An Introduction To Vascular Neurosurgery

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COORDINATOR:
IOAN TEFAN FLORIAN, MD, PhD
VICTOR VOLOVICI, MD
CRISTINA-CATERINA ALDEA
IOAN-ALEXANDRU FLORIAN
Intraoperative photographs, CT, MRI, CTA, MRA were provided by

Professor Ioan-tefan Florian, MD, PhD, from his personal
collection.
Angiographies from Chapter 4 were offered by Lucian Mrginean,
MD, PhD.
Artwork: Ioan-Alexandru Florian
Rare Micov
Desktop publishing and design: Adrian Zoican
CONTENTS
FOREWORD....5
SECTION I:
Anatomy.....7
SECTION II:
Imaging in vascular lesions.47
SECTION III:
Cerebrovascular disease.63
SECTION IV:
Aneurysms and AVMs85
FOREWORD
Vascular neurosurgery, while not the youngest subspecialty of neurosurgery, is by far the
most challenging and with an amazing evolution in terms of possibilities and options for the
treatment of vascular intracranial pathology.
Starting from very humble beginnings in the late 1700's it has evolved into one of
the most challenging domains that exists on the planet, with its specialists being able to
perform what is sometimes rightfully considered to be acts of magic inside the delicate
tissue of the brain with minimal or no damage. Aneurysms and intracranial vascular
malformations have been around as long as human history but it is only very recently that
they have also been recognized and treated. From the first use of a Cushing silver clip by
Dandy in 1935, the aneurysm clip has become a cornerstone and a symbol of what
neurosurgery is today. Even in the era of minimally invasive procedures, endovascular
treatment and progressively more aversion towards open surgery, good microsurgery still
remains the best, safest, most important manner to treat intracranial vascular pathology.
It is because of these and many other reasons that we decided to set up the second
edition of the Masterclass as a vascular-dedicated endeavour, to inspire and teach the
generation of future vascular neurosurgeons who are just now realizing where their loyalties
lie in this extraordinary field of ours.
We also thought it would be a welcome addition if next to the course participants
could receive a book detailing several more important aspects which will be discussed
during the course and this lies here before you in an electronic format.
We wish all the participants an open mind and to enjoy the second edition of the
Neurosurgical Masterclass in Cluj!
Professor Ioan Stefan Florian, MD, PhD

Cluj-Napoca, 28.02.2014
Victor Volovici, MD
Cristina-Caterina Aldea
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Medial dissection of the Internal Carotid Artery in order to expose the optic chiasm
anatomical relationships
CHAPTER 1
THE ARTERIAL ANATOMY OF THE BRAIN
VICTOR VOLOVICI
THE CAROTID ARTERY AND THE ANTERIOR CIRCULATION

Operating succesfully in Neurosurgery requires an in-depth three-dimensional
anatomical knowledge, good knowledge of radiology and of the imaging options
used in diagnosis of the pathology to be operated upon and much practice in the
operating room.
The cerebrum receives blood flow from the two internal carotid arteries
and from the two vertebral arteries, namely from their terminal arteries, the
anterior, middle and posterior cerebral arteries, interconnected to form the socalled circle of Willis (Figure 1.1) at the base of the cerebral hemispheres.
The Common Carotid artery arises from the brachiocephalic trunk on
the right side and from the aortic arch on the left side, resepctively, and courses
laterally to the trachea in the vagina carotica in the anterior portion of the neck
together with the internal jugular vein and the vagus nerve. It bifurcates into the
external and internal carotid arteries at the level of C4.
An article form Rhoton in 1981 provides an excellent anatomical study of
the carotid artery at a point in time where microsurgery for intracerebral
aneurysms, already pioneerd by Yasargil in the 60's, begun to take off at an
extremely rapid pace and in-depth microsurgical anatomical studies were required.
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VASCULAR NEUROSURGERY
.
Figure 1.1 Circle of Willis
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CHAPTER 1: THE ARTERIAL ANATOMY OF THE BRAIN
The Internal Carotid (Figure 1.2) may be divided thus into several
segments, each with anatomic particularities and different approaches. It is not the
purpose of this very short review to go in-depth into, for example the Dolenc
approach to the cavernous sinus and its very complicated anatomy, so we shall
only present a quick run-throug of concepts aiding and laying the foundation even
for the study of cerebrovascular disease.
There are many modalities to divide the carotid artery into segments and
there is no international consensus, but a useful division to remember is as follows:
C1- cervical segment, C2- petrous segment, C3- cavernous segment,
C4- supraclinoid segment, which can be further divided into C4- clinoid segment,
C5- ophtalmic segment, C6- communicating segment, C7- choroidal segment.
Figure 1.2 Carotid artery segments

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The divison into segments helps with the precise localisation of an

aneurysm in the course of the internal carotid and with anatomical correlations
with the digital subtraction angiography, allows planning of the operative
approach and establishes in one instance all anatomical relationships related to
one segment in particular. E.g. a lesion in the cavernous sinus automatically
implies an intimate relationship with cranial nerves III, IV, VI , V1 and V2, which
should be taken into consideration when plannin g the approach.
The cervical carotid, C1, does not present any branches and courses in
the carotid canal to become the petrous portion. C2 usually sends off 2 branches,
the tiny caroticotympanic and pterygoid arteries, which enter the tympanic
cavity via a foramen in the canalus caroticum and the pterygoid canal together
with the vidian nerve respectively.
The C2 portion then courses over the foramen lacerum- without passing
through it, to enter the cavernous sinus. Here C3 gives off inconstantly 4 branches,
the dorsal meningeal branch for the dura of the upper clivus, the tentorial artery
and the inferior hypophyseal artery. These are usually grouped in a meningohypophyseal trunk, barely visible on the DSA, save for rare situations where
there is a dural fistula involving the a. meningea posterior. The last branch is the
infero-lateral trunk, which runs to the lateral wall of the cavernous sinus.
Inconstantly, an artery for the capsule of the pituitary has been described, known
as the McConell capsular artery.
The most relevant portion of the internal carotid is the intracranial
supraclinoid portion, after the emergence of the carotid from the cavernous sinus.
Here the artery gives off the 3 important branches which also divide this portion
into 3 segments, each with its own particular anatomical correlations, the
ophtalmic artery which represents the proximal boundary of the ophtalmic
segment, the posterior comunicating artery, setting the proximal boundary for
the communicating segment C6, and the anterior choroidal, as the proximal
boundary for the choroidal segment. In C7 the internal carotid suffers the
bifurcation in its terminal branches, the anterior and middle cerebral arteries.
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Before we move on to the terminal arteries of the internal carotid, we

need to have a short look at the other 3 important intracranial branches. The
ophtalmic artery arises under the optic nerve and pases anteriorly and laterally to
assume a superolateral position to the internal carotid, entering the optic canal
together with the optic nerve heading towards the orbit. It initially sits inferiorly to
the nerve, but then crosses over it to assume a medial position in the orbit. Its
exposure during surgery usually requires a so-called Dolenc approach, with
removal of the anterior clinoid process with the help of a 1-mm diamond drill. The
perforating arteries arising from the artery serve the stalk of the pituitary, the optic
chiasm and the optic nerves.
The next branch of the supraclionoid portion of the carotid is often not
encountered during her surgical exposure and may present itself in a variable
number, ranging from one relatively bigger trunk to 5 thin arteries, namely the
superior hypophyseal artery(ies). They supply the anterior lobe of the
pituitary, but not the infundibulum and the floor of the 3rd ventricle which owe
their blood supply to the next branch.
The posterior communicating artery, embirologically the origin of the
posterior cerebral artery, poses a series of problems with reagard to its enormous
variability and anatomical relationships. Aside from being a common site for
aneurysms(its point of origin from the internal carotid), it can range from being
hypoplastic to being the primary source of blood flow to the posterior circulation
in the case of a "fetal" PCom. It passes posteromedially to join the posterior
cerebral artery in the interpeduncular cistern. Its trajectory is in a subarachnoid
cisternal compartment limited medially by the pituitary stalk and infundibulum,
laterally by the medial surface of the uncus, superiorly by the optic tract and
floor of 3rd ventricle and inferiorly by the roof of the cavernous sinus and
dorsum sellae. As mentioned before, its exact trajectory is extremely variable and
not the subject of this review. About 4-14 perforating arteries arise from the
PCom, supplying blood to the infundibulum and to the floor of the 3rd ventricle.
The largest and most important branch is the premamillary artery, also known as
the "anterior thalamoperforating artery".
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AN INTRODUCTION TO
The next and final collateral artery before the bifurcation of the ICA is the
anterior choroidal artery. It courses posteriorly and laterally under the optic
tract, entering the temporal horn through the inferior choroidal point posteriorly to
the uncus, which marks the beginning of the choroidal fissure. The AChA sends
off branches to the optic tract, crus cerebri, lateral geniculate bodies and uncus in
its cisternal segment. Furthermore, it provides numerous branches for the optic
radiation, globus pallidus, mesencephalon, thalamus, posterior limb of the internal
capsule. Inside the temporal horn it anastomoses with the lateral posterior
choroidal artery (PLChA).
Variably, 1-9 perforating arteries arise from the choroidal segment(C7) of
the carotid artery, and occupy the posterior half of the central region of the anterior
perforated substance.
The anterior perforated substance is also the landmark anterior to which
the carotid artery bifurcates into its terminal branches, the anterior and middle
cerebral arteries.
The Anterior Cerebral Artery (Figures 1.3 and 1.4) is the medial
terminal branch of the internal carotid. It courses on the medial side of the
hemispheres, providing vascularization mainly to the frontopolar region, part of
the superior frontal gyrus and the mesiofrontal structures, paracentral lobule
and precuneus and to deep structures. There are multiple systems which attempt
to divide the anterior cerebral artery in segments, and we find the angiographical
method most useful, as the it is easy to correlate the DSA findings with the
microsurgical anatomy encountered intraoperatively. There are, thus, 5 segments:
A1, extending from the bifurcation to the ACom(anterior communicating artery),
A2, extending from the ACom to the junction between the rostrum and the genu of
the coprus callosum, A3, extending from the genu of the corpus callosum to the
point where the artery turns sharply and posteriorly over the corpus callosum
following its course, A4 and A5, extending above the corpus callosum from the
genu to the splenium. The limit between A4 and A5 is a plane passing
posteriorly to the coronal suture and intersecting the A4- A5 segment, also called
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ANATOMY
the horizontal segment. The A2-A3 segment is also known as the ascending
segment, and the distal portion of the anterior cerebral artery to the anterior
communicating is commonly known as the pericalosal artery. Of its many
branches, the discussion needs to fan out to the most important ones. Thus, 1-11
medial lenticulostriate perforators arise usually from the posterior aspect of A1 and
enter the medial half of the anterior perforated substance. The anterior
communicating artery ensures communication between the 2 A1 segments, which
are in only about 25% of equal calibre. It originates embriologically from a
multitude of vascular channels which will coalesce and form one communicating
channels in about 75% of cases, explaining the high degree of variability of the
ACom anatomy which needs to be properly diagnosed before the first incison is
made. The Acom may also present 1-4 perforators, supplying the infudibulum,
the anterior perforated substance, the subcallosal area and the preoptic areas
of the hypothalamus. A very important branch, the recurrent artery of
Heubner, appears in 78% of cases from the procimal A2 and is usually seen upon
retraction of the frontal lobe prior to the visualization of the A1 segment. It is the
largest and longest branch heading towards the anterior perforated substance,
initially accompanying M1 in the first medial part if the Sylvian fissure before
entering the anterior perforated substance in its full mediolateral extent. Last but
not least, the basal perforators, passing posteriorly to enter the optic chiasm and
lamina terminalis. It is also worth mentioning that the 2 medial branches the
orbitofrontal and frontopolar arteries usually arise from the A2 segment and that
most of the vascularization of the medial hemisphere coming from the anterior
cerebral artery usually only arises from the pericalossal artery and very rarely from
the calosomarginal artery.
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AN INTRODUCTION TO
Figure 1.3 Anterior cerebral artery frontal view
Figure 1.4 Anterior cerebral artery sagittal view
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The second terminal branch of the internal carotid artery is the Middle
Cerebral Artery (Figures 1.5 and 1.6). It is divided into 4 segments, to allow for a
better microsurgical-radiological correlation. M1, or spehnoidal segment, M2, or
insular segment, M3, the opercular segment and M4, the cortical segment. The
M1 segment extends from the bifurcation of the internal carotid anteriorly to the
anterior perforated substance to the limen insulae. Anatomically, the proximal
segment is in relationship with the anteromedial uncus, the ala minor of the
sphenoid and the anterior perforated substance. The distal segment rests on the
planum polare, all the way to the apex of the insula of Reil called the monticulus.
M1 gives off 2 types of branches, the lateral lenticulostriate arteries which mostly
arise from its posterior aspect and the early branches usually temporopolar, which
arise before the bifurcation of M1, that occurs in 86% of cases before the limen
insulae. M2 or the insular segment extends from the limen insulae to the circular
or limiting sulcus of the insula. It most often appears as a superior and an inferior
trunk and at the edges of the limiting sulcus it fans out into the opercular
compartment as M3 branches. Extremely essential for operative exposure of the
middle cerebral artery is the relationship with the pars triangularis of the inferior
frontal gyrus. The genu of the middle cerebral artery is the sharp turn it makes at
the level of the monticulus, or insular apex, in order to pass from the basal surface
of the hemisphere to the lateral surface of the cerebrum. The genu is located a few
milimeters deep and ventral to the pars triangularis of the inferior frontal gyrus,
limited by the horizontal and ascending sulci. This relationship is useful for a rapid
intraoperative orientation: should the aneurysm be located in the vincinity of the
genu of the middle cerebral artery, then opening the fissure should start proximally
to the pars triangularis. If it is located at the level of the genu, then splitting the
sylvian fissure may start just proximally to the pars triangularis and if it is distal to
the genu then splitting may begin at the level of the pars triangularis, ensuring a
minimal exposure with good proximal control. The M3 or opercular segment has
an anatomical relationship with the frontoparietal operculum superiorly and the
temporal operculum inferiorly. An anatomical landmark of great importance is the
so-called M-point of Sylvian point, visible on the angiography. It is defined as the
point which is located behind the insula, above the medial end of the longest of the
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transverse temporal gyrus, the gyrus of Heschl. It displays on the angiography the
posterior end of the insula and the central core, atrium, thalamus and its endpoint
the pulvinar. The last segment is the M4 or cortical segment. It extends from the
opercula superiorly and inferiorly on the convexity, supplying a very large area
with blood.
Figure 1.5 Middle cerebral artery axial section
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Figure 1.6 Middle cerebral artery segments

THE POSTERIOR CIRCULATION
To complete the Circle of Willis, we will now refer to the Posterior Cerebral
Arteries. These are actually the terminal branches of the Basilar artery, but they
are the direct link of the posterior circulation to the anterior circulation via the
previously described posterior communicating artery, subject to extreme
anatomical variability. Moreover, they are embirologically branches of the
internal carotid and only after birth do they develop as terminal branches of the
basilar, hence the need to present them after the anterior circulation. The posterior
cerebral artery is divided into 4 segments. The P1 segment reaches from the basilar
bifurcation in the interpeduncular cistern to the place where the PCom joins the
posterior cerebral artery. The P2 segment begins at the union of the PCom with
the PCA to the quadrigeminal cistern. This segment is further divided, in order to
aid operative planning into P2A and P2P segments. P2A begins at the union with
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AN INTRODUCTION TO
the PCom and courses around the crus cerebri. At the posterior margin of the crus
begins the P2P and it courses in the ambient cistern to the tegmentum of the
midbrain, paralelly and inferiorly to the basal vein, inferolaterally to the lateral
geniculate bodies and pulvinar and medially to the parahypocampal gyrus, entering
the quadrigeminal cistern. The P3 segment begins under the pulvinar and ends at
the anterior limit of the anterior calcarine sulcus, being in most cases already
divided in its terminal branches, the calcarine and parieto-occipital arteries before
reaching this point. A point of interest on DSAs is the quadrigeminal point,
which marks the posterior limit of the mesencephalon on an angiography, defined
as the point where the 2 PCAs are closest to each other in the quadrigeminal
cistern. The P4 segment represents the cortical branches of the PCA. PCA gives
off the main branches in the shape of posterior thalamoperforating, direct
perforating, short and long circumflex, thalamogeniculate, MPChA and LPChA,
inferior temporal, parieto-occipital, calcarine and posterior pericallosal arteries.
The many and essential posterior thalamogeniculate arteries arise from P1 and
enter the brain through the posterior perforated substance and interpeduncular
fossa, supplying the posterior thalamus, hypothalamus, subthalamus, substantia
nigra, nucleus rubrum, oculomotor and trochlear nuclei, oculomotor nerve,
mesencephalic reticular formation, pretectum, posterior floor of 3rd ventricle and
posterior portion of the internal capsule. The direct perforating arteries mainly
arise from P2A and supply the crus cerebri. The short and long circumflex arteries
arise from P1 and supply the lateral geniculate body and the colliculi respectively.
The thalamogeniculate arteries arise from P2A and P2P equally. The medial
posterior choroidal artery (MPChA) usually arises from P2A, coursing laterally
to the mesencephalon, then turning sharply at the level of the pulvinar to proceed
laterally to the colliculi and epyphysis to enter the 3rd ventricle via the velum
interpositum and via the foramen of Monro in the choroid plexus of the lateral
ventricles. It supplies the crus cerebri, tegmentum, geniculate bodies, colliculi,
pulvinar, pineal gland and medial thalamic nuclei. On a lateral projection on a
DSA the MPChA is easiest recongizable by its shape resembling the number 3,
with the inferior curve being its sharp turn at the level of the puvinar and the
superior curve being the point where int crosses the colliculi before entering the
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velum interpositum. The lateral posterior choroidal artery (LPChA) usually

arises from P2P, passing directly laterally to enter the choroidal fissure to supply
the choroid plexus in the atrium and the temporal horn, and anastomosing with the
AChA. Inferior temporal arteries provide blood supply to the basal surface of the
temporal and occipital lobes, being made up of the hippocampal, anterior, middle
and posterior arteries, the former 2 usually arising from P2A and the latter 2
arising from P2P. The terminal branches of the PCA are the pariet-occipital and
calcarine arteries, each coursing in the homonymous fissure. The parieto-occipital
artery gives off the posterior paericallosal artery in 65% of the cases, providing
blood supply to the splenium of the corpus callosum.
In order to conclude the brief presentation of the blood supply of the
brain, essential for understanding the basics of cerebrovascular disease, we will
present the infratentorial circulation, beginning with the vertebral and basilar
arteries and proceeding to the essential 3 branches, the superior cerebellar artery
(SCA), the anterior inferior cerebellar artery (AICA) and the posterior inferior
cerebellar artery (PICA) Figure 1.7. It is of interest to note the endeavour of
scholars such as Prof. Rhoton to find a logic in the extremely complicated
infratentorial circulation. As such, he describes the "rule of 3", as such the
brainstem presents 3 parts, the cerebellum 3 surfaces (petrosal, tentorial and
suboccipital), 3 cerebellar peduncles, 3 fissures (cerebellomesencephalic,
cerebellopontine, cerebellomedullary), 3 main arteries mentioned earlier, 3 venous
draining groups (petrosal, galenic and tentorial). As such, we define 3
neurovascular complexes: the superior complex, SCA, and cranial nerves III, IV,
V and mesencephalon, the middle complex, AICA, nerves VI, VII, VIII, pons and
inferior complex, PICA, IX, X, XI, XII and medulla.
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Figure 1.7 - Posterior fossa blood supply

The Vertebral Artery arises from the subclavian artery as one of the 2
main superior collateral branches. It courses medially and superiorly to reach the
lowest foramen transversarium, usually C6, after which it ascends through all
foramina in front of the cervical nerve roots. At C2 it deviates laterally to enter a
more laterally placed foramen transversarium of the atlas. It then passes behind
the lateral mass of the atlas and atlanto-condylar joint, being pressed into the
groove on the upper surface of the posterior arch of the atlas, coursing along the
floor of the suboccipital triangle, entering the vertebral canal by passing
anteriorly to the atlanto-occipital membrane in order to pierce the dura. Here, it
gives off the posterior meningeal artery, the posterior spinal artery, muscular
branches to the deep cervical musculature and very infrequently the PICA. The
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intradural aspect begins here, at the edge of the foramen magnum, where the dura
thickens to form a funnel-like structure around the artery. It is also bound by
fibrous dependencies of the dura with the first cervical nerve and the posterior
spinal artery exiting through this foramen with the vertebral artery. The intradural
portion is divided academically into 2 segments, the lateral medullary coursing
until the preolivary sulcus and the anterior medullary segment coursing until the
union with the VA on the opposite site in front of the pontomedullary sulcus to
form the basilar artery. This latter segment also rests on the clivus. The branches
that arise in this region from the vertebral artery are the posterior spinal, anterior
spinal, PICA and anterior and posterior meningeal arteries.
The Basilar Artery, created from the union of the vertebral arteries,
courses in a very shallow groove on the surface of the pons. Its length spans the
distance between the pontomedullary sulcus to the level of the emergence of the
3rd cranial nerves from the pedunculli cerebri. It may sometimes have a tortous
trajectory and may even deviate so laterally as far as the origin of the abducens or
of the facial nerve. After crossing the oculomotor nerves it divides in its terminal
branches, the posterior cerebral arteries, discussed earlier. It gives off pontine,
labyrinthine, AICA, SCA and posterior cerebral arteries. The pontine branches
are perforators that either enter the pons directly or navigate it circumferentially
on its lateral aspect and give off small vessels which penetrate the pons.
From superior to inferior, the first artery to be discussed, representing the
first neurovascular complex is the Superior Cerebellar Artery. It is closely
related to the cerebellomesencephalic fissure, the oculomotor, trochlear and
trigeminal nerves and the mesencephalon. They usually arise close to the basilar
apex, under the oculomotor nerve. In 75% of cases there is a point of contact with
it, 100% of cases have a point of contact with the trochlear. As it encircles the
brainstem it sometimes makes a caudal loop which can reach all the way to the
trigeminal nerve on its posterior or posteriomedial surfaces, causing the
neruovascular conflict leading to trigeminal neuralgia. The proximal SCA courses
medially to the free edge of the tentorium and after passing above the trigeminal
nerve it enters the cerebellomesencephalic fissure, where its branches fan out into
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the precerebellar arteries. After exiting the cerebellomesencephalic fissure, it is

once again medial to the free edge of the tentorium and its branches pass
posteriorly under the tentorial edge to be distributed to the tentorial surface of the
cerebellum. The SCA usually bifurcates into a rostral and a caudal trunk, and it
gives off perforating arteries tot he brainstem and cerebellar peduncles. The rostral
trunk usually supplies the vermis and surrounding paravermian areas, whilst the
caudal trunk supplies blood to the hemisphere on the suboccipital surface.
Academically, it is divided in several segments. The anterior pontomesencephalic
segment extends to the anterolateral margin of the brainstem. The lateral
pontomesencephalic segment loops caudally and sometimes reaches the Vth nerve
root entry and terminates at the anterior margin of the cerebellomesencephalic
fissure. The basal vein and PCA course parallel to this segment. The
cerebellomesencephalic segment can be found in the homonymous fissure, which
deepens medially and is deepest in the midline above the superior medullary
velum. It then fans out in the shape of cortical branches, with the rostral trunk
supplying the medial area and the caudal trunk supplying the lateral area of the
tentorial surface of the cerebellum. The branches of the SCA are perforating,
precerebellar and cortical. The perforating ones may be of a direct or circumflex
type, with the direct ones entering the brainstem directly and the circumflex
encircling the brainstem before entering it. The latter circumflex ones may also be
divided into long and short circumflex, with the short ones travelling less than 90
degrees around the brainstem. The perforators arise from the main, rostral and
caudal trunks, the most frequent type of which is circumflex. The precerebellar
arteries arise in the cerebellomesencephalic fissure to supply the deep cerebellar
grey matter. They are divided in a medial group that passes between the superior
medullary velum and the central lobule and a lateral group that passes between
the superior and middle cerebellar peduncles and the wings of the central
lobule. After leaving the cerebellomesencephalic fissure, the trunks of the SCA
give off hemispheric/vermian arteries. The hemispheric ones are usually divided
into medial intermediate and lateral, depending on the third of hemisphere which
the vascularize. The vermian branches, usually 2, supply blood to the median strip
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which borders the midline and a paramedian strip bordeing the hemispheric
surface.
More inferiorly, we encounter the Anterior Inferior Cerebellar
Artery(AICA). It usually arises from the lower third of the basilar artery,
constituting together with the abducens, facial and vestibulocochlear nerves and
the pons the second neurovascular complex, around the cerebellopontine angle. Its
anatomical relationships are with important structures related to many operations
of the posterior fossa, namely the pons, lateral recess, foramen of Luschka,
cerebellopontine fissure, petrosal surface of the cerebellum. After it arises from the
basilar artery, it encircles the pons near the abducens and the facial, sensing
branches to them and to the internal acoustic meatus. It then passes in relationship
to the flocculus, on the middle cerebellar peduncle and supplies blood to the
petrosal surface of the cerebellum. Near the facial-vestibulocochlear complex it
divides into a rostral and a caudal trunk. The former usually courses above the
flocculus and at the level of the middle cerebellar peduncle distributes itself to the
superior lip of the cerebellopontine fissure and to the superior part of the petrosal
surface of the cerebellum. The caudal trunk supplies the inferior petrosal surface of
the cerebellum, with tha adjacent flocculus and choroid plexus coming out of
Luschka. Academically, we divide AICA into several segments. The anterior
pontine ends at the level of the long axis of the olive, usually being in contact with
the abducens at this point. The lateral pontine segment passes through the CPA,
above, below or throught the facial nerve and is related to the internal acoustic
meatus, sometimes looping in to form an arterial loop going into the meatus itself.
It is moreover intimately in contact with lateral recess and the choroid plexus
from the foramen of Luschka. This is where AICA gives off its nerve-related
branches, which we will describe shortly. The flocculonodular segment begins
where the trunks pass above or under the flocculus to the middle cerebellar
peduncle and cerebellopontine fissure. The final segment is composed of the
cortical branches supplying the petrosal part of the cerebellum. The branches of
the AICA are subject to a great deal of variability, beginning with the place of
bifurcation, as the vascularized territory is significantly different when the main
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trunk splits proximally or distally to the facial-verstibulocochlear complex.

