SPINAL AVMS

CLASSIFICATION AND SURGICAL MANAGEMENT OF

SPINAL ARTERIOVENOUS LESIONS: ARTERIOVENOUS
FISTULAE AND ARTERIOVENOUS MALFORMATIONS
Louis J. Kim, M.D.
Division of Neurological Surgery,
Barrow Neurological Institute,
St. Josephs Hospital
and Medical Center,
Phoenix, Arizona

Robert F. Spetzler, M.D.

Division of Neurological Surgery,
Barrow Neurological Institute,
St. Josephs Hospital
and Medical Center,
Phoenix, Arizona
Reprint requests:
Robert F. Spetzler, M.D.,
Neuroscience Publications,
Barrow Neurological Institute,
350 West Thomas Road,
Phoenix, AZ 85013.
Email: neuropub@chw.edu
Received, January 25, 2006.
Accepted, June 14, 2006.

OBJECTIVE: Preexisting spinal arteriovenous malformation nomenclature can be confusing. The aim of this article is to present a modified classification system for spinal
arteriovenous lesions and to discuss its implications for microsurgical strategies.
METHODS: Based on the literature review of prior classifications as well as on the
experience of the senior author (RFS), the authors delineate an anatomically and
pathophysiologically based classification to facilitate the description and treatment of
these uncommon entities.
RESULTS: Spinal arteriovenous lesions are composed of arteriovenous fistulae and
malformations. These lesions are classified as extradural, extradural-intradural, or
intradural. Intradural lesions are characterized further as ventral or dorsal fistulae or as
intramedullary lesions. Intramedullary lesions are characterized as compact or diffuse.
A new category, conus medullaris arteriovenous malformations, is described as a
distinct entity.
CONCLUSION: This updated classification system eliminates confusion related to
older nomenclature and is based on the anatomical and pathophysiological features of
these lesions. When treating these lesions, the neurovascular team must collaborate
closely with their microsurgical and endovascular colleagues. Finally, treatment
should be individualized, depending on lesional angioarchitecture and the patients
clinical status.
KEY WORDS: Classification, Nomenclature, Spinal arteriovenous fistula, Spinal arteriovenous malformation,
Surgical management
Neurosurgery 59:S3-195-S3-201, 2006

pinal arteriovenous lesions are a collection of disparate

and diverse entities. Our understanding of their pathophysiology has evolved significantly over the past century. As a byproduct of our gradual understanding of these
lesions, a cadre of nomenclature has developed over time.
Unfortunately, this terminology has served mostly to confound rather than to facilitate accurate descriptions of spinal
arteriovenous malformations (AVMs). Recently, anatomically
based classifications that offer accurate descriptions have been
developed.
In tandem with our understanding of the pathophysiology
of spinal AVMs, our technical ability to treat these lesions,
both microsurgically and endovascularly, has improved tremendously. This report describes the classification schemas of
spinal AVMs, pointing out the recent trend toward anatomical
nomenclature and the surgical strategies and techniques used
in the practice of contemporary neurosurgery.

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DOI: 10.1227/01.NEU.0000237335.82234.CE

www.neurosurgery-online.com

CLASSIFICATION OF ARTERIOVENOUS
FISTULAE AND AVMS
Spetzler et al. (44) proposed a modified classification system
for spinal arteriovenous lesions based on specific anatomical
and pathophysiological factors. Descriptions are based on extradural or intradural, ventral, dorsal, or intramedullary locations of the lesions and on the presence of single or multiple
feeding branches.

Extradural Arteriovenous Fistulae

Extradural arteriovenous fistulae (AVFs; Fig. 1), known as
epidural fistulae in older nomenclature, represent an abnormal communication between an extradural arterial branch
that usually arises from a branch of a radicular artery and an
epidural venous plexus. This entity results in significant engorgement of the venous system, leading to subsequent com-

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FIGURE 1. A, axial illustration demonstrating an extradural AVF along

a perforating branch of the left vertebral artery (arrow). B, illustration of
the posterior view demonstrating that engorgement of epidural veins can
produce symptomatic mass effect on adjacent nerve roots and spinal cord
(courtesy of Barrow Neurological Institute, Phoenix, Arizona).

pressive mass effect on adjacent nerve roots and spinal cord.

