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L. J. D. Sebastian et al.
close to the junction of the feeding artery with the nidal
compartment it supplies. A catheter tip in a partially
wedged position is desirable.
• Glue prepared in appropriate dilution is then injected
slowly and continuously under constant uoroscopic control in a blank roadmap. It is important to save appropriate
frames of microcatheter DSA in both planes for reference
on one side of the display screen or on separate monitors.
Progressive penetration of the glue into the nidus and
intercompartmental diffusion can be visualized and compared to the reference angiographic images. If the glue is
seen entering a compartmental draining vein or if it
reuxes in the feeding artery by more than a few millimeters, the injection is stopped and the catheter is withdrawn
swiftly.
• The above procedure is repeated for all nidal
compartments.
• Coils can be used sometimes to occlude larger stulous
components in mixed types of AVMs. A small amount of
glue after the coils could help in complete obliteration of
the stula.
• Glue either alone or along with coils is used for proximal
sealing of detachable-tip microcatheters in pressure
cooker technique (described later).
• Even in centers exclusively using copolymer liquid
embolics for AVM treatment, glue is still used for the last
two purposes mentioned above.
Embolization by Copolymers: Technical Aspects
Various techniques have evolved in the last two decades to
exploit the unique properties of copolymer-based embolic
agents, such that complete nidal obliteration is obtained by
injecting through a single or only a few feeder pedicles.
(i) Slow, prolonged nidal injection technique (plug and
push method) [17–21]: This was the basic method of
onyx injection adopted initially by many interventional
groups across the world. Prominent proponents of this
technique include S.Cekrige, J.Moret, and Van Rooiji,
among others. The essential steps are described next.
• After placing the microcatheter distally (close to the
nidus) in the feeder pedicle, the microcatheter is
ushed with DMSO, by a volume slightly higher
than the dead space of the microcatheter.
• Then the copolymer LEA is slowly injected over
approximately 40seconds to ll the dead space of
the microcatheter. This is to avoid the DMSO bolus
in the cerebral circulation. It has to be remembered
that DMSO can cause local toxic effects on the blood
vessels, potentially resulting in vasospasms, inammation of the vessel wall, or angionecrosis [22]. It
can also cause bradycardia or even asystole, mediated by the trigeminocardiac reex [23].
• LEA is further injected slowly under constant uoroscopic control, watching it penetrate the nidus.
• As soon as reux starts happening along the microcatheter, injection is stopped and resumed after
2minutes. If it migrates further into the nidus, the
injection is continued at the same pace. But if it
reuxes further, the injection is stopped again. The
cycle is repeated until a plug of onyx forms for a
short segment around the tip of the microcatheter. A
reux of up to 1.5cm may be allowed.
• Once a compact plug is formed, it is possible,
exploiting the unique solidication properties of
copolymers (outer solid coat with lava-like inner
core), to penetrate further into the deeper parts of
nidus and its multiple compartments.
• Note that in contrast to cyanoacrylates where reux
can cause catheter entrapment, deliberate shortsegment reux is an integral part of the technique
with embolization by copolymers.
• Anytime during the injection, if the embolic material
advances to the venous side, the injection is stopped
for some time so that on resuming, LEA is redirected
to other compartments of the nidus.
• Similarly, if further reux along the microcatheter
occurs, one has to pause. Excessive reux can lead to
non-target embolization and ischemic complications. Likewise, early venous penetration and premature draining vein occlusion can lead to dangerous
hemorrhagic complications.
• If during any phase of the injection, if the embolic
material advances to the venous side, the injection is
stopped immediately for some time so that on resuming injection, LEA is redirected to other compartments of the nidus.
• Deciding the end point of injection through a given
pedicle may be on one of the following counts: (i)
Injection of LEA through the microcatheter becomes
very difcult, and there is hardly any forward ow.
In this situation, embolization is stopped as further
injection may lead to catheter rupture. (ii) There is
continued reux along the microcatheter with little
nidal penetration. (iii) If there is complete elimination of the nidus. The last one is difcult to determine and it is critical to be sure of the same as
minimal residual AVM can rupture if the venous outow is already occluded.