However, constantly the branches of the rostral trunk anastomose with the
branches of the SCA and those of the caudal trunk anastomose with those of the
PICA. It also gives rise to perforating arteries to the brain stem, choroidal arteries
to the choroid plexus and nerve-related arteries. The nerve-related branches stem
in the CP angle and are related to the facial-vestibulocochlear complex. These
branches are the labyrinthine artery, which enter the internal auditory canal
and supply the bone and dura of this canal, as well as give off vestibular, cochlear
and vestibulocochlear branches, supplying the organs of the inner ear. The
recurrent perforating arteries arise in the close proximity of certain nerves
which they follow and supply blood to until the meatus and then they make a sharp
turn and return to the root of the nerves to vascularize this area and the brainstem
around it. The subarcuate artery originates medially to the porus acusticus and
enters the subarcuate canal via the subarcuate fossa. It is amenable to
coagulation safely when opening the internal acoustic meatus, it supplies the
petrous bone in the vincinity of the semicircular canals. The subarcuate canal may
be a route of extension of infections in complicated cases of mastoiditis to the
meninges and superior petrosal sinus. The terminal cortical branches of the rostral
and caudal trunks of AICA supply the superior and inferior petrosal surfaces of the
cerebellar hemisphere respectively, anastomosing as described with branches of
the SCA and PICA, subject to a high degree of variability with respect to the exact
area of vascularization.
The final and most complex artery is the Posterior Inferior Cerebellar
Artery (PICA). Infratentorially, it represents together with the medulla, the
glossopharyngeus, vagus, accesory and hypoglossus nerve the inferior
neruovascular complex. It has the most complex, tortous and variable course of
all the arteries. It is related to the cerebellomedullary fissure, the inferior
cerebellar peduncle and the suboccipital surface of the cerebellum. It arises
from the vertebral artery near the inferior olive, laterally or anteriorly to it. As it
courses towards the anterolateral edge of the medulla, it passes rostrally, caudally
or between the rootlets of XII, and at the posterolateral margin of the medulla
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ANATOMY
oblongata it courses between the fibers of the IX, X and XIth nerves. After that it
encircles the cerebellar tonsil and enters the cerebellomedullary fissure and passes
dorsally to the lower half of the roof of the 4th ventricle. After exiting the fissure,
its cortical branches are distributed to the vermis and the hemisphere of the
suboccipital surface. Academically, it is also divided into segments, but these are
more complex than those described for the SCA and the AICA. The anterior
medullary segment extends posteriorly past the hypoglossus to the level of the
boundary between the anterior and lateral medulla (a line that passes through the
most porminent part of the inferior olive). The lateral medullary segment ends at
the level of origin for the IX, X and XIth nerves. While the first segment is subject
to variability because of variability in origin form the vertebral artery, the lateral
medullary segment is one of the most constant ones. The third segment is called
the tonsillomedullary segment and it extends to the caudal half of the tonsil. The
proximal portion of this segment puts PICA in a relationship with the lateral recess
after which is dives posteriorly to reach the inferior pole of the tonsil. It then
turns rostrally on the medial side of the tonsil, forming a caudal loop easily
recognizable on the DSA and helpful for orientation. The fourth segment is called
the telovelotonsillar segment, which also happens to be the most complex one. It
begins during PICA's ascent on the medial side of the tonsil towards the roof of the
fourth ventricle and ends where it exits the fissures in orde to supply the vermis
and the hemispheres. It is here that PICA usually exhibits a convex loop called the
cranial loop, also useful for orientation on the DSA. An important anatomical
relationship of this loop is that it is caudal to the fastigium, being located between
the cerebellar tonsil and tela choroidea below and the inferior medullary velum
above, with the apex of the loop usually situated over the inferior medullary
velum, sometimes extending all the way to the fastigium, but usually remaining
under it. Branches that arise in this complex segment supply the tela choroidea and
the choroid plexus of the fourth ventricle. The final segment is the cortical
segment, which begins when the trunks of PICA exit between the vermis and
tonsil medially and the hemisphere laterally, and gives off the terminal branches.
The PICA bifurcates into lateral and medial trunks before it exits to the surface of
the hemisphere. The medial trunk usually climbs the vermohemispheric fissure to
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AN INTRODUCTION TO
reach the vermis and the lateral trunk passes via the telovelotonsillary fissure to
reach the suboccipital cerebellar surface. The medial trunk gives off terminal
branches for the inferior vermis and adjacent parts of the tonsil and hemisphere.
The lateral trunk divides into a large hemispheric trunk which supplies blood to
the hemisphere and several smaller tonsillar branches for the tonsilla. The
bifurcation occurs on the medial part of the tonsil. While passing through the
tonsilomedullary fissure, the turnks give branches for the medulla and while
passing through the telovelotonsillar fissure branches arise for the dentate
nucleus. Perforating arteries occur within the three medullary segments and are
either direct or circumflex. They enter the brainstem and intermingle with those
that arise from the vertebral arteries, usually from the part distal to the orogin of
the PICA. Other collaterals are the choroidal branches, which supply the tela
choroidea and the plexus of the fourth ventricle, near the midline or the medial part
of the lateral recess. Most of these arteries arise in the tonsillomedullary and
telovelotonsillar segments and the part of the plexus not supplied by PICA is
supplied by AICA. The cortical branches are the terminal branches of PICA and
they provide blood to the suboccipital surface of the cerebellum. They are divided
into hemispheric, vermian and tonsillar groups, the vermian usually arising from
the medial trunk and the rest from the lateral trunk, as previously mentioned. Each
half of the vermis is divided, just as in the case of the AICA, into paramedian and
median segments and the hemisphere is also divided in medial, intermediate and
lateral segments.
This has been a brief review of the most important aspects of the
immenisty and complexity which is the vascular system of the cerebrum. Without
permanent study of CTs, angiographies, dissectioons, books and intraoperative
anatomy one will never be able to reach a satisfying level in order to become a
vascular neurosurgeon. It is therefore of the essence that these concepts to be
repeated over and over again until one is able to juggle the concepts without
difficulty. It is our belief that this is the only path to proficiency and mastery of
cerebrovascular operations, most often the most challenging in all of neurosurgery.
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CHAPTER 2
CEREBRAL VENOUS BLOOD FLOW
CRISTINA C. ALDEA
C Cerebral Venous drainage patterns possess a high degree of variability not only
between different individuals but also when regarding the two hemispheres of a
given brain. These variations may pose limitations for detailed anatomic
understanding. However, normal anatomic variants characteristically display a
distinct set of common features (1).
Specific Anatomic and Physiologic Features

The cerebral venous system forms in the pia-arachnoid transitional area where
small venous channels drain the underlying brain parenchyma. These channels will
form the cerebral veins which will course through the subarachnoid space and
subarachnoid cisterns. The cerebral veins possess no valves and have thin walls
(owing to the absence of the tunica muscularis). Consequently blood flow within
these veins is possible in both directions and they have the capacity to remain
dilated and even become arterialized in certain pathological entities. The fact that
any change in the central venous pressure is transmitted to the intracranial
compartment is also explained by these two particularities with implications in
several pathological entities such as idiopathic intracranial hypertension (3). The
cerebral veins pierce the arachnoid membrane to cross the subdural space as
bridging veins in order to drain to the nearest dural venous sinus. The veins which
drain the central core and white matter course through the walls of the ventricles
and in the basal cisterns to collect into either the great vein of Galen, the basal
vein of Rosenthal or the internal cerebral vein. These in turn will drain into
dural venous sinuses.
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AN INTRODUCTION TO
In the jugular fossa, the sigmoid sinus will become the internal jugular
vein, which represents the major site of venous outflow from the intracranial
compartment. Other sites of venous outflow to the extracranial compartment are
the veins of the orbit and the venous plexuses around the vertebral arteries. The
diploe and scalp veins may act as collateral outflow pathways (2).
The diploic veins course between the external and internal tabulae of the
skull and connect the scalp veins with the underlying meningeal veins and dural
sinuses. Moreover these veins characteristically do not cross suture lines.
Damage to the diploic venous system may cause postoperative bleeding and may
impact the healing of the cranium after neurosurgical procedures. The parietal
bone harbors most of the diploic vessels whilst the squamous part of the temporal
bone presents no diploic veins. The anterior diploic system connects with the
superior sagittal sinus while the posterior diploic system displays connections
with the transverse and sigmoid sinuses. It is important to note that the point of
drainage for the frontal diploic vein is located near the supraorbital notch and that
the point of drainage of the anterior temporal diploic vein is located in the
pterional area. These vessels can be damaged during supraorbital, modified
orbitozygomatic, and pterional craniotomies (4).
The emissary veins connect the superficial veins with the underlying
dural sinuses by passing through the cranium. They pass through channels of
quite some variability. There are three commonly described groups: the parietal
emissary veins which connect the superior sagittal sinus with the overlying scalp
veins; the mastoid emissary veins which connect the transverse sinus with the
occipital and posterior auricular veins and passing through the mastoid foramen
and the anterior condylar emissary veins which connect the inferior petrosal sinus
with the suboccipital veins and passing through the hypoglossal canal (2).
The cerebral venous system can be didactically divided into a superficial

venous system and a deep venous system. The most important confluence point
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ANATOMY
CHAPTER 2: VENOUS BLOOD FLOW
between the superficial and deep venous systems is at the level of the straight
sinus. This sinus collects venous outflow from both great cerebral veins of Galen,
which are part of the deep cerebral venous system, as well as from superficial
veins draining the cerebral cortex. The key overlapping site of the extracranial
and intracranial venous systems is the cavernous sinus. At this level, venous
outflow from the ophthalmic veins is drained together with the venous outflow of
the sphenoparietal sinus, hypophyseal veins, the middle cerebral vein and
uncal vein (2). The cavernous sinus also receives venous drainage from the
pterygoid plexus, which lies outside the skull base through the foramen of
Vesalius, the foramen ovale and other foraminae innominata. Communication
between the intracranial and extracranial compartments is also aided by the
emissary and diploic veins.
DURAL VENOUS SINUSES

Dural venous sinuses are channels that form between two layers of dura. This
permits them to maintain their patency even if the intracranial pressure rises. As
the cerebral veins, they lack valves.
The superior sagittal sinus (Figure 2.1) courses along the midline
following the convexity of the calvarium. It extends from immediately posterior
to the foramen caecum all the way to the internal occipital protuberance where
it joins the transverse sinuses, the straight sinus and the occipital sinus to form the
confluence of sinuses. It receives blood from the inferior surface of the frontal
lobes and the superior portion of the medial and lateral surfaces of the frontal,
parietal and occipital lobes (5). The superior sagittal sinus drains to the left and
right transverse sinuses equally. When the drainage volume is not equal, the right
transverse sinus is usually the dominant one, receiving most of the venous outflow.
Lateral to the superior sagittal sinus are the venous lacunae. These are
enlarged venous spaces that communicate with the sinus through small openings.
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They drain the meningeal veins. The bridging veins coursing towards the superior
sagittal sinus characteristically pass beneath these lacunae. Pacchionian
granulations responsible for the resorption of the cerebrospinal fluid protrude into
the floor and walls of these spaces, becoming more prominent with age. These
lacunae must be kept in mind whenever performing an approach in the parasagittal
area and procedures which involve cannulation of the lateral ventricle.
The inferior sagittal sinus courses along the posterior two-thirds of the
inferior edge of the falx cerebri. It joins the great cerebral vein of Galen to form
the straight sinus. The anterior pericalossal vein is the largest tributary of this
sinus.
The occipital sinus is inconstant. It is the smallest of the cranial sinuses
and may be duplicated. When it is present, it drains superiorly towards the
confluence of sinuses. Alternatively, it may drain inferiorly towards the sigmoid
sinus or it can connect with the marginal sinus (which is located around the
foramen magnum). The occipital sinus is most prevalent in the pediatric
population, diminishing in size with age (7).
The transverse sinus courses laterally in the tentorium cerebelli until it
turns inferiorly to become the sigmoid sinus. The transverse sinus receives venous
outflow from important supratentorial veins from the occipital and parietal lobes.
The vein of Labb also drains into the transverse sinus. In addition, this sinus is
the draining point of some of the inferior cerebellar veins and the superior
petrosal sinus.
The superior petrosal sinus connects the transverse sinus with the
cavernous sinus. It receives the inferior cerebral veins, cerebellar veins and veins
from the tympanic cavity. The inferior petrosal sinus connects the cavernous
sinus with the internal jugular vein. It receives venous blood flow from the veins
of the pons, medulla oblongata and veins from the suboccipital surface of the
cerebellum. Internal auditory veins also drain into this sinus.
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ANATOMY
The sigmoid sinus represents the continuation of the transverse sinus. It

becomes the internal jugular vein in the jugular fossa. The sigmoid sinus may
also receive some venous channels from the pons and medulla oblongata.
The tentorial sinuses are located on each half of the tentorium cerebelli.
They are divided into a medial and a lateral group. The medial group of tentorial
sinuses collects the venous outflow of the superior cerebellar surface and drain
into the transverse sinus. The lateral group of tentorial sinuses receives the venous
blood from the basal and lateral surfaces of the parietal and occipital lobes.
They may drain in either the transverse or the straight sinus (6).
Figure 2.1 Dural sinuses and main veins of the cerebrum
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AN INTRODUCTION TO
DURAL VENOUS SINUSES

Dural venous sinuses are channels that form between two layers of dura. This
permits them to maintain their patency even if the intracranial pressure rises. As
the cerebral veins, they lack valves.
The superior sagittal sinus courses along the midline following the
convexity of the calvarium. It extends from immediately posterior to the foramen
caecum all the way to the internal occipital protuberance where it joins the
transverse sinuses, the straight sinus and the occipital sinus to form the confluence
of sinuses. It receives blood from the inferior surface of the frontal lobes and the
superior portion of the medial and lateral surfaces of the frontal, parietal and
occipital lobes (5). The superior sagittal sinus drains to the left and right transverse
sinuses equally. When the drainage volume is not equal, the right transverse sinus
is usually the dominant one, receiving most of the venous outflow.
Lateral to the superior sagittal sinus are the venous lacunae. These are
enlarged venous spaces that communicate with the sinus through small openings.
They drain the meningeal veins. The bridging veins coursing towards the superior
sagittal sinus characteristically pass beneath these lacunae. Pacchionian
granulations responsible for the resorption of the cerebrospinal fluid protrude into
the floor and walls of these spaces, becoming more prominent with age. These
lacunae must be kept in mind whenever performing an approach in the parasagittal
area and procedures which involve cannulation of the lateral ventricle.
The inferior sagittal sinus courses along the posterior two-thirds of the
inferior edge of the falx cerebri. It joins the great cerebral vein of Galen to form
the straight sinus. The anterior pericalossal vein is the largest tributary of this
sinus.
The occipital sinus is inconstant. It is the smallest of the cranial sinuses
and may be duplicated. When it is present, it drains superiorly towards the
confluence of sinuses. Alternatively, it may drain inferiorly towards the sigmoid
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ANATOMY
sinus or it can connect with the marginal sinus (which is located around the
foramen magnum). The occipital sinus is most prevalent in the pediatric
population, diminishing in size with age (7).
The transverse sinus courses laterally in the tentorium cerebelli until it
turns inferiorly to become the sigmoid sinus. The transverse sinus receives venous
outflow from important supratentorial veins from the occipital and parietal lobes.
The vein of Labb also drains into the transverse sinus. In addition, this sinus is
the draining point of some of the inferior cerebellar veins and the superior
petrosal sinus.
The superior petrosal sinus connects the transverse sinus with the
cavernous sinus. It receives the inferior cerebral veins, cerebellar veins and veins
from the tympanic cavity. The inferior petrosal sinus connects the cavernous
sinus with the internal jugular vein. It receives venous blood flow from the veins
of the pons, medulla oblongata and veins from the suboccipital surface of the
cerebellum. Internal auditory veins also drain into this sinus.
The sigmoid sinus represents the continuation of the transverse sinus. It
becomes the internal jugular vein in the jugular fossa. The sigmoid sinus may
also receive some venous channels from the pons and medulla oblongata.
The tentorial sinuses are located on each half of the tentorium cerebelli.
They are divided into a medial and a lateral group. The medial group of tentorial
sinuses collects the venous outflow of the superior cerebellar surface and drain
into the transverse sinus. The lateral group of tentorial sinuses receives the venous
blood from the basal and lateral surfaces of the parietal and occipital lobes.
They may drain in either the transverse or the straight sinus (6).
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AN INTRODUCTION TO
SUPRATENTORIAL VENOUS SYSTEM

Superficial Venous System
The superficial venous system drains the cortical surfaces of the cerebral
hemispheres. The cortical veins collect into bridging veins that carry the venous
blood through the subdural space to the nearest sinuses. It covers a depth of 1-2 cm
below the cerebral cortex. These veins are didactically divided into four groups:
superior sagittal, sphenoidal, tentorial and falcine.
The superior sagittal group is formed by the bridging veins that drain
the medial and lateral aspects of the frontal, parietal and occipital lobes. Part of
the orbital surface of the frontal lobe is also drained by this group of veins. This
group delivers blood to the superior sagittal sinus. The veins enter the sinus either
directly or through the meningeal sinuses adjoining the superior sagittal sinus.
The sphenoidal group of veins drains the cortical surfaces near the
Sylvian fissure corresponding to the frontal, temporal and parietal lobes. This
group carries blood to the sinuses on the inner part of the sphenoid bone: the
sphenoparietal or the cavernous sinus.
The tentorial group serves the basal and lateral aspects of the temporal
lobe, the basal surface of the occipital lobe and also serves as a draining point for
the vein of Labb.
The falcine groups anatomical drainage territory corresponds to that of
the limbic lobe. The venous blood is driven towards the inferior sagittal sinus or
the straight sinus. This may happen directly or via the deep cerebral veins.
There are two major anastomotic veins on the lateral surfaces of the
cerebral hemispheres: the vein of Trolard and the vein of Labb. The vein of
Trolard (the superior anastomotic vein or the frontoparietal vein) connects the
superior sagittal sinus to the veins coursing along the Sylvian fissure. The vein of
Labb (the inferior anastomotic vein or the temporooccipital vein) connects the
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ANATOMY
veins adjoining the Sylvian fissure with the transverse sinus. Together with two
other anastomotic veins (the vein of Rolando or the parietal vein and the vein of
Sylvius) they anastomose at the level of the insula (1). These four veins share a
close relationship with one another, the smaller one is, the larger the other. It is
also important to keep in mind the fact first demonstrated by di Chiro in 1962,
namely that the vein of Labb tends to be the dominant one in the dominant
hemisphere whilst the vein of Trolard tends to be more dominant the opposite side
(8).
Deep Venous System
This system drains the central core and white matter. Venous blood from these
regions is first collected into the deep cerebral venous system (internal cerebral
vein, basal vein of Rosenthal, great vein of Galen) and is eventually drained into
the straight sinus.
Thus, the straight sinus becomes a crucial meeting point between the
superficial and deep draining systems of the brain. This sinus originates at the
conjuncture of the inferior sagittal sinus and the great veins, behind the splenium
of the corpus callosum. It drains into the transverse sinus.
The internal cerebral vein originates behind the foramen of Monro and
courses posteriorly in the velum interpositum. It exits the velum above the pineal
body, enters the quadrigeminal cistern and joins the great vein of Galen. The
velum interpositum is a thin membranous partition in the roof of the third
ventricle. Between its folds many ventricular veins (among others, the
thalamostriate vein) course to reach the internal cerebral vein.
The basal vein of Rosenthal presents many anatomical variations. It
forms below the anterior perforated substance and courses posteriorly, between the
midbrain and temporal lobe to reach the vein of Galen. It drains the basal surfaces
of the cerebral hemispheres and is thus by didactic definition a superficial vein. It
is named together with the deep cerebral veins owing to its location.
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AN INTRODUCTION TO
The great vein of Galen passes posterosuperiorly behind the splenium of

the corpus callosum in the quadrigeminal cistern. Although only 1-2 cms in
length, it receives not only the basal and internal veins but also some of the veins
of the posterior fossa. It drains into the anterior end of the straight sinus.
INFRATENTORIAL VENOUS SYSTEM

Posterior Fossa Veins
The posterior fossa veins are best understood when cognitively linked with the two
main structures in the posterior fossa that they drain: the cerebellum and the
brainstem.
The cerebellar veins are named after the cerebellar structures which they
serve or the fissures where they course in.
The major veins related to the surface of the brainstem are named
according to their relationship to the mesencephalon, pons or medulla oblongata
and according to their course, either longitudinal or transversal. These medullary
veins also act as collecting veins for the small cerebellar veins.
The veins of the posterior fossa can be didactically divided into three
major groups according to the dural sinuses which receive their venous output: the
petrosal or anterior group, which drains to the superior and inferior petrosal
sinuses; the galenic or superior group, which collects into the great vein of Galen
and the tentorial or posterior group which gives its output to the sinuses adjacent
to the confluence of sinuses (6).
The petrosal group of veins is composed of five groups of veins: firstly
the veins which drain the anterior part of the brainstem, namely the anterior
pontomesencephalic vein, the transverse pontine vein, the lateral pontine vein,
the anterior medullary vein and the parenchymal perforating veins; secondly the
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ANATOMY
brachial veins, which course across the lateral aspect of the precentral cerebellar
fissure; thirdly the superior and inferior hemispheric veins and the veins of the
great horizontal fissure, which drain the superior and inferior surfaces of the
cerebellar hemispheres; and fourthly the veins which lie on the cerebellar side ( the
medial tonsillar vein) and the veins which lie on the medullary side (the retroolivary vein and the vein of the inferior cerebellar peduncle). The fifth group
consists of the vein of the lateral recess of the fourth ventricle.
The galenic group is composed of cerebellar tributaries (the precentral
cerebellar vein and the superior vein) and of mesencephalic tributaries (the
median anterior, the lateral anterior and lateral pontomesencephalic veins, the
lateral and posterior mesencephalic vein, the peduncular vein and the tectal
vein).
The tentorial group consists of the inferior vermian vein and the
superior and inferior hemispheric veins (6).
REFERENCE
1.
2.
3.
4.
5.
6.
Huber, Peter: Cerebral Angiography, Translated by George Bosse. Foreword by Hugo

Krayenbuhl and M. Gazi Yasargil- 2nd completely revised edition Stuttgart, NewYork- Thieme, 1982
Morris Pearse. : Practical Neuroangiography, Lippincott Williams and Wilkins, 2007
Bradac, Gianni Boris: Cerebral Angiography-Normal Anatomy and Vascular
Pathology, Springer, 2011
Garca-Gonzlez U, Cavalcanti DD, Agrawal A, Gonzalez LF, Wallace RC, Spetzler
RF, Preul MC: The diploic venous system: surgical anatomy and neurosurgical
implications. Neurosurg Focus. 2009 Nov;27(5)
Rhoton AL Jr. : The Supratentorial Cranial Space. Microsurgical Anatomy and
Surgical Approaches. Neurosurgery 51[Suppl 1]:159205, 2002
Rhoton AL Jr: The Posterior Fossa Veins. Neurosurgery, Vol. 47, No. 3, September
2000 Supplement
38 | P a g e
AN INTRODUCTION TO
7.
8.
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11.
12.
13.
14.
15.
16.
Ayanzen R.H., et al : Cerebral MR Venography: Normal Anatomy and diagnostic

pitfalls. AJNR 2000 21: 74-78
Di Chiro G : Angiographic Patterns of Cerebral Convexity Veins and Superficial Dural
Sinuses. AJR Am J Roentgenol Radium Ther Nuc Med :87. 301-321, 1962.
Duvernoy, Henry: Human Brain Stem Vessels-Second Edition, HeidelbergSpringer,1999
Osbron, Anne: Diagnostic Cerebral Angiography, Lippincott William and Wilkins,
1980
M.G. Yasargil: Microneurosurgery Vol.2, Thieme, 1994
Seeger, Wolgang: Microsurgery of Cerebral Veins, Springer-Verlag/Wien, 1984
Yasargil MG, Damur M. Thrombosis of the cerebral veins dural sinuses. In: Newton
TH, Potts DJ, eds Radiology of the Skull and Brain: Angiography St. Louis: MosbyYear Book; 1974;2:2375-2400
Browning H. The confluence of dural venous sinuses. Am J Anat 1953;93:307-329
Jin Wang. et al: Evaluation of the anatomy and variants of internal cerebral veins with
phase-sensitive MR imaging. Surgical & Radiologic Anatomy . Aug2010, Vol. 32
Issue 7, p669-674
Rhoton AL Jr: The Cerebral Veins. Neurosurgery. 2002 Oct;51(4 Suppl)
39 | P a g e
CHAPTER 3
SUBARACHNOID SPACE AND THE CEREBROSPINAL FLUID
INTRODUCTION
The meninges are three sequential membranous layers that cover the brain and
the spinal cord. They are named as follows:
The dura mater (L., tough mother) the outermost layer;

The arachnoid, beneath the dura;
The pia mater (L., tender mother), directly paving the surface of the brain
and spinal cord.
While the intracranial dura coats the bone through powerful adhesions,
the spinal dura is separated from the walls of the medullary canal. In truth, what
is considered the outer portion of the intracranial dura is actually the periosteum.
The genuine dura mater is the subjacent layer, closely adhering to the arachnoid
and forming the dural sinuses and the dural septa (the falx cerebri, falx cerebelli,
and tentorium cerebelli).
Both the arachnoid and the pia mater derive from the same mesenchymal
strata enveloping the brain. Therefore, they are commonly referred to as the piaarachnoid, with the former being the visceral portion, and the latter the parietal
portion of the same layer. Proof of this is the numerous trabeculae that bridge the
two within the so-called subarachnoid space.
The cerebrospinal fluid (CSF) is a clear, colorless fluid that fills up the
cerebral ventricles and the subarachnoid space. Only a tenth of its volume is found
within the ventricular system, the rest flowing in the subarachnoid space. CSF is
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AN INTRODUCTION TO
mostly produced in the choroid plexuses of the lateral, third and fourth ventricles,
and to a smaller degree in the spinal cord.
The importance of the subarachnoid space stems not only from the
circulation of the CSF, but also from the inclusion of the main vasculature of the
brain. Any injury brought onto the vessels supplying or draining the cerebral tissue
will most likely reverberate as a subarachnoid space hemorrhage. This chapter
is therefore dedicated to the anatomy of this space, as well as the physiology of the
cerebrospinal fluid.
THE ARACHNOID
The arachnoid is a slender and avascular membrane that borders the inner
surface of the dura, without being properly attached to it. It is weaved by fibrous
tissue and extends to the pia mater via subtle weblike trabeculae (from which it
derives its name). These trabeculae are composed of loose connective tissue fibers
including elongated fibroblasts and serve to anchor the blood vessels supplying
the brain. Underneath this layer of the meninges lies the subarachnoid space.
THE PIA MATER

The pia mater is also a subtle membrane comprised of connective tissue. Unlike
the arachnoid, however, it does contain blood vessels. It lies on the surface of the
brain and the spinal cord directly, closely following every nook and cranny. The
only regions where the pia is absent are the natural orifices between the
subarachnoid space and the fourth ventricle (foramen of Magendie and the
foramens of Luschka). The pia mater is also the continuation of the perivascular
connective tissue sheath of the blood vessels supplying these nervous structures.
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CHAPTER 3: SUBARACHNOID SPACE AND THE CEREBROSPINAL FLUID
Two layers compose this membrane: the pial intima situated deeply, and
the epipial layer that is superficial. The former penetrates the cerebral
parenchyma alongside blood vessels, whilst the latter continues the arachnoid
trabeculae. The subarachnoid space extends with the aforementioned blood vessels
as a perivascular space containing CSF, known as the Virchow-Robin space.
As a notice, both surfaces of the arachnoid, the inner surface of the pia,
and the weblike trabeculae are covered with a thin squamous epithelial layer. Both
the arachnoid and the pia mater fuse around the opening for the cranial and spinal
nerves as they emerge from underneath the dura.
SUBARACHNOID SPACE AND CISTERNS

