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Fig. 2.8 Intramedullary glomerular cervical AVM. (a)

Sagittal T2-weighted image shows the intramedullary

position of the AVM and enlarged supercial draining

veins in the cervical subarachnoid space extending intra-

cranially to the perimedullary region. (b

) Contrast-

enhanced MR angiography revealing the nidus and spatial

extent of venous drainage of AVM.Spinal AVM supplied

by the feeders from bilateral vertebral arteries at C6 level

on the right (c) and C5 level on the left (d). (e) Dilated

arterialized veins extending superiorly through the fora-

men magnum to the level of the clivus

M. Panigrahi et al.

https://t.me/med1917

Key Messages

• Spinal vascular malformations are a poten-

tially treatable cause of myelopathy.

• Spinal MRI and angiography are the main

diagnostic tools.

• Patient selection after careful evaluation of

angio-architecture of the spinal vascular mal-

formation is an important factor in achieving

good results, to avoid variations in treatment

outcomes and to minimize complications.

• Choice of surgery or embolization depends on

the type and location of lesions.

• Surgery gives outstanding results (98% suc-

cess), provided draining vein is correctly iden-

tied in sDAVF.

• Endovascular treatment is getting preference

over surgical obliteration.

References

1. Ferch RD, Morgan MK, Sears WR.Spinal arteriove-

nous malformations: a review with case illustrations.

J Clin Neurosci. 2001;8(4):299–304.

2. Oldeld EH.Surgical treatment of spinal dural arte-

riovenous stulas. SeminCerebrovasc Dis Stroke.

2002;2(3):209–26.

3. Thron A.Vascular anatomy of the spinal cord: radio-

anatomy as the key to diagnosis and treatment. 2nd

ed. Springer; 2016.

4. Nishio A, Ohata K, Takami T, Nishikawa M, Hara

M. Atypical spinal dural arteriovenous stula with

supply from the lateral sacral artery. J Clin Neurosci.

2007;14(1):65–8.

5. Takai K. Spinal Arteriovenous Shunts:

Angioarchitecture and Historical Changes

in Classication. Neurol Med Chir (Tokyo).

2017;57(7):356–65.

6. Cenzato M, Debernardi A, Steni R, et al. Spinal

dural arteriovenous stulas: outcome and prognostic

factors. Neurosurg Focus. 2012;32(5):E11.

7. Sivakumar W, Zada G, Yashar P, Giannotta SL,

Teitelbaum G, Larsen DW. Endovascular manage-

ment of spinal dural arteriovenous stulas. A review

Neurosurg Focus. 2009;26(5):E15.

8. Gross BA, Du R. Spinal pial (type IV) arteriove-

nous stulae: a systematic pooled analysis of demo-

graphics, hemorrhage risk, and treatment results.

Neurosurgery. 2013;73(1):141–51.

9. Endo T, Endo H, Sato K, Matsumoto Y, Tominaga

T. Surgical and Endovascular Treatment for Spinal

Arteriovenous Malformations. Neurol Med Chir

(Tokyo). 2016;56(8):457–64.

10. Zhan PL, Jahromi BS, Kruser TJ, Potts

MB.Stereotactic radiosurgery and fractionated radio-

therapy for spinal arteriovenous malformations: a

systematic review of the literature. J Clin Neurosci.

2019;62:83–7.

2 Types ofSpinal Vascular Malformations

https://t.me/med1917

X. Lv (ed.), Endovascular and Neurovascular Surgery for Spinal Vascular Malformations,

https://doi.org/10.1007/978-981-97-4661-3_3

Current Concept ofVascular

Structures ofSpinal Arteriovenous

Lesions

KirillYurievichOrlov

andDmitryS.Kislitsin

Abstract

Understanding of current concepts of spinal

arteriovenous lesions strictly depends on

understanding of spatial vascular anatomy and

visualization of focal vascular structures.

Most classications up to date are based on

either topical localization of stula or arteries

that form arteriovenous shunt. Regardless of

the implied classication, the major point of

discrimination of the pathology is the possibil-

ity to treat it weighted against certain possibil-

ity to cause neurological symptoms. Hence,

understanding of angiographic ndings is the

most crucial skill that neurovascular specialist

should develop. Multiple classication sys-

tems are proposed nowadays, but the so-called

“combined effort” system is the most widely

used one. According to this classication, all

spinal AV lesions are divided into the follow-

ing subgroups: type I, radicular arteriovenous

stulas; type II, glomus AVMs; type III, juve-

nile AVMs; type IV, perimedullary pial stu-

las; and type V, extradural shunts. Type V

comprise of heterogeneous group that is

slightly out of the scope of this chapter. While

established classication system somewhat

lacks in risk stratication and decision-

making, it is the best tool in the development

of understanding of complex pathological

anatomy. Despite rapid development of nonin-

vasive imaging techniques, catheter spinal

angiography is still the gold standard of spinal

vascular lesion visualization. Thus, the most

important skill that neurovascular specialist is

ought to have is the ability to “read” spinal

angiogram, to differentiate normal structures

from pathology. This ability comes with a lot

of diligence, as spinal angiography is more

tricky and tedious than cerebral

DSA. Experience in open spinal surgery is

also a valuable asset.