(ii) Embolization using detachable tip microcatheters:
The high probability for reux of LEA along the microcatheter and consequent entrapment of the later led to
the development of detachable tip microcatheter. Sonic
(Balt Extrusion), introduced in 2006, was the rst
detachable tip microcatheter approved for copolymer
injection in brain AVMs. Later Appollo (Medtronics)
13 Interventions inIntracranial andSpinal Arteriovenous Malformations
141
Fig. 13.13 (a) Right ICA
angiogram shows
orbitofrontal AVM with
supply from ACA; (b)
Detachable microcatheter
angiogram; (c) Onyx cast; (d)
Control angiogram showing
complete exclusion of AVM
a
b
c
d
was introduced and got FDA approval in 2014. Apart
from raising the safety of copolymer embolization, the
use of a detachable tip microcatheter helped achieve a
higher obliteration rate in a single embolization session
(Fig.13.13) [24].
(iii) Pressure cooker Technique: Rene Chapot et al. rst
described this technique [25]. It consists of essentially
two steps: navigating a detachable microcatheter to a
suitable position such as to inject the copolymer LEA
and navigating another microcatheter, e.g., Magic 1.2F
or Echelon 1.0, to a position between the tip of the rst
microcatheter and its detachment zone. Then one or two
micro coils or ow coils are deployed through the second microcatheter followed by injection of 30–50%
glue such that a focal plug of glue and coils is formed.
The plug so formed facilitates the AVM embolization in
the following ways: (i) The plug prevents reux of LEA
along the microcatheter and helps avert non-target
embolization. (ii) It helps to push continuously into the
nidus. (iii) The microcatheter detaches easily without
any trauma to the nidal region as the plug holds the dis-
tal segment rmly and the pulling force is hardly transmitted to the tip. (iv) Another additional advantage is
that the plug creates a wedge condition for the rst
microcatheter, and hence, better depiction of AVM
architecture during selective microcatheter angiograms
as contrast is not easily washed away.
(iv) Multiplug ow control Technique: Saruhan et al.
described this technique whereby all or majority of the
arterial feeders of an AVM are superselectively navigated by multiple microcatheters via bifemoral and
radial accesses. LEA is injected through multiple pedicles simultaneously by two or more operators. This
technique aims to better control of LEA deposition at
the nidus by preventing embolic agent wash-off.
Monitoring multiple microcatheter injections and synchrony between multiple operators are the major challenges in this technique.
(v) Transvenous embolization: In many of the AVMs,
arterial feeders may not be accessible for embolization
due to their narrow caliber, tortuosity, and eloquence
[26]. Venous side embolization may be the solution in
142
L. J. D. Sebastian et al.
some of these cases. Careful selection of cases is essential to avoid complications [27]. This technique requires
both arterial and venous-side selective navigation. The
venous side pressure cooker technique is often employed
to inject copolymer LEA from the venous side retrogradely into the nidus [28]. A detailed description of the
technique is beyond the scope of this chapter. Currently,
TVE is not a rst-line therapy for brain AVMs and is
reserved for deep-seated ones and large AVMs pretreated by multiple embolizations.
13.3 Intracranial Dural Arterio-Venous Fistulas (DAVFs)
Dural AVFs are particularly interesting for a neurointerventionist for the following reasons:
i. The mainstay of their treatment is endovascular.
ii. Understanding them means recognizing the complexities
of neurovascular anatomy and hemodynamics in normal
and diseased states and their clinical implications as well.
Pathogenesis
• Dural AVFs can be acquired or congenital.
• Congenital dural AVFs can present relatively early in life
(from infancy to early adulthood) and are frequently associated with dural sinus malformations [29].
• Acquired dAVFs occur due to the development of high-
ow stulae in otherwise redundant AV shunts in the
dura, in response to appropriate stimuli such as sinus
thrombosis/trauma [30].
• Primary AVFs can cause secondary dural sinus
thrombosis.
Clinical
Congenital dural AVMs are different from those occurring in
older age groups. Congenital ones are generally extensive,
often associated with dural sinus malformations, and have a
generally aggressive natural history. On the other hand, the
DAVFs in older populations are generally acquired and can
be less aggressive in their clinical course.
Clinical features are determined mostly by the location
and venous outow pattern of the DAVF.Symptoms can be
mild, e.g., headache, tinnitus, or propotosis [31]. Severe
symptoms include seizures, intracranial bleeding, psychiatric manifestation, or features of raised ICT.
Analysis and Classication
Analysis in a dural AVF patient should start with the location
of the stula, arterial feeders, venous drainage pattern, presence of cortical venous reux, and any parenchymal strain.
Topographical classication is based on the location of
the stula, e.g., TS/SS, SSS, cavernous, foraminal, and
tentorial.