Venous hypertension and vascular steal also may contribute to
myelopathic symptoms.

Intradural Dorsal AVFs

Intradural dorsal AVFs (Fig. 2), which correlate with Type 1
dural AVFs, are composed of a radicular feeding artery that
communicates abnormally with the venous system of the spinal cord at the dural sleeve of the nerve root. Inherent to the
pathophysiology is obstruction of spinal cord venous outflow,
which ostensibly contributes to the formation of the fistula. In
turn, arterialization of the coronal venous plexus, venous hypertension, and myelopathy ensue.

Intradural Ventral AVF

Intradural ventral AVFs (Fig. 3) are ventral midline lesions
located in the subarachnoid space. The fistulous site occurs between the anterior spinal artery (ASA) and an enlarged venous

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FIGURE 2. A, axial illustration of an intradural dorsal AVF demonstrating an abnormal radicular feeding artery along the nerve root on the
right. The glomerular network of tiny branches coalesces at the site of the
fistula along the dural root sleeve. B, illustration of the posterior view
demonstrating the dilatation of the coronal venous plexus. In addition to
venous outflow obstruction (not shown), arterialization of these veins produces venous hypertension. Focal disruption of the point of the fistula by
endovascular or microsurgical methods will obliterate the lesion (courtesy
of Barrow Neurological Institute, Phoenix, Arizona).

network. The lesions have been subclassified as Types A, B, and

C (1). Type A intradural ventral AVFs are small and have a single
feeder. The size of Type B lesions is intermediate. They have a
major feeder from the ASA and minor feeders at the level of the

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SPINAL ARTERIOVENOUS MALFORMATIONS

FIGURE 4. Axial illustration demonstrating an extradural-intradural

AVM. These treacherous lesions can encompass soft tissues, bone, spinal
canal, spinal cord, and spinal nerve roots along an entire spinal level.
Considerable involvement of multiple structures makes these entities
extremely difficult to treat. Although cures have been reported, the primary goal of treatment is usually palliative (courtesy of Barrow Neurological Institute, Phoenix, Arizona).

vested along a discrete somite level. Typically, they involve

bone, muscle, skin, spinal canal, spinal cord, and nerve roots.
Complete involvement of an AVM along an entire somite level
has been described as Cobbs syndrome.

Intramedullary AVMs
Intramedullary AVMs are analogous to intracranial AVMs,
located entirely in the spinal cord parenchyma. These lesions
may have single or multiple feeding arteries from branches of
the ASA and posterior spinal artery. They are classified further as compact or diffuse (Figs. 5 and 6), depending on the
angioarchitecture of the nidus.

Conus Medullaris AVMs

FIGURE 3. A, axial illustration demonstrating an intradural ventral AVF, a
midline lesion derived from a fistulous connection (arrow) between the anterior
spinal artery and coronal venous plexus. B, illustration of the anterior view
demonstrating the fistula along the anteroinferior aspect of the spinal cord.
Proximal and distal to this Type A lesion, the course of the anterior spinal artery
is normal (courtesy of Barrow Neurological Institute, Phoenix, Arizona).

fistula. Type C lesions are giant. They are multipediculated and

have massively dilated venous channels. Extraordinarily high
flow through these lesions leads to the phenomenon of vascular
steal from the intrinsic spinal cord arterial supply and to the
sequelae of ischemic symptoms.

Conus medullaris lesions (Fig. 7) occupy a separate category

(44). Conus lesions typically exhibit multiple feeders from the
ASA and posterior spinal artery with direct arteriovenous
shunts and large dilated veins. The pathophysiology underlying neurological decline includes venous hypertension, ischemia, and mass effect from hugely dilated venous structures.
Because the location and angioarchitecture of these lesions are
unique, both upper and lower motor neuron symptoms can
occur. Elimination of mass effect on descending nerve roots of
the cauda equina can be associated with striking improvements.

