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Pial Arteriovenous Malformations 45
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the most useful classifi cation of aneurysms associated
with brain AVMs is probably that proposed by the
Joint Writing Group (Ogilvy et al. 2001). Aneurysms
are categorized as fl ow related, non-fl ow related, nidal,
proximal, and distal. Flow-related aneurysms are
located on a pathway supplying the brain AVM shunt.
Aneurysms are defi ned as saccular luminal dilatations
of the parent feeding vessel. Nidal is defi ned as contiguous with the nidus. Proximal aneurysms would
be located on the vessel or branch points of the circle
of Willis or proximal to it. Distal refers to locations
beyond the circle of Willis. A similar classifi cation was
recently used in a series dealing with brain AVMs associated with arterial aneurysms (Redekop et al. 1998).
Piotin et al. (2001) also defi ne proximal, distal, and
intranidal aneurysms but do not distinguish between
fl ow-related and non-fl ow-related aneurysms.
As outlined by Houdart et al.(1993), the depiction of intranidal aneurysms is diffi cult; it is often
performed at the time of superselective angiography.
Moreover, true arterial intranidal aneurysms have to
be distinguished from pseudoaneurysms, which are
at the point of rupture of the nidus or of the venous
drainage.
The signifi cance of aneurysms associated with
brain AVMs in the occurrence of bleeding is unclear.
Pollock et al. (1996) fi nd no association between
proximal or nidal associated aneurysms and intracranial bleeding. The univariate and multivariate
analysis performed by Mansmann et al. (2000) in
a large series of patients revealed no association
between aneurysms in the feeders or intranidal
aneurysms and intracranial hemorrhage. In other
series, arterial aneurysms and intranidal aneurysms
are associated with a high prevalence of hemorrhage
(Marks et al. 1990; Turjman et al. 1995; Thompson
et al. 1998; Redekop et al. 1998; Piotin et al. 2001).
In the series of Cunha e Sa et al. (1992) the site of
rupture was the aneurysm in 46% of cases, the AVM
in 33% of cases, and undetermined in 21% of cases.
In other series (Batjer et al. 1986; Piotin et al. 2001),
the source of hemorrhage in patients harboring brain
AVMs and associated aneurysms was identifi ed as an
aneurysm in approximately 80% of cases.
Thus, we can postulate with Berenstein et al.
(1992) that intranidal aneurysms represent a weakness of the angioarchitecture and should infl uence
treatment strategy. This is probably also true for
other associated aneurysms.
A higher percentage of multiple aneurysms has
been reported in the population of patients with
brain AVMs (Batjer et al. 1986; Brown et al. 1990;
Cunha e Sa et al. 1992; Thompson et al. 1998), but
this feature seems not to be associated with a higher
risk of hemorrhage (Piotin et al. 2001).
Feeders from the External Carotid Artery
Some brain AVMs are fed by branches of external
carotid arteries, and the signifi cance of this anatomic
situation is uncertain. Is there an intradural compartment of the AVM? Or is there a vascularization of
the nidus through arterial anastomosis coming from
external branches? Whatever, it seems that the incidence of bleeding is not increased when the brain
AVM is fed by branches of the external arteries.
Others
Turjman et al. (1995a) have shown an increased risk
of bleeding in case of feeding by perforators and by
the vertebrobasilar system. As outlined by Turjman,
perforators are involved in the supply of deep AVMs,
such as corpus callosum and basal ganglia AVMs, and
it is diffi cult to evaluate which feature is the most
important for determination of the bleeding risk.
Regarding feeders coming from the vertebrobasilar system, the discussion is the same as for the location of AVMs (see below).
Nidus
Size
A relationship between the size of an AVM and its
tendency to rupture has been suggested. In the series
of Graf et al. (1983), the risk of hemorrhage at 5
years was 10% for large AVMs (>3.0 cm in diameter)
and 52% for small AVMs (<3 cm in diameter). In the
series of Spetzler et al. (1992), 82% of patients with
small AVMs (less than 3 cm), 29% of patients with
medium-sized AVMs (3–6 cm), and 12% of patients
with large AVM (greater than 6 cm) presented with
hemorrhage. The same relation between nidus size
and bleeding was found by other authors (Itoyama
et al. 1989; Kader et al. 1994; Duong et al. 1998). The
multivariate analysis performed in the large series
of patients studied by Mansmann et al. (2000) also
identifi ed AVM size of more than 3 cm as a factor
negatively associated with intracranial hemorrhage.
