Intracranial Vascular Lesions and Anatomical

Variants All Residents Should Know

Gloria Julia Guzmán Pérez-Carrillo, MD, and Jeffery P. Hogg, MD

The purpose of this article is to extensively illustrate patho-

logically and clinically proven cases of intracranial vascular
lesions and variants accumulated at a tertiary referral
center. These are organized by normal anatomy and
variants, arterial lesions, and venous lesions. High-quality
computed tomography, computed tomographic angiogra-
phy, magnetic resonance imaging, magnetic resonance
angiography, 3D reconstruction, and angiographic figures
illustrate the findings and complement a succinct review of
this category of disease. Some cases are accompanied by
histopathologic correlation. The reader of this article will
gain or refresh information about intracranial vascular
lesions and variants for clinical practice and for prepara-
tion for certifying examinations and clinical practice. The
text and figures aid recognition of these entities and
emphasize anatomy, clinical context, and differential diag-
nosis. These can aid the radiologist in arriving at the
appropriate diagnosis.

Normal Vascular Anatomy

Due to the limits of space, only a sample of the
different anatomical variants is included in this pre-
sentation. An exhaustive review of intracranial vascu-
lar anatomy, embryology, and anatomical variants is
found in the Atlas of Neuroradiologic Embryology, FIG 1. Normal anatomy of the anterior circulation as seen on AP
Anatomy and Variants by J. Randy Jinkins.1 The angiography after contrast injection of the right common carotid artery.
diagnostic test with the highest resolution is catheter
angiography, but owing to its invasive nature, com-
puted tomographic angiography and magnetic reso- Arterial
nance angiography are gradually supplanting catheter
The intracranial arterial circulation (Figs 1-8) forms
angiography.
the circle of Willis (Fig 5), which is composed of the
anterior cerebral artery (ACA), middle cerebral artery
(MCA), posterior cerebral artery (PCA), the anterior
From the Department of Radiology, Robert C. Byrd Health Sciences communicating arteries (Acomm), and posterior commu-
Center of West Virginia University, Morgantown, WV.
nicating arteries. It is complete only in approximately
Reprint requests: Jeffery P. Hogg, MD, Department of Radiology, Robert
C. Byrd Health Sciences Center of West Virginia University, PO Box 20%-25% of patients.2 The anterior circulation is formed
9235, Morgantown, WV 26506-9235. E-mail: jhogg@hsc.wvu.edu. by the internal carotid artery, which divides into the ACA
Curr Probl Diagn Radiol 2010;39:91-109.
and PCA. The right and left ACAs usually are connected
© 2010 Mosby, Inc. All rights reserved.
0363-0188/2010/$36.00 ⫹ 0 through an Acomm, although this is highly variable. The
doi:10.1067/j.cpradiol.2009.07.005 posterior circulation is formed from the union of 2

Curr Probl Diagn Radiol, May/June 2010 91

FIG 2. Normal anatomy of the anterior circulation as seen on lateral
angiography after contrast injection of the right common carotid artery.
FIG 3. Normal anatomy of the posterior circulation as seen on AP
angiography after contrast injection of the left vertebral artery.
vertebral arteries to form the basilar artery, which gives
off the following branches: anterior inferior cerebellar
artery, superior cerebellar artery, and PCA in ascending
order. The posterior inferior cerebellar artery (PICA)
usually arises from the intracranial vertebral artery prox-
imal to their confluence to form the basilar trunk. Usually
there is an anastomosis between the anterior and poste-
rior circulation through a posterior communicating ar-
tery; however, as mentioned before, this is highly vari-
able.
The ACA, MCA, and PCA are divided into differ-
ent segments depending on how proximal or distal
92
FIG 4. Normal anatomy of the posterior circulation as seen on lateral
angiography after contrast injection of the left vertebral artery.
FIG 5. Normal anatomy of the anterior and posterior circulation as
seen on 3D volumetric CT angiography. (Color version of figure is
available online.)
they are located. For example, the ACA is called A2
after the origin of the anterior communicating artery
(Acomm) and A3 at the level of the pericallosal artery.
The MCA is called M2 after the initial bifurcation/
trifurcation and the M3 segments are located at the
level of the sylvian fissure and beyond. The PCA is
Curr Probl Diagn Radiol, May/June 2010
 FIG 8. Normal anatomy of the anterior and posterior circulation as
seen in AP projection MIP MR angiography.

FIG 6. Normal anatomy of the anterior circulation as seen on 3D

volumetric CT angiography. (Color version of figure is available online.)