DISCUSSION

Extradural-Intradural AVM

Historical Perspective and Previous Classifications

Extradural-intradural AVMs (Fig. 4) correspond with juvenile or metameric AVMs. These formidable lesions are in-

In 1888, Gaupp (16) provided the earliest description of a

spinal AVM. In 1910, Krause (25) reported the first surgically

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FIGURE 5. A, axial illustration demonstrating a compact intramedullary AVM. In this figure, an arterial feeder from the anterior spinal artery
is identified. Note the discrete, compact mass of the AVM. B, posterior
view demonstrating additional feeding branches from the posterior spinal
artery and reemphasizing the compact nature of this type of spinal AVM.
Portions of the AVM are evident along the surface of the spinal cord. Surgical resection is the mainstay of treatment. Preoperative embolization is
reserved for select cases only (courtesy of Barrow Neurological Institute,
Phoenix, Arizona).

treated spinal dural fistula, and in 1916, Elsberg (14) described

the successful surgical treatment of a spinal epidural AVM. In
1926, Foix and Alajouanine (15) reported the syndrome of
subacute necrotic myelopathy associated with rapidly progressive onset of paraplegia and subsequent death.
Subsequent investigators recognized that Foix-Alajouanine
syndrome was associated with spinal AVMs after acute
thrombosis of the pathological vessels (28, 39). It is now un-

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FIGURE 6. A, axial illustration demonstrating a diffuse intramedullary

AVM with areas of intervening neural tissue between the intraparenchymal loops of AVM. Portions of the AVM also course along the pial surface
and subarachnoid space. B, illustration of the oblique posterior view demonstrating the loops of the AVM coursing in and out of the spinal cord.
Normal neural tissue is evident between intraparenchymal portions of the
AVM. This view accentuates the diffuse character of these lesions (courtesy of Barrow Neurological Institute, Phoenix, Arizona).

derstood that the syndrome can occur after acute exacerbation

of underlying venous hypertension. If treated sufficiently
early, the condition can be reversed in some cases. In 1943,
Wyburn-Mason (49) reported 110 spinal AVMs, which he
classified histologically into arteriovenous angiomas and
purely venous angiomas. The latter category accounted for
more than two-thirds of all cases. Consistent with Virchows
original classification of vascular lesions, Wyburn-Mason perpetuated the older nomenclature by popularizing the terms

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FIGURE 7. A, axial illustration demonstrating a conus medullaris AVM

and the feeding arteries and draining veins from both the anterior and
posterior aspects of the spinal cord. Note the proximity of the AVM to
branches of the cauda equina. B, illustration of the posterior view recapitulating the complexity of the angioarchitecture of these lesions. Anterior
and posterior spinal arteries, radicular arteries, and anterior and posteriorly draining veins are involved simultaneously. Portions of the AVM can
consist of direct AV shunts as well as regions of true AVM nidus. During endovascular treatment, surgical treatment, or both, it is crucial to
identify the en passage branches of the anterior and posterior spinal arteries (courtesy of Barrow Neurological Institute, Phoenix, Arizona).

for these lesions as angioma racemosum venosum and angioma

racemosum arteriovenosum (49).
As spinal angiographic techniques evolved (5, 1013), radiographic imaging of spinal AVMs afforded the opportunity to
develop anatomically based classifications. The most common
classification scheme for spinal AVMs uses the Type 1 to 4