The subarachnoid space is the only gap between the meningeal layers that is
constantly filled with fluid. As the arachnoid does not follow the contour of the
brain as intimately as the pia, an anatomic space is formed between the two. As a
result, subarachnoid space does not have the same depth as it surrounds the brain.
The more shallow portions are those respective to the gyri, while the depth
increases at the level of the brain sulci. At the base of the brain (adjacent to the
cerebral peduncles, in front of the brainstem, around the optic chasm and so forth),
the distance between the arachnoid and the pia mater is at its greatest, thus forming
the subarachnoid cisterns.
There are two types of cisterns, according to symmetry: median cisterns,
which are odd in number and situated along the median line, and lateral cisterns,
paired and placed symmetrically on both sides of the brain.
The median subarachnoid cisterns are as follows:
The cerebellomedullary cistern (cisterna magna) is the largest. It is situated

between the cerebellum and the medulla oblongata, continuous with the
fourth ventricle via the foramens of Luschka and the foramen of Magendie.
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AN INTRODUCTION TO
Found within it are the vertebral arteries, the origin of the PICA, cranial
nerves IX through XII, and the choroid plexus that protrudes from the fourth
ventricle through the foramens of Luschka.
The pontine cistern surrounds the pons anteriorly. It is most notable for
containing the basilar artery, along with the origins of the AICA and the
SCA from both sides, as well as the sixth cranial nerve.
The interpenduncular cistern, as its name suggests, lies between the two
cerebral peduncles. It is here that the basilar artery branches, forming the
posterior portion of the Circle of Willis. Also included are the PCoA, the
basal vein of Rosenthal, and the third cranial nerve.
The retrochiasmatic cistern is located just posteriorly to the optic chasm
and sets the continuation between the interpeduncular and prechiasmatic
cisterns.
The prechiasmatic cistern contains the origin of the ACA, the anterior
portion of the optic chasm and the intracranial segment of the optic nerves,
and the pituitary stalk.
The lamina terminalis cistern is situated anteriorly and superiorly to the
prechiasmatic cistern, merely rostral to the third ventricle. Found here are
arteries comprising the anterior portion of the Circle of Willis (the A1 and
proximal A2 of the ACA, and the ACoA), as well as the hypothalamic
arteries, the origin of the fronto-orbital arteries, and the recurrent artery of
Heubner (a branch arising from the proximal A2 or distal A1 and supplying
segments of the caudate nucleus, internal capsule, putamen, and septal
nuclei).
The superior cistern, or ambient cistern as it is also called, is located around
and dorsal to the midbrain. Its importance derives from containing the great
vein of Galen, the PCA, the SCA, the posterior pericallosal arteries, and the
fourth cranial nerve.
The lateral subarachnoid cisterns are as follows:
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ANATOMY
The cerebellopontine cisterns are situated in the angles formed between

the pons and the cerebellum. On each side, they contain the AICA, cranial
nerves V, VII and VIII, and the petrosal vein.
The lateral cisterns of Sylvius are found in the fissures (bearing the same
name) between the frontal and temporal lobes and they include the MCA as
well as the medial cerebral vein.
The carotid cisterns are located between the internal carotid arteries and
the respective optic nerve. Aside from the ICA, they contain the origin of
the PCoA.
In the proximity of the superior sagittal sinus, the pia mater and the
arachnoid send out small processes that pass through the dura and protrude into the
superior sagittal sinus. These are known as the arachnoid granulations of
Pacchioni. Although variable in quantity and placement, these formations have the
common purpose to drain the CSF from the subarachnoid space into the venous
system. This is achieved through the pressure gradient between the two
compartments, the venous system having the lower value.
The arachnoid villi are microscopic extensions of these granulations.
They are comprised of single-layered epithelium on the outside, a network of
connective and elastic tissue fibers on the inside, and a thin outer limiting
membrane in between.
The granulations of Pacchioni tend to increase in size and calcify with
age. The effect of these alterations on normal function is not fully understood. A
subarachnoid hemorrhage may lead to scarring of the granulations, with poor
CSF absorption as a consequence.
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AN INTRODUCTION TO
THE CEREBROSPINAL FLUID

As briefly stated above, CSF is a clear, colorless, and virtually acellular fluid that
occupies the most of the subarachnoid space and ventricles. In normal adults, the
total amount of CSF contained is approximately 125-150 ml, the majority of
which (90%) is situated solely in the subarachnoid space. All of the plasmatic
components (for example potassium, glucose, proteins, and especially sodium
chloride) are found within, however in different quantities.
The circulation rate of CSF is around 500-700 ml per day. The main sites
of production are the choroid plexuses found in every ventricle (and to some
extent the cisterna magna as well). A choroid plexus consists of numerous villi,
each one made of a single layer of cuboidal epithelial cells overlaying a highly
vascularized core of connective tissue. Plasma is processed by these cuboidal cells
and diffuses into the ventricles as CSF. This newly formed fluid escapes from the
ventricle system through the foramens of Luschka and the foramen of
Magendie, regardless from which of the choroid plexus it derives. Once inside the
cerebellomedullary cistern, CSF flows throughout the entire subarachnoid space,
bathing the brain and the spinal cord alike. A noteworthy difference between
production and drainage of CSF is that, while drainage ensues passively (at the
arachnoid granulations) in virtue of hydrostatic pressure gradient, production is
dependent on sodium-potassium ATPase and carbonic anhydrase.
CSF has multiple roles in protecting the cerebrospinal axis. As any
liquid, it acts as a mechanical dampener, diminishing traumatic forces that may
harm the brain. Also, by completely immersing the brain, it physically reduces its
weight from 1500 grams to a mere 50. Aside from mechanical protection, CSF
grants thermal stability, thus assuring optimal functionality of the nervous
system.
Cerebral nutrition is also a role provided by CSF, as well as discarding
many of the neuronal catabolism products and hematologically disseminated
pathogenic agents. Since the intracranial cavity of the adult is inextensible, any
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SECTION I:
ANATOMY
increase of intracranial pressure may damage the brain. CSF volume is the major
compensatory mechanism for intracranial pressure, any excessive production or
reduced drainage being able to cause possibly grave and irreversible injuries. As
such, internal hydrocephalus is caused by disproportionate accumulation of CSF
within the ventricles, whereas external hydrocephalus is the result of poor
absorption through the arachnoid granulations. Either of them may be the
complication of a subarachnoid space hemorrhage.
REFERENCE
1.
2.
3.
4.
5.
Sido FG. Tratat de Neuroanatomie Funcional i Disecia Nevraxului. Second

edition. Casa Crii de tiin, 2007; VII: 632-45
Ross MH, Pawlina W. Histology, a Text and Atlas. Sixth edition. Lippincott Williams
& Wilkins, 2011; 12: 383-5
Drake RL, Vogl AW, Mitchell AWM. Grays Anatomy Pentru Studeni. Second
edition. Churchill Livingstone, 2010; 8: 830-4
Wang PP, Avellino AM. Hydrocephalus in Children. In: Rengarchary SS, Ellenbogen
RG. Principles of Neurosurgery. Second Edition. Elsevier Mosby 2008; 8: 117
Dnil L, tefnescu F. Anevrismele Cerebrale. Editura Academiei Romne, 2007;
3: 45
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Left Frontal Spetzler Martin Grade 3 AVM- venous phase demonstrating superficial
drainage into the superior sagittal sinus
CHAPTER 4
IMAGING OPTIONS IN CEREBRAL VASCULAR LESIONS
CRISTINA C. ALDEA, LUCIAN MRGINEAN
COMPUTED TOMOGRAPHY (CT)

A patient with clinical diagnosis of stroke should immediately undergo an
emergency non-enhanced CT scan. This is done primarily to differentiate
between haemorrhagic and ischemic stroke. If an ischemic stroke is found, the
CT can point out whether the cause is an arterial or a venous infarction. If
intracranial hemorrhage is confirmed, this investigation permits localization of the
bleeding (table 1) and establishes whether the cause is vascular or non-vascular
(tumor, infection).
Intracranial hemorrhage
Intraaxial hemorrhage
Extraaxial hemorrhage
Intracerebral
Intraventricular
Epidural Hemorrhage
Hemorrhage
Hemorrhage
Basal ganglia
Subdural Hemorrhage
Hemorrhage
Lobar Hemorrhage
Subarachnoid Hemorrhage
Pontine
Hemorrhage
Cerebellar
Hemorrhage
Table 4.1: Classification of Intracranial Hemorrhage Based on its Location
CT is ideal in emergency settings because of its cost-time efficiency and
its high sensitivity in detecting acute blood in the intracranial compartment. Acute
blood is markedly hyperdense in comparison with normal brain parenchyma;
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AN INTRODUCTION TO
consecutively if the amount of hemorrhage is large enough and the scan is

performed early, the diagnosis is seldomly missed. In case of spontaneous
intracerebral hematoma, the hematoma appears on CT as a markedly hyperdense
area surrounded by a ring of low density (corresponding to the area of perifocal
edema). At 7-10 days from the onset of the hemorrhage the hyperdensity of the
blood attenuates from the periphery towards the center of the hematoma. If the
hematoma is small, it will become izodense in 2-3 weeks and in 2 months if it is
larger in size. After 2-4 months the space occupied by the hematoma will be
replaced by a liquid cavity. In case of an ischemic stroke, the region corresponding
to the territory of the obstructed vessel appears hypodense in comparison with
normal brain parenchyma (3) .
Image 4.1: Left Lobar Hemorrhage on non-e. CT
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VASCULAR LESIONS
CHAPTER 4: IMAGING OPTIONS IN CEREBRAL VASCULAR

LESIONS
Clinical suspicion of subarachnoid hemorrhage is always followed by

investigations which permit confirmation of the clinical diagnosis and establishing
the underlying cause (the source of hemorrhage). CT provides information about
the location and type of intracranial hematoma (if it exists), the coexistence of
hemorrhage in other intracranial compartments (e.g. acute subdural hematoma),
size of the ventricles (literature data reports the incidence of acute hydrocephalus
following SAH in the range of 15 to 31 % (5,6) ), the presence of ischemic
lesions (due to vasospasm), the amount of SAH (important prognostic factor for
vasospasm and pretruncal hemorrhage), the location of the aneurysm in 70 % of
cases (e.g. ACoA aneurysm- predominantly interhemispheric hemorrhage, ACM
and ACoP hemorrhage in Sylvian fissure) and it may point out the source of
bleeding in case of multiple intracranial aneurysms.
SAH appears as hyperdense substance filling the normally hypodense,
CSF- filled subarachnoid spaces. These findings are most visible in the larger
subarachnoid spaces such as the suprasellar cistern and the Sylvian fissure.
Blood in these two spaces appears as the characteristic star-sign on the CT-scan.
Non-contrast CT scan detects SAH in 95% of cases in the first 48 hours
from aneurysmal rupture. After 5 days, 58% of patients have normal CT scans (1) .
CT can confirm SAH but can rarely detect the underlying cause. If the
source of bleeding is not found, the patient must undergo a CTA and afterwards, if
there is still no certitude about the source of bleeding, an angiography. If the
angiography is also negative, an occult aneurysm or other cause of SAH must be
considered.
Contrast enhanced CT is performed for differential diagnosis with other
intracranial processes or if the examination is done late after the onset of the
bleeding. Between the 1st and 6th week a ring enhancement can be observed, this
disappears in 2-6 months and is due to the peripheral hypervascularisation of
the hematoma and damage to the blood-brain barrier.
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AN INTRODUCTION TO
The diagnosis of AVMs is dependent on imagistic studies. These studies

will confirm the existence, the characteristics, dimensions and will identify the
afferent and efferent vascular components of the malformation.
Clinical symptoms of AVMs are highly suggestive. Most patients present
with ictal debut (bleeding of AVM) consecutive to an epileptic fit without family
history of epilepsy or previous seizure history or pregressive neurologic deficit.
All these symptoms pointing towards an expansive intracranial process must be
investigated through an emergency CT scan (hemorrhagic the lesion or not). This
investigation provides data regarding the localization of the AVM, its
dimensions, and, if it has ruptured, the location of the hematoma.
On non-contrast enhanced (or native) CT, the AVM appears as a
hyperdense lesion. It can be located anywhere in the brain and is usually observed
as a triangular formation with the base of the triangle oriented towards a
ventricle. Other aspects may be encountered, the form and extent of AVMs being
extremely variable. Small calcifications at the level of lesion or in perilesional
area may be noted. Contrast enhanced CT will contour the AVM, as well as its
feeding arteries and draining veins. In case of a ruptured AVM the dimensions and
the extent of hemorrhage can be evaluated. The lesion itself is difficult to
visualize on native CT, but enhancement will make the lesion and/or its tributary
vessels visible, if the hematomas effect is not that huge to mask the AVM.
If the AVM or the hematoma resulting from its rupture was confirmed
with CT and the clinical data also indicates a vascular malformation (young patient
without significant history of hypertension, suggestive localization) will oblige to
continue the investigations in order to precisely characterize the lesion. CT is
also a helpful aid in postoperative evaluation of patients, when clinical evolution is
not favorable or for follow up of the lesion in time.
Cavernomas appear on CT as hyperdense lesions (because of their
impregnation with hemosiderin). They have an inhomogeneous, well contoured,
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LESIONS
round shape. Some may present calcifications and/or contrast enhancement

(tardive, due to the low flow inside the lesion).
COMPUTED TOMOGRAPHY ANGIOGRAPHY (CTA)

CTA is used to search for an underlying vascular cause of a bleeding prior
confirmed by conventional CT. It is especially useful in SAH and
intraparenchymal hematoma where primary hemorrhage is less likely based on
patient history.
Some centers report a sensibility of 98% of detection of aneurysms up to
2,2 mms (1). A number of authors advocate that CTA should be the most
important method of evaluation and preoperative planning both for aneurysms and
for AVMs (2) . The advantages of CTA are many: it is fast and non-invasive, it
offers the possibility of three dimensional evaluation of structures with digital
subtraction, which excludes the artifacts caused by bony structures (e.g. osseous
subtraction shows ACoP aneurysms), it allows the morphologic reconstruction of
the aneurysm and is not dependent on the permeability of the parent vessel or by
the aneurysmal sac. It is also an important aspect that CTA is readily available in
emergency conditions which allows immediate precise diagnosis and surgical
treatment .
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AN INTRODUCTION TO
Image 4.2: CTA reconstruction demonstrating a left MCA aneurysm

MAGNETIC RESONANCE IMAGING (MRI)
MRI is requested particularly in search of an underlying pathology, especially if a
tumor is suspected. Identifying the hemorrhage on MRI is challenging because the
blood changes in its appearance based on the sequence, the size and location of
bleed and the time elapsed from the onset of the hemorrhage. These parameters
modify the type and distribution of paramagnetic substances in the affected brain
parenchyma.
In the first 48 hours after the hemorrhage MRI has low sensibility for
detecting the acute blood. This investigation offers useful information after 4-7
days. MRIs most important aid is that it is of help in detecting SAH after 10-20
days from the onset. After this interval it can detect the source of the hemorrhage
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LESIONS
and it can point towards the location of an aneurysm, if this is the cause of the
bleeding. The fact that the pathologic modifications remain visible for a long time
period is very useful in multiple intracranial aneurysms (1) .
Image 4.3: MRI demonstrating 2 right MCA aneurysms

In case of a previously confirmed AVM on CT, performing an MRI offers
a helpful aid. It is a high accuracy non-invasive investigation, it demonstrates the
exact dimensions and the relationship of the lesion with the surrounding neural
structures. On MRI an AVM appears as a tangle of serpentine curvilinear
hypointense tubules. The high flow velocity inside the lesion may mask
Gadolinium enhancement. AVMs typically do not present perilesional edema.
This fact allows the differential diagnosis with a tumor with recent hemorrhage.
Often, in complementing the CT with help of the MRI information is gained
regarding the microanatomy of the nidus, feeding arteries and draining veins.
Association with MRA completes the anatomic details and offers invaluable
information for planning the surgical approach.
MRI is the gold standard for the diagnosis of cavernomas. They appear
as inhomogeneous, well circumscribed lesions with a characteristic salt and
pepper appearance. They may be surrounded by a ring of low signal because of
54 | P a g e
AN INTRODUCTION TO
the peripheral deposits o hemosiderine. Cavernomas are not contrast enhancing

lesions.
Image 4.4: Typical Appearence of Cavernoma on MRI in T2 sequence

MAGNETIC RESONANCE ANGIOGRAPHY (MRA)
Multicenter studies demonstrated that MRA routinely detects aneurysms as small
as 3mms in diameter (1,6). With this method the morphology of aneurysms can
accurately be studied. Its major advantage is that it offers the possibility of three
dimensional study of the aneurysm and the surrounding neural structures. This is
a major advantage also in the preoperative planning preceeding AVM surgery.
MRA can also be used to complement angiographic studies, especially in
cases when angiography failed to locate the source of the hemorrhage despite the
CT being very suggestive for aneurysmal rupture. In elderly patients and in those
allergic to iodinated contrast material used in both CT and angiography, MRA
remains the only diagnostic option.
MRA allows watchful waiting in case of aneurysms or AVMs found
incidentally, and helps the therapeutic decision by monitoring the evolution of the
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LESIONS
lesion. It can also be performed as a screening test in patients with first degree
relatives with cerebral aneurysms. This category of patients have a high risk for
developing cerebral aneurysms themselves.
Image 4.5: MRA reconstruction demonstratin a right occipital AVM

ANGIOGRAPHY
Catheter angiography is an invasive procedure which is only performed in cases
in which an underlying vascular abnormality is clinically suspected, but the
previously performed CTA was failed to identify the underlying cause. It is also
used in cases where further details about a previously identified lesion are needed
or if the further endovascular treatment of the identified lesion is desired.
In the past, in the absence of non-invasive imaging procedures like CT
and MRI, angiography was used as a method for investigating intracerebral
hematomas, midline shifting of vessels (particularly veins which are more
56 | P a g e
AN INTRODUCTION TO
adherent to the surrounding brain parenchyma than arteries) being an indicator of

an intraparenchymal hematoma and its mass effect (4).
Today, angiography is still considered to be the gold standard in
evaluating cerebral aneurysms. Angiography demonstrates the source of the
bleeding, in up to 80-85% of cases and it also shows the presence of vasospasm
(narrowed vessels).
Typically, a four-vessel angiography is carried out in every patient
(examining the two internal carotid arteries and the two vertebral arteries). This
is done in order to detect other possible aneurysms and the stat of the collateral
circulation. In performing an angiography the vessel with highest suspicion of
harboring the aneurysm is the first to be examined, in case the procedure has to be
prematurely abandoned. Before concluding the angiography it is necessary to
study the emergence of the PICA bilaterally and the flow in the ACoA (3).
Image 4.6: Aneurysm of the Carotid Artery

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LESIONS
In case of a previously demonstrated AVM, angiography provides

information on the flow velocity inside the lesion and additional information
regarding its anatomic relationships.
Using high velocity imaging, image zoom and different angles details
about the AVM feeders, draining veins and nidus can be obtained. Regarding the
flow dynamics inside the lesion, angiography is the sole investigation that can be
implied. If the chosen treatment modality is not endovascular obliteration of the
lesion the angiographic evaluation should be performed as close to the operative
moment as possible, because AVMs have the tendency of modifying their
dimensions and draining trajectories, especially if the initial presentation was
bleeding. Supplementary feeders or draining veins may appear which were either
masked by the hematoma in the acute phase or thrombosed. The four vessel
angiography allows identification of clinically silent lesions. It is important to
note that not every AVM can be identified with routine angiography.
Angiographically occult AVMs are small, high velocity lesions with partial
thrombosis at the level of the nidus.
Cavernomas are the classic prototype of angiographically occult
lesions. The site of the cavernoma appears as an avascular region with a high
density of capillaries. This is due to the fact that the cavernoma does not possess
feeding vessels and that the blood stagnates inside the lesion. Consequently
angiography is not used in their diagnosis and endovascular techniques cannot be
applied in their treatment.
Complications of angiography may include ischemic events; alteration of
the patients neurologic status after 24-72 hours; high intraluminal pressure
changes during the injection of the contrast agent which may precipitate
aneurysmal rupture; systemic hypertension; vasospasm; complications at the site
of catheterization (hematoma, pseudoaneurysm).
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AN INTRODUCTION TO
Image 4.7: Left Frontal Spetzler Martin Grade 3 AVM arterial phase
demonstrating the feeding arteries from the left ACA
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LESIONS
Image 4.8: Left Frontal Spetzler Martin Grade 3 AVM- venous phase
demonstrating superficial drainage into the SSS
REFERENCE
1.
2.
3.
4.
5.
Florian IS, Perju-Dumbrav L. Opiuni Terapeutice n Accidentele Vasculare

Hemoragice. Editura Medical Universitar IuliuHaieganu Cluj-Napoca 2007
Morris Pearse. : Practical Neuroangiography, Lippincott Williams and Wilkins, 2007
Osbron, Anne: Diagnostic Cerebral Angiography, Lippincott William and Wilkins,
1980
Huber, Peter: Cerebral Angiography, Translated by George Bosse. Foreword by Hugo
Krayenbuhl and M. GaziYasargil- 2nd completely revised edition Stuttgart, NewYork- Thieme, 1982
Woernle CM, Winkler KM, Burkhardt JK, Haile SR, Bellut D, Neidert MC, Bozinov
O, Krayenbhl N, Bernays RL:Hydrocephalus in 389 patients with aneurysm-
60 | P a g e
AN INTRODUCTION TO
6.
associated subarachnoid hemorrhage, J ClinNeurosci. 2013 Jun;20(6):824-6. doi:

10.1016/j.jocn.2012.07.015. Epub 2013 Apr 4
Pierot L, Portefaix C, Rodriguez-Rgent C, Gallas S, Meder JF, Oppenheim C: Role of
MRA in the detection of intracranial aneurysm in the acute phase of subarachnoid
hemorrhage. J Neuroradiol. 2013 Jul;40(3):204-10
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Main aneurysm sites
CHAPTER 5
SUBARACHNOID SPACE HEMORRHAGE
INTRODUCTION
The term subarachnoid space hemorrhage (SAH) denotes the extravasation of
blood in the space between the pial and arachnoid membranes of the meninges. It
can be either spontaneous, or as a result of trauma. However, the more common
usage of this term indicates non-traumatic hemorrhage (as a consequence of either
aneurysmal or arteriovenous malformation rupture). From a quantitative point
of view, SAH can range from insignificant to a massive amount. The blood may
originate from a vessel situated in the subarachnoid space (mostly arteries, while
veins rupture in the case of arteriovenous malformations), or from a parenchymal
hemorrhagic lesion that invades the ventricle system or lacerates the pia mater.
The arachnoid is a thin meningeal membrane weaved of fibrous tissue. It
stands underneath the dura mater and, although not attached, the two layers
strongly adhere to one another. On the other hand, the pia mater is more reclusive
in relationship with the arachnoid, and the weak bonds between the two are
comprised of fibrous trabeculas and connective tissue. As a result, a seemingly
virtual space is formed, namely the subarachnoid space.
The subarachnoid space houses cranial nerves and the main vessels
(including the arterial Circle of Willis). It can be divided into numerous chambers,
known as cisterns. The cerebrospinal fluid (CSF) originating from the ventricle
system passes through the medial foramen of Magendie and the two lateral
foramens of Luschka (belonging to the fourth ventricle) and into the cisterna
magna (the largest of cisterns, as its name suggests). From here on, the CSF can
either flow inferiorly into the spinal subarachnoid space, or anteriorly and laterally
into the other subarachnoid cisterns. Subarachnoid vessels resting in the cerebral
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AN INTRODUCTION TO
sulci send (or receive) branches into (or from) the parenchyma. These branches are
also included in a narrow continuation of the subarachnoid space, a perivascular
space filled with CSF, commonly referred to as the Virchow-Robin space.
Subarachnoid space hemorrhages account for a small number of strokes,
most of which are caused by aneurysmal rupture. Patients with arteriovenous
malformations or an unknown cause of SAH usually have a higher outcome than
patients harboring aneurysms. The most dreaded complication of SAH is
vasospasm, aggravating cerebral perfusion in an already damaged brain. It is
obvious why the causes of SAH need to be researched quickly and thoroughly, and
why treatment must be established to minimize not only the hemorrhage itself, but
the effects of vasospasm as well.
CLASSIFICATION (CLINICAL GRADING)

Clinical grading is essential in determining the patients condition on arrival, the
prognostic and possibilities of treatment. The Hunt and Hess Grade and the
Fisher Grade are detailed below. The Hunt and Hess grades are given in
accordance to the patients symptomatology and the Fisher Grade classifies the
appearance of SAH on CT scan.
A common rule is shared by these grading scales: the lower the grade,
the better the outcome. In the Hunt and Hess system, grades I-III are generally
associated with a favorable prognostic, while grades IV and V imply a poor
scenario. Patients diagnosed with a higher score generally require stabilization to
grade III before surgery can be performed. This system correlates well with patient
outcome. Fisher Grade has been shown to accurately predict the likelihood of
symptomatic cerebral vasospasm.
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CEREBROVASCULAR DISEASE
CHAPTER 5: SUBARACHNOID SPACE HEMORRHAGE
Grade
Description
Asymptomatic / mild headache / slight nuchal rigidity
II
Moderate to severe headache and nuchal rigidity / no deficits other

than cranial nerve palsy
Drowsiness / confusion with mild focal neurologic deficit
III
IV
V
Stupor, moderate to severe hemiparesis, early decerebration and

vegetative state
Deep coma, decerebration, moribund state
Table 5.1: Hunt and Hesss Grading of SAH
Grade
Appearance of Blood on Head CT Scan
No blood detected
II
Diffuse deposition / thin layer with all vertical strata of blood (in
interhemispheric fissure, insular cistern, or ambient cistern) less
than 1 mm in thickness
III
Localized clots and/or vertical strata of blood 1 mm or more in

thickness
IV
Intracerebral / intraventricular clots with diffuse or no

subarachnoid blood
Table 5.2: Fishers Grading

Because a recent grading scale has gained widespread usage among
neurosurgeons, it should be mentioned. The World Federation of Neurologic
Surgeons (WFNS) has established a SAH grading scale based on the onadmission Glasgow Coma Scale of the patient, associated with the presence of the
motor deficit.
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EPIDEMIOLOGY
Aneurysmal rupture stands at an annual rate of 12 cases per 100,000 population.
This is especially the case of patients in the 5th or 6th decades. The risk is higher
in Afro-Americans than in Caucasians and the incidence of SAH is greater in
women. SAH from aneurysmal rupture is a prominent cause of maternal
mortality (up to 25% of maternal deaths), being expressly heightened in the third
trimester of pregnancy.
Although mortality rates have decreased in the last 30 years, SAH still
stands as an overwhelming neurologic problem, with an estimated 10-15% of
patients dying before ever reaching the hospital. Death occurs in about 25% of
patients within the first 24 hours, regardless of medical attention received. Nearly
half of the affected individuals do not survive over 6 months, and a third of those
who endure have major, irreversible neurologic deficits.
ETIOLOGY
Traumatic head injury is by far the leading cause of subarachnoid hemorrhage.
In the case of spontaneous (or non-traumatic) SAH, rupture of saccular
aneurysms account for 80% of instances, while the rest result from the rupture of
mycotic aneurysms, arteriovenous malformations, neoplasm, or cortical
thrombosis. A lacerated intraparenchymal hematoma may also result in the
presence of blood in the subarachnoid space.
Both congenital and acquired factors are believed to take part in the
etiology of SAH. This is particularly emphasized by the association of aneurysms
with specific congenital diseases (Marfan syndrome, Ehlers-Danlos syndrome,
polycystic kidney disease, coarctation of the aorta, fibromuscular dysplasia).
Also, patients harboring multiple aneurysms have a significantly higher risk of
SAH. Aside from these, any acquired cause of aneurysmal rupture (factors that
brusquely heighten arterial hypertension) is considered an etiologic factor.
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PATHOPHYSIOLOGY
The blood escaping from an aneurysmal breach can vary from minute warning
leaks to massive amounts that lead to death. In most instances, probability of
rupture is directly proportional to the size of the aneurysm (based on La Places
Law stating that the larger the vessel radius, the larger the wall tension required to
withstand a given internal fluid pressure). Therefore, aneurysms with a diameter of
up to 5 mm have only a 2% chance to rupture, 40% of those with diameters
between 6-10 mm are already bleeding upon discovery. Paradoxically, large and
giant aneurysms rupture less frequently, so the rule seems to apply only to small
aneurysms (below 12 mm).
The consequences of SAH may change with the location of the bleed,
volume of CSF space, patient age, premorbid conditions (if present), cerebral
metabolism, systemic dysfunctions and electrolyte disturbances. Hypertension is
not only a cause of HAS of aneurysmal origin, but also a leading factor in
aneurysmal development. Because of hypertension, blood is released into CSF
space under high pressure, this in itself being able to engender damage to local
tissues. High flow rates of aneurysms with wide breaches produce large volume
SAH in a short amount of time. In this scenario, intracranial pressure rises
abruptly. Conversely, an aneurysm with a continuous leak may gradually escalate
SAH, progressively increasing intracranial pressure and slowly worsening the
clinical Grade of the patient. Blood extravasation elevates intracranial pressure,
while the presence of blood can irritate the meningeal layers. Its toxic effects can
result in global ischemia, mitochondrial respiration alterations with lactic
acidosis and cellular membrane ATPase dysfunction, and disturbances in calcium
and potassium serum levels.
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Figure 5.1 Aneurysm rupture