However, the absolute risk of spontaneous intracranial hemorrhage from small and large brain AVMs
is still a matter of controversy. In the series of Craw-
ford et al. (1986), 21% small and 18% large AVM
rebled within 5 years. Small and large AVMs may have
the same risk of bleeding. Large AVMs can more often
present in other ways than hemorrhage (seizures, progressive defi cits, headache), and this may lead to an
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overestimation of the rate of bleeding of small AVMs.
In this case, age at the time of presentation would
be higher in the group of patients with hemorrhage
than in the group without. However, age at the time
of presentation is the same in both groups (Kader et
al. 1994), supporting the idea that small AVMs have a
higher risk of hemorrhage. Moreover, by measuring
the feeding artery pressure intraoperatively, Spetzler
et al. (1992) demonstrated that the pressure is higher
in small brain AVMs, which could explain the higher
rate of bleeding of small AVMs (see below).
Hematoma size seems to be inversely related to the
size of the AVM (Spetzler et al. 1992).
Location
The risk of bleeding of brain AVMs depending on
their location has not been evaluated systematically.
Some authors suggest that AVMs in deep locations,
such as in the basal ganglia or in the periventricular
or intraventricular space, have an increased risk of
bleeding (Marks et al. 1990; Turjmann et al. 1995).
Willinski et al. (1988) concluded that hemorrhage
is more likely to occur in deep lesions and posterior fossa AVMs. However, Crawford et al. (1986)
showed that the depth of the AVM had no infl uence
on the risk of hemorrhage. Moreover, the high prevalence of hemorrhage in deep-seated AVMs identifi ed
in some series may be partially explained by the fact
that the patients are less likely to present with focal
neurologic defi cits or seizure disorders.
The results published by Stapf et al. (2000) sug-
gest that an arterial border zone location of brain
AVMs is an independent determinant of lower risk of
incident AVM hemorrhage.
Angiogenesis
This factor was defi ned as transdural anastomosis
or secondarily acquired perilesional angiogenesis
(Mansmann et al. 2000). When it is combined with
arterial stenosis or dural venous stenosis, this factor
may increase the risk of intracranial hemorrhage.
Venous Drainage
Deep Venous Drainage
Deep venous drainage is associated with a higher
risk of bleeding (Marks et al. 1990; Miyasaka et al.
1992; Kader et al. 1994; Nataf et al. 1997; Duong et
al. 1998). Superfi cial and deep venous drainage are
different from an anatomic point of view. The veins
of the central drainage have one fi nal common pathway which is the vein of Galen and the straight sinus.
On the other hand, superfi cial veins have more connections and may drain posteriorly via the superior
sagittal sinus and anteriorly via the sylvian vein. The
superfi cial venous system is probably more fl exible in
adaptation to the hemodynamic situation created by
the presence of the AVM.
Venous Stenosis
The presence of a stenosis on the venous drainage of
a brain AVM is associated with an increased risk of
bleeding (Miyasaka et al. 1992; Nataf et al. 1997),
probably due to proximal venous hypertension.
This factor was also identifi ed in the large series of
patients analyzed by Mansmann et al. (2000), but
venous stenosis was not statistically associated with
intracranial hemorrhage for cortical AVMs. Venous
dilatation was correlated to an increased risk of hemorrhagic presentation in dural arteriovenous fi stulas
(Cognard et al. 1995).
The suggested mechanisms for venous stenosis in
AVMs are varied: endovascular proliferation in reaction to increased venous fl ow or pressure (Fry 1968),
congenital extrinsic anatomic narrowing of the
lumen as it traverses the dura mater or curves around
bone (Crawford et al. 1986; Willinsky et al. 1988),
kinking in ectatic veins (Nataf et al. 1997).
Others
The presence of a single draining vein may be associated with an increased risk of bleeding (Miyasaka et
al. 1992; Pollock et al. 1996).
Venous refl ux into a sinus or a deep vein seems to
be positively correlated with the risk of hemorrhage
(Nataf et al. 1997), but this feature has seldom been
studied. In contrast, venous recruitment seems to be
protective against bleeding.