Classical Borden and Cognard classications are functional ones, based on venous drainage pattern (antegrade/retrograde), cortical venous reux, and spinal venous reux [32].
Most recent classication systems take into consideration
whether or not the stula is associated with a dural sinus, and
the presence/absence of cortical venous reux and parenchymal strain [33]. Cortical venous reux (CVR) should be further assessed for cortical strain (CVR with ectatic veins) and
parenchymal strain (phlebitic pattern of parenchymal veins).
Treatment (Figs.13.14 and 13.15)
Dural AVFs can be treated surgically or endovascularly.
Surgical treatment is preferred for single-hole, extra-sinus
dural AVFs, fed by non-accessible ECA branches.
Endovascular modality is the ideal mode of treatment for
most of cases, and it can either be trans-arterial, trans-venous,
or a mixed approach [34]. Liquid embolic agents (LEA)—
Cyanoacrylate (glue) and copolymers (e.g., Onyx, Squid)
and detachable coils are used as the embolic agents used in
the treatment of DAVFs. Various embolic agents can be used
alone or in various combinations. Copolymers often help
achieve curative embolization [35]. Glue is reserved for
high-ow components [36].
Large compliant balloons are useful for venous/sinus protection during embolic agent injection from the arterial side.
Small balloon microcatheters are used sometimes for ow control during LEA injection. DMSO-compatible mini- balloon
catheters are also available nowadays for LEA injection and
ow control at the same time. Sinoplasty using a balloon or
venous stenting is also employed in select cases [37].
Treatment intent can either be curative obliteration or
hemodynamic stabilization (for extensive dural AVFs with
deep venous reux) or palliation (for example in extensive
congenital dural sinus malformations). Arterial anatomy is
important to assess suitable and navigable feeders for the
embolization of stulae. Copolymer LEA is usually injected
with or without venous protection after cannulating the
feeder and injected till all possible stulae are obliterated
and no signicant venous reux is noted [35].
a
d
e
b
bc
13 Interventions inIntracranial andSpinal Arteriovenous Malformations
c
143
Fig. 13.14 An example of DAVF embolization with sinus protection
by using a large compliant balloon. A 50years old man who presented
with headache and tinnitus. (a) Right ECA angiogram showing transverse-sigmoid sinus dural AVF fed by middle meningeal artery
a
d
ef
branches; (b) Selective middle meningeal angiogram; (c) Inated balloon in the right transverse-sigmoid junction; (d) The onyx cast. (e)
Check angiogram showing complete embolization of the DAVF
Fig. 13.15 A middle aged lady presented with head ache and behavioural disturbances. (a) Axial T2 image shows enlarged ow voids in
the posterior third ventricular region. DSA images (b, c) shoe a tentorial
notch dural AVF fed by middle meningeal and meningohypophyseal
branches and draining into the Galenic system. Glue was injected (d)
via a microcatheter placed in a middle meningeal feeder. Control angiograms (e and f) show complete elimination of the stulae. The patient
made a remarkable clinical recovery
144
L. J. D. Sebastian et al.
13.4 VGAM
13.4.1 Embryological andMorphological
Considerations
Vein of Galen aneurysmal malformation (VGAM) is a congenital vascular malformation with the causative or triggering
event occurring between 6 and 12 weeks of embryonic life
[38]. The characteristic, numerous arterio-venous shunts
appear in the developing choroid, which is drained by the precursor of the vein of Galen which is the median vein of the
prosencephalon (MVP) [39]. This specic timing and location
of the malformation dene the unique clinical and angiographic
features of VGAM, which are summarized as follows:
1. The malformation is present at birth. In fact, most of the
patients reported in the literature are neonates, though
we, in India, encounter a sizeable number of older children and even adults [40].
2. Choroid is the site of AV shunts. Accordingly, anterior
and posterior choroidal arteries are the main feeders.
Subependymal and thalamic-perforator arteries can be
secondarily recruited due to the venous sump effect.
Persistent limbic arterial arch, which bridges the cortical
branches of the anterior choroidal artery and posterior
cerebral artery with the pericallosal artery, is seen in half
the cases4. On the other hand, the presence of transmesencephalic feeders points toward an AVM other than
VGAM like tectal plate or other mesencephalic AVM.
3. The median vein of the prosencephalon is persistent and
dilated, and is the main draining vein. So is the case about
Falcine sinus. VGAM is a misnomer as the vein of Galen
does not develop.