Cerebral perfusion is altogether reduced following SAH, and even more
so in the case of cerebral vasospasm. The cerebral metabolic rate of oxygen is
also significantly diminished. These values remain decreased for a few weeks after
this event, possibly foreshowing cerebral infarction. Autoregulation suffers
impairment (causing vasomotor paralysis), as evidenced by alterations in systemic
blood pressure and partial pressure of carbon dioxide.
CLINICAL FEATURES
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Sudden onset of excruciating headache is the central feature of SAH. It is

described appearing as a bolt out of the blue (hence named thunderclap
headache) and patients refer to it as the worst headache of my life. Some
individuals present with warning bleeds that trigger cephalgia of variable
intensity and possibly associated with nausea, vomiting, and giddiness. This
warning hemorrhage is exceedingly important to identify on time to prevent a
catastrophic SAH.
Sudden loss of consciousness (LOC) occurs as intracranial pressure
exceeds cerebral perfusion pressure. It affects 45% of patients and the severity
varies from a state of drowsiness and mild confusion to deep coma. The amount
of bleeding and the location of the aneurysm have a strong influence on the
duration of the comatose state.
Meningeal irritation syndrome (nuchal rigidity and pain, photophobia)
is caused by the presence of blood and its irritative effect in the subarachnoid
space. It is highly evocative and can occur in as many as two thirds of patients,
although only after a delay of several hours following the rupture event.
Visual loss manifests as a consequence of venous hypertension and
disruption of retinal veins and retinochoroidal anastomoses. The mechanism of
this is either compression, or increase of the intracranial pressure. Three types of
ocular hemorrhages have been described: subhyaloid (pre-retinal), intra-retinal,
and vitreous (the so-called Terson syndrome). Visual loss may spontaneously
resolve in 6-12 months, or may lead to irreparable visual deficit.
Among the focal neurologic deficits described, mono- and hemiparesis,
diplopia, and extraocular movement impairment are the most common. 3rd
cranial nerve palsy (the eye is angled down and out) is most likely the result
of compression from a Posterior Communicating Artery aneurysm.
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MANAGEMENT STRATEGIES
First of all, it is recommended that all patients suffering from SAH (regardless of
their clinical condition) should be admitted into the intensive care unit until the
etiology of hemorrhage is identified. Patients must not be allowed out of bed and
mobilization should be reduced to a minimum (just enough to prevent deep
venous thrombosis). Limited visitors and external stimulation (including
lighting) are also highly suggested. Nevertheless, it is mandatory to maintain
frequent neurologic evaluation, analgesia (but cautiously), pulse, hematocrit and
oxygen monitoring. Fluid intake should also be regulated.
Proper history of the patient, physical examination and assessing
Airway, Breathing and Circulation (properly coined the medical ABC) are
obligatory, since treatment is based on these variables. Endotracheal intubation
should be performed for comatose patients and those unable to protect their
airway. Intratecal thrombolytics such as recombined tissue plasminogen
activator (rtPA) may be required to reduce the risk of rebleeding. Because the
patient should be kept abed, placing a Foley catheter for urine output is
recommended.
The traditional medical treatment consisted of strict blood pressure
control with antihypertensive therapy and fluid restriction. Nowadays,
antihypertensive agents are advocated only when mean arterial pressure surpasses
130 mmHg, as the traditional treatment was incriminated for having high
mortality and morbidity rates. Arterial pressure should be kept at optimal levels, so
that cerebral perfusion is not affected. Most clinicians avoid using nitrates
(nitroglycerin), which increase intracranial pressure. Instead, the agents of
choice in patients without contraindications are beta-blockers, easily titrated and
have little if no influence on intracranial pressure. Calcium channel blockers
(nimodipine) do have a tendency to increase intracranial pressure, although not as
much as nitrates. The advantages of Triple H therapy (hypertension, hypervolemia
and hemodilution) are controversial.
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An angiogram can reveal the site of rupture, although some studies

debate on whether the use of angiographic dye may cause cerebral vasospasm. If
intracranial pressure is well controlled and, in general, the age of the patient is
under 65 years, a craniotomy can be performed immediately. Is preferable to
remove large flaps of bone, as to avoid brain herniation and strangulation. In
elderly patients who present with co-morbidities, or improperly controlled
intracranial pressure, the prospect of endovascular approach can be considered.
The treatment of complications ensuing SAH will be presented in the following
chapter.
REFERENCE
1.
2.
3.
4.
5.

Hemoragice. Editura Medical Universitar Iuliu Haieganu Cluj-Napoca 2007;
2.2.3: 107-116
4: 73-85
Kato Y, Sano H. Subarachnoid Hemorrhage. In: Kalangu KKN, Kato Y,
Dechambenoit G. Essential Practice of Neurosurgery. Access Publishing Co., Ltd,
2009; IV.3: 446-458
Becske T, Lutsep HL. Subarachnoid Hemorrhage. Medscape Reference. Cited 11 th
Jan 2014
Greenberg MS. Handbook of Neurosurgery. Seventh Edition. Thieme, 2010; 30:
1034-1044
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CHAPTER 6
COMPLICATIONS OF SUBARACHNOID SPACE HEMORRHAGE
INTRODUCTION
Complications following SAH can be divided into two categories, neurological
and medical. Although it was believed that the elevated mortality and morbidity
rates of SAH were assigned to neurologic complications, recent evidence tends to
confer medical complications a much more substantial role than before. Usually,
the poorer the patients state on admission means the higher the probability to
develop complications.
1.
Neurological complications:
Rebleeding
Hydrocephalus
Seizures
Vasospasm
2. Medical complications:
Cardiovascular dysfunction
Hypertension
Hyperglycemia
Hyponatremia
Deep Venous Thrombosis (DVT)
Pulmonary dysfunction
Gastrointestinal dysfunction
The two most dreaded of these are definitely rebleeding and
vasospasm. The most scarring and disabling of all, these two have the highest
mortality rates of all SAH complications. The majority of authors therefore
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AN INTRODUCTION TO
recommend a more assertive approach toward these patients, starting with

admission in intensive care, even should their general condition be good.
A. NEUROLOGICAL COMPLICATIONS
REBLEEDING
The incidence of rebleeding is greatest within the first 2 weeks, the peak looming
between the initial 24-48 hours and affecting about 4% of the patients. Afterward,
the incidence hovers at around 1.5% per day, thus 12-20% of individuals present
with rebleeding in the later 12 days and 50% in the following 6 months. Mortality
stands at staggering 50% within the first month. A high grade on the Hunt and
Hess scale indicates a great chance of this complication. The best chance for the
patient is either immediate surgical clipping of the ruptured berry aneurysm, or
endovascular obliteration, the choice depending on the location and neck of the
aneurysm, and, of course, hospital staff experience and availability.
Patients who have survived the initial SAH have a greater chance of
redeveloping SAH than the general population. Even though the aneurysmal cause
is identified and properly treated, the long-term risk of re-rupture remains.
Therefore, efficient screening for new aneurysms in these patients is enormously
worthwhile.
HYDROCEPHALUS
Hydrocephalus can either be an acute or a delayed complication of SAH. An
obstructive mechanism of acute post-SAH hydrocephalus is considered, with the
greatest implications being the impediment of CSF flow through the Sylvian
aqueduct, the fourth ventricle, or absorption through the arachnoid
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CHAPTER 6: COMPLICATIONS OF SUBARACHNOID

HEMORRHAGE
granulations. The onset is within the first 24 hours, although it can be postponed
to as much as one week.
Risk factors that precipitate the development of hydrocephalus include
increased age of the patient, radiologic factors (intraventricular hemorrhage,
diffuse SAH and intraparenchymal hematoma), use of antifibrinolytic drugs,
arterial hypertension, seizures, loss of consciousness, and certain locations of
aneurysms (especially those involving the posterior cerebral circulation).
Among the most evocative clinical features are abrupt mental status changes, such
as lethargy, stupor, or coma. The most lethal alterations are brainstem
compression and occlusion of blood vessels.
Nearly half of cases of acute post-SAH hydrocephalus resolve
spontaneously. In case sudden improvement does not occur, ventriculostomy is
the recommended course of action. Precautions must be taken in order to avoid
sudden decrease of intracranial pressure (which may itself increase the risk of
rebleeding) or infections.
Chronic or delayed hydrocephalus is caused by increased adhesion
between the arachnoid and the pia mater, and the scarring of the arachnoid
granulations of Pacchioni. It occurs in 3 weeks following SAH and manifests with
incontinence, gait instability, and progressive cognitive dysfunction. Half of
patients may require permanent ventricular drainage in order to achieve
amelioration.
SEIZURES
Rupture of aneurysms situated in the middle cerebral artery territory typically
results in seizures. These appear in 13-24% of patients within the first 24 hours
and can be partial, generalized or complex-partial. Seizures are inherently a risk
factor for rebleeding, as they may lead to hypertension, increased cerebral blood
flow, and elevated intracranial pressure.
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Since phenytoin can attain rapid therapeutic concentration through

intravenous load and does not cause alterations in consciousness, it is the agent
of choice in treating this complication. Long-term anticonvulsants are not
recommended if the patient is without a history of seizures prior to SAH.
CEREBRAL VASOSPASM
Cerebral vasospasm is the most severe, and therefore most feared, complication
following SAH of aneurysmal origin. Rarely, it can also occur after trauma, in
which case hemorrhage may or may not be present. Vasospasm has two
definitions:
1.
Delayed Ischemic Neurological Deficit (DIND), also known as

symptomatic vasospasm, is characterized by decreased level of
consciousness with focal neurological deficits. As its name suggests, a
variable time gap stands between the onset of SAH and the neurologic
deficit.
2. Radiographic vasospasm, or angiographic vasospasm, is described as
arterial lumen narrowing shown on angiography, with slowing of contrast
filling.
These two entities may coexist, or appear independently. Most patients
(20-70%) present with radiologic vasospasm, while only a fraction (20-30%)
develop neurological deficit.
From a clinical standpoint, vasospasm may be indistinguishable from
rebleeding or delayed hydrocephalus. It is usually insidious and manifests with
general symptoms such as decrease in level of consciousness, meningeal signs and
confusion, and focal symptoms, for example headache, focal motor deficit and
cranial nerve palsy.
Depending on the location of the ruptured aneurysm (or cause of SAH),
two syndromes have been described:
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HEMORRHAGE
Anterior Cerebral Artery (ACA) syndrome, essentially comprised of

frontal lobe deficit (apathy, confusion, attention deficit, bradypsychia,
urinary incontinence);
Medial Cerebral Artery (MCA) syndrome, as evidenced by hemiparesis,
aphasia and apraxia (inability to perform complex movements).
Vasospasm has a typical onset on the 3rd day after SAH has occurred, but
no later than 17 days following hemorrhage. This, however, depends on whether
the patient has had a prior SAH. In patients with previous SAH, the day of onset
is nearer to the earlier limit, while the patients experiencing the first SAH
develop vasospasm closer to the later limit of the interval. The culmination of
vasospasm is around days 6-8 after hemorrhage and the resolution is usually on the
12th day.
Pathophysiology is still disputed. There are many theories regarding the
narrowing of arteries, although studies in humans and animals have revealed that it
is not the result of architectural thickening of the vessel walls (thus disaffirming
the hypothesis of endothelial proliferation). Most likely, vasospasm is actually a
multifactorial, profound vasoconstriction as a response to vasoactive substances
(noradrenaline, prostaglandins, plasmin, fibrin degradation products, angiotensin,
or serotonin) in the subarachnoid space. Presently, the most studied etiologic
factors are hemoglobin and endothelin. Inflammation and immunoreactive
processes might also be incriminated.
Among the known risk factors of vasospasm are as follows:
1.
2.
3.
4.
5.
6.
7.
8.
High Hunt and Hess grade on admission

Placement and number of blood clots (high Fisher Grade)
Clinically severe SAH
Large volume of blood in the subarachnoid space
Female sex
Age less than 35 and more than 65 years
Smoking
Arterial hypertension
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AN INTRODUCTION TO
9.
10.
11.
12.
Hypovolemia
Location near the proximal 9 cm of ACA or MCA
Incomplete Circle of Willis
Angiographic dye administration (controversial)
Diagnosis of vasospasm is by method of exclusion of other causes of

neurological deficit, which are rebleeding, hydrocephalus, cerebral edema,
seizures, cerebral hypoxia, sepsis, and metabolic disturbances (hyponatremia).
Transcranial Doppler (TCD) is a non-invasive method for diagnosing cerebral
vasospasm. Whenever vasospasm is present, the velocity of blood flow increases
(above 200 cm/s), which is detected by the TCD. MCA is the most often used
vessel in this purpose. Increased blood flow may yield false negative results,
which should be taken into consideration.
Prevention of vasospasm is primarily achieved trough early surgery (by
evacuation of clots, ventricular drains of blood and reducing the chances of
rebleeding), although tempestuous handling of vessels may actually increase the
chance of vasospasm. Avoidance and treatment of hypertension, hypovolemia,
infection and anemia may also alleviate the severity of this complication.
Early surgical treatment of rebleeding represents the most important
method of prevention of vasospasm. Conversely, aneurysmal clipping can
essentially increase the risk of vasospasm by aggressive behavior toward arteries.
The risk of this complication can be diminished through intraoperative irrigation
of the subarachnoid space with thrombolytic substances (such as urokinase,
recombined tissue Plasminogen Activator, papaverine and, more recently,
nicardipine). In the case of refractory vasospasm affecting larger vessels, Trans
luminal Balloon Angioplasty can be used to dilate the narrowed arteries. Cervical
sympathectomy has fallen into desuetude.
Medical management targets vasospasm, with the additional goal of
granting neuroprotection. At the core of this method lies the Triple-H therapy,
represented by hypertension, hypervolemia and hemodilution, which has
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HEMORRHAGE
promising results. Calcium channel blockers (such as Nimodipine and

Nicardipine) are also used due to their smooth muscle relaxation effect and their
neuroprotective action (Nimodipine especially). Other neuroprotective agents are
NMDA receptor antagonists (Nuedexta) and Free Radical scavengers
(antioxidants).
Patient monitoring should include maintenance of systolic pressure
above 120 mmHg, isotonic substance perfusions and normal maintenance of
systemic vascular resistance. Electrocardiography may be performed for elderly
patients. Careful monitoring of the side effects of medical treatment is also
mandatory.
B. MEDICAL COMPLICATIONS
CARDIOVASCULAR DISFUNCTIONS
Arrhythmias occur in the initial stages of SAH and can affect as many as 90% of
patients. They are the result of subendocardial and myocardial infarction, and
coronary vasospasm due to high levels of systemic and myocardial noradrenalin
(released as a response to stress and pain during SAH) and potassium depletion.
Mostly benign, only those associated with hypokalemia are considered life
threatening.
The most common examples of arrhythmias following SAH include:
Premature ventricular complexes

Bradyarrhythmias
Supraventricular tachycardia
Ventricular flutter
Ventricular fibrillation
Torsade de Pointes
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AN INTRODUCTION TO
Treatment of this complication is rather difficult. The Triple H therapy

employed to prevent secondary cerebral infarction may actually exacerbate an
already existent myocardial ischemia. Contrariwise, myocardial infarction therapy
(such as nitrates) may in fact increase intracranial pressure, lower cerebral
perfusion pressure, and aggravate cerebral ischemia. Some patients may require
insertion of a pacemaker in the event of sustained bradycardia. However this may
also decrease cerebral perfusion pressure.
HYPERTENSION
Arterial pressure may increase prior to aneurysmal rupture as a response to stress
factors, or after this event as a means to compensate for the decrease in cerebral
perfusion pressure. The latter situation is known as the Cushing phenomenon.
Mild sedation might prove sufficient in the maintenance of arterial
pressure, whereas antihypertensive medication may only be given should
sedatives fail. The true purpose of treating hypertension is not a rapid decrease in
arterial pressure, but preserving a balance between maintaining cerebral perfusion
pressure and diminishing the risk of vasospasm and rebleeding.
HYPERGLYCEMIA
This complication arises mostly because of stress and mainly affect elderly
patients with already manifest diabetes mellitus. Increased glycaemia may alter the
state of consciousness and trigger partial or generalized seizures.
Cortisone therapy would likely worsen hyperglycemia. Recommended
treatment should aim for dehydration correction, since the benefits of insulin are
disputed in these cases.
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HEMORRHAGE
HYPONATREMIA
Hyponatremia is the most common and most important of the hydrolytic
disturbances following SAH. It occurs in 35% of patients, with a peak incidence
between days 2-10 after the event. The exact mechanism is still uncertain, however
elevated levels of antidiuretic hormone (ADH) and atrial natriuretic factor
(ANF) have been incriminated.
ADH levels increase when plasma osmolality is high (as a consequence
of hyperglycemia, for instance), thus resulting in hypervolemia with an apparent
decrease in serum sodium levels (although technically there is no urinary loss of
sodium in this case). On the other hand, ANF secretion is stimulated by increased
intravascular volume and blocks sodium reabsorption in the distal ducts of the
nephrons. It is important to clinically differentiate between the two causes. In
inappropriate secretion of ADH (SIADH), the patient presents with
hypervolemia and fluid retention, whereas cerebral salt wasting syndrome
(CSW) manifests with hypovolemia and requires an additional supply of liquids.
Anterior circulation aneurysms are likely to result in diabetes
insipidus (since perforating arteries from this level provide for the hypothalamus).
This may remit in a matter of days up to weeks, yet some patients need intranasal
administration of desmopressin as diabetes insipidus may become permanent.
DEEP VENOUS THROMBOSIS

The incidence of DVT is 2%, with half of these patients developing pulmonary
thromboembolism. Therefore, prevention must be achieved by any means
necessary.
Intermittent compression of the inferior limbs and passive movement
exercises are the most favorable prophylactic measures, however anticoagulant
therapy is expressly prohibited in the case of an unclipped aneurysm.
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PULMONARY DYSFUNCTIONS
These complications are the most life threatening, affecting nearly half of the
patients with SAH. Pulmonary edema is of neurogenic origin and occurs after
acute neurological injuries that determine an increase of intracranial pressure. It
is caused by an alteration in pulmonary capillary permeability. Although its
incidence lessens with the time elapsed since SAH, it makes way for pneumonia
and thromboembolism.
Treatment of acute pulmonary edema may comprise of gentle diuresis,
dobutamine, and positive end-expiratory pressure. Triple H therapy is not
associated with neurogenic pulmonary edema, however it may be the cause of
fluid overload.
DIGESTIVE DISFUNCTIONS
Upper gastrointestinal bleeding arises from stress gastritis and mucosal ulcers
formed as result of elevation in intracranial pressure. These bear the name of
Cushing ulcers. They affect a significant number of patients with SAH (around
4%).
As a rule, all medical and surgical centers administer antacids and
antihistamines as prophylaxis. However, there is no study that supports the
efficacy of this treatment.
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REFERENCE
1.
2.
3.
4.
5.
6.

2.2.3: 107-116; 2.6: 149-158
4: 73-85; 8: 129-130
Kato Y, Sano H. Subarachnoid Hemorrhage. In: Kalangu KKN, Kato Y,
Dechambenoit G. Essential Practice of Neurosurgery. Access Publishing Co., Ltd,
2009; IV.3: 446-458
Mally R. Cerebral Vasospasm. In: Kalangu KKN, Kato Y, Dechambenoit G.
Essential Practice of Neurosurgery. Access Publishing Co., Ltd, 2009; IV.4: 472-476
Becske T, Lutsep HL. Subarachnoid Hemorrhage. Medscape Reference. Cited 12 th
Jan 2014
Kassel NF, Shaffrey ME, Shaffrey CI. Cerebral Vasospasm Following Aneurysmal
Subarachnoid Hemorrhage. In: Apuzzo MLJ. Brain Surgery. Churchill Livingstone,
1993; Vol.1, 27: 847-856
84 | P a g e
Resection of a temporal lobe AVM situated on both sides of the vein of Labbe, with
anatomical and functional preservation of the aforementioned vein
CHAPTER 7
CEREBRAL ANEURYSMS - GENERAL ASPECTS
INTRODUCTION
Cerebral aneurysms are pathologic focal dilatations of the blood vessels
comprising the cerebral circulation. This implies a thinning of all the layers of the
vessel wall, representing its point of minimal resistance.
Numerous factors have been incriminated in the development of
aneurysms, although not one can be declared the sole cause of their manifestation.
Thus, careful evaluation of all the risk factors and predispositions is crucial. Their
frequency, however, is nearly impossible to determine.
One of their main features, and also most perilous, is their propensity to
rupture. This often leads to the dreaded subarachnoid space hemorrhage
(SAH), with diffuse or focal forms of vasospasm resulting in the infarction of the
cerebral parenchyma.
Clinical presentation is mostly nonspecific, raging from a silent and
asymptomatic state, to mild headache, to even uncommon onsets of sudden death.
Though a SAH of an aneurysmal origin usually has characteristic historical
features, the pattern of symptoms differs with the size and placement of the
aneurysm itself.
All things considered, it is obvious why this subject has been considered a
challenge for neurosurgeons across the ages and why so many efforts were made
into understanding, diagnosing and treating cerebral aneurysms. The last decade
alone brought along considerable progress in these fields.
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CLASSIFICATION
Based on morphology, aneurysms can be divided as follows:
Saccular (berry or congenital, Figure 7.1) represent the majority (90%) of

all intracranial aneurysms and are usually placed at the branching points of
subarachnoid conducting arteries. In most cases (85-95%), saccular
aneurysms are situated in the anterior circulation. Rupture is frequent
within this variant, accounting for 70-80% of spontaneous SAH.
Figure 7.1 Saccular aneurysm
Dolichoectatic (fusiform) aneurysms (Figure 7.2) are elongated

outpouchings of proximal arteries, having mainly an arteriosclerotic origin.
They are by far fewer than the saccular type (only 7%) and are generally
less likely to rupture. They predominantly affect the vertebrobasilar
circulation.
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AND AVMs
CHAPTER 7: ANEURYSMS GENERAL ASPECTS
Figure 7.2 fusiform aneurysm
Mycotic (infectious) aneurysms are stationed peripherally, being the least

common type (0.5% of all cases). They are secondary to vascular wall
infection, due to hematogenous dissemination (for example, from a site of
infectious endocarditis). Frequently, infectious aneurysms are multiple.
Their high rate of rupture is noted.
The diameter of an aneurysm may vary from a few millimeters (below 5

mm it is considered a microaneurysm) to a few centimeters. Small aneurysms
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range from 5 to 12 mm. A large aneurysm has a diameter between 12 and 25 mm,
while a giant aneurysm surpasses the higher limit (Figure 7.3)
Figure 7.3 Giant aneurysm
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AND AVMs
EPIDEMIOLOGY
The actual prevalence of aneurysms in the general population is problematic to
estimate, since autopsy series differ in terms of age of the individuals assessed.
Most authors agree on an average of 5% of the general populace. Around half of
these aneurysms eventually rupture. It is unmistakable, however, that the
frequency of aneurysm detection increases with age.
Peak incidence of rupture varies between the fifth and seventh decades of
life, with only 2% of pediatric patients presenting intracranial aneurysms and a
significantly lower risk of bleeding. The great majority of aneurysms are
asymptomatic until this event.
Aside from age, aneurysm size has been repeatedly found as a
contributing factor of rupture. Thus, an aneurysm with a diameter between 4 and
7 mm has the maximum risk, while the giant variants seem to have a much less
pronounced tendency (possibly due to a thrombus reinforcing the thin vessel wall).
Most of cerebral aneurysms are situated in the anterior portion of the
Circle of Willis. Although it is debated whether this is a cause of limited diagnoses
rather than the actual prevalence.
Gender distribution of aneurysms tends to favor women, with a male to
female ratio of 1:1.6. This may suggest a hormonal determinism in their
development. Most of the aneurysms in men are situated either in the anterior
communicating artery (ACoA), or the anterior cerebral artery (ACA), while the
most common site in women is at the junction of the internal carotid artery (ICA)
with the posterior communicating artery (PCoA). Giant aneurysms are three
times more often in women and the prognosis for aneurismal SAH is also worse
for this sex.
Survival ratio after the firs episode of rupture is merely 50%. Only a
third of these patients may present an adequate long-term prognosis.
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ETIOLOGY
The cause of aneurysmal development is as of yet shrouded in mystery. The
pathogenesis is inherently tied to cerebrovascular structure aberrations and a
multifactorial etiology is currently widely accepted. Three types of factors are
involved in aneurysmal manifestation: A. risk factors, B. adjuvant factors and C.
rupture-triggering factors.
A. In comparison to extracranial arteries, the intracranial vessels present a thicker
internal elastic lamina, despite lacking the external elastic lamina. Also, the
muscular media has fewer muscle fibers, while the elastic tissue is sparser within
the media and the adventitia. The fibrous adventitia has the greatest input in
maintaining the structural integrity of the vessel wall. Despite this, the
subarachnoid space does not confer the same support as conjunctive tissue does.
Thus a genetic predisposition may be assessed. More recently, a substantial genetic
contribution to sporadic intracranial aneurysms has been discovered (Alg et al).
The researchers identified 19 single-nucleotide polymorphisms (SNPs) associated
with this disease, the most important of which were on chromosomes 9, 8 and 4.
The genes involved are related to vascular endothelial maintenance.
While atherosclerosis has been definitely impeached in the genesis of
dolochoectatic aneurysms, many authors associate this factor with hypertension
(along with a possible familial inheritance pattern) to the origin of saccular
aneurysms. The embolic factor has been tied to atrial myxoma (causing
neoplastic aneurysm formation).
The infectious factor determines the appearance of mycotic aneurysms,
typically in the distal branches of the middle cerebral artery (MCA). This suggests
the embolic origin of this type of lesion. Direct extension from arterial lumen to
adventitia of septic emboli containing Staphylococcus aureus or Streptococcus
viridans is thought to lead to wall degradation, thus causing mycotic aneurysms.
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AND AVMs
Last, but not least, craniocerebral trauma may hold a key role in
instigating these lesions. In this case, aneurysms affect the peripheral cortical
branches as a result of the contact with the edge of the falx cerebri or skull
fracture. While not true aneurysms (due to the absence of all layers of the vessel
wall), traumatic dissecting aneurysms are generally located at the skull base and
are a consequence of the expansion of intramural hematomas.
Recent studies highlighted a direct relationship between aneurysmal
rupture and the intensity of apoptosis within the aneurysmal wall 1 or 2 days prior
to rupture itself.
B. Recurrently cited adjuvant factors are as follows:
Smoking (apparently the most important of all)