Venous ectasia may be intra- or paranidal and the
sign of a previous hemorrhage. Venous ectasia may
also be remote from the nidus. The link between venous
ectasia and bleeding is unclear (Nataf et al. 1997).
Hemodynamic Factors
Feeding Artery Pressures
In a relatively small series of patients, Spetzler et al.
(1992) evaluated the perfusion pressure of AVM arterial
feeders. The difference between mean arterial blood
pressure and the feeding artery pressure was higher
in ruptured than in non-ruptured AVMs. Moreover,
smaller AVMs had signifi cantly higher feeding artery
pressure than larger AVMs and were associated with
larger hematomas. These results were partially con-
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fi rmed by Kader et al. (1994), who found that patients
presenting with hemorrhage had higher feeding artery
pressure than patients in the nonhemorrhage group.
The feeding artery pressure was only weakly related
to the size of the lesion, but measurements were performed only in medium and large-sized AVMs.
In a large series of patients, Duong et al. (1998)
also found that feeding arterial pressure was positively correlated with the occurrence of bleeding.
In the study performed by Norbash et al. (1994),
feeding arterial pressure was not statistically different in the hemorrhage and nonhemorrhage groups
and was not related to the size. A non-statistically signifi cant trend to decreasing feeding arterial pressures
from AVMs having a central venous drainage to those
having peripheral venous drainage was observed.
Moreover, the feeding arterial pressure was lower
when the feeding artery was longer, and the length of
the feeding artery was also correlated to the type of
venous drainage (deep or superfi cial).
Draining Vein Pressures
The draining vein pressure did not differ between
patients with hemorrhage and those without (Kader
et al. 1994).
3.3.2.2
Factors Decreasing the Risk of Bleeding
Very few studies have evaluated anatomic factors
decreasing the risk of bleeding of a brain AVM. Two
factors were identifi ed on the arterial side as having
a protective effect against bleeding (Mansmann et
al. 2000):
Arterial stenosis, which is defi ned as a reduction in
arterial caliber and could be intrinsic (concentric
narrowing by intraluminal protrusions related to
high-fl ow angiopathy) or extrinsic (bony, dural or
venous compression)
Arterial angioectasia, which is defi ned as segmen-
tal arterial capillary dilatation in the collateral
system in the vicinity of the AVMs (with recruit-
ment and enlargement of leptomeningeal and
subependymal anastomoses) and hemodynamic
enlargement of preexisting feeding arteries
These two factors probably contribute to the
decrease of the pressure inside the nidus.
Arteriovenous fi stulas, defi ned as large arteriovenous communications between the arterial and
venous components of AVMs with high fl ow velocity and a visible shunting transition, seem to be also
associated with a lower risk of bleeding (Mansmann
et al. 2000).
In summary, several factors have been identifi ed
which potentially modify the risk of bleeding of
brain AVMs. However, there is clearly a general bias
in many studies regarding the evaluation of bleeding
rates. Indeed, some anatomic characteristics identifi ed as increasing the risk of bleeding are also related
to a less frequent nonhemorrhagic presentation
such as epilepsy or focal defi cit, e.g., small size of the
AVM, deep location, and deep venous drainage. If a
group of brain AVMs can be only asymptomatic or
hemorrhagic, then the percentage of bleeding in this
group will be 100%, except if asymptomatic AVMs are
detected for any reason by CT or MRI.
3.3.2.3
Annual Rate of Bleeding
The natural history of brain AVMs has been studied in
different series of untreated patients (Graf et al. 1983;
Fults and Kelly 1984; Crawford et al. 1986; Brown et
al. 1988; Itoyama et al. 1989; Ondra et al. 1990). There
are a number of biases in these different studies:
– Generally, studies were conducted at centers
specialized in the treatment of cerebrovascular
disorders, thus creating a recruitment bias.
– The number of patients included in these series is
usually small (50 to 343 patients).
– In the majority of series, natural history was stud-
ied in the group of patients managed nonsurgically,
and this is a very important recruitment bias.
– Most studies are retrospective.
For all these reasons, we have to be careful with the
data provided by these series.
Graf et al. (1983) reported a series of 191 patients
presenting with unruptured or ruptured AVMs.
