and balloon catheter for ICAS treatment
Diameter
and
length
Product name
Drug-eluting balloon catheter
AcoArt-Litos
(Acotec) [57]
Drug-eluting stent
NOVA
(Sinomed) [40]
Maurora (Alain
Biotechnology)
CE European conformity; FDA US Food and Drug administration; ID
internal diameter; NA Not available
(mm)
2–4mm
20–
300mm
NA NA Paclitaxel No
NA NA Rapamycin No
Minimum
microcatheter
ID (inch) Drug
4F Paclitaxel No
CE or
FDA
approved
antiproliferative drugs. Altogether, this new device might
reduce the risk of restenosis and improve clinical outcome.
The optimal management of ICAD-related LVO has yet to
be dened. There are two ongoing studies aiming to evaluate
the safety and efcacy of rescue intracranial angioplasty/
stenting in acute LVO patients who have failed standard
MT.The Acandis Credo Intracranial Stent for Unsuccessful
Recanalization After Thrombectomy (ACUTE) trial [58] is a
prospective, single-arm, open-label, multicenter trial including patients using the Credo/NeuroSpeed system. The Rescue
Stenting for Failed Endovascular Thrombectomy in Acute
Ischemic Stroke (ReSET) study [59] is a prospective, openlabel, multicenter registry using Solitaire device detachment.
The results of the aforementioned studies will hopefully
provide pragmatic data regarding the implications for intracranial stenting in acute ICAD and other more refractory
forms of LVOS.
Illustrative Case
Due to the recurrent stroke despite adequate medical treatment, the patient was transferred to a comprehensive stroke
center to perform endovascular treatment of the known left
middle cerebral artery stenosis.
She was treated under general anesthesia. The patient was
under continuous heparin drip, after an initial bolus of
5000IU.
A right femoral puncture was performed, and a Destination
6Fr catheter (Terumo, Tokyo, Japan) was placed into the left
common carotid artery. Coaxially, a Fargo Max 6Fr (Balt,
Montmorency, France) supporting catheter was positioned in
the intrapetrous internal carotid. The initial angiographic
evaluation revealed a 5-mm-long critical M1 stenosis, with a
clear downstream circulatory ow reduction (Fig. 28.1c).
The left M1 stenosis was crossed with a Traxcess 0.014″
28 Intracranial Atheromatous Stenosis
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289
guidewire, and a balloon angioplasty was rst performed
with a 2 × 12 mm Gateway balloon (Fig. 28.1d). Then a
2.5× 15mm Wingspan stent was placed along the stenosis
(Fig.28.1e), allowing a satisfying angiographic result without residual stenosis (Fig.28.1f). Control angiograms conrmed a good stent expansion and showed a normal left
sylvian and anterior cerebral circulation (Fig.28.1f). The CT
scan at the end of the procedure does not reveal any additional complication.
After the procedure, the patient remained perfectly neuro-
logically stable with preserved vigilance and no new decit.
The patient was discharged on double antiplatelet therapy
for 3 months, followed by simple antiplatelet therapy for
another 3months.
Follow-up imaging showed good stent permeability with
no new ischemic lesions. Clinically, the patient retained very
moderate right hemiparesis and a discrete word-nding difculty but presented no new neurological symptoms.
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Arch Vessel Dissection
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KirillAlektoro andPanagiotisPapanagiotou
29
Case Report
A 33-year-old female patient presented at the emergency
department with acute dysarthria and a high-grade left-side
sensorimotor hemiparesis. The non-enhanced CT of the
head revealed no intracranial bleeding or signs of ischemia.
The CT-angiography showed an occlusion of the right extracranial internal carotid artery due to vessel dissection
ab c
(Fig. 29.1b, c). No occlusion of intracranial arteries was
present.
Systemic thrombolytic therapy was administered after
ruling out contraindications. Due to further neurological
deterioration (reaching an NIHSS of 14) and unchanged
CT-imaging ndings, the patient was transferred to the angiographic suite for endovascular therapy.
