1
Posterior inferior cerebellar artery
aneurysms: An institutional series
Thesis submitted in fulfillment of the rules and regulations for MCh Degree Examination of Sree
Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram
By
Dr. Manish Ganesh Pai
Resident in Neurosurgery
Month and Year of Submission: October 2011
Pos
Submitte
Program
Month &
sterior in
ed by
mme
& year of
nferior cins
f submiss
2
cerebellastitution
:
:
sion :
ar arterynal series
Dr. Ma
MCh N
Octobe
y aneurys
anish Gan
Neurosurg
er, 2011
ysms: A
nesh Pai
gery
An
3
CERTIFICATE
This is to certify that the thesis entitled “Posterior inferior cerebellar artery
aneurysms: An institutional series” is a bonafide work of Dr. Manish Ganesh
Pai and was conducted in the Department of Neurosurgery, Sree Chitra
Tirunal Institute for Medical Sciences & Technology, Thiruvananthapuram
(SCTIMST), under my guidance and supervision.
Dr. Suresh Nair
Professor and Head
Department of Neurosurgery
SCTIMST, Thiruvananthapuram
4
DECLARATION
This thesis titled “Posterior inferior cerebellar artery aneurysms: An
institutional series” is a consolidated report based on a bonafide study
done by me during the period from January 2009 to September 2011,
under the Department of Neurosurgery, Sree Chitra Tirunal Institute for
Medical Sciences & Technology, Thiruvananthapuram.
This thesis is submitted to SCTIMST in partial fulfillment of rules and
regulations of MCh Neurosurgery examination.
Dr. Manish Ganesh Pai
Department of Neurosurgery,
SCTIMST, Thiruvananthapuram.
Formatted: Font: (Default) Times New Roman
Formatted: Justified, Right: -0.92"
5
ACKNOWLEDGEMENT
The guidance of Dr. Suresh Nair, Professor and Head of the Department of Neurosurgery, has been invaluable and I am extremely grateful and indebted for his contributions and suggestions, which were of invaluable help during the entire work. He will always be a constant source of inspiration to me.
I owe a deep sense of gratitude to Dr. Girish Menon for his invaluable advice, encouragement and guidance, without which this work would not have been possible.
The critical remarks, suggestions of Dr. Gopalakrishnan C. V, helped me in achieving a high standard of work.
I am deeply indebted to Dr. Mathew Abraham, Dr. Easwer H. V, Dr. Krishnakumar K, Dr. George Vilanilam, Dr. Jayanand Sudhir and thank them for their constant encouragement and support.
I wish to sincerely thank all my colleagues for their support.
Last but not the least, I owe a deep sense of gratitude to all my patients without whom this work would not have been possible.
6
INDEX
INTRODUCTION 7-8
REVIEW OF LITERATURE 9-60
AIMS AND OBJECTIVES 61
MATERIALS AND METHODS 62
RESULTS 63-74
DISCUSSION 75-96
CONCLUSIONS 97-98
REFERENCES 99-109
PROFORMA 110-111
ABBREVIATIONS 112-113
7
INTRODUCTION
Aneurysms arising from the posterior inferior cerebellar artery (PICA),
either at its junction with the vertebral artery or more peripherally along
its course, are rare, representing approximately 0.49% of intracranial
aneurysms (1). Aneurysms of the PICA-VA complex combine a narrow
range of clinical presentation with unusual anatomical variability. Their
strategic location and the tortuousness of the vertebral arteries require
special consideration during diagnostic evaluation and surgical planning.
Aneurysms of the vertebrobasilar system have several characteristic
features which distinguish them from aneurysms of the anterior
circulation. First of all, they are relatively uncommon, accounting for
only about 3% of the intracranial aneurysms. This is the reason why the
majority of neurosurgeons have little experience with the management of
these lesions. Secondly, these aneurysms show great variability in size,
location, and morphology. The percentage of dissecting and fusiform
aneurysms is much higher than in the other intracranial compartments.
Thirdly, most of the aneurysms of the vertebral artery (VA) and the
posterior inferior cerebellar artery (PICA) are located deeply in the
posterior fossa and have a close relationship to the lower brainstem and
8
the caudal cranial nerves. The variability of the anatomy of the VA and
the PICA add further to the complexity of the lesions and increase the
risk of surgical management (2). It is sometimes even difficult to pick the
side from which the surgical approach should be made, unless the
angiographic size and delineation of the aneurysm, the general height and
shape of the vertebral artery, and the pattern of collateral supply are
carefully evaluated. Relatively little guidance is available in the literature
in regard to these matters. Posterior inferior cerebellar artery (PICA)
aneurysms are uncommon and their underlying pathology, natural history
and clinical management are poorly understood. Surgical treatment of
PICA aneurysms is challenging in view of their close neurovascular
relationship. Evaluation of these aneurysms with relation to outcome after
treatment is scant in the neurosurgical literature. Analysis of outcome is
critical, however, if surgeons are to understand the likely consequences of
their actions.