The average yearly risk of bleeding was estimated
to be between 2% and 3%. Crawford et al. (1986)
reported a series of 217 patients harboring AVMs
who were managed without surgery with a mean
follow-up period of 10.4 years. There was 42% risk of
hemorrhage, 29% risk of death, 18% risk of epilepsy,
and 27% risk of having a neurological handicap at 20
years after diagnosis.
Brown et al. (1988) reported a series of 168
patients with unruptured AVMs followed for a mean
period of 8.2 years. The mean risk of hemorrhage was
estimated to 2.2% per year. The risk of death from
rupture was 29%.
The series of Ondra et al. (1990) included 166
patients with a mean follow-up of 24 years (Ondra
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et al. 1990). The annual rate of bleeding was 4% per
year and the mortality was 1% per year. The combined rate of major morbidity and mortality was
2.7% per year. Overall, the percentages are relatively
close between the different series, with annual rates
of bleeding between 2% and 4% (Jomin et al. 1993).
The occurrence of a fi rst hemorrhage seems to
be associated with an increased risk of subsequent
hemorrhage (Graf et al. 1983; Itoyama et al. 1989;
Mast et al. 1997). In the series of Graf et al., patients
with ruptured AVMs had a 6% risk of rebleeding in
the fi rst year after hemorrhage and 2% thereafter
(Graf et al. 1983). Itoyama et al. found relatively
similar results (Itoyama et al. 1989). The incidence
of rebleeding after a fi rst hemorrhage is 6.9% in the
fi rst year, 1.9% per year after 5 years and 0.9% after
15 years.
Pregnancy does not appear to signifi cantly
increase the likelihood of hemorrhage from an AVM
(Finnerty et al. 1999). In a large retrospective study
of 451 women (Horton et al. 1990), the hemorrhage rate for pregnant and nonpregnant women
of childbearing age with an unruptured AVM was
respectively 0.035 per person-year and 0.032 per
person-year. Women with an AVM have a 3.5% risk
of hemorrhage during pregnancy. In this series, none
of the hemorrhages occurred during labor, vaginal
delivery, or cesarean section. Thus, the route of
delivery should be based on obstetric considerations
(Horton et al. 1990; Dias and Shekhar 1990).
3.3.2.4
Severity of the Hemorrhage
On the basis of retrospective analysis, the rupture of
brain AVMs is estimated to be less severe than that
of intracranial aneurysms, with mortality between
10% and 15% and an overall morbidity of less than
50% (The Arteriovenous Malformation Study
Group 1999). Hemorrhages of brain AVMs are subarachnoidal (30%), parenchymal (23%), intraventricular (16%), and in combined locations in 31% of
cases (Hartmann et al. 1998). Parenchymal hemorrhages were most likely to result in a neurological
defi cit (52%). Overall, in the series of Hartmann et
al. (1998), 47% of patients had a good outcome after
the bleeding and an additional 37% of patients were
independent in their daily life.
In fact, as was shown by Hillman (2001), the
rupture of an AVM is as devastating as that of an
aneurysm. While aneurysm rupture is more lethal
than AVM rupture (21% versus 9%), a good outcome
is obtained less frequently in AVM than in aneurysm
ruptures (49% versus 56%), due to the high incidence
of parenchymal hematoma.
3.3.3
Epilepsy
Seizures are the initial symptom in 16%–53% of
patients, with a mean of 34% (Mast et al. 1995). In
the majority of cases, seizures are partial or partial
complex (Osipov et al. 1997). Grand mal seizures
are encountered in 27%–35% of cases (Osipov et
al. 1997).
Cortical AVMs are more often associated with
seizures (Turjman et al. 1995). In a large number
of cases antiepileptic drugs provide good control of
seizures (Osipov et al. 1997).
3.3.4
Headache
Chronic headache is the initial symptom in 7%–48%
(mean: 31%) of cases (Mast et al. 1995). The relation between headache, migraine, and arteriovenous
malformations is unclear. In a large review of the
literature, Frishberg concluded that “while most
patients with AVM who have headache have it on
the side of the AVM, migraine patients with strictly
unilateral location of headache are very unlikely to
have an AVM” (Frishberg 1997).
There is no feature such as frequency, duration, or
severity suggesting the diagnosis of AVM (The AVM
Study Group 1999).