Fig. 29.1 CT-images of a 33-year-old-patient with severe left-side
stroke symptoms. Non-enhanced axial computed tomography of the
head (a) shows no evidence of bleeding or ischemia. Sagittal multiplanar reconstruction of the CT-angiography shows an occlusion of the
K. Alektoroff
Department of Diagnostic and Interventional Neuroradiology,
Klinikum Bremen-Mitte/Bremen-Ost, Bremen, Germany
e-mail: alektoroff@gmx.de
P. Papanagiotou (*)
Department of Diagnostic and Interventional Neuroradiology,
Klinikum Bremen-Mitte/Bremen-Ost, Bremen, Germany
Department of Radiology, Aretaieion University Hospital, National
and Kapodistrian University of Athens, Athens, Greece
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
G. Geroulakos et al. (eds.), Mastering Endovascular Techniques, https://doi.org/10.1007/978-3-031-42735-0_29
right internal carotid artery and a “candle ame”-like narrowing of the
ICA-lumen (b). The axial image (c) shows a severe lumen narrowing of
the extracranial ICA (straight arrow), caused by an intramural hematoma (curved arrow)
291
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K. Alektoro and P. Papanagiotou
Introduction
Supra-aortic arterial vessel dissection represents a common
cause of strokes in young and middle-aged patients and
accounts for 10–25% of stroke cases in patients under
50 years of age. Dissections may occur spontaneously or
traumatically [1]. They result from a tear in the vessel wall,
leading to an intramural hematoma between vessel wall layers (usually intima and media or media and adventitia). The
intramural blood collection causes aneurysmatic dilatation
of the vessel wall as well as lumen stenosis, potentially compromising normal blood ow. Intimal injury and altered
hemodynamics may be complicated by thrombus formation
at the dissection site, which may become a source of distal
emboli, causing neurological decits. Distention and thinning of the affected arterial wall can lead to pseudoaneurysm
formation.
Among arch vessels, extracranial internal carotid artery
dissection represents the most common dissection type (estimated yearly incidence of 2.5–3/100,000), followed by
extracranial vertebral artery dissections (1–1.5/100,000) [2,
3]. Subclavian artery dissections are rarely reported [4–6].
Risk factors of arch vessel dissections include trauma,
connective tissue disorders (e.g., Ehlers-Danlos syndrome,
Fibromuscular Dysplasia, Marfan syndrome) and acute
infections. Simultaneous bilateral dissections are observed
in some patients [7].
Clinical Features
The most common symptoms of supra-aortic or cervical
artery dissection are neck pain, headache or facial/jaw
pain, cranial nerve palsies, as well as neurological decits
corresponding to the affected vascular territory. Partial
Horner’s syndrome (ipsilateral ptosis and miosis) may be
observed in patients with carotid artery dissection resulting from compression of perivascular sympathetic nerve
bers.
Table 29.1 Borgess classication of spontaneous cervical artery dissection. (Modied from [8])
Type Description
IA Intact intima. Lumen stenosis with persistent antegrade blood
ow
IB Intact intima. Complete lumen occlusion due to intramural
hematoma
IIA Small intimal disruption
IIB Large intimal disruption with intimal ap formation
Table 29.2 Bif classication of blunt carotid arterial injuries.
(Modied from [9])
Grade Description
I Dissection or luminal irregularity with luminal narrowing
<25%
II
Dissection or intramural hematoma with ≥25% luminal
narrowing, intraluminal thrombus, or raised intimal ap
III Pseudoaneurysm
IV Lumen occlusion
V Transection with free extravasation
Treatment Options
Symptomatic arterial dissections are most commonly treated
conservatively using antithrombotic medication (anticoagulants and antiplatelet drugs) [10]. The main therapy goal is to
prevent thrombus formation at the injured arterial wall and
thereby avoid potential thromboembolic complications.
Patients presenting with acute neurological symptoms may
be treated by systemic thrombolysis during the rst 4.5 h
from symptom onset.
The endovascular treatment of arterial dissections is usually reserved for patients with acute severe cerebral perfusion decits, simultaneous large cerebral artery occlusions,
and persistent (or recurring) neurological symptoms despite
receiving sufcient antithrombotic therapy [11–16].
Endovascular Treatment ofArch Vessel
Dissections
Classication ofArterial Dissections
The spontaneous dissections can be classied according to
the Borgess classication. Based on the presence or absence
of the intimal tear, the dissections are divided into type I (no
intimal tear) and type II (intimal tear present). Both type I
and II dissections are further divided into two subtypes, A
and B (Table29.1).
To describe the traumatic blunt carotid arterial injuries,
the Bif grading scale is often used, which classies the dissections into ve types (Table29.2).