Pregnancy and labor (presence of aneurysms during late pregnancy and
childbirth commonly leads to rupture)
Oral contraceptives
Alcoholism
Drug abuse
Exaggerated food consumption
C. A few authors describe rupture-triggering factors, circumstances causing rapid

heightening of arterial tension:
Defecation
Coitus
Stress
Lumbar puncture
Cerebral angiography
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Intracranial aneurysms have been repeatedly associated with systemic

conditions and intracranial vascular malformations, among which:
1)
2)
3)
4)
5)
6)
7)
8)
9)
10)
11)
12)
Autosomal dominant inherited polycystic kidney disease (ADPKD)

Coarctation of the aorta
Fibromuscular dysplasia (intra- and extracranial alike)
Marfan syndrome
Ehlers-Danlos syndrome (type IV especially)
Arteriovenous malformations
Osler-Weber-Rendu syndrome
Tuberous sclerosis
Systemic lupus erythematosus
Sickle cell anemia
Von Recklinghausen disease
Moyamoya syndrome (explained in its respective chapter)
MORPHOLOGY
Typically, an aneurysm is comprised of three elements: the neck, which connects
it to the originating artery (it is also the site for clipping); the body (or the sac),
making up the majority of the aneurysm itself; the fundus, or the distal portion
(usually the point of minimal resistance, most likely to rupture). As previously
mentioned, saccular aneurysms represent the net majority and this description is
mostly suited for them. There are four rules regarding saccular aneurysm
anatomy, crucial to surgical approach:
1) They usually arise at the branching point of an artery;
2) They may also appear at the turning point of an artery, on its convex
portion;
3) They develop on the presumed trajectory of the blood flow had the
branching point or turn not existed;
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4) A constant feature is the perforating vessels that reside at the aneurysmal

point of origin. These must be preserved at all costs!
Fusiform (dolichoectatic) aneurysms are, as their name suggests,
elongated dilatations in the vascular wall, sometimes tortuous, innately deprived
of a true aneurysmal neck. They frequently contain a laminated thrombus. SAH
through rupture may occur, however these lesions more often exert mass effect on
cerebral parenchyma, with brainstem compression and cranial neuropathies.
Sometimes, their presence may result in the obstruction of cerebrospinal fluid
outflow.
Mycotic aneurysms are usually multiple and located at the distal
branches of the MCA. While meager in size, their propensity to bleed is
alarming. Because of these qualities, clipping is not recommended, if not entirely
impossible.
There are five major sites, accounting for almost 90% of all aneurysmal
placements:
1)
2)
3)
4)
5)
The point of emergence of the PCoA from the ICA

The AcoA
The branching point of the ICA
The MCA point of bifurcation
The junction between the PCA and the basilar artery
Histologically, brownish pigmentation (hemosiderin) and fibrous

adhesions surrounding the adjacent brain parenchyma can be seen in gross
postmortem examinations. Shape and size may change after the onset of death.
Aneurysmal calcifications and intraluminal thrombus may also be sighted.
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Figure 7.4 Localisation of aneurysms

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Microscopically, the thinned wall of an aneurysm might present all layers

of normal intracranial vessel wall. However, the internal elastic lamina may be
deteriorated and fragmented, while the tunica media may all the while be entirely
absent. Phagocytes laden with hemosiderin and lymphocytic infiltration may also
be present. An infected embolus adhering to a necrotic arterial wall within a
mycotic aneurysm is not uncommon. In this instance, the intima and internal
elastic lamina may be intensely affected, with an inflammatory infiltrate comprised
of polymorphonuclear cells, lymphocytes and macrophages. Vasospastic arteries
may display sarcolemmal destruction and myofilament fragmentation.
Figure 7.5 comparrison between aneurysm wall structure (upper arrow)

and normal arterial wall structure (lower arrow)
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NEUROLOGY
Since most aneurysms are clinically silent prior to rupture, symptoms usually
describe the event of an acute SAH. Even though SAH of aneurysmal origin has
distinctive historical features, these may vary with placement, shape and size of
the aneurysm itself. The most typical symptoms of cerebral aneurysms and SAH
are along these lines:
Severe acute headache, it is commonly reported as the worst headache

ever. Pain can also be caused by aneurysmal expansion, intramural
hemorrhage or thrombosis and it may or may not accompany SAH. In most
neurosurgeons experience, there is a history of a warning leak a few days
before the onset of rupture (in up to patients). Though these may be
mild, sudden headache or minor focal neurologic deficit should rouse the
physicians awareness.
Facial pain can be caused by cavernous carotid aneurysms.
Alterations in consciousness, brought on by the sudden elevation of
intracranial pressure (possibly rupture-related) and a swift decline of cerebral
arterial perfusion pressure, may range from confusion, to mild impairment, to
even syncope in 50% of cases.
Palsy of the third cranial nerve (the eye is infraducted and abducted, or
down and out), particularly with a fixed dilated pupil and palpebral ptosis,
is pathognomonic for PCoA aneurysms. It requires diagnostic studies to
exclude a posterior carotid wall aneurysm or a distal basilar aneurysm.
Focal or generalized seizures occur within 24 hours of the onset of rupture
in up to 25% of patients.
Visual loss, blurred vision or diplopia may be manifest.
Weakness, hemisensory loss, language disturbances, memory loss, attention
deficit and olfactory disturbances are focal deficits produced by hemorrhage
or ischemia, although more commonly associated with giant aneurysms.
Photophobia, sonophobia or stiffness of the neck (caused by meningeal
irritation) may also be present.
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Autonomic disturbances such as fever, nausea, vomiting, diaphoresis and

chills are a result of blood degradation products being accumulated in the
subarachnoid space. Cardiac arrhythmias might have a different trigger.
Respiratory dysfunction and cardiovascular instability herald brainstem
compression.
Pituitary function may be altered due to intrasellar aneurysms.
The presentation of a traumatic aneurysm may be belated, with intracranial
hemorrhage or recurrent epistaxis.
First of all, it should be emphasized that there is no such thing as two clinically
identical patients. Therefore, the most effective way to approach a patient is not
simply objectivizing the superfluity of diagnostic information, but to employ a
subjective medical sense for the patients neurologic and systemic status.
Because the risk of rebleeding is at its highest within the first 48 hours
after the initial rupture, the surgical strategy is to minimize this threat by securing
the ruptured aneurysm as soon as humanly possible. Alas, the possibilities of
referring to neurosurgical centers are not the same for all patients; thus, many
arrive at least one or two days following the bleeding incident. This aside, it is not
always in the patients best interest to undergo surgery at night, citing the fatigue
of the neurosurgeon and the possibly suboptimal operating room staff. Last, but
not least, not aneurysms are alike, just as the patients are not. While some may
tolerate extensive retraction and dissection, those in poorer conditions may worsen
with hasty surgery. In this situation, it would be best if the brain was permitted a
few days to recover and even palliative endovascular approach might prove
attractive.
Prehospital care should include a thorough evaluation of vital signs and
neurological status. Endotracheal intubation and intravenous access may be
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necessary. The prevention of complications and supportive measures are the key
objectives of medical therapy for patients in the periprocedural period or poor
surgical candidates.
Prior to definitive aneurysm treatment, medical approaches imply the
control of hypertension, calcium channel blocker administration and seizure
prevention.
Following surgical or endovascular treatment, blood pressure must be
maintained higher as to lessen the complications of vasospasm. Antifibrinolytic
therapy (-aminocaproic acid) was introduced more than two decades ago, aiming
to prevent or delay rebleeding. However, cerebral ischemia resulting from
vasospasm proved more frequent if antifibrinolytics were used than if they were
not.
Pressors remain a pillar in the therapy of aneurysms. Their safety and
efficacy appear to be profusely enhanced by volume expansion, the combination of
hypertension and hypervolemia having the greatest outcome in the medical
treatment of symptomatic vasospasm.
Mainly, there are two major invasive strategies in the treatment of
cerebral aneurysms. Surgical therapy focuses on excluding the aneurysm from
the cerebral circulation and reducing mass effect on neighboring structures.
Numerous approaches have been developed and perfected to suit the location and
the anatomy of the lesion. In this purpose, a surgical clip (Yaargil clip) is placed
across the neck of the aneurysm, preserving the parent vessel and eliminating any
aneurysmal rest that may develop afterward. Endovascular techniques, on the
other hand, are an alternative that may be employed even in the onset of acute
aneurysmal SAH. They also allow parent vessel preservation and rely on
electrolytically detachable platinum coils (Guglielmi detachable coils, or GDC),
pliable stents (self-expanding or balloon-expandable), balloons or glue. GDC may
be deployed within the lumen of the aneurysm, promoting thrombosis and eventual
obliteration (See the following chapters for further details).
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REFERENCES
1.
2.
3.

2.1: 91-102
Liebeskind DS, Lutsep HL. Cerebral Aneurysms. Medscape Reference, cited Dec
2013
Batjer HH, Chandler JP, Getch CC, Gravely L, Bendok BR. Intracranial Aneurysm.
In: Rengarchary SS, Ellenbogen RG. Principles of Neurosurgery. Second Edition.
Elsevier Mosby 2008; 14: 215-239
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CHAPTER 8
ANEURYSMS OF THE POSTERIOR CIRCULATION
VICTOR VOLOVICI
EPIDEMIOLOGY, TREATMENT, PROGNOSIS

The incidence of subarachnoid hemorrhage is estimated at 10-15 cases per 100
000, with major geographical, ethnic and gender variations[1]. Although a
common incidental finding at postmortem examination, with prevalence ranging
from 1% to 6% in large autopsy series[2,3] it is also estimated that per year 50%
or more from the patients with an SAH secondary to a ruptured intracranial
aneurysm die or are severely disabled, corresponding to about 14.000 people[2].
The outcome depends on various factors, 6 of which are the most relevant, age,
accessibility to a care facility, patients clinical status as described by the Hunt
and Hess and WFNS grading scales, the amount of intracerebral hemorrhage
according to Fishers grading scale, aneurysmal location and the presence of
vasospasm.
Aneurysms of the posterior circulation are estimated at 8-15% of all
intracranial aneurysms, according to multiple authors[6,8,9]. They are most
frequently located at the top of the basilar artery or at the junction of the
vertebral artery and the ipsilateral posterior inferior cerebellar artery[5,6]. In
20-30% of patients there were multiple aneurysms, usually 2 or 3, with as many as
13 described in one single patient[5,6,7,10].
Schievink and collaborators describe in the 1997 review published in the
New England Journal of Medicine that of the patients with spontaneous
subarachnoid hemorrhage approximately 12% die before reaching a hospital,
40% die within 30 days from the rupture and ~30% of the survivors are left
with severe neurological disability. Mayberg and colleagues describe in 1994 in
the guidelines for the management of aneurysmal subarachnoid hemorrhage that 5102 | P a g e
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15% of patients presenting with clinical symptoms of a stroke actually have a

subarachnoid hemorrhage and that the advice for this group of patients is early
treatment as early as 24-72 hours because of the high risk of repeat rupture
within the first 2 weeks after the subarachnoid hemorrhage episode[11].
SURGICAL OPTIONS
Some of the most burdensome lesions that a cerebrovascular neurosurgeon has to
face are posterior circulation aneurysms[26]. As stated earlier, disparaging
anatomy, lengthy complicated approaches and prolonged operation and ischemia
time all factor in to provide a considerable challenge for even the most skilled
neurosurgeon[14,15]. As with all intracranial aneurysms, a thorough plan has to be
thought out preoperatively and intraoperatively, a thorough and deep knowledge of
neuroradiology has to be employed for this purpose, and one must also make
judicious use of intraoperative monitoring, angiography, Doppler, whilst bearing
in mind proximal control, preservation of perforators and sharp dissection, to name
a few precepts[25].
There are 4 classical preferred approaches to posterior circulation
aneurysms, as well as combinations of these: the pterional approach, transpetrosal
approaches, retrosigmoid approach and extended far-lateral approach[25].
Lawton, Spetzler and collaborators divide posterior circulation aneurysms
in 3 groups with respect to their relationship to the basilar artery, as follows:
The first is the the upper basilar zone comprising the upper 2/5 of the basilar
artery, approached via an pterional approach [23].
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CHAPTER 8: ANEURYSMS OF THE POSTERIOR CIRCULATION
Figure 8.1 - Periosteum removal for craniotomy.

The second area of interest is the midbasilar zone, the middle fifth of the
basilar artery. These are approached via transpetrosal-type approaches: the
retrolabyrinthine approach, which spares the semicircular canals and cochlea,
and provides access to the neck of the basilar aneurysm, the translabyrinthine
approach, which implies sacrificing hearing and the elimination of semicircular
canals [29] and the transcochlear approach, which although offers a broad and
elegant exposure of the brain stem and clivus, does so at the expense of the most
part of the petrous bone, cochlea and extended manipulation of the facial nerve
[13,14]. For aneurysms involving the AICA the retrosigmoid approach is the most
widely used [25].
The third area of interest with respect to the basilar artery is the
vertebrobasilar zone, involving the lower 2/5 of the basilar artery as well as the
intradural part of the vertebral artery. These lesions are commonly approached via
a far-lateral approach [30,31], whereby classically 1/3 of the occipital condyle
would be drilled away and the foramen magnum would be resected laterally
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AN INTRODUCTION TO
towards it while also removing the arc of C1 all the way to the anterior sulcus of
the vertebral artery. Experience has taught that it is also safe to drill 1/2 to 2/3 of
the condyle without sacrificing stability [25,30].
In selected cases where a giant aneurysm of the area needs to be
microsurgically treated, combinations of the aforementioned approaches may be
required, for example a combined far lateral- transpetrosal approach, in which
both the tentorium and the sinus sigmoideus are both sectioned to provide a wide
exposure of the antero-lateral brainstem [32,33].
Figure 8.2 - X-shaped or Y-shaped dura mater incision offers a wide

surgical field.
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Figure 8.3 - PICA aneurysm clipping performed while avoiding

damage to the cranial nerves and arterial perforators.
ENDOVASCULAR OPTIONS
As stated earlier, after the first experiments with Hunterian balloons as means of
occluding the parental artery[18, 19]. After the revolutionary invention of Guido
Guglielmi in 1991, the platinum detachable coils[35, 36], experiments began to be
more focused on the patient group deemed too difficult to clip: anatomically
undesirable location, poor neurological status, advanced age and poor overall
prognosis. Vinuela reports in the first multicenter study using coils in 1997 403
patients, 57% of which had posterior circulation aneurysms[22], as opposed to the
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AN INTRODUCTION TO
regular 8-15%[8]. The breakthrough moment for the endovascular treatment of

aneurysms came after the publication in 1997 of the study by Raymond en
colleagues where 23 basilar tip aneurysms were treated by coiling and prevented
rebleeding, with mortality and poor outcome rates of 8.7% each and one death and
one minor permanent deficit as a direct result of endovascular treatment[38]. The
largest series of basilar tips aneurysms ever published, by Peerless and colleagues
in 1994 also had a mortality rate of 8% and a morbidity rate of 9.7%, which were
both linked, as in the case of the coiling procedures, to initial or recurrent bleeding,
vasospasm or technical complications. However, this series of patients was very
large, comprising 1767 vertebrobasilar aneurysms[37].
The studies reviews by Lozier et al regarding the endovascular treatment
of basilar apex aneurysms had diverse indications for coiling, failed clipping, poor
neurological status, physician or patient preference and anticipated surgical
difficulty on preoperative scans[9, 45-49], with a preponderance for the latter as
main reasons, namely anticipated operative difficulty and personal preference. The
size of the aneurysm was small(<10 mm) in 57.5% of cases, large(11-25 mm) in
34.6% of cases and giant(>25 mm) in 7% of cases, with 60.1% of them exhibiting
a broad neck(>4 mm). The Hunt and Hess score upon admittance was in 33.2% of
cases grade 1, in 31.4% grade 2, in 22.1% grade 3, in 8% grade 4 and in 4% of
cases grade 5. 220 aneurysms were treated with GDC coils. Of these, on analysis
of the immediate postprocedural angiography 100% occlusion was achieved in
43.2% of cases, 90-99% occlusion in 44.6% of cases and less than 90% occlusion
in 12.3%. The overall complication rate procedure-related was 14%(32 cases), the
most relevant being coil protrusion 9 cases(3.9%), parent artery thrombosis 9
cases(3.9%) and aneurysm rupture 7 cases(3.1%). Of these, 2 patients suffered
considerable neurological deterioration with a poor outcome and 2 patients
expired.
Subsequent articles, so far as 2013 confirmed the findings of Lozier et al
and despite the evolution of techniques figures hover around the same point[57].
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Even after 10 years, with the experience gathered and in spite of all new
techniques, a retrospective study performed by Tykocki et al in 2013 on 63
posterior circulation aneurysms, reveals similar figures[58]. 51 of these aneurysms
were ruptured and 12 unruptured. Complete occlusion was achieved in 36 (57.1%),
incomplete in 15 (23.8%), and partial in 12 (19%) patients. In patients with the
neck size of 1-2 mm the complete occlusion was in 75% (24/32) andincomplete in
12,5% (4/32). A neck size of 2-4 mm corresponds to obliteration rates of 38.7%
(12/31) complete occlusion and 29% (9/31) incomplete occlusion. The predictor of
total occlusion in Probit and linear regression models consisted of only one
independent variable, the narrow neck size. In this study there were no aneurysms
commonly regarded as broad-necked(>4 mm)[58], which could be considered a
selection bias.
As mentioned earlier, the most frequent localization of aneurysms of the
posterior circulation besides the basilar apex is the superior cerebellar artery,
13.5%[9]. Studies on other localizations are relatively scarce and are limited to
single-center experiences with small numbers of patients. Haw et al publish one
such study in 2004 in which 12 superior cerebellar artery aneurysms were treated
by endovascular coiling in eleven patients between 1992 and 2001[59]. 7 patients
presented with subarachnoid hemorrhage, 2 with neurologic deficit, and 2 with
unruptured aneurysms. 6 patients had a complete obliteration and 6 an incomplete
obliteration, with no further subarachnoid hemorrhage occuring during the followup period(duration of follow-up between 6 and 119 months, mean follow-up 50
months). Procedural morbidity was one superior cerebellar artery infarct with good
recovery, and the outcome was satisfying, with 9 out of 11 patients on follow-up
were performing at Glasgow Outcome Scale (GOS) 5. One patient with GOS 3
presented with a poor grade subarachnoid hemorrhage and the other patient with
GOS 4 presented with a parenchymal hemorrhage due to an arteriovenous
malformation[59].
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RANDOMIZED TRIALS
The four trials which will be reviewed are the Helsinki prospective study of 1999,
the ISAT study of 2002, the ISUIA trial of 1998 and the Barrow Ruptured
Aneurysm Trial results of 2013.
The first randomized clinical trial which compared microsurgery with
endovascular procedure was published by Hernesniemi and his collaborators in
1999, and included 109 patients with SAH and an aneurysm which could be
treated by either method. The follow-up was clinical at 3 months, angiography at
3, 6, and 12 months and neuropsychological testing at 3 and 12 months. The
relevant figures show a technical mortality of 4% in the surgery group and 2% in
the endovascular group, with better initial angiographical results for posterior
circulation aneurysms in the endovascular group(11 patients, p=0.045)[65].
In 2002 in the Lancet Molyneux et al published the International
Subarachnoid Aneurysm Trial(ISAT)[66], providing level I evidence on the
subject. The study was a randomized prospective trial which enrolled 2143
patients with aneurysms which could be treated by either option, 1070 of which
were included in the clipping group and 1073 included in the coiling group. Over
90% of these aneurysms were under 6 mm and the majority involved the anterior
cerebral artery(50.5%), followed in frequency by the internal carotid(with the
posterior communicating included in this group). For the purposes of this review
we find in the study a figure of 2.7% posterior circulation aneurysms. When
compared to the normal 8 to 15%[6], we are faced with a selection bias of the
adjudicating committee, where there was unanimity among neuroradiologists and
neurosurgeons that most of the aneurysms needed to be treated by enodvascular
techinques. The overwhelming majority of patients were in excellent clinical
condition prior to the intervention. Follow-up involved using the modified Rankin
scale(mRS) at 2 months and 1 year. The study was halted when an interim analysis
revealed significantly better (p=0.0019) death and disability rates in the
endovascular group, where 30.6% of the patients treated microsurgically(243 of
793) had expired or were dependant at 1-year follow-up, compared with
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23.7%(190 of 801) in the endovascular group. A risk reduction for death and
dependancy of 22.6% and an absolute reduction of 6.9% for the endovascular
option[66].
The ISUIA(International Study of Unruptured Intracranial Aneurysms)
study published in the New England Journal of Medicine in 1998[67] explored a
different, subtly more complex issue: that of the treatment options for unruptured
aneurysms, which far outnumber those presenting with subarachnoid hemorrhage,
basing their discussion of the following key-point: what variables can predict the
moment of rupture for an aneurysm. The strongest predictors are thus the size of
the aneurysm, the location and the patient's gender and history(herein included
previously ruptured aneurysms). 1449 patients with 1937 were retrospectively
studied. The cohort was split in 2 groups: Group 1, 727 patients, no history of
SAH and Group 2, 722, with a history of a previously ruptured and treated
aneurysm, which presented another, unruptured, one.
For Group 1 the rupture rate was proven to be 0.05% per year with aneurysms
under 10 mm in diameter, and 1% per year for aneurysms over 10 mm in diameter.
Giant aneurysms posed a significantly higher risk, experiencing a 6% rupture rate
in the first year. As well as size, location was also a predictor for rupture: posterior
circulation aneurysms tend to rupture regardless of size.
Group 2 already had a history of SAH with a treated aneurysms and had another,
not ruptured aneurysm. Here the risk for rupture was 0.5% per year for aneurysms
less than 10 mm in diameter and less than 1% for aneurysms over 10 mm in
diameter. Size was in this group not an independent risk factor, but location and
age were, with basilar tip aneurysms showing a 5.1 relative risk and older age a 1.3
relative risk.
There is a discrepancy between the rupture rates encountered in clinical
practice and the rates exposed by the ISUIA study[6,67]. Thus, the same
investigators published in 2003 a prospective study following a larger cohort
recently, 4060 patients being assessed, 1692 without aneurysmal repair, 1917 had
open surgery, and 451 had endovascular procedures. The critical size for rupture
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was deemed 7 mm, with an evident higher risk for rupture of posterior circulation
aneurysms relative to that of anterior circulation aneurysms.
The results of the ISAT study of 2002 have to be viewed in light of the
new prospective randomized study carried out on 471 patients at The Barrow
Neurological Institute by Spetzler and his collaborators, the 3-year follow-up being
published in 2013[68]. 238 patients were assigned to clip occlusion and 233 to
coil embolization, with no exclusions based on anatomical criteria. Crossovers
were possible based on the physician's preference and evaluation and/or the
patient's wish and it is very interesting to note that of the 170 patients who had
been originally assigned to coiling, 64 (38%) crossed over to clipping, whereas 4
(2%) of 179 patients assigned to surgery crossed over to coiling. There was on the
6 months' 1 year and 3 year follow-up no significant difference in outcome
between anterior(339 cases) and posterior(69 cases) circulation aneurysms. The
only concern was raised by posterior circulation aneurysms: there was a
significantly better outcome in the coiling group than in the clipping group which
persisted at 3-year follow-up, but these figures have to be viewed taking into
considerations that the 3 groups are strongly inhomogeneous: anatomical matching
differs strongly, with for example 18 of the 21 posterior inferior cerebellar artery
cases being assigned to clipping.
CONCLUSION
It is easy to draw drastical conclusions based upon, for example, the ISAT study,
and say that all aneurysms need to be coiled or to take another extremist stand and
deem all aneurysms suitable for clipping based on the experience of renowned
centers with incommensurable experience in the microsurgical treatment of such
diseases. It is clear that there is a place for endovascular techniques in the
treatment of intracranial aneurysms, even with the recurrence rates and
reintervention rates. The question is if the patient who is admitted with an SAH or
the patient who discovered as a chance finding an aneurysm should be primarily
referred to the endovascular specialist or to the neurosurgeon (or to a vascular
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neurologist, who, in turn runs a multidisciplinary team) and in this respect it seems
rather evident that a multidisciplinary team is needed where the neurosurgeon the
lead role plays and the final word enounces for any given case. Moreover, it is
very easy to dismiss posterior circulation aneurysms as "coilable, with few
exceptions", when studies such as the one by Krisht in 2007[73] clearly show that
is not only endovascular techniques who are evolving, but also microsurgical ones,
with excellent results(no procedure-related mortality, mRS 0-2 in 92.8% of cases
for basilar apex aneurysms, traditionally considered a per excellence coilable
aneurysm). It should be evident, thus, that microsurgery has to continue to evolve
in providing the medical world with new techniques and new solutions for old
problems in the case of posterior circulation and should not, under any
circumstance, take a step back to allow coiling to automatically be the treatment
of choice for this anatomical location, but rather to set the tone and the standard of
care with respect to these lesions.
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endovascular treatment of acutely ruptured aneurysms: report on 69 cases. J
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41. Phillips LH. The unchianging pattern of subarachnoid hemorrhage in a community.
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aneurysmal subarachnoid hemorrhage. Neurology 1995;45(5):871-874
44. Vallee JN, Aymard A, Vicaut E, Reis M, Merland JJ. Endovascular treatment of
basilar tip aneurysms with Guglielmi detachable coils: predictors of immediate and
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45. Tateshima S, Murayama Y, Gobin YP, Duckwiler GR, Guglielmi G, Vinuela F.
Endovascular treatment of basilar tip aneurysms using Guglielmi detachable coils:
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aneurysms. J Neurosurg 1990;90(5):868-874
47. McDougall CG, Halbach VV, Dowd CF, Higashida RT, Larsen DW, Hieshima GB.
Enodvascular treatment of basilar tip aneurysms using electrolytically detachable
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48. Bavinzki G, Killer M, Gruber A, Reinprecht A, Gross CE, Richling B. Treatment of
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experience. J Neurosurg 1999;90(5):843-852
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endovascular treatment with Guglielmi detachable coils - midterm results. Radiology
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50. Steiger HJ, Medele R, Bruckmann H, Schroth G, Reulen HJ. Interdisciplinary
management results in 100 patients with ruptured and unruptured posterior circulation
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51. Uda K, Murayama Y, Gobin YP, Duckwiler GR, Vinuela F. Enodvascular treatment
of basilar apex aneurysms with Guglielmi detachable coils: clinical experience with
41 aneurysms in 39 patients. J Neurosurg 2001;95(4):624-632
52. Lempert TE, Malek AM, Halbach VV, et al. Endovascular treatment of ruptured
posterior circulation cerebral aneurysms. Clinical and angiographic outcomes. Stroke
2000;31(1):100-110
53. Nicholas DA, Brown Rd Jr, Thielen KR, Meyer FB, Atkinson JL, Piepgras DG.
Endovascular treatment of ruptured posterior circulation aneurysms using
electrolytically detachable coils. J Neurosurg 1997;87(3):374-380
54. Birchall D, Khangure M, McAuliffe W, Apsimon H, Knuckey N. Endovascular
treatment of posterior circulation aneurysms. Br J Neurosurg 2001;15(1):39-43
55. Pierot I, Boulin A, Castaings L, Rey A, Moret J. Selective occlusion of basilar artery
aneurysms using controlled detachable coils: report of 35 cases. Neurosurgery
1996;38(5):948-953 discussion 953-954
56. Le Roux PD, Winn HR. Management of cerebral aneurysms. How can current
management be improved? Neurosurg Clin N Am 1998;9(3):421-433
57. Jennett B, Bond M. Assesement of outcome after severe brain damage. Lancet
1975;1(7905):480-484
58. Tykocki T, Nauman P, Kostkiewicz B. Endovascular embolization of ruptured and
unruptured posterior circulation aneurysms. A multi-factor analysis. Turk Neurosurg.
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59. Haw C, Willinsky R, Agid R, TerBrugge K. The endovascular management of
superior cerebellar artery aneurysms. Can J Neurol Sci. 2004 Feb;31(1):53-7
60. Jin SC, Park ES, Kwon do H, Ahn JS, Kwun BD, Kim CJ, Choi CG. Endovascular
and microsurgical treatment of superior cerebellar artery aneurysms. J Cerebrovasc
Endovasc Neurosurg. 2012 Mar;14(1):29-36
61. Milosevic Medenica S. Endovascular treatment of wide-neck, ruptured and
unruptured aneurysms without supporting devices. A single center experience.
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62. Mukonoweshuro W, Laitt RD, Hughes DG. Endovascular treatment of PICA
aneurysms. Neuroradiology 2003;45(3):188-192
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65. Vanninen R, Kovisto T, Saari T, Hernesniemi JA, Vapalahti M. Ruptured intracranial
aneurysms: acute endovascular treatment with electrolytically detachable coils- a
prospective randomized study. Radiology 1999;211(2):325-336
66. Molyneux A, Kerr R, Stratton I, et al. International Subarachnoid Aneurysm Trial
Collaborative Group(ISAT). ISAT of neurosurgical clipping versus endovascular
coiling in 2143 patients with ruptured intracranial aneurysms: a randomised trial.
Lancet 2002;360(9342):1267-1274
67. International Study of Unruptured Intracranial Aneurysms Investigators. Unruptured
intracranial aneurysms- risk of rupture and risks of surgical intervention. N Engl J
Med 1998;339(24):1725-1733
68. Spetzler RF, McDougall CG, Albuquerque FC, Zabramski JM, Hills NK, Partovi S,
Nakaji P, Wallace RC. The Barrow Ruptured Aneurysm Trial: 3-year results. J
Neurosurg. 2013 Jul;119(1):146-57
69. Wiebers DO, Whisnant JP, Huston J III, et al; International Study of Unruptured
Intracranial Aneurysms Investigators. Unruptured intracranial aneurysms: natural
history, clinical outcome, and risks of surgical and endovascular treatment. Lancet
2003;362(9378):103-110
70. McCormick WF, Acosta-Rua GJ. The size of intracranial saccular aneurysms. An
autopsy study. J Neurosurg 1970;33(4):422-427
71. Juvela S, Porras M, Poussa K. Natural history of unruptured intracranial aneurysms:
probability and risk factors for aneurysm rupture. J Neurosurg 2000;93(3):379-387
72. Hacein-Bey L, Connolly ES Jr, Mayer SA, Young WL, Pile-Spellman J, Solomon
RA. Complex intracranial aneurysms: combined operative and endovascular
approaches. Neurosurgery. 1998 Dec;43(6):1304-12; discussion 1312-3
73. Krisht AF, Krayenbuhl N, Sercl D, Bikmaz K, Kadri PA. Results of microsurgical
clipping of 50 high complexity basilar apex aneurysms. Neurosurgery 2007
Feb;60(2):242-250 discussion 250-252
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CHAPTER 9
SURGICAL MANAGEMENT OF INTRACRANIAL ANEURYSMS
IOAN-TEFAN FLORIAN, CLAUDIU POPA, IOAN-ALEXANDRU FLORIAN
INTRODUCTION
The purpose of surgical treatment of intracranial aneurysms is preventing
aneurysmal enlargement and/or rupture while at the same time preserving the
integrity of normal vasculature, cranial nerves and cerebral parenchyma.
Usually, this objective is achieved by placing a clip at the neck of the aneurysm.
SURGICAL EXPOSURE
The ideal surgical exposure involves adequate brain relaxation and a sufficiently
wide bone opening. The former is vital in certain placements of aneurysms, such
as ACoA or basilar apex aneurysms. However, when aneurysms are more easily
accessible (as is the case of MCA and PCoA aneurysms), brain relaxation is not as
important. Methods for realizing brain relaxation are:
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Hyperventilation
CSF drainage, which offers a dry surgical field and helps removing
blood and fibrin degradation products. This is realized through:
Ventriculostomy: the ventriculostomy catheter can be placed pre- or
intraoperatively and may have a number of complications (seizures,
bleeding at point-of-insertion, infection, heightened risk of
vasospasm)
Lumbar drainage: this is performed usually after anesthesia as to
avoid inducing arterial hypertension. In our unit, we use two types of
lumbar drainage:
AN INTRODUCTION TO
Through a lumbar puncture needle, which offers swifter