3.3.5
Focal Neurologic Deficits
Focal neurologic defi cits without hemorrhage are
the initial symptom in 1%–40% of patients (Mast
et al. 1995). In fact, this clinical presentation is probably infrequent (The AVM Study Group 1999). As
outlined by Mast et al. (1995), focal neurologic defi cits encountered in patients harboring brain AVMs
may be progressive, stable, or reversible. Reversible
focal neurologic defi cits are questionable regarding
their mechanism, since a post-ictal etiology cannot
be ruled out. The progression of neurologic defi cit
may have different explanations: steal phenomenon
(Carter and Gumerlock 1995), venous hyperten-
sion, or mass effect (Miyasaka et al. 1997). The
relevance of the steal phenomenon is in fact very
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diffi cult to demonstrate in patients presenting with
progressive neurologic defi cits (Mast et al. 1995).
Indeed, positron emission tomography studies (Fink
1992; Kaminaga et al. 1999) showed a decrease of
cerebral blood fl ow in brain tissues surrounding
AVMs, but without increase in parenchymal blood
volume or modifi cations of glucose and oxygen
extraction fractions.
Mass effect is detected in a relatively high percent-
age of nonhemorrhagic cases (44%, Miyasaka et al.
1997). Cortical sulci obliteration and lateral ventricle
displacement are frequently observed. Mass effect
could be related to the size of the AVM itself or to
the presence of large dilated venous sacs or ectatic
veins. White-matter edema is rarely the cause of mass
effect.
3.4
Diagnostic Imaging
3.4.1
Goals of Imaging
Imaging has several roles and goals:
1 To establish the diagnosis of brain AVM in various
clinical situations
2 To make a pretherapeutic evaluation of the AVM
to help in decision-making
3 To treat the AVM as a sole therapy or in associa-
tion with surgery or radiosurgery
4 To perform post-therapeutic evaluation
3.4.2
Imaging Modalities
3.4.2.1
CT Scan
In patients with a sudden-onset of a neurological
defi cit, a CT scan is usually the fi rst imaging modality used, mainly to rule out hemorrhage (Ducreux et
al. 2001). CT is able to show very early parenchymal,
subarachnoid, and intraventricular bleeding. The
diagnosis of brain AVM should be discussed when
the patient is young, if the parenchymal hematoma
has a lobar topography, and if calcifi cations or spontaneously hyperdense serpiginous structures are
visible (Fig. 3.2).
In case of unruptured AVM, non-contrast-enhanced
CT scans can be normal. However, in some patients
slightly hyperdense serpiginous structures can be seen
(Fig. 3.3). Parenchymatous calcifi cations are observed
in 20% of cases, related to intravascular thrombosis or
evolution of an old hematoma. Contrast agent injection is absolutely mandatory to depict the brain AVM
(Figs. 3.4, 3.5) on CT. Abnormalities of the parenchymal density are visible in approximately 25% of cases,
related to the presence of gliosis or an old hematoma.
Abnormalities of the ventricular system can be
observed: focal dilatation in case of associated parenchymal atrophy; compression of the ventricular system
in case of mass effect caused by the AVM. Hydrocephalus can be observed in case of previous hemorrhage or
if the ventricular system is compressed by enlarged
draining veins of the AVM.
The role of CT angiography in the diagnostic
workup of brain AVMs is not precisely defi ned. Aoki
et al. (1998) showed that 3D CT angiography provided
precise anatomic information on nidus and draining
veins but did not demonstrate small feeders.
In patients with a large hematoma for which emergency evacuation is necessary, CTA may be useful to
detect a brain AVM preoperatively and thus give the
surgeon some idea about the surgical strategy to be
followed. However, small AVMs can be misdiagnosed
by this technique.
3.4.2.2
MR
Patients presenting with ruptured AVMs are usually
examined in the acute phase by a CT scan. MRI is
currently used in case of unruptured AVM or to fi nd
the underlying lesion in case of lobar hematoma,
generally days or weeks after the bleeding.
Given the different sequences available in MR
imaging, MRI is able to give three levels of analysis
of the AVM:
– Anatomic analysis using conventional sequences
– Vascular analysis using MR angiography
– Functional analysis using fMRI
Anatomic Analysis
Conventional sequences (T1, T2, T1 with gadolinium)
enable a very precise analysis of the brain AVM
(Smith et al. 1988b). On T1- and T2-weighted images,
circulating vessels have no signal because of the fl ow
void phenomenon (Fig. 3.5). On T1-weighted images
with gadolinium, vessels are enhanced.