FIG 7. Normal anatomy of the posterior circulation as seen on 3D

volumetric CT angiography. (Color version of figure is available online.)
called P2 after the first bifurcation and P3 at the level
of the lateral occipital artery.
Venous
There is a superficial cortical and a deep venous
system. Venous anatomy is more individually variable
than arterial anatomy, especially the superficial corti-
cal venous system (Figs 9-13).
FIG 9. Normal anatomy of the venous circulation as seen on AP
angiography after contrast injection of the left common carotid
artery.
Anatomical Variants
Persistent Trigeminal Artery
Persistent trigeminal artery is the most common
persistent carotid-basilar anastomosis. It is located

Curr Probl Diagn Radiol, May/June 2010 93

FIG 10. Normal anatomy of the venous circulation as seen on lateral
angiography after contrast injection of the left common carotid artery.
FIG 12. Normal anatomy of the venous circulation as seen on AP
oblique MIP MR venography.

FIG 13. Normal anatomy of the venous circulation as seen on T1W with
FIG 11. Normal anatomy of the venous circulation as seen on lateral gadolinium sagittal magnetic resonance imaging (MRI) of the brain. This
projection MIP MR venography. patient incidentally also has a capillary telangiectasia in the pons.

between precavernous ICA and basilar artery. The have been described: Saltzman type 1 and 2, each of
caudad portion of the basilar artery is usually hypo- which is divided into medial and lateral components.
plastic. It is commonly associated with aneurysms due This variant may be identified by the presence of the
to abnormal flow dynamics. The following 4 types Tau sign3 (blue arrow, lower left on Fig 14H).

94 Curr Probl Diagn Radiol, May/June 2010

FIG 14. Persistent trigeminal artery. (A) Axial CTA, (B) MIP MRA, (C) Axial MRA, (D-F) MIP MRA, and (G-H) lateral projection cerebral angiogram.
Persistent trigeminal artery is identified (red arrows) starting at the distal ICA canal. Tau sign (blue arrow, lower left in H only). (Color version of
figure is available online.)

FIG 15. Persistent hypoglossal artery. (A, B) 3D reconstruction CTA, (C) lateral projection cerebral angiogram, (D) CTA axial, and (E) MIP MRA.
Abnormal bifurcating internal carotid artery (red arrows, A, B and E) giving off persistent hypoglossal artery, which enters the hypoglossal canal
(gold arrow, D). (Color version of figure is available online.)

Curr Probl Diagn Radiol, May/June 2010 95

FIG 16. Persistent stapedial artery. (A) Axial temporal bone CT, (B) coned-down axial temporal bone CT, (C) lateral projection cerebral
angiogram, and (D) coned-down lateral projection cerebral angiogram. (Color version of figure is available online.)

Persistent Hypoglossal Artery Persistent Stapedial Artery

Persistent hypoglossal artery is the second most
common persistent carotid-basilar anastomosis after
persistent trigeminal artery. It connects the cervical
ICA to the basilar artery. It enters through the hypo-
glossal canal, not the foramen magnum, and usually
parallels the course of the hypoglossal nerve. Often it
is associated with vertebral artery aplasia or hypopla-
sia, aneurysms, and subarachnoid bleeds. Typically no
posterior communicating arteries are present (Fig 15).
Persistent stapedial artery is a persistent fetal branch of
the hyoid artery. It gives rise to the middle meningeal
artery (red arrows, Fig 16C and D); thus, the normal
foramen spinosum is absent. It presents as a soft-tissue
mass along the horizontal portion of the tympanic facial
nerve (yellow arrows, Fig 16A and B). It coexists with
aberrant ICA in 60% of cases. Typically, they are
asymptomatic and rarely can present with tinnitus and
pulsatile retro tympanic mass (Fig 16).

96 Curr Probl Diagn Radiol, May/June 2010

FIG 17. Aberrant internal carotid artery. (A) Axial CT through temporal bone with normal internal carotid artery canal wall in inset and (B)
coned-down view of the abnormal side on axial (top) and coronal (bottom) projections. Red arrows point to lack of normal internal carotid artery
canal wall (B). Compare with normal internal carotid artery canal wall (yellow arrow [A]). (Color version of figure is available online.)

FIG 18. Infraoptic anterior cerebral artery. (A) Axial MR T2W, (B) axial CTA, (C) coronal MR T1W with gadolinium, and (D) sagittal CTA. In this
case, infraoptic ACA arises extradurally directly from the ICA, near the ophthalmic artery origin. (Color version of figure is available online.)