decompression, but can cause aneurysmal rupture. This drainage
method implies removing the needle only after lifting the
craniotomy flap. Drainage is allowed only up to 20-30 ml of CSF,
resulting in moderate brain relaxation and avoiding aneurysmal
rupture.
Through a drainage catheter, which grants a slower decompression,
but has the advantage of removing large amounts of CSF through a
Touhy 16 needle. On the one hand, there is a risk to abruptly
decompress the brain and rupture the aneurysm if this maneuver is
performed before surgery. On the other, catheter drainage provides
an adequate postoperative control of the aspect of CSF, avoids
painful repeated lumbar punctures, and offers protection against
fistulas in the event of an accidental opening of the frontal sinus.
Accidents reported in this maneuver are: aneurysmal rupture (0.3%),
chronic lumbar pains, drainage malfunction (5%), drainage fracture
in the subarachnoid space and consecutive CSF fistula, headache,
infection, neuropathy, and epidural spinal hematoma.
Intracisternal drainage: in our opinion, this is the most effective method of
intraoperative brain relaxation. Opening the basal cisternae and the Sylvian
valley, and extracting the occasional blood clots allows surgical comfort and
sufficient brain relaxation in the great majority of cases.
Administration of diuretics: Mannitol and Furosemide may, in theory,
elevate the risk of rupture.
CRANIOTOMY
The bone opening (craniotomy) must be:
Utterly adapted to the location, size and morphology of the aneurysm;

Able to reveal the Circle of Willis as basally as possible, thus reducing
the traction suffered by the brain;
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Spacious enough for the surgeon to explore the main blood vessels and to
allow ample room in case of unforeseen events (aneurysmal rupture or
detachment, lesion of the proximal artery and so forth)
The classical pterional flap described by Yaargil is the pathway most
authors employ in the case of anterior circulation aneurysms, as well as the
majority of basilar apex aneurysms. We utilize a slightly modified pterional
craniotomy (frontal-temporal) for anterior circulation and supraclinoid basilar
aneurysms. We also used this approach to treat multiple bilateral aneurysms, with
one exception (in which case the bleeding emerged from the distal segment of A2
and we were required to use a bifrontal-pterional approach).
The indications for frontal-temporal approach are suprasellar and
parasellar lesions. On a sagittal plane, this approach can extend from the anterior
planum sfenoidale to the basilar artery level. On a frontal level, it can range
from the sellar diaphragm to a perpendicular level 1.5-2 cm away from it. Based
on the majority of authors and their reports, the greatest disadvantage of the
pterional approach is compromising the visibility of the contralateral optical nerve
and internal carotid artery. In our surgical experience, however, this disadvantage
persists only concerning the visibility of aneurysms of the contralateral PCoA and
anterior choroidian artery. This said, we have had only two cases of multiple
aneurysms in which we succeeded in clipping a contralateral PCoA aneurysm.
Using this approach, even the opposite MCA bifurcation may be accessed.
This type of craniotomy offers lateral subfrontal and Sylvian valley
access of aneurysms. Interstitial spaces of access are the interoptic-carotid,
ineroptic-chasm, suprachasmatic translaminaterminalis, and supracarotid
spaces, and the triangle made by the carotid artery and the oculomotor nerve. By
enlarging the craniotomy posteriorly (half-and-half), one can even clip
aneurysms near the basilar apex (superior cerebellar, posterior inferior cerebellar,
and posterior-superior-oriented basilar apex aneurysms).
Patient positioning. Generally, dorsal decubitus with a soft support of
the ipsilateral shoulder is recommended.
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The scalp incision starts at approximately 1 cm anterior to the tragus, just

above the zygomatic arch. Based on the location of the aneurysm, a slightly
anterior-driven incision will be performed. This allows a trepanation hole to be
placed above the middle of the superciliary arch (Figure 9.1)
Figure 9.1 - Frontal craniotomy incision. In this case, an anterior frontal

extension of the incision was performed to assure larger access of the
subfrontal region.
To preserve the frontal branch of the facial nerve, we perform an
interfascial dissection, exposing the flap on its entire surface and inferiorly until
this reaches the zygomatic arch (Figure 9.2).
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Figure 9.2 - Interfascicular dissection of the cutaneous flap.
Figure 9.3 - Bone flap periosteum removal.

We have modified the classical method of craniotomy, described as
having 4 burr holes, by placing the anterior hole above the middle of the
supraorbital margin. The so-called key-hole, the most important of the four, is
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AN INTRODUCTION TO
positioned at the orbital-frontal angle. The second hole is made at the middle of
the coronal suture. The third one is made in the mediotemporal region and the
fourth in the temporal fossa, as low as possible (Figure 9.4).
Image 9.4 - Burr hole placement.

Once the bone flap is lifted, resection of the sphenoid wing is performed,
as close to the anterior cranial fossa as possible. Simultaneously, subtemporal
craniotomy is executed. The importance of this maneuver is great, since it
provides a large access toward deep structures while also diminishing the need for
brain retraction (Figure 9.5).
Decompressive lumbar puncture is usually practiced before opening the
dura mater. Its effects are almost immediate, the brain becoming pulsatile. Thus,
the tension in the dura mater decreases and the epidural space broadens.
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Figure 9.5 - Resection of the external 1/3 of the sphenoid wing.
DURA MATER INCISION

The dura mater is incised in an arch, from the posteriormost trepanation hole to
the anteriormost, at a distance of 2 cm from the sphenoid bone. The dural flap is
suspended inferiorly while the rest of the dura mater is left in its place, thus
protecting the brain (Figures 9.7 and 9.8).
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Figures 9.7 & 9.8 - Arcuate opening of the dura mater.

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DISSECTION
For adequately exploring the optochiasmatic region, opening the Sylvian valley is
mandatory. This operation may sometimes be challenging due to extant arachnoid
adhesions. Opening the Sylvian valley is simplified firstly by decompressive
lumbar puncture (performed earlier), and secondly by the aperture of the
pericarotid cistern deep within this valley. We begin opening the valley just above
the optic nerve, at the site where the arachnoid is further from the cortex,
regardless of whether this space is situated more laterally or medially. Afterward,
we dissect the valley until obtaining a sufficiently wide breach, extending it both
laterally and medially. At first, we do not employ any surgical instruments other
than a fine aspirator and a pair of microsurgical scissors. This way, we avoid
generating any decubitus lesions of the basal surface of the brain. Once we make a
small breach within the cistern, spontaneous CSF evacuation is achieved through a
soft tampon applied at the tip of the aspirator. Thus, an additional brain relaxation
is accomplished. By now the brain is suitably relaxed as to permit continuing the
dissection.
From this point on, the dissection may resume toward the location of the
aneurysm. For ACoA aneurysms, we dissect medially, whereas for aneurysms
involving the PCoA and choroidal arteries we continue laterally from the ICA
(Figures 9.9, 9.10, 9.11 and 9.12)
Regarding ICA bifurcation aneurysms, dissecting along this artery itself is
required. We usually focus on the lateral portion of the Sylvian valley, which we
dissect medially. The reason for this is to circumvent any chance to apply
excessive traction on the frontal lobe, traction that may detach a thrombus off the
ICA bifurcation aneurysm. Once the valley is entirely open, the ICA bifurcation is
visible. Above this element, the neck of the aneurysm can be distinguished, and
then dissected and isolated from the surrounding perforating vessels.
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Images 9.9 & 9.10 - Anatomic relationships include the optic nerve,
which is the first to appear in the surgical field. Careful dissection of
the arachnoid permits the visualization of the ipsilateral ICA, situated
on a deeper plane than the optic nerve (with which it forms the opticocarotid triangle).
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Figures 9.11 & 9.12: Medial dissection permits total exposure of the
optic chasm, the contralateral A1 segment, as well as the contralateral
ICA. Continuation of the dissection allows access of the contralateral
M1 bifurcation.
Concerning MCA aneurysms, we recommend dissecting the ICA laterally

toward the bifurcation, as well as the initial portion of the MCA, so as to attain
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proper access of the vessel proximal to the aneurysm. Lateral dissection of the
valley can then be resumed, thus allowing for a shorter and relatively safer path
toward the aneurysm. Should intraoperative rupture of the aneurysm occur, we
discourage applying the temporary clip on the initial portion of the MCA longer
than 2-3 minutes (even if proximal control of this artery is attained). This amount
is usually more than enough to identify the M1 proximal to the aneurysm, where
the temporary clip may be reapplied for longer periods of time (8-10 minutes).
Basilar apex aneurysms can be approached through the
interopticocarotid triangle. Because the first aneurysmal component that pops
up in the surgical field is the fundus, access to this type of aneurysm raises a
number of difficulties. In the case of rupture, the situation may become dire, since
applying a temporary clip on an undissected and unisolated basilar artery is
performed at random and with the risk of affecting small-caliber vessels. These
vessels may be vital from a functional standpoint. Therefore, controlled
hypotension is recommended in this scenario (60-70 mmHg), along with placing a
clip on the dome of the ruptured aneurysm (to reduce the hemorrhage), and
dissecting and isolating the aneurysmal neck. Once the neck is in reach and as long
as the conditions are optimal, a permanent clip may then be applied.
CLOSURE
Closure is unexceptionally performed after rigorous hemostasis. This requires not
only frequently used hemostatic materials (such as Surgicel and Gelfoam), but also
a great amount of patience.
In all of our cases, we have used periosteum patch plasty to close the
dura mater. The periosteum is the most readily available material, as well as the
one having the greatest plasticity and tissue tolerance.
Nonresorbable threads are utilized to close the anatomic layers.
Subgaleal external drainage for a 48-hour period is, in our opinion, mandatory.
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We have employed this approach for 220 out of our 224 surgically treated
cases. The other types of opening will be presented in the chapters committed to
the anterior and posterior circulation aneurysms respectively.
INTRAOPERATIVE CEREBRAL PROTECTION

From a pathophysiological perspective, cerebral metabolism changes occur when
the cerebral metabolic rate of oxygen consumption (CMRO2) falls under a
certain threshold, due to an occluded artery. The territory supplied by said artery is
comprised of an ischemic tissue core, where neurons die in mere minutes, and a
penumbra (where marginal oxygenation is maintained, usually through the
leptomeningeal vessels). It may take up to several hours for the cells in the
penumbra to suffer irreversible damage. Cerebral protection against ischemia is
achieved by raising cerebral tissue tolerance to hypoxia. Protective agents act
through either preserving CMRO2 (Calcium channel blockers, free radical
scavengers, or Mannitol), or reducing CMRO2 by lowering neuronal electric
activity (barbiturates, Etomidate, or Isoflurane) or decreasing neuronal
maintenance energy (hypothermia remains the sole factor that can achieve this
purpose). Hypothermia has four grades:
Mild hypothermia, with core temperature down to 33OC may have

beneficial effects;
Moderate hypothermia, with temperatures between 32.5 and 33 OC has been
used for head trauma;
Deep hypothermia from 32 to 18OC allows the brain to tolerate circulatory
arrest for up to 1 hour;
Profound hypothermia, with temperatures lower than 10OC, permits several
hours of complete ischemia (although this has unconfirmed clinical efficacy)
Adjunctive cerebral protection techniques: Systemic hypotension is
usually employed during manipulation and dissection of the aneurysm and has two
theoretic purposes, namely reducing aneurysmal turgor (to facilitate clip closure
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especially in the case of atherosclerotic neck) and diminishing transmural pressure

(to decrease the risk on intraoperative rupture). Some surgeons avoid this method
because of possible systemic hypoxia injuries.
Focal hypotension is achieved through the use of temporary clips,
specifically devised to avoid intimal injury of the vessel. These are placed on the
parent arteries, upstream of the aneurysm. Systemic hypertension may be
adjoined with this method to increase collateral flow. The proximal segment of the
ICA can sometimes tolerate an hour or more of occlusion, although perforatorbearing portions of the MCA and the basilar apex may only abide several minutes
of temporary clipping. Among the most noted complications are intravascular
thrombosis and thromboembolism subsequent to removing the clip.
Some authors deem the use of temporary clips as being necessary in these
following cases: giant aneurysms, calcified neck, slender and fragile domes,
adhesion of dome to vital structures, perforators that arise from the vicinity of
the neck, and intraoperative aneurysmal rupture. Likewise, heparin might be used
to prevent thrombosis, whereas Thiopental, Etomidate, and Propofol may be
utilized when temporary clipping surpasses 10 minutes (so as to reduce neuronal
metabolism).
Circulatory arrest is used in conjunction with deep hypothermia. This
technique may be employed for patients harboring large aneurysms with
atherosclerosis and/or thrombosis and when the aneurysmal dome adheres to vital
cerebral structures.
ANEURYSMAL REST
Aneurysmal rest refers to the case in which clipping of the entire neck is not
feasible, leaving a free triangular-shaped section. This is not entirely harmless,
retaining a tendency to rupture throughout the years even at dimensions of 1-2
mm. The classification of aneurysmal rest is accredited to Drake (1967). More
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recently, Sidou et al. have proposed a new method of classification that may also
present reasons for additional clipping. Other surgeons encourage the necessity of
careful planning concerning adequate therapy of these aneurysmal rests:
endovascular approach, or direct surgical treatment. The incidence of
rebleeding in these cases stands at 3.7%. Postoperative follow-up must include
seriate angiography examinations. Any and all signs of aneurysmal rest growth
sanction either surgical or endovascular approach. A rebleeding incidence of 25%
has been cited at a 10-year postoperative follow-up of patients presenting with
aneurysmal rest.
ANATOMIC PRINCIPLES OF SURGICAL APPROACH
1) The parent vessel of the aneurysm must be exposed proximally to establish
blood flow control in the event of intraoperative aneurysmal rupture.
2) If possible, the main ipsi-/contralateral main vessel must be dissected
before the aneurysmal neck.
3) Dissection of the neck should precede fundus anatomization.
4) Before placing the permanent clip, all perforators must be separated from
the aneurysmal neck.
5) In the case of intraoperative rupture, certain objectives must be met:
tamponing, temporary occlusion, and lowering arterial pressure.
6) The permeability of large vessels and perforators should be confirmed
immediately after inserting the clip.
7) Bipolar coagulation can adjust the diameter of a large neck.
INTRAOPERATIVE ANEURYSMAL RUPTURE

Intraoperative aneurysmal rupture (IAR) is an undesirable event that should be
prevented and considered as integrating part of the surgical treatment of ruptured
intracranial aneurysms. Authors report an IAR incidence between 18 and 40%.
The epidemiology is on a continuous decline especially as a result of increasing
worldwide surgical experience and a greater expertise of rupture probability
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AN INTRODUCTION TO
factors. If we consider that this risk peaked at 50% in the pre-microscopic age,
current data reveals that the number might have actually dropped to around 8.6%.
Morbidity and mortality of aneurysms increase with rupture by 20-25%.
This complication is exceptionally more threatening the earlier it occurs, during
anesthesia or opening of the dura mater. The aims of the neurosurgeon in this
scenario are: hemostasis, avoiding further aneurysmal damage, preventing
accidentally injuring main vessels and perforators, and clipping the aneurysm.
Precluding aneurysmal rupture involves certain measures: positioning the
patient in a way such that cerebral reduction is minimized, careful induction of
anesthesia, preventing hypertension during the painful stages of surgery, and
incision or head support fixation; eradicating the causes of transmural pressure
increase; simplification of access and aneurysmal dissection through a sufficiently
wide craniotomy and brain relaxation; using sharp instruments and dissecting
carefully so as to reduce the risk of extensive aneurysmal damage. Any method
that decreases cerebral retraction can lower the risk of rupture. Tempestuous
cerebral retraction in the initial phases of surgery can induce additional stress upon
the aneurysmal fundus and lead to overwhelming rupture and hemorrhage.
Lumbar or external ventricular drainage also assist in brain relaxation.
Some authors recommend cannulation of the frontal lobe as soon as the dura mater
has been opened (no occurrence of IAR in a series of 1500 patients who underwent
this maneuver), while also oppose lumbar drainage (which decreases intracranial
pressure in a chaotic manner). Frontal lobe cannulation also allows for better
control over intracranial pressure reduction.
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Operative stage
Initial exposure
Characteristics and treatment procedures

Rare. Cerebral mass becomes tensioned.
Causes:
Vibrations during drilling;
Intramural pressure growth upon opening the
dura;
Painful-phase hypertension;
Measures:
Decreasing arterial pressure;
Applying temporary clip, or ICA compression;
Frontal/Temporal cerebral resection.
Aneurysm
Causes:
dissection
Blunt surgical instruments: proximally from the
neck, difficult to control;
Sharp surgical instruments: minimal fundus
lesions;
Measures:
Damage caused by blunt instruments: temporary clip,
or lesion microsuture;
Damage caused by sharp instruments: tamponing,
suction, or coagulation.
Applying the clip Causes:
Insufficient aneurysmal exposure (blunt injury);
Flaws of the clip.
Based on Mark S. Greenberg, 2006.
Table 9.1: Characteristics of IAR
The phase of aneurysmal neck microdissection is associated with the highest
occurrence of IAR prior to applying the clip. Currently, there is a consensus
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regarding the use of sharp surgical instruments, which generate much more easily
controllable lesions.
In the event of early surgical phase aneurysmal rupture (preceding
aneurysmal microdissection), regional corticotomy might be sanctioned.
Sometimes, frontal or temporal lobectomy may be required to attain control over
the hemorrhage. The reasons for early IAR appear to be inadequate management
of arterial pressure, technical aspects that are correlated to lifting the craniotomy
flap, or uncontrolled drainage of CSF.
The basic rule of microdissection is obtaining proximal and distal
vascular control in its initial stages. In some cases, this may consent extracranial
exposure of vessels (for example, the cervical segment of the ICA, or the atlas
portion of the vertebral artery). This method of external compression of the
cervical ICA (performed by the anesthetist during aneurysmal rupture) seems to
subject the patient to unnecessary additional risks, as well as creating a lowvisibility surgical field.
Another aspect that should be taken into consideration is the path chosen
by the neurosurgeon to expose and dissect the region through the subarachnoid
space. If feasible, dissection must follow the natural anatomic path toward an area
concealed by a blood clot. Tempestuous aspiration of said clot ought to be
avoided, instead utilizing sharp instruments.
Temporary arterial occlusion is believed by most surgeons to be one of
the paramount measures in both prevention and control of aneurysmal rupture.
This maneuver can be coupled with the administration of certain agents that
protect the brain from ischemia.
In our practice, we apply temporary clips only in case we anticipate a
challenging dissection: giant aneurysms, polylobated aneurysms, or lesions that
have recently bled. Emergency surgical treatment builds the foundation for
aneurysmal rupture, while generally impressive cerebral edema makes for difficult
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brain retraction. This is the reason why, in case of early IAR (during induction,
craniotomy, or the initial stages of dissection), first and foremost we dissect the
ICA and apply a temporary clip at this level (preferably distal to the emergence of
the anterior choroidal artery). In some cases, this desideratum is not possible and
therefore the temporary clip is placed on the ICA just laterally to the optic nerve,
offering some measure of surgical comfort. The time gap is no longer than 8-10
minutes, however repeatedly removing and reapplying the clip (also in 8-minute
intervals) may allow for successful dissection of the ruptured aneurysm. A
permanent clip is then placed at the aneurysmal neck in 20-25 minutes at most.
The challenges that may arise as a result of rupture are a hemorrhagic
microsurgical field, accidental occlusion of the parent vessel or the perforators,
and substantial blood loss. Each and every location of intracranial aneurysms has
its own unique features concerning regional anatomy. These features can be used
in conceiving a targeted surgical approach, so as to effectively avoid or amend
aneurysmal rupture.
Ophthalmic artery IAR can be problematic to manage in the situation of
deficient proximal exposure and aneurysmal placement below the optic nerve or
the anterior clinoid process. This type of IAR is usually early, due to adhesions
between the aneurysmal dome and the optic nerve, although rupture can also
occur during neck dissection and clipping. Therefore, some authors support the
necessity of cervical ICA exposure before craniotomy, a method that can be useful
in the event of performing intraoperative angiography. In a few cases of surgically
treated ophthalmic artery aneurysms, resection of the anterior clinoid and
eventually opening the optic canal on a length of 2-3mm were sufficient for
aneurysmal clipping, rendering cervical ICA exposure unnecessary.
PCoA aneurysms have a more pronounced tendency to rupture because
of the adhesions between the aneurysmal dome and the medial surface of the
temporal lobe, or the anterior choroid artery. Thus, bleeding happens at the time of
temporal lobe retraction, or neck microdissection and clipping. In the last
scenario, clipping should be paused while temporary occlusion is initiated. This is
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AN INTRODUCTION TO
the exact reason why we start the dissection in the subfrontal region, above the
optic nerve. From this level, we begin isolating and dissecting the ICA,
establishing vigilant proximal control. In the case of a subtentorially extended
aneurysm, any sudden movement can lead to rupture and therefore applying a
temporary clip on the ICA may be the necessary course of action.
There are three possible circumstances in which ACoA aneurysms
rupture: in the initial stages of microdissection (rough retraction of the frontal
lobe must be avoided, especially in the anteriorly or posteriorly oriented variants
which adhere to the optic chasm or the floor of the anterior fossa), microdissection
of an aneurysmal neck arising at the origin of the A2 (temporary occlusion of both
A1 segments is required), or the final stages of neck dissection (which necessitates
temporary bilateral occlusion of both the A1 and the A2). Resection of the gyrus
rectus proves highly useful, mostly succeeding the dissection of both A1
segments. The anatomy of these aneurysms is generally complex and angiographic
exploration does not always yield adequate coordination. On the other hand,
frontal lobe traction may alter normal anatomic rapports. These are the motives for
which we recommend proximal control on both A1 segments in all cases of ACoA
aneurysms. In the event of rupture, clipping will take place as near to the neck as
possible, firstly on the same side, and, should this not generate sufficient
hemorrhage reduction, a second clip will be placed on the contralateral A1.
ICA bifurcation aneurysms are in most cases adherent to the inferior
surface of the frontal lobe and have a higher leaning toward rupture than
aneurysms of the same caliber and different location. Frontal lobe retraction can be
limited if the ipsilateral Sylvian valley is dissected. Temporary occlusion is
performed above the origin of the anterior choroidal artery, which is a terminaltype artery and can only endure occlusions of up to 15 minutes. A1 temporary
occlusion is executed if the ACoA receives blood flow from both A2 segments.
MCA aneurysms rupture either early during Sylvian valley dissection
procedures (when a second aspirator, dissection, and clipping of the M1 are
required), or during neck microdissection (in this scenario, we recommend
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temporary clips placed on both the M1 and the M2). Although, in theory, these are
much more easily approached, MCA aneurysms raise a series of difficulties
regarding valley dissection (the arachnoid can sometimes be thickened and
adherent, especially when hemorrhage occurred more than 14 days prior to
surgery), large aneurysmal neck, the emergence of the M2 segments on a long
portion of the neck, and the occasional presence of a trifurcation. All of these
features, along with a diminished occlusion tolerance of the M2, are decisive in
labeling the MCA as a challenging placement for aneurysms.
One of the most demanding complications of surgery is early rupture of a
basilar apex aneurysm. Consequently, adequate craniotomy is essential, as well
as CSF drainage, large basal exposure, and proximal vascular control (basilar
artery, superior cerebellar artery, PCA). Rupture occurs either during initial
dissection, or while clipping (in both cases, temporary occlusion and additional
aspiration are used).
Considering the anatomic features of the region, aneurysms affecting the
inferior portion of the basilar artery, PICA, or AICA are prone to rupture. Hence,
proximal arterial control and temporary clipping must be performed as soon as
possible during dissection.
Translated by Ioan-Alexandru Florian from: Florian IS, Perju-Dumbrav L.