9
REVIEW OF LITERATURE
Incidence
Aneurysms arising from the posteroinferior cerebellar artery (PICA),
either at its junction with the vertebral artery or more peripherally along
its course, are rare. Vertebrobasilar aneurysms constitute approximately
15% of all intracranial aneurysms, most of which arise from the
basilar apex (3). VA aneurysms represent 20 to 30% of posterior fossa
aneurysms. One-fifth of these posterior fossa lesions originate from
the posterior inferior cerebellar artery (PICA), thus accounting for
3% of all intracranial aneurysms (4). Aneurysms that arise at the PICA-
VA complex are relatively uncommon, comprising less than 0.5% to 3%
of all intracranial aneurysms (5).
In a cooperative study of 2672 intracranial aneurysms, the incidence of
PICA aneurysms was 0.49% (1). In a study by McDonald and Korb (6) in
1939 the incidence of PICA aneurysms was reported as 0.8%. Majority of
the aneurysms on the vertebral artery arise at the origin of the PICA (7).
Aneurysms of the PICA are usually found on the bifurcation of the
10
vertebral artery-PICA junction (4, 8). Aneurysms arising from the
peripheral segment of the PICA are quite rare. Distal PICA aneurysms are
relatively rare, constituting less than 30% of all PICA aneurysms (4, 8, 9,
10). Aneurysms arising on the PICA distal to the origin represent only 0.5
to 1 % of all intracranial aneurysms (7, 11). Rothman et al. noted that two
thirds of aneurysms involving the PICA arose at the origin and one-third
arose distal to the origin (11). PICA-vertebral aneurysms usually arise
along the rostral one-half of the origin of the PICA, point superiorly and
slightly posteriorly, and lay against the medulla (7, 12, 13). Rarely, the
PICA-vertebral junction may be the site of a dissecting aneurysm (14,
15).
Historical Perspective
Cruveilhier described a spherical aneurysm arising from the PICA-
vertebral junction in 1829 (16). Fernet (17) reported the first case of an
aneurysm arising from a distal segment of the PICA in 1864. But it was
not until 1947 that Rizzoli and Hayes (18) performed the first surgical
procedure on an aneurysm known to arise from this vessel. In their case,
preoperative angiography was not done, and the posterior fossa location
of the lesion was deduced from a shift of the fourth ventricle seen at
ventriculography. The aneurysm was trapped between silver clips.
Schwartz reported the first successful obliteration of a posterior fossa
11
aneurysm in 1948 (19). The rare peripheral PICA aneurysm was first
operated by Olivecrona in 1932(20). Richardson's study (21) of the
natural history of aneurysms following SAH revealed that those arising
from the vertebrobasilar system were associated with the highest
mortality rate. Uihlein and Hughes (22) reported a series of 14 posterior
fossa aneurysms treated without definitive surgery; eight of these patients
died of aneurysm rupture. Routine utilization of vertebral angiography
after normal carotid angiography in patients with SAH enhanced the
recognition of these aneurysms. In 1958, DeSaussure, et al., reported the
successful trapping of two PICA aneurysms that had been defined by
preoperative angiography (23). Further refinements, including
transfemoral catheterization, subtraction, and magnification, have
enhanced the preoperative angiographic assessment of size, location,
and position of such aneurysms. In 1967, Rand and Jannetta (24)
recognized the benefit of the operating microscope for aneurysms of
the vertebrobasilar system, both for the delicate dissection of the neck
of the aneurysm and for preventing inadvertent occlusion of the small
perforating arteries at the time of clipping. The excellent results enjoyed
by Drake (25) and others confirm these benefits.
ANATOMY OF PICA (26, 27)
12
The PICA has the most complex, tortuous, and variable course and area
of supply of the cerebellar arteries. It may be exposed in surgical
approaches to the foramen magnum, fourth ventricle, cerebellar
hemisphere, brainstem, jugular foramen, cerebellopontine angle, petrous
apex, clivus and trigeminal nerve (26). The PICA is intimately related to
the cerebellomedullary fissure, the inferior half of the ventricular roof, the
inferior cerebellar peduncle, and the suboccipital surface.
Origin of the PICA and its course (26, 27):
The PICA, by definition, arises from the vertebral artery near the inferior
olive and passes posteriorly around the medulla. Warwick and Williams
in Gray’s Anatomy have also defined the PICA as arising solely from the
vertebral artery (28). The PICA is less commonly defined as the
cerebellar artery that supplies the posteroinferior part of the cerebellum
and generally arises from the vertebral artery. The PICA may also arise
from the basilar artery (29, 30).