4. Early development of a high-pressure shunt precludes
connection of other normal deep venous channels with
MVP. These deep veins nd some other collateral
drainage.
5. Parenchymal or choroidal AVMs which develop late in
the fetal life (>12weeks) can be drained by a mature or
well-developed vein of Galen in which case it is called
VGAD (vein of Galen dilatation) rather than VGAM.
6. Yasargil initially proposed a comprehensive classication
of all the AVMs/AVFs involving the vein of Galen drainage (i.e., including VGAM and VGAD). Lasjaunias later
separated out VGAM and classied them based on angiomorphology [41].
7. Based on the stulae morphology, VGAM is divided
into choroidal type, mural type, and mixed type. The
choroidal type corresponds to the choroidal arteries
opening into an interposed network before opening
into the large venous pouch. In the mural type, direct
stulae are seen; that is, feeding choroidal arteries
open directly within the wall of the median vein of
prosencephalon.
8. The angio-architectural features are depicted in
Figs.13.16, 13.17 and 13.18.
13.4.2 Natural History andClinical
Presentations
The clinical presentation depends on the developmental
stage the child presents. The natural history depends on the
severity of the shunt and host response. VGAM is generally
considered a severe disease with relentless progression in the
majority of cases. A small proportion of the patients may
Fig. 13.16 VGAM—
Angioarchitectural types. (a)
Mural type (b) Choroidal type
a
b
13 Interventions inIntracranial andSpinal Arteriovenous Malformations
145
a
b
c
d
Fig. 13.17 Arterial feeders in VGAM. (a) Posterior choroidal artery (b) Thalamotuberous, subependymal arteries (c) Coroidal branch of perical-
losal artery (ACA), (d) Dural branches
Fig. 13.18 Venous drainage in VGAM.The dilated venous collecting
venous sac (black arrow in left rst image) represents the median vein
of proscencephalon (MVP) and the embryonic precursor of vein of
Galen. Also note the persistence of falcine sinus (white arrow in the
same image). The early development of stulae in VGAM precludes
deep venous connection to the MVP. This is depicted in the middle
image, another case of VGAM where deep veins are seen draining
(white arrows) through alternate route (known as the epsilan sign). The
right image from a different individual shows normal deep venous connection to the vein of Galen (white arrows)
146
L. J. D. Sebastian et al.
exhibit spontaneous closure of the stulae and remarkable
clinical normalization.
• Antenatal.
– Can be diagnosed as early as the 25th week; not all are
seen in utero.
– There is no brain damage in utero in the absence of
cardiac failure.
• Cardiac failure must be distinguished from cardiac
hypertrophy as it is the major cause of mortality in
neonates.
• Antenatal imaging, especially fetal MRI, can be used
to predict aggressive early post-natal course [42].
• Neonatal.
– The clinical presentation may vary from no symptoms
to severe congestive heart failure (CHF) with multiorgan failure.
– Timing of interference is very important with the main
goal to restore normal growth conditions rather than a
normal angiographic appearance.
– If the cardiac and multi-organ failure is severe, then the
patient will have a poor prognosis. Lasjuanias etal.
developed a scoring system popularly known as
Bicetre score. It takes into consideration ve organ
systems—cardiac, cerebral, respiratory, hepatic, and
renal—and assigns a score of 0–5 for the rst three and
a score of 0–4 for the remaining two based on their
functional status, as shown by clinical and laboratory
examinations. A higher score indicates functional status with the maximum score of 21 indicating a normal
baby.
– A score of less than 8/21 results in a decision not to
treat; shrinkage of head circumference in the rst few
days of life is stigmata of a melting brain, which portends a very poor prognosis.
– A score of 8–12 entails emergency endovascular
management.
– A score of >12 managed with medical treatment as
long as possible or until 5months of age; best balance
between the maximum benet of treatment against the
minimum risk of cerebral maturation delay.
• Infants.
– Hydrovenous disorders is the hallmark of next stage of
VGAM in kids surviving the neonatal CHF or those
who don’t develop CHF.
– Increased venous pressure decreases the CSF-venous
gradient which in turn increase the CSF pressure
accounts for hydrovenous disorders.
– Macrocrania, ventriculomegaly, and then hydrocepha-
lus appear in that order. Left untreated, this will lead
eventually to mental retardation or delayed
milestones.
– Status of jugular bulbs also dictates the clinical course
in a given patient. In patient’s jugular bulbs, overloading of the heart is seen, and if bulbs are closed, the
venous drainage must reux, into the orbits, face, also
resulting in epistaxis.