The main goal of the endovascular treatment is reconstruction of arterial lumen integrity to restore normal hemodynamics and prevent thromboembolic events to distal vessel
territories. This is usually achieved by a stent implantation
into the vessel lumen to relieve the stenosis caused by intramural hematoma or intimal ap. Sometimes, implantation of
multiple stents in a telescopic manner may be necessary to
sufciently treat a long-segment dissection.
The main advantages of endovascular dissection treatment are rapid removal of the vessel stenosis and increasing
of blood ow to relieve cerebral perfusion decits. Stent
placement may also facilitate the healing of dissection-
cd
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293
induced pseudoaneurysms by altering intra-aneurysmal ow
velocity and promoting pseudoaneurysm thrombosis.
Endovascular Technique
The endovascular treatment of arch vessel dissections is performed on an interventional (preferably biplanar) angiography system. Self-expanding stents are usually used for
extracranial dissection treatment. Whenever possible, the
patient should start receiving dual antiplatelet medication
before the stent placement (e.g., loading dose of 100–500mg
acetylsalicylic acid (ASA) and 300mg clopidogrel). In case
of acute stent implantation, glycoprotein IIb/IIIa antagonists
(Eptibatide, Tiroban, etc.) may be used as a bridging therapy for sufcient thrombocyte function inhibition [17].
After obtaining a digital subtraction angiography of the
dissected vessel, it is necessary to access the true vessel
lumen before a stent can be placed. First, a microwire and a
microcatheter are carefully navigated through the true lumen
until the intact distal portion of the artery is reached. An
angiographic run through the microcatheter should be performed to conrm its correct location inside the true lumen.
Flexible stents (e.g., Leo) or ow diverters are often used
in curved vessel portions. These stents are usually introduced
directly through the microcatheter and are released inside the
true lumen during microcatheter retraction.
The stiffer “over-the-wire” stent systems (e.g., Wallstent,
Casper) are usually used in straight arterial segments. An
exchange-length microwire is then rst advanced through
the microcatheter. After removing the microcatheter, a folded
stent is navigated over the microwire and released inside the
true vessel lumen at the level of dissection.
Finally, a balloon angioplasty may be performed inside
the stent to treat remaining stenosis. Depending on the dissection length, several stents sometimes need to be placed in
a telescopic manner to ensure the dissected vessel portion is
sufciently treated.
After stent implantation, dual antiplatelet medication
should be maintained for 1.5–3 months (usually 100 mg
ASA and 75 mg clopidogrel daily) to prevent in-stent
thrombosis.
Case Report (Procedure and Outcome)
During a digital subtraction angiography of the right ICA,
the extracranial dissection was conrmed (Fig.29.2a). After
advancing a microcatheter and a distal access catheter over
a microwire into the distal ICA segment, the true lumen
location was conrmed by an angiographic run (b). A long
self- expanding stent (Wallstent) was advanced into the dissected cervical ICA segment and was gradually released
into the true lumen (c). The dissection part in the curvy distal ICA portion was treated by an overlapping exible stent
(Leo, d). The nal angiographic run showed a good radio-
ab
Fig. 29.2 Digital subtraction angiography (DSA) images of a 33-yearold-patient with an ICA-dissection. First angiographic run (a) showing
a “candle ame”-like narrowing of the ICA-lumen. The dissected vessel portion was passed by a microcatheter and a distal access catheter
(Rebar and Soa, arrows in b) over a microwire (Traxcess). The loca-
tion of the catheters inside the true lumen was conrmed by an angiographic run (b). Long self-expanding stent (straight arrows in c) was
advanced into the dissected vessel portion (curved arrows in c). Final
angiographic run (d), showing the reconstructed ICA-lumen with an
expanded Wallstent (straight arrows) and a Leo stent (curved arrows)
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K. Alektoro and P. Papanagiotou
logical result of an ACI reconstruction without periprocedural complications. The patient’s symptoms gradually
improved from NIHSS 14 to NIHSS 8 during the clinical
stay, and further rehabilitation treatment has been started
soon.
Toolkit
– Use self-expanding stents to reconstruct the dissected
vessel lumen (exible stents (e.g., Leo) for curvy segments and stiffer stents (e.g., Wallstent, Roadsaver,
Casper) for straight segments.
– Use a microcatheter and microwire or a microcatheter
alone to carefully navigate through the true vessel lumen
to reach the intact distal vessel segment.
– Conrm the true lumen location by a DSA run through a
microcatheter before deploying the stent.