If a PICA is present, it is the largest branch of the vertebral artery. It is
rarely absent bilaterally, but may arise as a double or duplicate PICA.
Salamon and Huang found the PICA to be absent unilaterally in 26% and
bilaterally in 2% of the brains examined (31). Margolis and Newton
found it to be absent in 15% and double in 2.5% of the brains examined
(32).
13
The site of origin of the PICA from the vertebral artery varied in location
from below the foramen magnum to the vertebrobasilar junction. The
origin was located between 14mm below and 26mm above the level of
the foramen magnum (average, 8.6mm above the foramen). A few of the
PICAs arising below the foramen magnum may arise from the vertebral
artery in an extradural location.
The PICA arises from the posterior or lateral surfaces of the vertebral
artery more often than from the medial or anterior surfaces. On leaving
the parent vessel, the initial course of the PICA is posterior, lateral, or
superior more often than anterior,medial, or inferior. The diameter of the
PICA at its origin ranges from 0.5 to 3.4 mm (average, 2.0 mm). The
PICA has been reported to be hypoplastic in 5 to 16% of cerebellar
hemispheres (31, 32).
At the anterolateral margin of the medulla, it passes rostral or caudal to or
between the rootlets of the hypoglossal nerve, and at the posterolateral
margin of the medulla it courses rostral to or between the fila of the
glossopharyngeal, vagus, and accessory nerves. After passing the latter
nerves, it courses around the cerebellar tonsil and enters the
cerebellomedullary fissure and passes posterior to the lower half of the
roof of the fourth ventricle. On exiting the cerebellomedullary fissure, its
branches are distributed to the vermis and hemisphere of the suboccipital
14
surface. The medial trunk supplies the vermis and adjacent part of the
hemisphere, and the lateral trunk supplies the cortical surface of the tonsil
and the hemisphere. The PICA gives off perforating, choroidal, and
cortical arteries. The cortical arteries are divided into vermian, tonsillar,
and hemispheric groups.
Segments
The PICA is divided into five segments (26): 1) anterior medullary, 2)
lateral medullary, 3) tonsillo-medullary, 4) telovelotonsillar, and 5)
cortical. These segments are often longer than the distance around the
medulla or the tonsil because the PICA frequently has a tortuous course
and forms complex loops on the side of the brainstem among the lower
cranial nerves, near the tonsil, and caudal to the roof of the fourth
ventricle. Each segment may include more than one trunk, depending on
the level of bifurcation of the artery.
15
Figure 1: Drawing demonstrating lateral view of PICA anatomy and
nomenclature. Green portion (1) = anterior medullary segment; orange
portion (2) = lateral medullary segment; blue portion (3) =
tonsillomedullary segment; yellow portion (4) = telovelotonsillary
segment; and red portion (5) =cortical segment.
16
Figure 2: Drawing demonstrating posterior view of PICA anatomy and
nomenclature. Green portion (1) = anterior medullary segment; orange
portion (2) = lateral medullary segment; blue portion (3) =
tonsillomedullary segment; yellow portion (4) = telovelotonsillary
segment; and red portion (5) =cortical segment.
Anterior medullary segment
This segment lies anterior to the medulla. It begins at the origin of the
PICA anterior to the medulla and extends backward past the hypoglossal
rootlets to the level of a rostrocaudal line through the most prominent part
17
of the inferior olive that marks the boundary between the anterior and
lateral surfaces of the medulla.
Those PICAs arising lateral rather than anterior to the medulla do not
have an anterior medullary segment. An anterior medullary segment is
more likely to be present if the PICA arises from the superior part of the
vertebral artery, because the vertebral artery courses from the lateral side
of the medulla below to the anterior surface of the medulla above. An
anterior medullary segment is present if the vertebral artery at the level of
origin of the PICA has passed to the anterior surface of the brainstem.
From its origin, the PICA usually passes posteriorly around or between
the hypoglossal rootlets, but occasionally loops upward, downward,
laterally, or medially before passing posteriorly around or between the
hypoglossal rootlets.
Lateral medullary segment
This segment begins where the artery passes the most prominent point of
the olive and ends at the level of the origin of the glossopharyngeal,
vagus, and accessory rootlets. This segment is present in most PICAs. Its
course varies from passing directly posterior to reach the
glossopharyngeal, vagal, and accessory rootlets to ascending, descending,
18
or passing laterally or medially to form one or more complex loops in the
cistern on the side of the brainstem before passing between these nerves.