Keywords

Spinal arteriovenous malformation · Spinal

dural arteriovenous stula · Spinal pial

arteriovenous stula · Spinal arteriovenous

lesion · Spinal vascular pathology

The classication proposed by Di Chiro etal. [1]

in 1967 was the rst stage in the creation of com-

plex nomenclature of spinal lesions. A lot of

attempts to clarify and classify spinal lesions

were made later; Borden and colleagues [2] in

K. Y. Orlov (*)

Federal Center of Brain Research and

Neurotechnologies of Federal Medical Biological

Agency of Russia, Russian Federation,

Moscow, Russia

e-mail: kirill.orlov@rens-russia.org

D. S. Kislitsin

E.N.Meshalkin National Medical Research Center of

Ministry of Healthcare of Russia, Russian Federation,

Novosibirsk, Russia

https://t.me/med1917

1995 proposed to stage spinal arteriovenous

pathology based on the anatomy of venous drain-

age, and Bao etal. in 1997 proposed the nomen-

clature with the greatest emphasis on anatomical

relation of the AVMs to the spinal cord [3].

Spetzler and colleagues, in 2002, proposed the

most complex classication that would cover

almost every single possible spinal lesion [4].

The result of multiple, often unrelated, scientic

effort resulted in the appearance of the so-called

combined effort classication [5, 6], which

includes four types of lesions: radicular sleeve

stulas (type I), intramedullary glomus AVMs

(type II), juvenile metameric lesions (type III),

and perimedullary AVFs (type IV). There is still a

lack of general consensus of denitive classica-

tion, and multiple centers propose new models of

nomenclature [7], and though “modern” classi-

cations tend to rely more on angiographic nd-

ings or allow to stratify risks precisely, for

teaching purposes, in this chapter, we are going

to stand with the most widespread “combined

effort” system.

3.1 Type I

By far, the most common among all spinal AV

lesions are radicular arteriovenous stulas,

which account for up to 60–70% of all spinal

vascular conditions [8, 9]. It is presumed that

the pathology is of acquired nature [10] though

precise etiology is still unknown. The most

prominent common feature of the lesions in this

group is the anatomical relation to the dural

root sleeve. The vessel of origin is always a

radicular artery with the drainage into the

radicular vein. That drainage is not always

direct, and pathological vessel net can often be

visualized (see Fig.3.1 as an illustrative case).

As most of those lesions are located posteriorly,

they are a great subject for microsurgical treat-

ment [11], though the role of endovascular

methods gains much more weight with the

progress of the techniques [12].

The cornerstone of endovascular emboliza-

tion, for radicular stulas, is the ability to visual-

ize radiculomedullary artery (RMA). Those

arteries are irregular and of variable origin [13],

and thus, neurovascular specialist can only rely

on his understanding of local spatial anatomy to

discriminate them. The rule of thumb is to never

embolize unless one guarantees the patency of

RMA.

Although clinically most radicular stulas

appear in adult and elderly patients, the authors

of this chapter have had an extremely unusual

experience with high-ow thoracic radicular s-

tula, of highly likely congenital origin, in the

9-year-old child, who manifested with pleural

effusion due to distention of the common tho-

racic duct. See Fig.3.2 for an illustrative case.

K. Y. Orlov and D. S. Kislitsin

https://t.me/med1917

Fig. 3.1 (a) Sagittal plane of T2-weighted MRI with

typical “ow voids” corresponding to dilated posterior

median vein. (b) DSA with left thoracic segmental artery

injection; radicular artery (white arrow) gives origin to the

arteriovenous net inside the radicular sleeve; note the

extended and tortuous due to excessive drainage posterior

median vein (black arrow). (c) Superselective distal injec-

tion; reux of the contrast material shows intercostal

branch (black arrow) unseen on previous angiogram

3 Current Concept ofVascular Structures ofSpinal Arteriovenous Lesions

https://t.me/med1917

Fig. 3.2 (a) Thoracic slice of the T2W MRI of a 9-year-

old child reveals signicant “ow void” in the region of

left radicular sleeve (white arrow). (b) DSA with left tho-

racic segmental injection showing prominent AV shunting

between posterior radicular artery and posterior radicular

vein with prominent varix (white arrow) at the fusion site.

Note the retrograde lling of the coronal veins (black

arrows). (c) Microcatheter tip is navigated into the stula.