– Ventriculoperitoneal shunting increases the CSF-
venous pressure gradient, and causes enlargement
of the size of the venous pouch; so it is
contraindicated.
• Children.
– They can present mental retardation or seizures. Rarely
children with VGAM can be asymptomatic.
13.4.3 Management (Fig.13.19)
• The treatment of VGAM is essentially endovascular at
any stage of its presentation (Fig.13.19).
• In neonates presenting with heart failure, therapeutic
decisions are best taken based on the Bicetre score.
Aggressive medical therapy to manage cardiac failure is
instituted with the intention to delay vascular intervention. Urgent interventional treatment is given in indicated
cases (Bicetre score: 8–12).
• For infants, the best time for endovascular treatment is
around 5–6months.
• Ventricular shunt for hydrocephalus is never advised
before embolization.
• Complete exclusion of stula in the lowest number of
sessions possible, in the safest manner is the goal of
endovascular treatment.
• Transarterial femoral approach with a 20G needle is pre-
ferred. 4F/5F femoral sheath is used in infants.
• One to three angiographic runs are sufcient to gauge the
information needed in an infant. A vertebral artery angiogram in Towne’s and lateral projections is the rst one to
be obtained. If a posterior cerebral artery is not visible,
corresponding internal carotid artery run may be taken in
lateral projection. The other internal carotid angiogram
may be useful for venous information2.
• Trans-arterial embolization is the best mode. Transvenous
embolization is often hazardous and generally nor
advised. The trans-torcular approach is also associated
with a higher rate of complications.
• Flow-guided microcatheters—Magic 1.8 F/Marathon
1.5F—are used for superselective navigation.
• The embolizing agent of choice is concentrated glue
(NBCA). Lipiodol and tantalum powder are added for
radio-opacity.
• Run of the ow embolization technique is adopted for
injecting glue. Lower blood pressure, i.e., systolic around
70 mm Hg, is maintained at the time of embolization.
13 Interventions inIntracranial andSpinal Arteriovenous Malformations
147
a
d
b
e
c
Fig. 13.19 Endovascular treatment of VGAM.Antenatally diagnosed
case of VGAM, referred at 3months with failure to thrive and fast
breathing; cardiac failure had been well managed in the rst 2months
with drugs. Echocardiogram at our institution revealed pulmonary arterial hypertension. The baby weighed 2.5 kg. Diagnostic DSA (a)
showed mixed type of VGAM.The mural type of stula was embolized
using concentrated glue (b). Post-embolization angiogram (c) showed
signicant reduction in ow with a few residual choroidal type of stulae. Subsequent microcatheter angiogram (d) in an attempt to embolize
the residual showed almost complete obliteration of the malformation.
Post-procedure CT in sagittal reconstruction (E) showing the glue cast.
The baby made excellent clinical recover, catching up weight and normal milestones
148
L. J. D. Sebastian et al.
Occluding the distal-most feeder segment and the stulous site is aimed at. The venous sac should not be lled
with embolic material.
• Flow control balloons, coils + glue, and copolymer
embolic agents are various techniques used in some
centers.
• Every attempt is made to keep the procedure time to a
minimum.
• Post procedure, the patient is managed in a pediatric
intensive care unit.
• For subsequent sittings, alternate femoral puncture is
done.
• Complications include hemorrhage due to venous sac
rupture, arterial perforations, and complete venous occlusion. Mortality rate is very high in low Bicetre score
infants even if the embolization is technically perfect.
13.5 Spinal Vascular Malformations
13.5.1 Introduction
Spinal vascular malformations are uncommon and are generally viewed as complex disorders, difcult to diagnose and
treat. However, a systematic approach to the clinical and
angiographic aspects can make it easier to understand them.
From a developmental and anatomic perspectives, spine and
spinal cord represent the most basic form of neural organiza-
tion in general and neurovascular in particular. Hence, a
review of spinal vascular anatomy is essential before proceeding further.
13.5.2 Anatomy
The spinal cord is supplied by one solitary anterior spinal
artery or axis and two posterior spinal arteries or axes [43].