Tonsillomedullary segment
This segment begins where the PICA passes posterior to the
glossopharyngeal, vagus, and accessory nerves and extends medially
across the posterior aspect of the medulla near the caudal half of the
tonsil. It ends where the artery ascends to the midlevel of the medial
surface of the tonsil. The proximal portion of this segment usually
courses near the lateral recess and then posteriorly to reach the inferior
pole of the tonsil. This segment commonly passes medially between the
lower margin of the tonsil and the medulla before turning rostrally along
the medial surface of the tonsil.
The loop passing near the lower part of the tonsil, referred to as the
caudal or infratonsillar loop, has been reported to form a caudally convex
loop that coincides with the caudal pole of the tonsil, but it may also
course superior or inferior to the caudal pole of the tonsil without forming
a loop. In some cases it dips below the caudal margin of the tonsil and
even below the level of the foramen magnum. A caudally convex loop is
not present if the PICA passes directly medial between the tonsil and
19
medulla, if the PICA ascends along the lateral surface of the tonsil to
reach the hemispheric surface, or if the artery has a low origin from the
vertebral artery and ascends posterior to the medulla to reach the tonsil.
The relationship between the tonsillomedullary segment and the
cerebellar tonsil and foramen magnum varies.
Figure 3: PICAs passage through the cerebellomedullary fissure and
around the tonsil. The artery frequently forms a caudal loop at the lower
margin of the tonsil and a cranial or supratonsillar loop that wraps around
the rostral pole of the tonsil
Telovelotonsillar segment
This is the most complex of the segments. It begins at the midportion of
the PICA’s ascent along the medial surface of the tonsil toward the roof
20
of the fourth ventricle and ends where it exits the fissures between the
vermis, tonsil, and hemisphere to reach the suboccipital surface. In most,
but not all, hemispheres, this segment often forms a loop with a convex
rostral curve, called the cranial loop. This loop is located caudal to the
fastigium between the cerebellar tonsil below and the tela choroidea and
posterior medullary velum above. The apex of the cranial loop usually
overlies the central part of the inferior medullary velum. This segment
gives rise to branches that supply the tela choroidea and choroid plexus of
the fourth ventricle.
Cortical segment
This segment begins where the trunks and branches leave the groove
between the vermis medially and the tonsil and the hemisphere laterally,
and includes the terminal cortical branches. The bifurcation of the PICA
often occurs near the origin of this segment. The cortical branches radiate
outward from the superior and lateral borders of the tonsil to the
remainder of the vermis and hemisphere.
Bifurcation
Most PICAs bifurcate into a smaller medial and a larger lateral trunk; the
trunk before the bifurcation is referred to as the main trunk. The medial
trunk supplies the vermis and adjacent part of the hemisphere and the
21
lateral trunk supplies most of the hemispheric and tonsillar parts of the
suboccipital surface. The bifurcation usually occurs posterior to the
brainstem as the PICA courses around the tonsil. The most common site
of the bifurcation is in the telovelotonsillar fissure as the artery courses
around the rostral pole of the tonsil. The medial trunk usually ascends in
the vermohemispheric fissure to reach the vermis, and the lateral trunk
passes laterally out of the telovelotonsillar fissure to reach the
hemispheric surface. The medial trunk terminates by sending branches
over the inferior part of the vermis and adjacent part of the tonsil and
hemisphere. The lateral trunk divides into a larger hemispheric trunk that
gives off multiple branches to the hemisphere and smaller tonsillar
branches that supply the posterior and inferior surfaces of the tonsil.
Figure 4: The PICAs divide into a medial trunk, which supplies the
vermis and adjacent part of the hemisphere, and a caudal trunk, which
22
loops around the tonsil to supply the largest part of the hemispheric
surface. Choroidal branches pass to the tela choroidea and choroid plexus
in the roof.
Branches
The PICA gives rise to perforating branches to the medulla, choroidal
arteries that supply the tela choroidea and choroid plexus, and cortical
arteries. The cortical arteries are divided into median and paramedian
vermian, tonsillar, and medial, intermediate, and lateral hemispheric
arteries. The cortical branches arising near the superior pole of the tonsil
send branches upward to supply the dentate nucleus.
Perforating arteries
The perforating arteries are small arteries that arise from the three
medullary segments and terminate in the brainstem. They are divided into
direct and circumflex types. The direct type pursues a straight course to
enter the brainstem. The circumflex type passes around the brainstem
before terminating in it.
The circumflex perforating arteries are divided into short and long types.
The short circumflex type does not travel more than 90 degrees around
the circumference of the brainstem. The long circumflex type travels a
greater distance to reach the opposite surface. Both types of circumflex
23
arteries send branches into the brainstem along their course. The
perforating arteries have numerous branches and anasto-moses that create
a plexiform pattern on the medullary surface. They terminate in the lateral
and posterior surfaces of the medulla.