– Use telescopic stenting to reconstruct long dissected ves-
sel segments.Conict of InterestThe authors declare no
conicts of interest.
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Endovascular Approach forCurative
https://t.me/medicina_free
Embolization ofBrain AVMs: Insights
fromAngio-architectonics
andAngio-anatomy
RahulKumar, DeepDas, ArpanDutta, SubhadeepGupta,
KalyanSajja, andTrilochanSrivastava
30
Background
Curative endovascular embolization of brain arteriovenous
malformations (AVMs) is possible and is being done routinely in selected centres around the world. However, in the
spectrum of disorders amenable to endovascular treatment, it
is not as simple as coil embolization of an aneurysm or stenting of a carotid stenosis. The complexity of the treatment is
a direct result of the complexity seen in the disease process.
This in turn is a function of the extreme degree of evolution
of the cerebral vasculature that has carried forward elements
from the vasculature of our most primitive ancestors. Any
discussion on AVM treatment by embolization must therefore look at this truly fascinating process, in order to understand and master the complexities of the human cerebral
vasculature.
The human brain, as we know today, is the result of a
progressive evolution over the last 250–500 million years
(Fig. 30.1). Starting from a clustering of neurons in the
Hydra to the non-lamellated but enclosed, non-laminar brain
of the Amphioxus containing only seawater in its primitive
ventricular cavity, we have come a long way in terms of size,
R. Kumar (*)
G S Neuroscience Clinic and Research Center, Interventional
Neurology, Patna, India
D. Das
Department of Neurology, Bangur Institute of Neurosciences,
Institute of Post Graduate Medical Education and Research,
Kolkata, India
Woodlands Multi-speciality Hospital and C K Birla Hospitals,
Kolkata, India
A. Dutta · S. Gupta
Neurology Bangur Institute of Neurosciences, Institute of Post
Graduate Medical Education and Research, Kolkata, India
K. Sajja
Life Hospital, Guntur, India
T. Srivastava
SMS Medical College and Hospital, Jaipur, India
organization, and heterogeneity to see the brain as it is today,
in humans. Briey, the oldest parts of the brain to develop
from the non-lamellated structure to a lamellated structure
are referred to as the Paleopallium or old brain. Subsequently,
we have the appearance of the Archipallium, Subpallium,
and nally the Neopallium. This Neopallium is phylogenetically the “youngster” in the human brain. All these steps of
development are summarized in the diagram below. The
reader can also refer to dedicated monograms on the
subject.
Brain AVMs are a Neopallial disease, predominantly as
about 70% of these occur in the Neopallium. Therefore in
this entire manuscript, the detailed discussion will be on the
Architectonic, Angio-architectural properties and the embolization techniques that are used in Neopallial AVMs. An
attempt will be made to touch upon the peculiarities and precautions that need to be taken while dealing with, let us say,
choroidal AVMs that are Paleopallial and Archipallial in
nature.
There are three prerequisites to a successful curative
embolization of brain AVM. These are as follows:
1. The ability to place the lesion in a pre-dened
Architectonic compartment of the brain, with the intention of being able to predict the expected blood supply
and the angio-architecture of the lesion.
2. The ability to be able to access with a microcatheter, the
exact vascular pedicle(s) that is supplying only the AVM
and no other structures in the vicinity.
3. The ability to master the ow within the “nidus” and
thereafter the deposition of an embolic material within it.
This may be done with one or several successive catheterizations. It is imperative that, at the end of embolization,
the draining vein(s) be also occluded for a permanent
cure.
Each of these is equally important to the successful endovascular outcome in treating these extremely complex
lesions. In isolation, all are inadequate. But when used as a
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
G. Geroulakos et al. (eds.), Mastering Endovascular Techniques, https://doi.org/10.1007/978-3-031-42735-0_30
295
296
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R. Kumar et al.
combination, they become a powerful tool that has been considerably neglected over the last few decades. The rst point
of the Architectonic organization of the different brain
regions is beyond the scope of this chapter. However it is also
the most important part in the entire planning process and
will be touched upon in brief. The second and third points
regarding the microcatheterization and the embolic material
deposition will be the main focus of this manuscript.