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grading system (11, 13, 22, 29, 37). Type 1 lesions are dural
AVFs in which a dural branch from a radicular artery forms an
abnormal communication with the dural veins at the nerve
root sleeve. Arterialization of the perimedullary coronal venous plexus results. Type 2 refers to glomus or intramedullary
lesions. Type 3 lesions are juvenile or metameric AVMs associated with both extradural and intradural extension of the
spinal AVM. Type 4 spinal AVMs, as first described by Djindjian et al. (12) and categorized as Type 4 by Heros et al. (22),
refer to perimedullary fistulae. These ventrally located fistula
primarily receive arterial contributions from the ASA.
Borden et al. (8) described a three-point classification for
both intracranial and spinal dural AVFs using the term dural
arteriovenous fistulous malformation. Type 1 referred to extradural AVFs or epidural types, with direct drainage of the
feeding artery into Batsons venous plexus. Type 2 referred to
dural artery feeders draining into both epidural and intradural venous systems. Type 3 referred to what is known as
intradural dorsal AVFs, or Type 1 AVMs, according to the
description of Di Chiro et al. (11).
More recent spinal vascular lesion classifications are based
on descriptive anatomic considerations. Niimi and Berenstein
(35) divided vascular lesions of the spine into spinal vascular
lesions and spinal cord vascular lesions. They subdivided
spinal vascular lesions into spinal dural fistulae and extradural fistulae. Spinal cord vascular lesions are referred to as
spinal cord vascular malformations, of which there are two types:
isolated, which includes AVMs and AVFs, and multiple,
which includes metameric and nonmetameric forms.
Bao and Ling (6) classified spinal cord vascular lesions as
intramedullary AVMs, intradural AVFs, dural AVFs, paravertebral AVMs, and Cobbs syndrome. Intramedullary lesions
include glomus and juvenile forms. Intradural AVFs are subdivided into Types 1 to 3, as the size of the lesion and degree
of AVF flow increase.
Rosenblum et al. (42) differentiated spinal AVFs from
AVMs based on their experience with 81 treated patients.
Intradural AVMs were divided into intramedullary and direct
AVFs. Intramedullary lesions included glomus and juvenile
AVMs. Direct AVFs occupied either an intramedullary or
extramedullary location. Intramedullary lesions were supplied by medullary arteries, and the arteriovenous shunt was
located partially in the spinal cord or pia mater. Dural AVFs
were supplied by a radicular branch along the dural nerve
root sleeve, which drained via an AVF into the coronal venous
plexus.
Our classification system represents an evolution that incorporates our enhanced understanding of these entities in recent
decades (7, 27). This classification system offers several advantages. First, it includes all spinal AVFs and AVMs, including
the recently proposed conus medullaris category (41, 44). Second, the system is based on the anatomic location of each
lesion with its corresponding pathophysiological mechanism.
Finally, it eliminates potential confusion inherent in the older
nomenclature.

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Treatment Strategies
Three pathophysiologic mechanisms underlying spinal
AVMs can cause neurological injury: hemorrhage, mass effect,
or vascular steal. Venous hypertension tends to be associated
with either intradural spinal AVFs or conus medullaris-type
spinal AVMs. Clinical manifestations can include pain, acute
or progressive myelopathy, and radiculopathy. Magnetic resonance imaging and a thorough catheter-based angiogram
provide the most important diagnostic information.
In contemporary neurosurgical settings, these lesions
should be approached in a team-oriented fashion. Optimal
patient care depends on direct collaboration between open
vascular and endovascular neurosurgeons. The role of each
half of this neurovascular team depends on the lesion, and
treatment must be individualized to the specifics of each situation. The following surgical strategies and technical consideration serve only as a guide.
At our institution, monitoring somatosensory and motor
evoked potentials has become a routine part of spinal AVM
surgery. Intraoperative angiography should be used in selected cases when residual AVM may remain. When intraoperative angiography is unwarranted or indeterminate, immediate postoperative, as well as long-term, follow-up catheterbased angiography is the mainstay of our treatment paradigm.