The perforating branches of the PICA intermingle and overlap with those
arising from the vertebral artery. The segment of the vertebral artery
distal to the origin of the PICA more frequently gives rise to perforating
arteries than the segment proximal to the PICA origin. The perforating
branches arising between the entrance of the vertebral artery into the dura
mater and origin of the PICA are most commonly of the short circumflex
or direct type and terminate predominately on the lateral side of the
medulla. Those arising between the PICA origin and the vertebrobasilar
junction are predominately of the short circumflex type and terminate on
the anterior and lateral surfaces of the medulla.
Choroidal arteries
The PICA gives rise to branches that supply the tela choroidea and
choroid plexus of the fourth ventricle, usually supplying the choroid
plexus near the midline of the roof of the fourth ventricle and in the
medial part of the lateral recess. This includes all of the medial segment
and the adjacent part of the lateral segment of the choroid plexus. More
choroidal branches arise from the tonsillomedullary and telovelotonsillar
24
segments than from the lateral or anterior medullary segment. The
segment of the vertebral artery distal to the PICA origin also gives rise to
a few branches that enter the choroid plexus protruding from the foramen
of Luschka.
Cortical arteries
The most constant area supplied by the PICA includes the majority of the
ipsilateral half of the suboccipital surface of the cerebellum. This includes
the majority of the suboccipital surface of the ipsilateral hemisphere and
tonsil, the ipsilateral half of the vermis, and the anterior aspect of the
tonsil. If the PICA is absent on one side, the contralateral PICA or the
ipsilateral AICA supplies most of the area normally supplied by the
absent PICA.
The cortical branches are divided into hemispheric, vermian, and tonsillar
groups. The vermian branches usually arise from the medial trunk, and
the hemispheric and tonsillar branches from the lateral trunk. Each half of
the vermis is divided into median and paramedian segments, and the
hemisphere lateral to the vermis is divided into medial, intermediate, and
lateral segments. There is a reciprocal relationship with frequent overlap
in the areas supplied by the tonsillar, hemispheric, and vermian branches.
25
Hemispheric branches
The hemispheric branches most commonly arise from the lateral trunk
within or distal to the vermo-hemispheric fissure. They appear to radiate
outward to the hemispheric surface from the superior and lateral margin
of the tonsil. A common pattern is three branches with an individual
branch being directed to the medial, intermediate, and lateral segments of
the suboccipital surface.
Vermian arteries
The vermian arteries usually arise from the medial trunk in the
vermohemispheric fissure. A common pattern is for there to be one or
two vermian branches. If two are present, they are often directed to the
median and paramedian segments. If no vermian branches are present, the
vermian area is usually supplied by the contralateral PICA.
Tonsillar branches
The tonsillar branches usually arise from the lateral trunk and most
commonly supply the medial, posterior, inferior, and part of the anterior
surfaces of the tonsil. If there are no branches directed predominantly to
26
the tonsil, the tonsil is supplied by the adjacent hemispheric and vermian
branches.
Relationship to the cranial nerves
The PICA has the most complex relationship to the cranial nerves of any
artery (26, 33, 34). The vertebral artery courses anterior to
glossopharyngeal, vagus, accessory, and hypoglossal nerves, and the
proximal part of the PICA passes around or between and often stretches
or distorts the rootlets of these and adjacent nerves.
The inferior olive protrudes from the anterolateral surface of the medulla
near the vertebral artery and the origin of the PICA. The hypoglossal
nerve joins the brainstem on its anterior border and the glossopharyngeal,
vagus, and accessory nerves on its posterior border. Most PICAs arise at
the level of the olive, but some will arise rostral or caudal to that level.
The PICA origins at the level of the olive are either lateral or anterior to
the olive. The PICA origin is anterior to the olive if the vertebral artery
pursues its usual course anterior to the olive, but if the vertebral artery is
tortuous and kinked posteriorly, the PICA origin is lateral to the olive.
27
Figure 5: Illustration showing the complex relationships of the rootlets of
the lower cranial nerves to the origin and initial segments of the right
PICA.
Hypoglossal rootlets
The hypoglossal nerve arises as a line of rootlets that exits the brainstem
along the anterior margin of the caudal two-thirds of the olive in the
preolivary sulcus, a groove between the olive and the medullary pyramid.
The hypoglossal rootlets, in their course from the preolivary sulcus to the
hypoglossal canal, pass posterior to the vertebral artery, except in the rare
instance in which they pass anterior to the artery. If the vertebral artery is
28
elongated or tortuous and courses lateral to the olive, it stretches the
hypoglossal rootlets dorsally over its posterior surface.