ASA is reinforced by radiculo-medullary arteries (RMA)
(Fig.13.20) at 4–8 levels, which originate from the radicular
branches of the corresponding segmental artery at every vertebral level. The largest of them is named the artery of
Adamkiewicz. These arteries follow the corresponding nerve
roots and ascend up to reach the cord surface where they give
off superior and inferior limbs that join the anterior spinal
axis, forming a hairpin conguration. ASA gives off sulcocommisural branches which further branch out in a radial
fashion, perfusing the cord in a centrifugal pattern. On the
other hand, PSA forms an extensive coronal anastomotic network over the cord surface, which gives off centripetal
branches that supply the cord. There are two PSAs—one on
each side of the posterolateral aspect of the cord—and they
are reinforced at multiple levels by radiculopial arteries
(RPA) (Fig.13.20). ASA supplies anterior one-third of cord
substance, while PSAs supply posterior two-thirds and a
watershed zone exist between the two. Venous drainage is
anteriorly via the anterior spinal vein, which lies in the ante-
Fig. 13.20 Normal spinal
vascular anatomy. Native (a)
and DSA (b) images of a
radiculomedullary artery
(arrows) and anterior spinal
axis (arrowheads). Note the
midline disposition of
ASA.Similarly, (c) and (d)
demonstrate a radiculo-pial
artery (arrows), which lies
postero-laterally
a
b
c
d
13 Interventions inIntracranial andSpinal Arteriovenous Malformations
149
rior commissure along the ASA, and posteriorly via the coronal plexus. The latter drains out to the epidural (systemic)
venous system through a limited number of “medullary” or
“bridging” veins. A functional valve-like system is noted at
the intradural-extradural transition, which prevents the transmission of external pressures to the intradural venous
system.
13.5.3 Classication andClinical Features
Dura serves as the planar landmark to compartmentalize and
classify different types of spinal vascular malformations, as
enlisted in Table13.4 [44–46]. Interestingly, each of these
types has its own distinctive demographic and clinical features, as highlighted. General clinical presentations include
motor symptoms (hemiparesis/paraparesis), sensory symptoms (paresthesias, sensory loss), and autonomic symptoms
relating to the bowel/bladder or erectile dysfunction along
with constitutional symptoms of headache and backache.
The mode of presentation may be either acute or chronic progressive or acute on a chronic course.
13.5.4 Treatment ofSpinal Vascular
Malformations
Treatment strategy depends on the type of SVM (Figs.13.21,
13.22 and 13.23). Accordingly, each group is managed as
follows:
13.5.4.1 SDAVF (Fig.13.21)
Surgery and embolization are equally effective. The goal, in
either approach, is the disconnection of the draining/reuxing medullary vein from the AVF situated in the dural sleeves
[47].
The endovascular approach consists of the following
steps which can be sometimes technically demanding.
1. Stable guide catheter access is important but can be often
difcult to achieve, especially in the elderly with atherosclerotic aorta where the origin of segmental arteries can
be torturous.
2. Identifying the often thin and tortuous radiculomenigeal
feeder and negotiating a microcatheter to a sufciently
distal position suitable for glue injection.
Table 13.4 Classication of spinal AVMs
Type Subtype Location Age Presentation Remarks
Intradural (based on type of shunt and location)
SCAVM Nidus within parenchyma Adolescence Hematomyelia and
Glomerular Single axial section
Multi-
myelomeric
SCAVF Fistula on cord surface Cord edema, spinal
Micro-stula Low-ow direct shunt Middle aged
Macro-stula/
giant stula
Filar AVF Over piamater of lum
Dural/extra-dural (based on shunt location)
SDAVF Within dural sleeves,
EPIDURAL/
OSTEODURAL
Metameric syndromes
All embryonic layers (e.g., spinal cord, bone, paraspinal musculature, subcutaneous tissues, and skin)
Hereditary Klippel-Trenauney syndrome, parks Weber
Non-hereditary
Multiple axial sections
High-ow direct shunt Pediatric
terminale
Elderly
commonly in the vicinity
of nerve root exit
Over the dura/anterior
epidural space/posterior
epidural space epidural +
vertebral body
male
spinal SAH
SAH
Cord edema Feeder from radiculo-
Cord compression by
dilated extradural
venous pouches
Feeder from RMA/RPA,
draining to ASV/perimedullary
venous plexus
One/many feeders from RMA/
RPA, draining into ectatic/
non-ectatic ASV/perimedullary
venous plexus.
Association with HHT
Supply from ASA extension, or
lumbar/sacral spinal segmental
arteries
meningeal artery drainage into
coronal plexus/ASV via
reuxing medullary vein
Feeder from anterior/posterior
epidural artery; drainage to
epidural venous plexus (rarely
intradural)