Architectonic Organization
oftheTelencephalon andLocation ofBrain
AVMs
The telencephalon consists of 16 distinct, interdigitating histogenetic units, in each hemisphere. The rst aim is to identify the limits of the telencephalon. The telencephalon, or
“end-brain”, as it is called is the newest component of the
human brain in terms of evolution (Fig.30.1). It has also
been established that the Insula is the rst component of the
neopallium to develop, and the subsequent evolution of the
Neopallium takes place from the Insula. Regular discussion
on imaging in modern medical literature has completely
neglected these evolutionary landmarks and has not allowed
us to look at the details for the simple reason that all the data
available on the brain is dependent on axial sections of the
brain that show a piecemeal view of all these structures
rather than show us a holistic picture.
For detailed understanding of the different Architectonic
compartments of the brain and the different landmarks that
separate these structures, one needs to understand the orientation in a coronal/sagittal plane. Also the interaction between
the various structures can only be studied when all these are
visible in a single cut. To understand the boundaries between
the old and the new brain, we are therefore moving to the
coronal section at the midventricular level, passing through
the corpus striatum, which is ideal, as is shown in the image
below.
The three oldest sulci in the order of appearance, both
during phylogeny and embryologic ontogeny, are the
Cingulate Sulcus, the superior and inferior limbs of the
Circular Sulcus, demarcating the Insula, and the Collateral
Sulcus (Fig.30.2a). An imaginary line passing through these
on both sides ultimately creates a boundary, with the long
association bre bundles of the white matter at this interface
(Fig.30.2b). Any part of the brain that is within this “phylogenetic circle” is old brain and contains the Archipallium,
Paleopallium, and Subpallium. The entire structure that is
seen outside this phylogenetic circle is the Neopallium and
will remain the main focus of this description.
Once we have identied the telencephalon, we now have
to move away from the coronal orientation and look at each
hemisphere in toto, in a sagittal orientation. This helps us in
understanding the location and the organization of the 16
histogenetic units in each hemisphere. For ease of understanding, we are showing these concepts in the diagram
below (Figs.30.3 and 30.4).
The Central Sulcus of the Insula divides it into an anterosuperior part containing the gyri brevi, and a postero-inferior
part containing the gyri longi. Anatomically, the Central
Sulcus of the telencephalon can be conceptualized as a continuation of the Central Sulcus of the Insula. Thus when we
connect these two, the entire Neopallium gets divided into
two parts as illustrated. The anterior part is referred to as the
“Epistriatal Zone” as it straddles the Corpus Striatum, and
the posterior part is referred to as the “Epihippocampal
Fig. 30.1 Composite image
showing the evolution of the
telencephalon from the
Paleopallium that consisted of
a non-layered conglomerate
of nerve cells surrounding a
cavity lled with ocean water
instead of CSF to the complex
structure that it is today in
terms of the Full Neopallium.
All the structures shown in
dark blue colour represent the
Paleopallium, those in green
represent the Archipallium,
Turquoise represents the
Medial and Lateral
Ganglionic Eminences that
ultimately form the
Subpallium, and Red
represents the Insula and the
Neopallium
ab
30 Endovascular Approach forCurative Embolization ofBrain AVMs: Insights fromAngio-architectonics andAngio-anatomy
https://t.me/medicina_free
Fig. 30.2 (a) A coronal MR
through the corpus striatum
showing the three primordial
sulci. These are the Cingulate
Sulcus (1), the superior and
inferior limbs of the Circular
Sulcus (2,3), and the
Collateral Sulcus (4). (b) The
DTI image with the
reconstruction of the
association bre systems in
green also shows the presence
of a long association bre
bundle at all these locations
(1, 2, 3, and 4)
297
ab c
de f
Fig. 30.3 This gure shows the placement of the phylogenetic circle
on coronal MR IR images (a). The upper panel also shows the expected
extent of the supply from the supercial and deep systems in terms of
arterial supply and venous drainage (b and c respectively). The arterial
supply is marked in red and the venous drainage is marked in blue. As
far as the arterial system is concerned, the demarcation is very strict and
is right at the ventricular edge. This also corresponds to the phylogenetic circle. All the areas within the phylogenetic circle will be supplied
by either the striate system or the choroidal system (d). All the areas
outside the phylogenetic circle will be supplied by the leptomeningeal
arterial arcade (d). The lower panel shows the vessels, as seen on cone
beam CT angiographic exploration in relation to the circle, the extent of
supply of the striates, and the penetrating supply from the leptomeningeal arcade (e). Also seen is the minimal territory of drainage of the
cortical veins (f)
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