Opiuni Terapeutice n Accidentele Vasculare Hemoragice. Editura Medical
Universitar Iuliu Haieganu Cluj-Napoca 2007
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CHAPTER 10
ARTERIOVENOUS MALFORMATIONS
INTRODUCTION
Among the non-neoplastic cerebral lesions, arteriovenous malformations
(AVMs) account for the majority of hemorrhagic strokes below the age of 35
years. AVMs are also the main cause of neurologic deficit or mortality in young
adults. Therefore, well-defined diagnostic and treatment algorithms are substantial
in the management of AVMs.
William Hunter received credit for providing many important early
concepts on extracranial arteriovenous malformations in his 1762 monograph. His
descriptions formed the basis for the analyzing conflicting theories regarding the
pathophysiology and development of AVMs. In the mid 19 th century, Rokitansky
was the first to comprehensively portray angiomas of the intracranial cavity.
However, in his opinion, these were vascular tumors. Not long after, Virchow and
others polished Rokitanskys description so as to include a somewhat rudimentary
classification of arterial, venous, arteriovenous and cystic angiomas, as well as
telangiectasias. It was Virchow who postulated that only a small percentage of
these lesions were neoplastic, and that the rest were, in fact, congenital anomalies.
The first well-documented case of a successful AVM excision was
performed in 1889 by Pean, a French general surgeon. The patient was a 15-yearold boy who presented left-sided seizures and a right-sided fronto-parietal lesion,
namely an AVM. Afterward, Cushing and Dandy contributed to the history of
AVM treatment with their individual series of 14 and 15 cases, respectively.
Even so, the most important event in the treatment of AVMs to this day is
considered to be the development of intracerebral angiography. The
development of embolization and endovascular procedures represent other
milestones in the treatment of these lesions, as does the progress of neuroimaging.
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Today, functional mapping and frameless stereotaxis assist the

localization of AVMs. Endovascular procedures are perpetually improved,
although regardless of these advancements some patients are currently beyond any
assistance. Also, there are still numerous questions left unanswered concerning
AVM from both a medical and a scientific point of view. Yasargil and colleagues,
who have written a comprehensive review on historical developments of AVMs,
assure us that these dilemmas have existed ever since their discovery. That is
precisely why AVMs are in a neurosurgical spotlight, as not only diagnosis and
excision are key aspects of their treatment, but understanding them as well.
CLASSIFICATION
An exact description of AVMs is challenging, since their characteristics depend on
the quality of the post-mortem specimen. They differ in terms of bleeding
tendency as well as growth rate. McCormick defines four types of vascular
malformations:
1.
True arteriovenous malformations share a common pathology, which is

direct arterial shunting into draining veins without the interposition of
capillaries. Most vessels within an AVM resemble veins in morphology,
although transitional vessels have also been described. Focal lesions are
usually compact, with no intervening neural tissue, while diffuse AVMs
include cerebral parenchyma between abnormal vessels. However, their
tendency to bleed depends on the histology and pathology of these lesions,
and not so much on their morphology. Hemosiderin deposits and atypical
gliotic tissue can be identified through microscopic examination after a
bleeding event. Consequently, thrombosis and reparative fibrosis (and in
some cases calcifications) ensue after these microhemorrhages. AVMs may
or may not be singular or associated with other vascular lesions. While
venous malformations do not present a clinical correlation, arterial
aneurysms have important clinical and surgical implications. These arterial
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CHAPTER 10: ARTERIOVENOUS MALFORMATIONS
aneurysms have been categorized as intranidal, flow-related, or unrelated to

the AVM nidus itself. The intranidal aneurysms add to the risk of bleeding of
the AVM, whereas patients with flow-related aneurysms may present
hemorrhage from either lesion.
2.
Venous malformations are composed of anomalous veins parted by normal

neural parenchyma. These malformations may represent a single tortuous,
profoundly dilated vein, or several veins converging at a single point. An
invariable trait is the absence of arterial input. They have been described as
the most frequent type revealed by autopsy. The venous phase of an
angiogram shows their characteristic appearance described as caput
medusae. On contrast-enhanced CT and conventional MRI, venous
malformations appear as linear signals in unusual locations. These lesions are
considered clinically benign, any hemorrhage arising from one being
secondary to a neighboring cavernous malformation.
3.
Cavernous malformations are comprised of cystic vascular spaces

belonging to sinuous vessels, lined by a single endothelial layer. Recently it
has been discovered that the endothelial cells lack tight junctions. The
ensuing compact mass leaves no room for neural parenchyma to develop
within. Gross examination reveals well-circumscribed focal areas of reddishpurple discoloration. Diameters tend to vary, reaching up to a few
centimeters. Hemorrhage leads to hemosiderin deposits, reactive gliosis and
possibly calcification. Since these lesions are in want of direct arterial input,
conventional angiography renders them almost undetectable. They are,
however, visible on MRI, having a specific appearance and heterogeneous
pattern.
4.
Capillary telangiectasias are formed entirely by capillary-type blood

vessels. They closely resemble normal capillaries and, as opposed to
cavernous malformations, are surrounded by normal cerebral parenchyma.
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They seldom leave sequelae such as thrombosis or bleeding, despite their

frequent occurrence in the pons. Because of their low propensity to bleed,
capillary telangiectasias do not present a hemosiderin rim. It has been
considered1 that capillary telangiectasias are in fact nascent forms of
cavernous malformations, as both were present in the same patients, along
with what they described as intermediary forms.
A fifth category has been considered, that of direct arteriovenous

fistulae, presenting an undeviating connection between one or more arteries and a
vein. The interposing nidus is absent. Blood flow occurs at high pressures. Such
examples are the vein of Galen aneurysm, dural aneurysms and the carotidcavernous fistula.
The Spetzler-Martin grading scale is currently the most employed. It
takes into account the size, placement and drainage method of the AVM.
Obviously, this classification offers precious data on prognosis, evolution and
treatment indications, albeit being considered somewhat rudimentary.
Small (<3 cm)
1 point
Medium (3-6 cm)
2 points
AVM size
Large (>6 cm)
3 points
Ineloquent
0 points
Adjacent cerebrum
eloquence
Eloquent
1 point
Superficial
0 points
Venous drainage
Deep
1 point
Table 10.1: Spetzler-Martin grading scale, with score for every criterion
An eloquent cerebral portion, through its lesions, leads to neurologic
motor or sensory deficit, or superior integration function deficit. The score given
Rigamonti et al, 1991

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AND AVMs
by this classification can have a value between 1 and 5, thus defining the SpetzlerMartin grade. As such, a medium-sized AVM in an ineloquent cerebral area with a
deep venous drainage has a grade III on the Spetzler-Martin scale. But so does a
small AVM affecting an eloquent cerebral area (for example the parietal lobe) and
a deep venous drainage.
In conclusion, grades I and II usually have a low mortality and morbidity
rate, while a grade V AVM may be considered inoperable, with severe neurologic
deficit. It is clear why this classification is not merely useful, but also imperative
before initiating the treatment of the patient.
EPIDEMIOLOGY
The true epidemiology and natural history of AVMs is difficult to determine, due
to the heterogeneity of patient populations and variable institutional bias towards
treatment. International detection rates range from 0.9 to 1.2 per 100,000 personyears, however the true number of these lesions is thought to be far greater. It is
considered that approximately 0.1% of the global populace harbors at least one
AVM, most of which belong to the clinically benign types. Only 2% of AVMs are
multiple lesions.
As previously mentioned, AVMs are the main cause of hemorrhagic
stroke episodes under the age of 35 years and the most frequent cause of
neurologic deficit or mortality of individuals under 20 years of age. Death occurs
in 10-15% of patients who present hemorrhage, while morbidity occurs in 30-50%.
In population-based studies, 38-70% of intracranial AVMs initially present with
hemorrhage. Initial presentation may be indiscernible from other causes of
hemorrhage. The risk or rebleeding is high, especially during the first year after the
initial hemorrhage. Features associated with the risk of bleeding are the male
gender, an AVM of small size, posterior fossa or basal ganglia location, deep
venous drainage, reduced number of draining veins, high pressure in feeding
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arteries (as measured during angiography) and arterial aneurysms (whether

intranidal or flow-related).
The neurological deficit in an AVM-related hemorrhage is usually less
severe than that caused by a non-AVM-related hemorrhage. Recovery tends to be
better, as a result of both the young age of patients and the functional
reorganization of the cerebral parenchyma in patients with AVMs.
Seizures and epilepsy (focal or secondarily generalized) that are
unrelated to hemorrhage occur as the principal symptom in 15-40% of patients
presenting an AVM. The young age of patients, large AVM diameter, location in
the temporal lobe and feeders from the middle cerebral artery (MCA) are usually
associated with seizures. Anticonvulsivants comprise the standard treatment.
AVMs rarely lead to headache, however this may be the presenting
symptom for 4-14% of patients. Headache may be typical for migraine, or (less
specifically) more generalized.
MORPHOLOGY
The morphologic characteristics of an arteriovenous malformation are the arterial
inflow, the nidus and the venous drainage.
1.
The arterial inflow consists of one or more arteries that supply the AVM
with arterial blood. They derive from the normal arterial circulation of the
cerebrum, however the vessel wall structure may present alterations. Blood
pressure in these abnormal arteries is lower than normal as a result of the
absence of peripheral resistance of the blood flow, normally generated by
capillary networks. As is the case with AVMs, the abnormal arteries drain
directly into low-pressure veins, causing the atrophy of the tunica media and
the adventitia. A high blood flow in these arteries may cause aneurysmal
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AND AVMs
dilation, which in turn may lead to subarachnoid or intraparenchymal

hemorrhage.
2.
The nidus is the main component of the AVM, the body, so to speak. It is
mainly an entanglement of abnormal, tortuous vessels that present variable
trajectories, calibers and lengths. Normal neural tissue usually cannot be
identified within the nidus. It is instead replaced by hemosiderin-impregnated
gliosis tissue, along with possibly thrombosis and even calcification.
Intranidal aneurysms possess a risk of rupture, adding the overall risk of
bleeding from the AVM itself. The size of the nidus can vary from just a few
millimeters to several centimeters (reaching even to an entire hemisphere), as
is the case of giant AVMs. Arteriovenous malformations tend to enlarge
where the arterial inflow is heightened, by engaging additional veins.
3.
The venous drainage concludes the malformed arteriovenous route by

routing the arterial blood (that has not participated in nutrient and oxygen
exchange) into the venous circulation. Since the pressure in these particular
veins is higher than normal, it may lead to the vascular steal phenomenon,
depriving adjacent cerebral tissue of blood supply. Drainage can take place
into the dural sinuses (constituting superficial drainage), or the deep veins.
Arterialization is a process suffered by many of the drainage veins,
becoming larger in diameter (sometimes even aneurysmal in appearance)
with thickened walls, a tortuous trajectory and can occasionally be pulsatile.
Although capillaries are absent within the AVM, a proliferation of

capillaries can be noted at the periphery of the malformation itself. As previously
stated, aneurysms may be identified inside or associated with the AVM. They can
be of the following types: intranidal, flow-related or unrelated to the malformation.
As placement, AVMs can be found anywhere in the cerebrum, but also
intramedullary. The majority is located supratentorial, especially at the branches
of the MCA.
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PATHOGENESIS
Regarding the pathogenesis of AVMs, two hypotheses have been widely
discussed: embryonic agenesis of the capillary system and retention of
primordial vascular connections between arteries and veins. However, capillary
network agenesis would most likely result in brains lacking capillaries entirely, not
just focally. This is the reason why a different etiology must be incriminated.
AVMs are most likely the result of a combination of factors: the arrest of capillary
development in a certain area and the induced development of dysplastic vessels
from primordial vascular connections (although the latter mechanism is still
debated).
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There are several similarities between the morphology of an AVM and

that of an anastomotic plexus of a developing vasculature in the embryo. As such,
it has been hypothesized 2 that AVM development begins during the sequential
formation and absorption of surface veins of the human embryotic growth.
Discordance between formation and absorption can potentially result in such an
anomaly. For example, the absence of the middle cerebral vein or its unsuccessful
communication with the cavernous sinus in patients harboring AVMs may signify
a late embryological development of that particular vein.
Aside from this, there are a few other embryological variants that tend to
correlate to arteriovenous malformations:
The entry of the superior ophthalmic vein into the cavernous sinus through
the inferior orbital fissure (rather than the superior one);
The relative infrequency of hemorrhage tied to the inferior petrosal sinus
fistula;
The occurrence of hemorrhage associated with a superior petrosal sinus
fistula;
The relative infrequency of blood backflow through the middle cerebral
vein in relation to a large cavernous sinus fistula;
A fusion deficit of the paired internal cerebral veins (which would explain
vein of Galen aneurysms).
Type 1 hereditary hemorrhagic telangiectasia (HHT), also known as OslerWeber-Rendu disease, has an autosomal dominant determination and is
represented by vascular dysplasia in multiple organs: cerebrum, gastrointestinal
duct and annexes and lungs. The AVMs concerning these cases have been reported
predominantly in adults. It is thought that mutation in the endoglin gene (on
chromosome 9) is the cause of this disease. Endoglin is a membrane glycoprotein
with a fundamental role in angiogenesis. Its level is reduced in the normal blood
vessels of these patients. HHT type 2 is caused by a mutation in the activin
receptor-like kinase gene (on chromosome 12) and is also autosomal dominantly
2
Mullan et al, 1996
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transmitted. However, the involvement of the endoglin gene in causing AVMs has
not been accurately demonstrated.
PATHOPHYSIOLOGY
The physiology of AVMs and the adjacent cerebral tissue can be affected by a
series of factors, including the size and location of the AVM itself, associated
vascular anomalies and the presence of hemorrhage. The key components to AVM
physiology models count the feeding artery of the lesion, the surrounding brain
(normally served by the same artery), and the arteriovenous shunt facilitated by the
AVM.
The unmediated connection between arteries and veins leads to the
abolition of peripheral capillary resistance. This in turn, eases blood flow
within these vessels, allowing for a higher velocity flow. As the arteriovenous
shunt becomes more pronounced, it will diverge blood flow towards the shunt
itself. This results in a reduction of cerebral perfusion in the vascular network
supplied by the feeding artery. This phenomenon is known as vascular steal and it
is inversely proportional to the hemodynamic resistance of the AVM. In normal
conditions, cerebral autoregulation would allow dilation of nutrient arterioles,
thus accommodating the reduced blood flow to the neighboring parenchyma.
However, long exposure to reduced perfusion pressures may result in permanent
dilation of the nutrient arterioles, which become pressure-dependent and passive
networks. Neither autonomic dilation nor constriction inputs function in this event.
Ischemia in the affected region occurs when the reduction in nutrient artery flow
exceeds the capacity for compensatory vasodilatation.
The nidus is also a site for important modifications. With the exception of
venous malformations and capillary telangiectasias, functioning brain parenchyma
is absent, being replaced by gliosis tissue (with calcifications and hemosiderin
impregnation). Blood vessel walls may also present with calcifications, hyalinosis,
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AND AVMs
and aneurysmal dilation as a result of increased velocity and pressure of blood

flow.
AVM vessels are tortuous and entangled, showing intermediary
characteristics between arteries and veins. The size of the nidus is directly
influenced by flow and pressure. The higher the pressure and the flow, the larger
the diameter and the length of the vessels become. However, the most significant
mechanism of AVM growth is represented by the recruitment of additional
vessels. This is believed to cause the progressive neurologic deficit in AVM
symptomatology. Because of the high-velocity blood flow through vessels with
varying calibers, the flow becomes turbulent, non-laminar. This might lead to
murmurs perceived by the patient, or heard through the auscultation of the eye.
Drainage veins present a higher-than-normal blood pressure that is
conveyed to the tributary veins. This phenomenon leads to the adaptation of the
vessel walls, namely arterialization. High pressure and vessel dilation may lead to
headache that is resistant to analgesics and frequently pulsatile. The presence of
AVMs in small children can even be the source of cardiac pathology, such as
congestive heart failure.
HISTOPATHOLOGICAL FEATURES AND MOLECULAR BIOLOGY

Cavernous malformations regularly have a poor blood supply through very
small arteries. It is believed that capillary telangiectasias and cavernous
malformations are variations of the same entity (the former being the early
evolution stage of the latter). The veins in vascular malformations possess
thickened and hyalinized walls, almost completely deprived of smooth muscle
and elastic tissue. These veins are generally interspersed with normal brain
parenchyma. In some situations, cavernous malformations have been shown to
drain directly into venous malformations.
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As opposed to cavernous malformations, true AVMs exhibit mature

vessel wall features, as well as a high bloodflow profile. These grant a tendency
to vascular recruitment, vein arterialization and adjacent brain tissue gliosis.
Immunohistochemistry revealed that cerebral AVMs present with actin and
myosin heavy-chains staining within vessel-wall media. SM2, a marker for the
contractible phenotype of smooth muscle cells, has also been found in the venous
components of AVMs, suggesting arterialization of these components.
The dynamic features of AVMs may be explained through recent
findings, such as the increased expression of growth factors (including Vascular
Endothelial Growth Factor, Fibroblastic Growth Factor and Transformation
Growth Factor-1) and their receptors, positive DNA fragmentation, high levels
of endothelial turnover and imbalance of matrix metalloproteinases and their
respective tissue inhibitors, as well as angiopoetin and its receptor (Tie-2). Cell
death through apoptosis is also detected in the affected vessel walls. These
findings imply that AVMs are not inert vascular anomalies, but biologically active
and dynamically changing vascular pathologies.
The perinidal brain parenchyma suffers not only neural dysfunction, but
also neural loss as a result of the disturbed circulation around the AVM itself. A
pathologically dilated capillary network is located in the vicinity of the AVM,
connected to the malformation. Also, the absence of blood-brain barrier in these
afflicted vessels has been described.
CLINICAL PRESENTATION
AVMs are generally silent from a clinical perspective. As such, diagnosis is made
at the time when the first presenting event has occurred, usually a seizure or a
hemorrhage.
Intracranial hemorrhage is evidently the most common presenting

symptom (between 50 to 75% of cases) for patients with intracranial AVMs.
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Although subarachnoid and intraventricular hemorrhages may also occur, the

most often are the intracerebral hemorrhages, due to the location of the
AVM inside the parenchyma. Intraventricular hemorrhage from an AVM has
significant differences from that of a ruptured aneurysm. First, the blood
originates from (possibly arterialized) venous channels carrying blood with
arterial pressure, and not actual arteries. Second, vasospasm is rarely
associated in these instances. And last, survival and recovery rates are
much higher than those of a ruptured aneurysm, patients improving overtime
as the parenchymal clot resorbs.
Seizures are the second most frequent symptom related to supratentorial
AVMs, affecting 25 to 50% of patients without obvious hemorrhage. The
presence of a seizure disorder alone does not warrant radical surgical
treatment of true AVMs or cavernous malformations, since effective medical
management is sufficient in controlling AVM-induced epilepsy.
Headaches are a common symptom in patients harboring AVMs, however
rare in other vascular lesions without the evidence of hemorrhage. The
headache disorder is usually unilateral and similar to classical migraine
headaches, with the notable difference being that the pain does not shift
from side to side. However, auras, visual symptomatology and severe
debilitating intermittent headaches have also been described in patients
with AVMs. Patients most prone to developing a migraine-like headache
disorder of this cause harbor AVMs in the occipital lobe.
Arterial steal is a rare, nevertheless important symptom. It is most relevant
in patients who develop progressive neurological deficits without
hemorrhage over the course of many years, as a result of high-flow AVMs.
Treatment planning for AVMs depends on the risk of subsequent hemorrhage.
Although seizure disorder is also an important factor in deciding medical or
surgical management, it alone cannot be the basis of radical surgical excision. The
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historical and angiographic features of the individual patient establish the risk of
hemorrhage. Therapeutic alternatives include:
1.
Operative resection or obliteration: Surgical treatment is the most

definitive and grants the best chance of an immediate cure. The least
important factor in deciding surgical approach is probably the presenting
symptom. The age of the patient, however, is significant. Non-symptomatic
patients over the age of 55 years present surgical risks equal to those of
allowing the lesions to develop naturally in the course of the lifetime.
Therefore, the risk of operative intervention in these patients is generally not
justified. Also crucial is the location of the AVM. Lesions in the basal
ganglia or brainstem should be treated surgically only in young patients
with symptomatic hemorrhage and important neurologic deficit. AVMs
situated in the medial hemisphere are also an operative challenge. As
opposed to these, small polar lesions can be treated even in older patients. As
previously stated, the Spetzler-Martin grading scale discriminates vascular
malformations on size, venous drainage and neurological eloquence of the
adjacent cerebral tissue. Surgical extirpation is highly recommended for
grades I and II, whereas grades IV and V are usually not amenable to this
approach alone. AVMs may be approached with craniotomy over the
cerebral convexity, through the base of the skull, or through the ventricular
system. The first step in resection in the isolation and ligation of the
arterial feeders. The nidus follows, while the draining veins are left for
last, so as not to increase the pressure while resecting the nidus.
2.
Embolization: Endovascular embolization is an important adjunct that has

known rapid improvement concerning safety and efficacy. The procedure is
facilitated by the access through the femoral artery and fluoroscopic
guidance of a catheter into the feeding artery of an AVM. The arterial supply
of the lesion is occluded through the controlled use of embolic materials
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AND AVMs
(such as wire coils, particulate slurries, pellets, small balloons or acrylate

glue). This method is almost never appropriate as the sole treatment, as a
partially treated AVM has a higher tendency to bleed than an untreated
lesion (through the increase of pressure inside the nidus). Embolization may
be performed in a single-stage, as well as a multistage approach, although
single-stage embolization offers higher safety and efficacy, despite the
apparent aggressiveness.
3.
Radiosurgery: After Cushing and Bailey first described radiation therapy for
patients with AVMs, great progress has been achieved in both improving
target resolution and associated reduction in treatment morbidity. Proton
beam, gamma knife and linear accelerator methods are used to deliver
high-energy radiation to a well-defined volume containing the AVM nidus.
Thus, the malformed blood vessels undergo gradual sclerosis over the
course of 1-2 years, obliterating the AVM. During this period, the patient is
not free from the risk of hemorrhage. The gamma knife instrument is
expensive and therefore not widely available. Proton beams and linear
accelerators are more readily available and can be easily interfaced with
standard CT and angiographically directed stereotactic equipment. Proper
dosimetry diminishes side effects to moderate occurrences of mild radiation
necrosis. However, studies also reveal that neurological sequellae may
develop following radiosurgery. Regardless of the stereotactic method
employed, radiosurgery is not effective for AVMs with a diameter larger
than 3 cm.
As a rule, venous malformations and capillary telangiectasias do not require

therapeutic intervention due to their harmless nature. Incidentally discovered
cavernous malformations are best left untreated, unless they present with
hemorrhage. Medical care is recommended for older patients or individuals
without the high-risk features of AVMs. In such patients, anticonvulsants
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(phenytoin, carbamazepine) and appropriate analgesia (either non-specific or

migraine-specific) may be sufficient.
REFERENCE
1.
2.
3.
4.
5.
Parsa AT, Solomon RA. Vascular Malformations Affecting the Nervous System.
In: Rengarchary SS, Ellenbogen RG. Principles of Neurosurgery. Second Edition.
Elsevier Mosby 2008; 14: 241-258
Hemoragice. Editura Medical Universitar Iuliu Haieganu Cluj-Napoca
2007; 2.1: 331-346
Hashimoto N, Nozaki K, Tagagi Y, Kikuta K, Mikuni N. Surgery of Cerebral
Arteriovenous Malformations. In: Apuzzo MLJ. Surgery of the Human Cerebrum.
Neurosurgery 2009; 375-389
Wurm G, Schnizer M, Fellner FA. Cerebral Cavernous Malformations Associated
with Venous Anomalies: Surgical Considerations. In: Apuzzo MLJ. Surgery of
the Human Cerebrum. Neurosurgery 2009; 390-406
Sen S, Lutsep HL. Arteriovenous Malformations. Medscape Reference. Cited 8
Jan 2014
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CHAPTER 11
ARTERIOVENOUS MALFORMATIONS CLASSIFICATION
SYSTEMS, DECISION MAKING AND CLINICAL
ORIENTATION
VICTOR VOLOVICI
Even though one would find in the old surgical/neurosurgical books references to
various attempts to handle this lesion sugically, true veritable surgery only took
place since 1960, with the most eloquent series up to this date being that of
Yasargil[1]. Around the same time, Luessenhop and Spence describe the first
embolization procedure[2]. It was only in 1980 with the appearance of the first
radiosurgical procedures that a three pylon treatment was established for
intracranial AVMs.
The same Luessenhop proposed in 1977 together with Gennarelli a
classification taking into consideration aspects of the arterial pedicles belonging
to the AVM[3], which din not take into account localization, size, age of the
patient or other criteria. In 1984 Luessenhop published another attempt at
classifying the AVMs based on their size[4,5]. In 1986, two complex classification
systems would be published, and one would be up to this date regarded as the
definitive one, even though new attempts are published every year. The first
system had 7 grades and was proposed by Shi and Chen in 1986, however it was
difficult to remember and had thus low applicability for the busy surgeon who had
to resort to sometimes rapid decisions when facing a patient[5]. The other
classification system which would remain is the one proposed by Spetzler and
Martin in the same year and published in Journal of Neurosurgery[4]. Its
unanimous acceptance is proof of its feasibility, easy application and relevance up
to this date. However, the Spetzler-Martin grade III poses a unique problem: it is
a very heterogenous group of lesions, which can range from a medium-sized
lesion in the brainstem to a small lesion in Broca with deep venous drainage, and
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all possible combinations inbetween. There is obviously a very big difference in

prognosis and treatment between these 2 lesions, which obviously with itself the
need to further develop the classification system in order to better classify the
grade III AVMs. This will then be known as the Lawton modified scale[6], who
in a study published in 2003 solves the dillemma in the following manner:
- Grade III- AVMs (S1V1E1) have a surgical risk similar to that of low-grade
AVMs and can be safely treated with microsurgical resection;
- Grade III+ AVMs (S2V0E1) have a surgical risk similar to that of high-grade
AVMs and were to be best managed conservatively;
- Grade III AVMs (S2V1E0) have intermediate surgical risks and require
judicious selection for surgery;
- Grade III* AVMs (S3V0E0) are either exceedingly rare, with a surgical risk
that is unclear, or theoretical lesions with no clinical relevance.
For the Grade III lesion described above of great relevance is the study by
Hernesniemi describing the natural history of the lesion and the bleeding chance
per year, whereby younger people would be much earlier and more aggresively
treated as opposed to older people[7].
In 1979 Drake published a paper about the management of AVMs whose
prerogatives hold true to this day[8]. These imply that a neurosurgeon has 5
options at hand when dealing with these lesions:
Expectant behavior (nothing except symptomatic treatment)