The relation of the origin and proximal part of the PICA to the
hypoglossal rootlets varies markedly. The PICA arises either rostral or
caudal or at the level of the hypoglossal rootlets. The majority of the
PICAs arise at the level of the hypoglossal rootlets near the junction of
the hypoglossal rootlets with the medulla. The PICAs that arise superior
or inferior to the hypoglossal rootlets usually course superior or inferior
to, rather than between, the hypoglossal rootlets. The hypoglossal rootlets
are frequently stretched around the origin and initial segment of the
PICAs that arise at the level of the caudal two-thirds of the olive, in
addition to being stretched posteriorly by the vertebral artery. About half
of the PICA origins are located anterior to and half posterior to or at the
level of the rostrocaudal line drawn through the exits of the hypoglossal
rootlets from the medulla.
29
Figure 6: The PICA loops upward before turning caudally and passing
between the rootlets of the vagus and accessory nerves. The hypoglossal
nerve arises from the brainstem in front of the olive. One of the rootlets
of the hypoglossal nerve loops upward around the origin of the PICA
before descending to join the other rootlets at the hypoglossal canal
The vertebral artery courses from the lateral side of the inferior part of the
medulla to the anterior surface of the superior part of the medulla. Those
PICAs arising inferior to the olive, arise posterior to the level of the
hypoglossal rootlets if the vertebral artery at the site of origin of the PICA
has not coursed far enough anterior to reach the level of the hypoglossal
rootlets. The PICA origin is anterior to the hypoglossal rootlets if the
vertebral artery, on reaching the hypoglossal rootlets, was anterior to the
olive. The PICA origin is located at the level of or posterior to the
hypoglossal rootlets if the vertebral artery at the site of origin of the PICA
30
courses lateral to the olive and stretches the hypoglossal rootlets
posteriorly.
The initial segment of the PICA has a variable course in relation to the
hypoglossal rootlets. The most common course is for the PICA to arise
from the vertebral artery and pass directly posteriorly around or between
the hypoglossal rootlets. However, some PICAs will loop upward,
downward, or laterally in front of the hypoglossal rootlets before passing
posteriorly between or around them.
Glossopharyngeal, vagus, and accessory nerves
After coursing posterior to the hypoglossal rootlets, the PICA encounters
the rootlets of the glosso-pharyngeal, vagus, and accessory nerves. These
nerves arise as a line of rootlets, which then exit the brainstem along the
posterior edge of the olive in the retro-olivary sulcus, a shallow groove
between the olive and the posterolateral surface of the medulla.
The glossopharyngeal nerve arises as one or rarely two rootlets posterior
to the superior third of the olive, just inferior to the pontomedullary
junction and anterior to the foramen of Luschka and the rhomboid lip of
the lateral recess of the fourth ventricle. The vagus nerve arises inferior
to the glossopharyngeal nerve as a line of tightly packed rootlets posterior
to the superior third of the olive. The accessory nerve arises as a widely
31
separated series of rootlets that originates from the medulla and upper
cervical cord, inferior to the vagus nerve below the level of the junction
of the upper and middle third of the olive. The glossopharyngeal and
vagus nerves arise rostral to the level of origin of the hypoglossal rootlets.
The accessory rootlets arise at both the level of and, inferior to the origin
of the hypoglossal rootlets.
The PICA commonly passes from the lateral to the posterior aspect of the
medulla by passing between the rootlets of the glossopharyngeal, vagus,
and accessory nerves. The PICA may be ascending, descending, or
passing laterally or medially or be involved in a complex loop that
stretches and distorts these nerves as it passes between them.
Facial and vestibulocochlear nerves
The facial and vestibulocochlear nerves arise superior to the
glossopharyngeal nerve at the level of the pontomedullary junction. The
proximal part of the PICA usually passes around the brainstem inferior to
the facial and vestibulocochlear nerves. However, in some
cerebellopontine angles, the proximal part of the PICA, after coursing
posterior to the level of the hypoglossal rootlets, loops superiorly toward,
even compressing, the facial and vestibulocochlear nerves before
descending to pass between the glosso-pharyngeal, vagus, and accessory
rootlets.
32
Embryology of PICA:
The embryological vascular development shows that basilar and vertebral
arteries are formed from plexiform formations around the brainstem, with
transverse branches connected by longitudinal remnants of the prominent
lateral channel (41). The PICA also develops from these plexiform
formations, which may lead to many anatomic variations of the PICA.
Such developmental characteristics would act as an important congenital
factor for aneurysm formation at the straight portion of arteries. In other
words, there would be fragile points at the straight portion of the PICA.
Types of PICA aneurysms:
PICA aneurysms can be divided into three distinct forms depending upon
their morphology: saccular, fusiform, and dissecting (35). It is sometimes
difficult to differentiate among these three types of aneurysm
radiographically. Yamaura (35) in his series of 94 vertebral aneurysms
reported that 90 of the aneurysms were arising at the VA-PICA junction
or from the distal segment of PICA reported that among PICA
aneurysms 61.1% were saccular aneurysms, 10% were fusiform
aneurysms, and 28.8% were dissecting aneurysms.