Aberrant Internal Carotid Artery recognized and properly documented, as failure to do

Aberrant ICA is located anteromedial to the hori-
zontal portion of the internal carotid artery canal. It
usually is located immediately adjacent to the cochlear
promontory and is seen as an enhancing mass with
identical attenuation as adjacent blood vessels. The
patient presents with pulsatile tinnitus. It must be
so could result in fatal exsanguination if biopsy is
performed. Dehiscence of the anterior carotid canal
wall is always present and identification of this finding
is very helpful in determining the appropriate diagno-
sis. It can be associated with persistent stapedial artery
(Fig 17).

Curr Probl Diagn Radiol, May/June 2010 97

FIG 19. Azygous anterior cerebral artery. (A) Coronal CTA, (B) sagittal MIP MRA, (C) sagittal CTA, (D) 3D reconstruction CTA, (E) MIP MRA, and
(F) axial CTA. (Color version of figure is available online.)

FIG 20. Fetal posterior cerebral artery. (A) Axial CTA, (B) axial MRA, (C) lateral projection cerebral angiogram after injection of left common
carotid artery, and (D) AP projection cerebral angiogram after injection of left common carotid artery. (Color version of figure is available online.)

98 Curr Probl Diagn Radiol, May/June 2010

FIG 21. Fenestrated basilar artery. (A) Sagittal CTA, (B) coned-down sagittal CTA, (C) coronal CTA, (D) AP projection cerebral angiogram after injection of
right vertebral artery, and (E) lateral projection cerebral angiogram after injection of right vertebral artery. (Color version of figure is available online.)

FIG 22. Fenestrated posterior cerebral artery. (A) Coronal CTA, (B) coronal MRA, and (C) coned-down coronal CTA. (Color version of figure is
available online.)

Infraoptic Anterior Cerebral Artery Azygous Anterior Cerebral Artery

Infraoptic ACA results from early origin of ACA
(red arrows, Fig 18B and D). It courses underneath and
between the optic nerve (yellow arrows, Fig 18A and
C) and can cause optic nerve compression. Anomalous
origins of the ACA are uncommon4 (Fig 18).
Azygous ACA is a single anterior cerebral artery
(yellow arrows) that branches more distally at the level
of the falx (red arrows, top arrow on Fig 19A, B, D
and E). It may be an isolated finding. It is commonly
associated with holoprosencephaly (Fig 19).

Curr Probl Diagn Radiol, May/June 2010 99

FIG 23. Vertebral artery origin from the aortic arch. (A) Coronal CTA, (B) sagittal CTA, (C, D) axial CTA, and (E) MIP MRA. (Color version of figure
is available online.)

Fetal Posterior Cerebral Artery formed due to failed regression of the primitive connec-
tion with the dorsal aorta during embryogenesis (Fig 23).
Persistent fetal origin from the ICA (red arrows) is
found in approximately 10% of patients (Fig 20). Vertebral Artery Terminates in Posterior
Inferior Cerebellar Artery
Fenestrated Basilar Artery
The contralateral vertebral artery is always en-
Fenestrated basilar artery, also known as neural
larged and it forms the basilar artery. Termination in
artery, results from the incomplete fusion of 2 primi-
PICA (blue arrows) must be recognized to avoid the
tive vertebral arteries, resulting in a vessel with a
improper diagnosis of intracranial vertebral artery
single origin that divides and forms 2 parallel seg-
occlusion and to avoid high-volume contrast injection,
ments that again unite along the vessel’s course5
which could lead to artery rupture and intracranial
(yellow arrows, Fig 21).
bleed (Fig 24).
Fenestrated Posterior Cerebral Artery Extradural Posterior Inferior
A fenestrated PCA is similar to basilar fenestration Cerebellar Artery
except that the vessel with a single origin that divides
PICA has the most variable origins of the posterior
and forms 2 parallel segments that again unite along
circulation. Note the origin of PICA (yellow arrow)
the vessel’s course is the PCA. It has an association
outside of the calvarium (red arrows, multiple arrows
with increased frequency of aneurysm6 (Fig 22).
on the right of Fig 25).
Vertebral Artery Origin from the Aortic
Arch
Arterial Lesions
Vertebral artery origin directly from the aortic arch is
present in approximately 5% of the population. They Arteriovenous Malformation
most commonly arise between the left common carotid These vascular malformations are defined by the
artery (CCA) and the left subclavian artery and are presence of an enlarged feeding artery (yellow arrow,