Surgery
Endovascular therapy
Radiosurgery
Combination of the aforementioned options
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With respect to decision-making, there are a series of studies published

providing guidelines for each Spetzler-Martin grade in particular (Vasquez and
Larrea in 2000, Ogilvy et al 2001 and Starke et al, 2009)[9,10,11]. They do not
differ much in their reccomendations, and these, resumed, would be as
following[12]:
Grade I and II: Must always be treated. They should not pose any
difficulty to the surgeon and have a curative rate of 100%. They can also be treated
endovascularily or radiosurgically, but radiosurgery in the case of grade I lesions
implies a period of about 2 years during which the malformation can bleed before
it disappears. Moreover, for grade II lesions of higher volume the nidus may not be
fully irradiated, leading to a recurrence with perhaps more risk of a bleeding
event. Endovascular options may show angiographical complete disappearance of
the lesion, but surgeons often see when operating on AVMs with complete
angiographical closure that there are often several arterial pedicles which are not
visible angiographically and which are at risk of bleeding.
Grade III: Must always be treated, as their heteorgenity predisposes
them to become problematic and symptomatic with time. Herein a
multidisciplinary team may be set up to preembolize the lesion (which would
intraoperatively bleed less) and it may also be combined ith radiosurgery. When
the lesions are treated they have a cure rate very close to 100%, but morbidity
reaches 25% even in the best series, especially with lesions in eloquent areas.
Grade IV: If the lesion has not bled and has no complications such as
flow-related aneurysms then it is amenable to wait-and-scan treatment. If it does
bleed then treatament should always be preeceded by endovascular treatment,
save for the most experienced surgical hands. There is high morbidity risk
associated with this entity.
Grade V: In principle, these should not be treated. When they are
treated, they have a very high morbidity and mortality rates and thus treatment is
for most surgeons of a palliative nature, to try to prevent bleeding. There are
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studies which suggest that operation without total excision involves a greater risk
of bleeding ultimately[12]. In principle, the lesion should be first embolized and
then operated on, keeping in mind the very high risk of postoperative sequelae.
In conclusion, AVMs are lesions which pose a number of risks even in
the most experienced hands and must thus only be treated by a handful of people
with the knowledge, experience and character, able to take on such a lesion, as
unforgiving as satisfactory as its obliteration can be.
REFERENCE
1.
2.
3.
4.
5.
6.
7.
8.
9.
M.G. Yasargil: `Microneurosurgery, vol. III B: AVM of the Brain.1998 Georg

Thieme Verlag Stuttgart 25-53
A.J. Luessenhop, W.T. Spence: Artificial embolization of brain arteries: report of
use in a case of arteriovenous malformation. JAMA.172:1153-1155 1960
E. Spagnuolo, L. Lemme-Plaghos, F. Revilla, et al.:Recomendaciones para el
manejo de las malformaciones arteriovenosas cerebrales. Neurociruga-Rev.
Espaola de Neurociencias. 20:5-14 2009
R.F. Spetzler, N.A. Martin, L.P. Carter, et al.: Surgical management of large
AVMs by staged embolization and operative excision. J Neurosurg. 67:17-28 1987
E. Spagnuolo: Deep arteriovenous
malformations. A.Pedroza L. Quintana T. Perilla Latinamerican Treaty of
Neurosurgery. 2008 FLANC Bogot 425-436 Chap: 30
M.T. Lawton: Spetzler-Martin grade III AVMs: surgical results and a modification
of the grading scale. Neurosurgery. 52:740-749 2003
A. Hernesniemi, R. Dashti, S. Juvela, et al.: Natural history of brain arteriovenous
malformations: a long-term follow-up study of risk of hemorrhage in 238
patients. Neurosurgery. 63 (5):823-831 2008
C. Drake: Brain arteriovenous malformations: considerations for and experience with
surgical treatment in 166 cases. Clin Neurosurg.26:145-208 1979
Vazquez F, Larrea, J: Guides of treatment of AVMs. Guides of endovascular
emoblization. In: GENI: Grupo espaol de neurorradiologa intervencionista
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10. C.L. Ogilvy, I. Awad, R. Brown, et al.: Recommendations for the management of
intracranial arteriovenous malformations: a statement for healthcare professionals
from a special writing group of Stroke Council, American Stroke
Association. Stroke. 32:1458-1471 2001
11. R. Starke, R. Komotor, B. Hwang: Treatment guidelines for arteriovenous
malformations microsurgery. BJNS. 23:376-385 2009
12. A. Quinones-Hinojosa, et al.: Schmidek and Sweet Operative Neurosurgical
Techniques, chap. 83, Elsevier Saunders 2012
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CHAPTER 12
SURGICAL MANAGEMENT OF ARTERVIOVENOUS MALFORMATIONS
IOAN-TEFAN FLORIAN, CRISTIAN PRJOL, IOAN-ALEXANDRU FLORIAN
INTRODUCTION
Quite a few treatment methods for AVMs have been inducted and applied into the
neurosurgical practice. All of them have one common element, which is the risk of
inflicting additional cerebral lesions and deficits. This calls for measuring both
the emergency of treatment initiation and the risk it implies along with
conservative attitude, as well as the risks of nonsurgical therapy. AVM
pathology counts among the few cases in which deciding if and how to treat a
lesion may prove difficult. In these scenarios especially, Hippocrates' dictum
"primum non nocere" truly finds its applicability.
As methods of treatment, microsurgical excision of AVMs has been the
standard option for the last 25 years. It has the advantage of permanently
eliminating the nidus and closing the arterial feeders. Also, treatment of AVMassociated aneurysms and hemorrhage control are practiced. It has been proven
that surgical resection grants an adequate control over AVM-induced strokes.
Currently, electing the treatment and adjuvant methods, as well as time of
surgery, are challenging decisions, being individualized for each and every case.
This depends on a series of risk factors tied to the features of the lesion, state of
the patient, and the patient's options. The aim is to avoid causing a worsening of
the deficit.
The indication of surgery is based upon significant symptomatology:
Hemorrhage with progressive clinical deterioration;

Gradual neurologic deficit;
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Severe, repeating, and incapacitating strokes that cannot be medicallymanaged;

Recurrent hemorrhage;
Mental status deterioration;
Persistent and medically unresponsive headache.
Radical surgical approach is also encouraged in the case of small
cortical, or subcortical AVMs, especially located in non-eloquent regions of
the brain.
SURGICAL TIMING
Surgical treatment of AVMs has had a long history. Along the course of time, a
few principles of application have been implemented.
Surgical resection must be done selectively, not as emergency
treatment. Exceptions to this are when surgery is mandatory, the life of the patient
hanging in the balance due to the mass effect produced by the hematoma
following AVM hemorrhage.
In case it is feasible, conservatory treatment for about 3-4 weeks is
preferred. This leads to amelioration of the patients clinical condition and may
stabilize neurologic deficits. During this period, the hematoma caused by AVM
rupture liquefies, allowing for an easier removal. After this interval, angiographic
reevaluation is made (even if this is the initial angiographic examination), since
the rapports between the lesion and adjacent vessels may change following edema
resorption and hematoma organization. This allows for a simpler and facile
surgical approach of the AVM, as the brain is relaxed and the hematoma is
liquefied.
In the case of emergency surgical intervention, determined by progressive
neurologic worsening of the patient and life-threatening AVM hemorrhage, some
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CHAPTER 12: SURGICAL MANAGEMENT OF ARTERIOVENOUS

MALFORMATIONS
authors recommend a more conservative attitude. They imply dividing surgery into
two separate times: initially, removal of the hematoma and avoiding tributary
vessels of the lesion; afterwards, once the patient is stabilized and the cerebral
edema has been resorbed, reintervention with radical excision of the AVM is
recommended. This algorithm offers operative comfort and alleviates surgical
dissection by reducing the acute effects of hemorrhage and assuring brain
relaxation at an interval from the moment of bleeding.
In patients harboring an aneurysm of the feeding artery of the nidus, if
this has ruptured, it is recommended to urgently clip the aneurysm, after which the
AVM can be approached. If the source of hemorrhage cannot be identified,
surgical treatment will also target the aneurysm first, and only then the AVM. It
should be mentioned that these patients present with a higher risk of bleed (7% per
year) than patients without AVM-associated aneurysms (4% per year). This is a
reason for early surgery. Aside from this, 50% of these patients carry multiple
aneurysms, 85% of which are situated on the feeding arteries or the major arteries
from which the feeders derive. This too encourages mainly surgery in favor of
other treatment options.
It must be emphasized that, form a clinical standpoint, hemorrhage arising
from AVMs are less severe than spontaneous bleed or aneurysmal rupture. As a
rule, after a rather dramatic start, progressive neurologic amelioration ensues,
permitting a delay of the surgical intervention. Even though neurological status
does not permit a postponement of more than 3-4 weeks, 4-5 days may seem
reasonable from the outlook of cerebral edema resorption and local
appeasement.
PREPARATIONS FOR SURGERY

As previously mentioned, preparatory steps must first include an angiographic
reevaluation. During this interval, selected cases would undergo main feeder
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vessel embolization, so as to reduce the risk of intraoperative bleeding. Also

during this period of time, the blood of the patient is collected for autotransfusion
(available for centers where this is performed as a routine), rheological values are
reassessed, and presumed hydric and electrolytic imbalances are adjusted.
If the patient is conscious and oriented, a series of neuropsychological
tests must be taken. All neurologic status elements must be well documented for a
more accurate comparison between preoperative and postoperative states.
POSITIONING OF THE PATIENT

The position of the patient on the operating table must be adjusted to a series of
principles. It should:
Be adapted to the location of the lesion;

Assure greater access of the lesion, offering the greatest amount of visibility
with the minimum degree of microscopic mobility;
Assure the greatest amount of brain relaxation, so as to avoid excessive
traction of the brain;
Not impede venous flow, even if this implies a slight intraoperative
repositioning of the patients head;
Guarantee a thoracic respiratory cycle as close to normal as possible.
Concerning supratentorial lesions, especially deep ones, we prefer dorsal
decubitus with turning the head sideways and eventually lifting the shoulder
(which allows lateral turning of the head without compromising venous flow in the
contralateral jugular vein). Lateral decubitus, especially for overweight patients,
cannot assure any degree of freedom of thoracic respiratory cycle, and may
sometimes at least encumber venous flow in the contralateral jugular vein.
Regarding posterior fossa AVMs, our opinion is that the sitting position
corresponds (Figure 12.1) in the highest degree to the principles presented earlier.
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Venous flow is greatly preserved, which is why we recommend this position,

along with all the measures of preventing air embolism.
Figure 12.1 - Median suboccipital craniotomy with the resection of the

superior of the posterior C1 arch, which grants an additional 2-3mm
enlargement of the surgical field without compromising vertebral
stability.
We considered highlighting these aspects of AVM surgery and patient

positioning as necessary, since personal experience revealed the dramatic shifts in
operative aspect and conduct just through alleviating venous flow. Therefore,
whenever we notice an increase of AVM pressure and volume during surgery
(without this being tied to a lesion of nidus drainage veins), we ask the anesthetic
personnel to establish whether the head had turned slightly, compressing the
jugular veins.
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CRANIOTOMY
It is obvious that the bone flap must be centered on the AVM. What is particular
in these certain cases is the size of the flap, which more often must be wide enough
to permit:
Direct access toward the nidus feeder vessels (which may have a distant
origin from the lesion itself), as well as toward the nidus and its drainage
vessels;
A multidirectional approach of the AVM, without exerting traction or
excessive compression of the brain;
Differentiating between the normal drainage vessels, which should be
preserved, and the pathological ones, which must be excised;
Postoperative decompression of the brain, when cerebral edema, normal
perfusion pressure breakthrough phenomenon, or eventually rebleeding
(though an insufficiently obliterated feeder artery or AVM remnant) might
occur.
For posterior fossa lesions, a large suboccipital craniotomy is
performed, eventually partially removing the posterior arch of the C1. This latter
element is implemented when MRI reveals descended cerebellar tonsils.
SURGICAL EXCISION OF AVMs

The basic aim of surgery is complete resection of the AVM, abolishing the risk of
ulterior hemorrhage. This is also the essential treatment of AVM-induced strokes.
Incomplete resection does not reduce the risk of either recurrent hemorrhage, or
further stroke episodes.
The AVM excision technique includes several well-established
objectives. These may be separated into five steps: identifying and eliminating
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feeder vessels, circumferential nidus dissection, apex dissection, venous pedicle

removal, and definitive hemostasis.
Identifying and eliminating the feeder vessels is the first step. This
implies dissecting AVM tributary arteries up to the level of the nidus, verifying
their role in AVM supply through temporary occlusion (with a temporary clip),
and removing them via coagulation or permanent clips. Also during this steps,
presumed en passage arteries are evaluated, which although traverse the nidus
have no connection to it whatsoever and must be preserved at all costs. These
supply the adjacent cerebral parenchyma.
In theory, this is a relatively easy step. In truth, this is a lot more
challenging due to the sinuous pathway of the arteries, their duplication, or
triplication sometimes further from the nidus. In this case, comparing
intraoperative aspects with angiographic imagery may offer valuable
indications, although these two facets may not always match perfectly. In many
cases, intraoperative observation shows the transformation of a normal artery into
a secondary feeder vessel, or numerous feeder arteries that provide perforators for
the normal brain. On the other hand, distal dissection of the nutrient vessels is not
without its risks of damaging the brain, even superficially, during opening the
sulci. An approach that is as close to the nidus as possible may increase the
difficulty of identifying these vessels and thus complicate surgery. Removal of the
nidus without proximal control on at least one major feeder vessel is also a delicate
procedure. This is the reason why there is no universally available technique for
AVM management (Figure 12.4).
In the case of superficial malformations, once the feeder artery has been
identified, it is dissected along its entire path adjacent to the AVM itself. This is
performed with great regard towards recognizing and maintaining the arteries as
well as the veins that serve the normal cortex (Figures 12.2 and 12.3).
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Figures 12.2 and 12.3 - In superficial malformations, identification of

the feeder artery and the nidus is easy. Placing a temporary clip
enables malformation collapse.
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Figure 12.4: Feeder artery dissection within the intergyral sulcus is

performed with the preservation of the normal draining veins, as well
as the normal arteries that supply the surface of the brain.
In the case of deep malformations, especially insular or medial temporal,
dissection must start from the main cerebral arteries: ICA and MCA. From these
on, dissection would progress until the nidus feeder has been identified, followed
by the malformation.
For medial line supratentorial AVMs, interemispheric approach may
appear as the most logical. Craniotomy should therefore be performed so as to
offer access of the A2 segment as proximally as possible. It should also allow
access of the drainage veins that usually flow into the sagittal sinus (frequently
posterior to the anteriormost third of said sinus). Interemispheric access must be
performed with the utmost care, so as to not generate compression or lesion of the
AVM drainage vein proximal to the malformation. The pericallosal artery must
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also be correctly distinguished and preserved. From this on, the feeder vessels
would be identified, coagulated and sectioned.
Paraventricular AVMs present a serious challenge: their feeder arteries
may have multiple origins (MCA, ACA as well as PCA). Clearly, there is no
craniotomy technique that allows dissection of all feeder arteries. Therefore, the
approach is made through the wide opening of the gyral sulcus that may lead
closest to the lesion. Angiographic data helps in pinpointing the superficial feeder
arteries, which will be dissected, later followed by the nidus itself.
For posterior fossa AVMs, finding the nutrient vessel may be difficult.
Our advice is to dissect the vertebral artery ipsilateral to the AVM, followed by
identifying the origin of the PICA, which most frequently generate the feeder
arteries. Dissection of the PICA and the nutrient arteries offers the possibility of
proximal control of the AVM, and by placing a temporary clip, nidus dissection
may ensue.
The most efficient method of occluding feeder arteries, which usually
have thin vascular walls, is bipolar coagulation, followed by microsurgical
sectioning. Few are the cases in which two vascular clips must be placed with the
arterial section made between them. Even arteries of remarkable diameters can be
coagulated, sometimes gradually, as to reduce its caliber until it no longer presents
a problem for ulterior coagulation and sectioning. The intensity of coagulation,
however, must receive great care. If this is too high, it may lead to hemorrhage of
remarkable proportions, complicating surgery from the very start (Figures 12.5 and
12.6).
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Figures 12.5 & 12.6 - Through progressive coagulation, even large

vessels can diminish their diameter, facilitating sectioning.
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Circumferential dissection of the nidus would be performed only after

the nutrient arteries have been individualized and eliminated. This step should be
taken as close to the margins of the lesion as possible, to avoid damaging adjacent
cerebral tissue (especially in the eloquent cerebral areas). Although some surgeons
prefer dissection in the glial plane surrounding the nidus, our experience revealed
that, in most cases, this plane does not exist to begin with, the monstrous nidus
being bordered by apparently normal cerebral tissue. Through coagulation of the
nidus walls, a progressively increasing dissection plane can be obtained. This is
performed circumferentially, while protecting the adjacent cortex with serum
soaked tampons. Gradual nidus coagulation leads to a decrease of its volume and
creating new dissection planes. As this increases in depth, newer feeder arteries
may be discovered, some of them small in size, which would also be coagulated
and dissected (Figure 12.7).
Figure 12.7 - Circumferential dissection of a deep malformation is

practically impossible. In cases such as this, the AVM is gradually
coagulated.
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Figure 12.8 - Circumferential dissection of a superficial AVM.

Accidental lesion of a nidus vessel represents a possible scenario with
impressive bleeding, which can be resolved with aspiration to pinpoint the origin
of hemorrhage and progressive coagulation along the entire path of the affected
vessel. Applying a small tampon and aspirating through it offers a neat cleansing
of the surgical field and the possibility of adequate reevaluation of the situation.
This event may seem a trial to the inexperienced neurosurgeon. The loss
of a relatively high amount of blood in short time, decrease of arterial pressure, the
pressure exerted by the event itself and possibly by the anesthetist team may lead
to a state of panic. From this moment on, precipitated gestures, tempestuous
maneuvers, and random coagulation of nidus vessels can lead to a cataclysmic
conclusion. That is precisely why we consider this type of surgery only available
to the high-experienced neurosurgeons. In our experience, we have not met with a
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single intraoperative AVM hemorrhage that we could not contain in the proper
amount of time, although this type of hemorrhage was not seldom encountered.
In the most frequent cases in which the AVM became apparent through
bleeding, the hematoma represents a pathway to the nidus simply by aspirating
the liquefied clot. If surgery is performed as an emergency to save the patient (due
to the increased volume of the hematoma), the aspired clots generally lead to a
bleeding nidus. Therefore, it is preferable to partially drain the hematoma at a
slight distance from the AVM, with the purpose of cerebral decompression,
followed by identifying the nutrient vessels and excluding them and only
afterwards returning to the nidus and removing it.
Apex dissection continues the previous step and represents the hardest
part of AVM surgery. The last nutrient vessels to be removed from circulation are
found at the AVM apex. Usually, vascular dissection, coagulation, and
hemostasis are challenging at this point, considering the depth of the field.
Dissection is also made difficult by the numerous small vessels that perforate the
white matter to reach the nidus. Isolating and coagulating them must be preformed
gently so as not to section them. Otherwise, coagulation within cerebral
parenchyma may determine further brain damage.
Venous pedicle removal and AVM excision are performed in this
relatively simplistic step, after circumferential and apex dissections. Great care
must especially be attributed to the small remaining feeder vessels that may be
situated underneath and masked by the venous pedicles. By any and all means,
normal veins must be carefully preserved (Figures 12.9 and 12.10).
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Figure 12.9 - Isolation and coagulation of the draining vein.
Figure 12.10 - Dissection of the draining vein.
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Figure 12.11 - Resection of a temporal malformation situated on both

sides of the vein of Labbe, with anatomical and functional preservation
of aforementioned vein.
Definitive hemostasis is the final step of AVM resection. It is achieved
through electrocoagulation or hemostatic materials. Any residual damage at the
border of the cavity must be identified. Hemostasis confirmation is made by
soliciting the anesthetist team to progressively increase arterial blood pressure
up to values of 150-160 mmHg. Venous return, on the other hand, is verified by
moderate jugular compression. In the case of residual lesions, these may bleed
upon either blood pressure increase, or jugular compression test. These lesions
must be subsequently removed. After complete hemostasis is attained, hemostatic
material (Surgicel) is placed in the surgical field.
Regarding the cases involved in our study, all patients received surgical
treatment, without preoperative intravascular embolization or radiosurgery. The
majority of cases included presented a profoundly altered neurologic status upon
admission. Therefore, the most important decision regarding treatment concerned
the optimal time for surgery.
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In the case of patients with severe neurologic status upon admission

(GCS=6 or less), presenting considerable cerebral hematomas, surgery was
performed in emergency as primary intention. It implied hematoma evacuation
with cerebral decompression, followed by complete removal of the AVM. This
goal, however, was not achieved in every case, rebleeding being present in 6 out of
the 48 cases included in the study. If the neurologic status of the patient does not
improve, or even deteriorates, a second intervention is necessary in the shortest
amount of time possible. For an increase in surgical ease and if the patients
neurological status allows it, it is preferred to postpone the second intervention for
a few days to permit a decrease of the cerebral edema.
For patients who presented with a GCS=7 or above, recommended
attitude was delaying the surgical intervention (for as long as the neurologic status
allowed it), until a significant remission of the cerebral edema was achieved,
leading to an increase of surgical comfort for both surgeon and patient.
Neurological follow-up presented the most important aspect of this strategy. Any
deterioration of the neurological status called for surgical intervention.
Translated by Ioan-Alexandru Florian from: Florian IS, Perju-Dumbrav L.

Opiuni Terapeutice n Accidentele Vasculare Hemoragice. Editura Medical
Universitar Iuliu Haieganu Cluj-Napoca 2007
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An Introduction To Vascular Neurosurgery

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Intraoperative photographs, CT, MRI, CTA, MRA were provided by

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Professor Ioan Stefan Florian, MD, PhD

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THE CAROTID ARTERY AND THE ANTERIOR CIRCULATION

CHAPTER 1: THE ARTERIAL ANATOMY OF THE BRAIN

Figure 1.2 Carotid artery segments

The divison into segments helps with the precise localisation of an

CHAPTER 1: THE ARTERIAL ANATOMY OF THE BRAIN

Before we move on to the terminal arteries of the internal carotid, we

CHAPTER 1: THE ARTERIAL ANATOMY OF THE BRAIN

Figure 1.3 Anterior cerebral artery frontal view

Figure 1.4 Anterior cerebral artery sagittal view

CHAPTER 1: THE ARTERIAL ANATOMY OF THE BRAIN

Figure 1.5 Middle cerebral artery axial section

CHAPTER 1: THE ARTERIAL ANATOMY OF THE BRAIN

Figure 1.6 Middle cerebral artery segments

CHAPTER 1: THE ARTERIAL ANATOMY OF THE BRAIN

velum interpositum. The lateral posterior choroidal artery (LPChA) usually

Figure 1.7 - Posterior fossa blood supply

CHAPTER 1: THE ARTERIAL ANATOMY OF THE BRAIN

the precerebellar arteries. After exiting the cerebellomesencephalic fissure, it is

CHAPTER 1: THE ARTERIAL ANATOMY OF THE BRAIN

trunk splits proximally or distally to the facial-verstibulocochlear complex.

CHAPTER 1: THE ARTERIAL ANATOMY OF THE BRAIN

Specific Anatomic and Physiologic Features

The cerebral venous system can be didactically divided into a superficial

CHAPTER 2: VENOUS BLOOD FLOW

DURAL VENOUS SINUSES

CHAPTER 2: VENOUS BLOOD FLOW

The sigmoid sinus represents the continuation of the transverse sinus. It

Figure 2.1 Dural sinuses and main veins of the cerebrum

DURAL VENOUS SINUSES

CHAPTER 2: VENOUS BLOOD FLOW

SUPRATENTORIAL VENOUS SYSTEM

CHAPTER 2: VENOUS BLOOD FLOW

The great vein of Galen passes posterosuperiorly behind the splenium of

INFRATENTORIAL VENOUS SYSTEM

CHAPTER 2: VENOUS BLOOD FLOW

Huber, Peter: Cerebral Angiography, Translated by George Bosse. Foreword by Hugo

Ayanzen R.H., et al : Cerebral MR Venography: Normal Anatomy and diagnostic

The dura mater (L., tough mother) the outermost layer;

THE PIA MATER

CHAPTER 3: SUBARACHNOID SPACE AND THE CEREBROSPINAL FLUID

SUBARACHNOID SPACE AND CISTERNS

The cerebellomedullary cistern (cisterna magna) is the largest. It is situated

The lateral subarachnoid cisterns are as follows:

CHAPTER 3: SUBARACHNOID SPACE AND THE CEREBROSPINAL FLUID

The cerebellopontine cisterns are situated in the angles formed between

THE CEREBROSPINAL FLUID

CHAPTER 3: SUBARACHNOID SPACE AND THE CEREBROSPINAL FLUID

Sido FG. Tratat de Neuroanatomie Funcional i Disecia Nevraxului. Second

COMPUTED TOMOGRAPHY (CT)

consecutively if the amount of hemorrhage is large enough and the scan is

Image 4.1: Left Lobar Hemorrhage on non-e. CT

SECTION II: IMAGING IN

CHAPTER 4: IMAGING OPTIONS IN CEREBRAL VASCULAR

Clinical suspicion of subarachnoid hemorrhage is always followed by