33
According to the location on the PICA they can be further characterised
as:
1) Junction PICA-VA aneurysms: usually arose at a curve where
the vertebral artery turned medially to join the contralateral
vertebral artery. Thus, they tended to arise just above the PICA
origin in the angle between the vertebral artery and PICA,
usually pointing superiorly and often partially embedded into the
anterolateral medulla (4).
2) Proximal segment aneurysms: those arising from anterior and
lateral medullary segments
3) Transitional segment aneurysms: those arising from
tonsillomedullary segment
4) Distal segment aneurysms: those arising from telovelotonsillar and
cortical segments
This is a surgical–anatomical classification schema, based on whether
the vessel lacks perforating vessels to the brainstem, is useful in
deciding whether the PICA can be potentially sacrificed at that point
without producing major functional impairment risks (36).
34
Figure 7: Surgical–anatomical classification schema used to determine
the need for PICA preservation. Segments of PICA: green portion =
anterior medullary segment; orange portion = lateral medullary segment;
blue portion = tonsillomedullary segment; yellow portion =
telovelotonsillary segment; and red portion = cortical segment
Pathogenesis of PICA aneurysms:
These lesions followed the habit of aneurysms, set forth by Rhoton (13),
in that they occurred at branching points and at curves, and pointed
35
in the direction that the blood flow would have taken if the curve had
not been present. Most of the evidence suggests that the predominant
contributor to their development is increased hemodynamic stress related
to hyperdynamic flow (37) and time (38, 39). When arising from small
peripheral vessels, particularly when associated with an AVM, these
lesions were often not associated with visible bifurcation sites, and the
length and pattern of the vessel wall that was affected resembled the
“side-wall blow out” often seen with dissecting aneurysms (36).
Although saccular intracranial aneurysms usually arise from the
bifurcation of arteries, distal PICA aneurysms occasionally have no
associated branching artery around the aneurysmal neck (4, 26, 40, 36).
Such branchless aneurysms can arise from a straight portion of the artery
in addition to a turning point (4, 10, 40). Hemodynamic stress and/or
congenital factors would be involved in the branchless aneurysm
formation at the distal PICA. The hemodynamic stress may cause
aneurysm formation at the hairpin curve of the PICA. Conversely, it is
not clear how the branchless aneurysm develops at the straight portion.
The PICA develops from the plexiform formations around the brainstem,
which may lead to many anatomic variations of the PICA (41). Such
developmental characteristics would act as an important congenital factor
36
for aneurysm formation at the straight portion of arteries. In other words,
there would be fragile points at the straight portion of the PICA (42).
Stehbens (43) stated that large fusiform aneurysms are the direct result of
severe atherosclerosis with weakening of the wall. Rupture can occur but
is rare. Their pressure effects depend on size and anatomical
displacement associated with elongation and tortuosity of the parent
artery.
CLINICAL PRESENTATION:
The most common presentation in the published series
(4,42,2,44,45,46,8,9,47,36) was headaches, decreased level of
consciousness, and meningismus without focal deficits. Laine (48)
described a syndrome of localizing value for ruptured vertebral and PICA
aneurysms. However, in most cases, the symptoms of aneurysms at
this location are related to subarachnoid hemorrhage. Altough focal
neurological deficits are rare (40), these aneurysms can present as
bilateral abducent palsy, hemiparesis and truncal ataxia and this has been
described earlier (49, 20, 50). Even when these aneurysms reach giant
proportions, the clinical characteristics are quite variable, and these
lesions have been reported to present as posterior fossa tumor (51),
foramen magnum syndrome (50), obstructive hydrocephalus (52), and
cerebellopontine angle syndrome (53). Early evacuation of blood from
37
the ruptured aneurysm at this location prevents severe neurological
impairment (54).
PATTERNS OF HEMORRHAGE:
The hemorrhage patterns shown on CT scans are generally specific to the
PICA segment from which the aneurysm arises. Blood in the fourth
ventricle without blood in the suprasellar, prepontine, and/or
circumesencephalic cisterns is said to be the typical CT appearance of
bleeding secondary to PICA-VA aneurysms (4). Some distal PICA
aneurysms present with only cerebellar or fourth ventricular hemorrhages
(55). Rupture of proximal PICA aneurysms is evidenced by presence of
clots within the ipsilateral basal cisterns, with or without extension into
the fourth ventricle. Isolated IVH without cisternal SAH is uncommonly
seen with proximal PICA aneurysms though more evident following
rupture of distal PICA aneurysms (4, 56, 55, 57). Aneurysms arising
from the tonsillomedullary segment are known to hemorrhage into the
fourth ventricle alone.