100 Curr Probl Diagn Radiol, May/June 2010

FIG 24. Vertebral artery terminates in posterior inferior cerebellar artery. (A) Coronal CTA, (B) coned-down coronal CTA, (C) axial CTA, (D)
coned-down coronal CTA, and (E) lateral projection cerebral angiogram after injection of the right subclavian artery. (Color version of figure is
available online.)
FIG 25. Extradural posterior inferior cerebellar artery. Coned-down
lateral projection cerebral angiogram. (Color version of figure is
available online.)
Fig 26H) and draining vein (blue arrow, Fig 26I) and
associated cluster of entangled vasculature called ni-
dus (purple arrows, Fig 26F, H [top arrow], I [top
arrow] and J). They require complete angiographic
Curr Probl Diagn Radiol, May/June 2010
workup, and they can hemorrhage or cause steal
phenomenon, which can result in seizures or neuro-
logical deficits. They are identified as flow voids on
magnetic resonance imaging (red arrow, Fig 26C).
They are associated with multiple syndromes includ-
ing Sturge-Weber, Wyburn-Mason, Klippel-Trenau-
nay-Weber syndrome, hemorrhagic hereditary telangi-
ectasia, Foix-Alajouanine disease, etc. Multiple
treatment modalities exist including stereotactic radio-
therapy if they are less than 3 cm in size, staged
embolization, or surgery. Histology demonstrates di-
lated abnormal blood vessels full of thrombus (green
arrows; Fig 26K).
Capillary Telangiectasia
Capillary telangiectasias (purple arrows, Fig 27A-D
and F-H) are angiographically occult and demon-
strate typical “brush-like” enhancement (red arrow,
Fig 27E only). They do not hemorrhage; thus, they
are commonly identified incidentally. They are
characterized by normal neural tissue between clus-
ters of abnormal capillaries. Most commonly they
are located in the pons and midbrain. Because
101
FIG 26. Arteriovenous malformation. Patient 1A-F: (A) Axial CTA, (B) axial MRI T1W post gadolinium, (C) axial MRI FLAIR, (D) coronal CTA, (E)
sagittal CTA, (F) AP cerebral angiogram. Patient 2G-I: (G) axial CT enhanced, (H-I) AP projection vertebral angiogram. Patient 3J: AP projection
vertebral angiogram; (K) histologic figure. (Color version of figure is available online.)

lesions do not bleed, there is no deposition of blood Cavernous Malformation

breakdown products and thus no abnormal low
signal on T2W images from hemosiderin deposition.
They are associated with Osler-Weber-Rendu syn-
drome and rarely with developmental venous anom-
alies (Fig 27).
Cavernous malformations are hemorrhagic lesions.
As they contain blood products with high protein
content, they present as high-density lesions on CT
and may calcify (red arrow, Fig 28D). They are
angiographically occult (see angiogram, Fig 28G) but

102 Curr Probl Diagn Radiol, May/June 2010

FIG 27. Capillary telangiectasia. (A) MRI of the brain axial T1W with gadolinium, (B) MRI of the brain axial T2W, (C) MRI of the brain coronal
T1W with gadolinium, (D) MRI of the brain sagittal T1W with gadolinium, (E) MRI of the brain axial T1W with gadolinium, (F) MRI of the brain
axial T1W GRE with gadolinium, (G) MRI of the brain axial GRE, and (H) MRI of the brain axial T2W. (Color version of figure is available online.)

FIG 28. Cavernous malformation. (A) MRI axial FLAIR, (B) MRI axial T2W, (C) MRI axial GRE, (D, E) CT axial unenhanced, (F) MRI axial perfusion
image, (G) lateral projection cerebral angiogram, and (H) MRI axial T2W. (Color version of figure is available online.)

can enhance. Characteristically, they demonstrate a
complete rim of hemosiderin (yellow arrows, Fig
28B, E and H). Hemosiderin deposition causes signal
dropout in magnetic resonance perfusion imaging due
to paramagnetic effect (black arrows, Fig 28F). A
“blooming” effect from blood product deposition is
seen on gradient echo (GRE) sequences (purple arrow,
Fig 28C). Histologically, we see vascular hamartomas
with associated immature blood vessels and hemor-
rhage and no interposed neural tissue (latter 2 charac-
teristics used to differentiate from capillary telangiec-
tasia) (Fig 28).
Moya Moya
Moya Moya represents leptomeningeal collater-
als in patients with occluded ICAs. Classically