Surgical Management
Extradural AVFs are treated primarily by endovascular
techniques (3, 18, 21, 32, 35, 43). In our experience, the purely
extradural fistula is an extremely uncommon lesion. The role
of surgery in treating these lesions is limited to patients requiring reduction of local compression.
In 1977, Kendall and Logue (24) accurately redefined the
pathophysiology of intradural dorsal AVFs. They recognized
that the fistulous point occurred at the level of the dural root
sleeve rather than along the dilated coronal venous plexus,
which can be striking in such patients. Earlier, it was common to
perform vein stripping procedures with no benefit or even worsening of symptoms (26) and with no effect on obliteration of the
fistula itself. It is worth reiterating that successful surgical management of these lesions requires a careful and thorough
catheter-based spinal angiogram to identify the arterial feeder(s)
and artery of Adamkiewicz. Although angiographic visualization is paramount, angiographically occult lesions in patients
under high clinical suspicion for intradural dorsal fistulae have
been associated with successful surgical exploration and fistula
disruption (36). These rare instances stress the importance of
recognizing the clinical manifestations of these fistulae.
As soon as the appropriate spinal level has been identified, the
surgical strategy involves its posterior exposure. We favor a
posterior approach and laminoplasty. High-powered magnification and illumination with the operating microscope are used to
perform intradural dissection along the appropriate nerve root.
Typically, an arterialized vein is identified along the nerve root
and can be dissected sharply to its exit point at the margin of the
dural root sleeve. Nonstick bipolar cauterization and microscis-

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sors are used to interrupt the fistula. The advantage of surgical

disruption is the relative ease of exposure and direct visualization of the vascular anatomy (2, 33, 36, 38, 42, 46).
Small intradural ventral AVFs (Subtypes A and B) are managed surgically (1, 17, 20, 40). These lesions may require an
anterior or anterolateral approach for adequate exposure; however, posterolateral approaches are feasible for ventrolateral lesions (23, 30). Therefore, a thorough understanding of complex
spinal approaches is essential for both the operative approach
and spinal stabilization. Key to surgical success is preservation of
the ASA branches during obliteration of the fistula. Giant (Subtype C) lesions, however, are best treated with endovascular
embolization techniques because of their complex angioarchitecture and multipedicled feeders (1, 19, 22, 31, 34, 40).
Extradural-intradural AVMs are formidable lesions involving neural structures, bone, and soft tissue along the affected
spinal level. They are treated primarily with endovascular
embolization; surgery is reserved for decompression of mass
effect along the nerve roots and spinal cord (22, 29, 30, 35, 38,
45). Although treatment cures have been reported (30, 45, 47),
the realistic goal in most cases is reduction of mass effect,
venous hypertension, and vascular steal to ameliorate the
patients neurological deficits.
Intradural-intramedullary AVMs have been treated successfully with embolization procedures (4). However, the mainstay of treatment remains surgical extirpation (9, 44). We
recommend preoperative embolization in selected cases, particularly for patients with complex, multipedicled lesions.
Typically, a posterior or posterolateral approach is suitable,
but an anterior approach may be warranted in selected cases
(9, 30, 48). For diffuse lesions (Fig. 6) situated superficially on
the spinal cord, it is prudent to avoid chasing vascular loops of
AVM that may invaginate into the spinal cord parenchyma.
Because the pathophysiology of this lesion defines it as a
superficial entity, it is best to truncate vessels embedded in the
parenchyma at the pial surface. This strategy minimizes
trauma to the tissue that could lead to inadvertent neurological injury yet still permits complete obliteration of the lesion.
We have achieved gross total resection of 92% of the intramedullary AVMs that we have treated (44).
Conus medullaris AVMs are treated with a combined endovascular and microsurgical approach. Careful identification
of ASA and posterior spinal artery branches separate from the
lesion is crucial. Because the venous structures associated with
conus AVMs are so hugely dilated, surgical decompression of
adjacent spinal cord and nerve roots can relieve neurological
symptoms significantly. Conus AVMs are usually easily accessible from a posterior approach. Our continuing experience
with these entities has demonstrated that aggressive combined treatment can result in good outcomes (44).

CONCLUSION
Our ability to identify and treat spinal AVMs has advanced
tremendously in the past several decades. This article describes a modified classification system of spinal arterio-

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venous lesions based on this current anatomic and pathophysiological understanding. Further advances in the treatment of
spinal AVMs mandate an integrated approach with microvascular and endovascular neurosurgeons.

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