The size and the anatomic location of the nidus
are precisely delineated by MRI (Figs. 3.4, 3.6). Smith
et al. (1988) showed that the size of the nidus was
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a
c
b
d
e
Fig. 3.2a–f. A 14-year-old girl presenting with sudden headaches and defi cit
of right lower limb. a CT-scan shows a subcortical frontoparietal hematoma
with hypodense structures. b Proton density MR, fl ow void serpiginous structures anterior to the hematoma very evocative of brain AVM. c Time of fl ight
(TOF) angio-MR shows feeding arteries and nidus size and morphology.
d Phase contrast (PC) angio-MR shows nidus and draining veins. Combined
information from TOF and PC concerning arterial feeders, nidus, and venous
drainage morphology were considered accurate enough to plan treatment.
Embolization was decided on fi rst and was performed 3 months after bleeding. Digital angiography in lateral and AP view (e, f) was done with the patient
under general anesthesia at beginning of embolization. Retrospectively, AVM
architecture was very precisely analyzed on angio-MR
f
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a
c
b
d
Fig. 3.3a–f. A 46-year-old man who presented with a parenchymal frontal hematoma in 1976, resulting in a slight residual right
hemiparesis predominating at the level of the lower limb. The patient came to our department in 2000 complaining of progressive
worsening of the defi cit, confi rmed by repeated clinical examination during the preceding 6 months. Contrast CT scan shows an
AVM of the left medial frontal lobe with calcifi cations (a) and an aneurysm of the anterior communicating (Acom) artery (b). Digital
angiography shows Acom aneurysm and huge frontoparietal AVM fed by both anterior and middle cerebral artery branches and
deeply involving the white matter (c, d). Acom aneurysm was considered the weakest point and treated fi rst (e, f). Treatment was dif-
fi cult due to aneurysm neck size and high fl ow. Oversized coils were necessary to keep them in the aneurysm cavity. The AVM is still
under an embolization protocol with the aim of reducing AVM volume and fl ow to improve progressively worsening symptoms
e
f
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a
c
b
d
e
f
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g
i
h
j
䉭
Fig. 3.4a–j. A 42-year-old woman presenting with two episodes of seizures. Pre- and post-contrast CT scans (a, b) show a right
䉰
temporal AVM. A slightly hyperdense structure is visible before and, strongly enhanced, after injection. Frontal and axial T
images perfectly localize the AVM within the white matter of the right temporal lobe, but determination of the nidus border is
diffi cult (c, d). 3D TOF image does not show the nidus limits precisely and affords poor understanding of the AVM architecture
(e). Digital angiography performed during embolization shows the arterial feeders, nidus size and venous drainage much better
(f). Superselective injection during embolization allows a much better understanding of nidus arteriovenous architecture. Distal
catheterization shows immediate opacifi cation of draining veins (g). Such arteriovenous anatomy allows very effi cient embolization with easy gluing of origin of draining veins (h). Three and 18 months after second embolization, follow-up angiography
showed complete occlusion (i, j)
2
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C. Cognard et al.
a
c
Fig. 3.5a–d. A 63-year-old woman presenting with common headaches. Post-contrast CT scan shows an abnormal vessel within
the right temporal lobe (a). Axial proton density image shows enlarged fl ow void vessel (b). Digital angiography depicts a very
small superfi cial temporal AVM draining into a single, slightly dilated, superfi cial vein (c, d). AVM is supplied by very short “en
passage” feeders. Due to patient’s age, absence of symptoms, and AVM morphology no therapy was planned
b
d
Fig. 3.6a–f. A 27-year-old man presenting with a small deep hematoma with ventricular hemorrhage. Axial proton density MR
image shows a left temporopolar small brain AVM (a) and the hematoma in a remote, more posterior location at the medial
aspect of the left temporal lobe (b). Internal carotid injection shows the temporal AVM with a deep venous drainage (c). An
intranidal aneurysm or false aneurysm is visible; this must be considered the most likely cause of the bleeding and should be
the fi rst target of embolization. Superselective catheterization of the lenticulostriate artery harboring the aneurysm allowed
gluing of both aneurysm and AVM (d). Final follow-up angiography after four embolizations showed incomplete obliteration
of the AVM with disappearance of any nidus but persistent early venous drainage (e, f)
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