(d) LEA cast with complete occlusion of the AV lesion

K. Y. Orlov and D. S. Kislitsin

https://t.me/med1917

3.2 Type II

This cohort includes nidus arteriovenous malfor-

mations (also known as glomus malformations).

The distinctive feature of type II lesions is the

presence of intramedullary arteriovenous nidus.

Pathophysiology and histological properties in

the group are identical to cerebral AVMs (with

adjustments for localization and distinct spatial

anatomy). Glomus malformations are the second

most common spinal AV lesions following radic-

ular DAVFs and account for approximately 30%

of cases [3]. Among them, 70% are located in the

thoracolumbar region, and 30% are located in the

cervical segments, with caudo-medullar AVMs

being a different nosological group associated

with tethered spinal cord syndrome [14]. In con-

trast with type I, where clinical presentation is

usually related to congestive myelopathy, type II

lesions (as well as their cerebral “siblings”) often

tend to manifest with hemorrhage (the annual

rate is estimated to be 4% for previously unrup-

tured AVMs and 10% for those with history of

hemorrhages) [15]. However, venous congestion

is still a factor in pathogenesis of spinal nidus

malformations [16]. Surgical treatment propos-

edly gains the most radical results [15], while

endovascular measures allow to achieve cure in

approximately 30% of cases [16, 17]. Needless to

say, that constant progress in endovascular mate-

rials and techniques should increase the endovas-

cular curability of spinal AVMs, though in

contrast with brain AVMs, even the large retro-

spective cohort studies seem to be impossible due

to the relative rarity of the lesions. Radiosurgery,

while hasn’t been proven as a curative method, is

still capable to obliterate some nodes and should

be considered as an option for the cases where

local anatomy rules out microsurgery or endovas-

cular intervention [18].

Vascular anatomy is the major factor in the

technical possibility of complete endovascular

obliteration. For thoracolumbar lesions, it is

important to recognize major spinal trunks warped

by the high-ow anomaly. Decision to embolize

should only be made when one can be sure that

the anterior or posterior spinal arteries will not be

compromised by either propagation of embolic

agent or by critical reux. Not to mention that in

comparison with cerebral AVMs, thoracolumbar

spine AVMs usually do not have multiple cathe-

terizable feeders, owing to the segmental nature

of spinal circulation. See Fig.3.3 for an illustra-

tive case of thoracolumbar type II AVM.

Cervical region differs from other segments

by more “rostral” multiple source inow, with the

involvement of costocervical and thyrocervical

trunks and vertebral arteries. Cervical AVMs

have more variability in the inow and outow,

but due to extremely high stakes of the cervical

medullar edema, open surgery should probably

routinely follow embolization at least in limited

decompressive form. See Fig.3.4 for an example

of cervical glomus AVM.

3 Current Concept ofVascular Structures ofSpinal Arteriovenous Lesions

https://t.me/med1917

c d

Fig. 3.3 (a) Axial plane of T2-weighted MRI with “ow

voids” in a pattern of intramedullary lesion. (b) Right

lumbar segmental artery injection (early phase) reveals

intranidal aneurysms (white arrow), which are common in

type II lesions. Note the characteristic “hairpin” turn of

the radiculomedullary artery (black arrow). (c) Late phase

shows the AVM nidus, along with the anterior spinal

artery (black arrows) and early lling of dilated anterior

spinal vein. (d) Single-shot uoroscopy image with

EVOH cast. Note that reux did not propagate further

than the point of “sharp turn” of the feeder, to avoid risks

of ASA occlusion. The patient, in this case, did not

develop additional neurological symptoms

Fig. 3.4

(a–c) AP (left) and lateral (right) DSA.Left thy-

rocervical trunk injection (a) showing intramedullary AV

nidus at the level of C4 with numerous intranidal aneu-

rysms (white arrows) and distinct venous varices (black

arrows) Superselective series conrms the intranidal posi-

tion of the catheter tip (b). LEA cast following complete

occlusion (c). (d) Axial (left) and sagittal (right) planes of

the at-panel scan showing the LEA cast; due to the risk

of medullary edema, the patient has been scheduled for

decompression surgery immediately following the

procedure

K. Y. Orlov and D. S. Kislitsin

https://t.me/med1917

3 Current Concept ofVascular Structures ofSpinal Arteriovenous Lesions

https://t.me/med1917

3.3 Type III

Juvenile spinal AVM is another distinct nosology

that comprises of lesions that involve not only the

spinal cord but also most of the tissues (i.e., ver-

tebrae and muscles) in the involved metamere,

thus the alternative name “metameric.” These

lesions are extremely rare and are thought to be

of congenital origin [19]. By far the most com-

plex among all spinal vascular lesions, metameric

Fig. 3.4 (continued)

K. Y. Orlov and D. S. Kislitsin

https://t.me/med1917

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