Curr Probl Diagn Radiol, May/June 2010 103

FIG 29. Moya Moya. (A) Coronal CTA, (B) AP projection cerebral angiogram after injection of right common carotid artery, (C) axial CTA, (D)
sagittal CTA, (E) MRA MIP, and (F) MR T1W with gadolinium.
described as having a puff of smoke appearance (Fig
29B), it is caused by high-grade stenosis or slow
occlusion, which is caused by vasculitides, sickle
cell, neurofibromatosis, or radiation arteriopathy.
Symptoms vary according to age of the patient. In
children, it presents as a transient ischemic attack
and stoke, whereas, in adults, it presents as intrapa-
renchymal or subarachnoid hemorrhage. Patent ce-
rebral arteries, perforating basal ganglionic arteries,
and transdural anastomosis from the external carotid
arteries form the main leptomeningeal collaterals
(Fig 29).
Aneurysms
Aneurysms are defined as focal abnormal dilatation
of a blood vessel. Rupturing results in subarachnoid
hemorrhage. The types include the following: berry or
saccular (most common), fusiform, mycotic, pseudo-
aneurysm (usually post traumatic), neoplastic, and
giant (⬎2.5 cm in size). The most common location is
the anterior communicating/anterior cerebral artery ⬎
middle cerebral artery ⬎ vertebrobasilar circulation. It
can have familial incidence and is associated with an
extensive list of disorders including adult polycystic
104
kidney disease, moya moya, fibromuscular dysplasia,
etc. (Fig 30).
Mixed: Carotid Cavernous Sinus Fistula
Carotid cavernous sinus fistula is defined as an
abnormal vascular connection between cavernous in-
ternal carotid artery and cavernous sinus. It is most
commonly seen with trauma but is also seen in elderly
patients, secondary to rupture of cavernous carotid
aneurysm, or a blow-out of diseased vessel wall
(Ehlers-Danlos, etc). Findings include enlarged lat-
erally bulging cavernous sinus, enlarged superior
ophthalmic vein (dashed red arrows, Fig 31A, F and
G), proptosis, and enlarged extraocular muscles (red
arrows, Fig 31F). Angiogram is the study of choice
to locate and guide endovascular treatment of the
fistula. Angiogram findings include abnormal opaci-
fication of cavernous sinus and abnormal retrograde
opacification of veins draining to cavernous sinus
[superior ophthalmic vein, inferior ophthalmic vein
(gold arrow, image G)] in the early arterial phase
(Fig 31).
Curr Probl Diagn Radiol, May/June 2010
FIG 30. Aneurysms. Mycotic aneurysm (A, B), giant aneurysm (C, D), basilar fusiform aneurysm (E, F, G), petrous ICA aneurysm (H, I, J; green
arrows in image I and J), basilar saccular aneurysms (K), pseudoaneurysm resulting in arteriovenous fistula (L), and Acomm aneurysm (M, N).
(Color version of figure is available online.)

Venous Lesions
Developmental Venous Anomaly
Developmental venous anomaly is an anatomical vari-
ant of normal venous drainage that presents as dilated or
tortuous intramedullary veins (yellow arrows, Fig 32A-G).
They usually converge onto a larger vein that drains into
the superficial or deep venous system. The lesions are
most often asymptomatic and may rarely hemorrhage. They
are visible with angiography (blue arrow, Fig 32H) and are
associated with cavernous hemangiomas (red arrow, lower
arrow in image D) (Fig 32).

Curr Probl Diagn Radiol, May/June 2010 105

FIG 31. Carotid cavernous sinus fistula. (A-C) Axial enhanced CT, (D) AP projection cerebral angiogram in patient with right CCF after injection
of the left common carotid artery, (E) lateral projection cerebral angiogram after injection of the left common carotid artery, (F) coronal enhanced
CT, (G) lateral projection cerebral angiogram after injection of the left common carotid artery, and (H) different patient from (F) lateral projection
cerebral angiogram after injection of the left common carotid artery. (Color version of figure is available online.)

FIG 32. Developmental venous anomaly. (A) MRI axial T1W with gadolinium, (B) MRI coronal T1W with gadolinium, (C) axial enhanced CT, (D)
MRI axial T1W with gadolinium, (E) MRI coronal T1W GRE with gadolinium, (F) MRI axial T1W with gadolinium, (G) coronal enhanced CT, and
(H) AP cerebral angiogram in venous phase after injection of the left common carotid artery. (Color version of figure is available online.)

Sinus Pericranii common location is frontal ⬎ parietal ⬎ occipital ⬎

Sinus pericranii is caused by an abnormal com- temporal. The superior sagittal sinus is most com-
munication between extracranial veins and dural monly involved. The lesion changes with position
sinuses. It may be direct or indirect (communicates and Valsalva maneuver and may cause bone thin-
via intracranial cortical vein or varix). The most ning and remodeling (Fig 33).

106 Curr Probl Diagn Radiol, May/June 2010

FIG 33. Sinus pericranii. (A) Coned-down axial CTA, (B, C) AP projection cerebral angiogram, (D) lateral projection cerebral angiogram, (E) axial
CTA, (F, G) MRI coronal T1W with gadolinium, and (H) MIP magnetic resonance venography (MRV). (Color version of figure is available online.)

FIG 34. Vein of galen aneurysm. (A) MRI axial T2, (B) T1W axial with gadolinium, (C) axial contrast-enhanced CT, and (D) MRI sagittal T1W.

Vein of Galen Aneurysm Sagittal Sinus Venous Lake

Vein of Galen aneurysm is a misnomer, as it involves
aneurysmal dilatation of the median prosencephalic vein
of Markowski, not the vein of Galen. They are located in
the quadrigeminal plate cistern and the cistern of velum
interpositum. Usually dilated arteries feeding a well-
defined tubular vein located midline in a neonate or
infant are identified. They may calcify. Most commonly
vein of Galen malformations present with high-output
heart failure and hydrocephalus (Fig 34).
Venous lakes (blue arrows) are benign, well-defined,
lucent skull lesion representing remodeled bone that
contains venous structures. Differential diagnosis in-
cludes, for example, metastasis, dermoid/epidermoid,
hemangioma, osteomyelitis, and postoperative osteol-
ysis. However, when a well-defined nonerosive
lesion of the skull is identified that contains only
venous structures, venous lake is the diagnosis of
choice (Fig 35).

Curr Probl Diagn Radiol, May/June 2010 107

FIG 35. Sagittal sinus venous lake. (A) Coronal CT, (B) AP projection cerebral angiogram, (C) MRI coronal T1W with gadolinium, (D) MRI axial
T1W with gadolinium, (E) axial early arterial phase CTA, and (F) axial CT bone algorithm images. (Color version of figure is available online.)

FIG 36. Fenestration of venous sinus with cephalocele. (A) MR axial T1W with gadolinium, (B) MIP MRV, (C) sagittal unenhanced CT, and (D)
histopathological image. (Color version of figure is available online.)

Fenestration of Venous Sinus TABLE 1. Cognard classification

With Cephalocele I. Venous drainage into dural venous sinus with antegrade flow;
Fenestration of venous sinus with cephalocele is benign clinical course
IIa. Venous drainage into dural venous sinus with retrograde flow
caused by herniation of meninges without any brain (not into cortical veins)
content through a skull defect. It is most commonly IIb. Venous drainage into dural venous sinus with antegrade flow
located in the parietal or occipital region and fre- and CVR; 10%-20% risk of hemorrhage
III. Venous drainage directly into cortical veins with no venous
quently coexists with venous sinus anomalies such as ectasia; 40% risk of hemorrhage
vertical embryonic positioning of the straight sinus IV. Type III with venous ectasias of the draining subarachnoid
(yellow arrow, center of Fig 36B), and fenestration of veins; 66% risk of hemorrhage
V. Spinal lesion
the superior sagittal sinus (red arrow, upper right on

108 Curr Probl Diagn Radiol, May/June 2010

FIG 37. Dural arteriovenous fistulas. Cerebral angiograms: Cognard type IV dural arteriovenous fistula (A-D); Cognard type IIa arteriovenous
fistula (E, F). (A) Lateral projection cerebral angiogram, (B, C) AP projection cerebral angiogram, (D, E) lateral projection cerebral angiogram, and
(F) sagittal CTA.
Fig 36B). Cephalocele (green arrows, Fig 36A and C)
can be associated with a variety of congenital anom-
alies such as porencephaly, corpus callosum agenesis,
Dandy-Walker malformation, etc, although they may
also be isolated (Fig 36).
Mixed: Dural Arteriovenous Fistulas
Dural arteriovenous fistulas are arteriovenous shunts
that occur within the dura and are most commonly
located at the skull base ⬎ cavernous sinus. The most
aggressive type is type IV in the Cognard classification
(Table 1). The most benign is type I. They are treated
with stereotactic radiosurgery, endovascular emboliza-
tion, and surgery7-9 (Fig 37).
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