Rupture of aneurysms along the cortical or telovelotonsillar segment may
cause an intracerebellar hematoma that secondarily extends into the
ventricular system. Identification of any small focal peri-fourth
ventricular clot should alert the clinician to this possibility.
j
Figure 8:
junction a
ventricula
Kal
cases of a
fossa SAH
present in
present. S
hemorrha
cases, wh
present in
93% of c
associated
IVH in 13
al. (47) fo
: Compute
aneurysm
ar blood.
llmes et a
angiograph
H was pre
n 30% of
Supratento
age (IVH)
hereas isola
n 95% of
cases. Oth
d with ru
3 (100%)
ound IVH
erized tom
showing d
al. (56) d
hicaly con
sent in 95
cases, but
orial SAH
with or w
ated IVH
cases. Bo
her author
ptured PI
of 13 case
in 83% of
38
mogram of
diffuse su
described
nfirmed ru
% of case
t in no ca
was prese
without as
was seen
oth IVH a
rs also ha
ICA aneur
es of ruptu
f cases.
f a patient
ubarachnoi
the patter
uptured PI
es. Isolated
se was iso
ent in 70%
ssociated
in 5% of
and hydro
ave noted
rysms. Sa
ured PICA
t with rup
id hemorrh
rns of he
ICA aneu
d posterior
olated sup
% of cases.
SAH was
cases. Hy
ocephalus
high freq
adato et a
A aneurysm
ptured PIC
hage with
emorrhage
urysms. Po
r fossa SA
pratentoria
. Intravent
seen in 9
ydrocephal
were pre
quencies o
al. (58) d
ms and An
CA-VA
h fourth
e in 44
osterior
AH was
al SAH
tricular
95% of
lus was
sent in
of IVH
etected
ndoh et
39
Therefore, a patient presenting with neither hydrocephalus nor IVH
would be highly unlikely to harbor a ruptured PICA aneurysm. The
presence of SAH along the convexity would further diminish the
likelihood of a ruptured PICA aneurysm. When encountering a pattern of
SAH highly atypical of ruptured PICA aneurysms, difficult vertebral
artery catheterizations might be deferred in the acute setting. Conversely,
encountering a pattern highly typical for ruptured PICA aneurysms would
mandate careful evaluation of the vertebral arteries, even if other
aneurysms had already been angiographically documented (56).
The possible patterns of bleeding due to other causes have to be
borne in mind. In nonhypertensive younger patients, vermian or
cerebellar hemisphere clots (often having extension into the ventricular
system) are most commonly caused by an underlying structural vascular
lesion such as an AVM. In contrast, hypertensive cerebellar hemorrhages
most commonly occur in men during their sixth through eighth decades,
originate in the dentate nucleus but may enlarge to involve the vermis
medially, and generally do not extend into the ventricular system unless
quite large (59, 60).
Most spontaneous IVH's result from rupture of a parenchymal
hematoma into the ventricles, but occasionally subarachnoid blood
refluxes into the ventricular system from the basal cisterns.
40
Hypertensive hemorrhage is the most common source of spontaneous
IVH, but the condition was recognized less frequently prior to
development of CT imaging of the brain (61, 62, 63). In a report of 54
adult patients with IVH, 14 cases were due to rupture of saccular
aneurysms (62).
Compared with other intracranial aneurysms, ruptured PICA
aneurysms represent a unique subset of intracranial aneurysms with a
higher incidence of IVH and secondary hydrocephalus (56, 64). The high
frequency of IVH in ruptured PICA aneurysms may result from the close
association between the PICA and the foramina of Luschka and
Magendie, with retrograde flow of extravasated blood into the fourth
ventricle (58, 65). It is likely that the higher frequency of hydrocephalus
associated with PICA aneurysms compared with other aneurysms is
related to the high frequency of IVH in ruptured PICA aneurysms (56).
Early CT literature suggested that extensive supratentorial SAH
was unusual with ruptured posterior fossa aneurysms. More recent
literature has noted extensive supratentorial SAH in as many as 50% of
ruptured posterior fossa aneurysms (58). Kallmes et al. (56), reported that
supratentorial SAH was present in 70% of cases.
41
ANGIOGRAPHIC FEATURES:
The digital subtraction angiography remains the "gold standard" in
preoperative neuroradiological imaging of aneurysms (2).
Figure 9: Antero-posterior view of a digital subtraction angiogram of a
patient with ruptured PICA aneurysm showing a small saccular aneurysm
arising at the VA-PICA junction.
The importance of performing a complete four-vessel angiogram in this
setting has been emphasized previously (66, 67). Although arteriography
of the dominant vertebral artery reveals the aneurysm, the necessity for
direct visualization of each VA and its PICA has been repeatedly stressed
42
by many authors. One should not depend on washout down the
contralateral VA to provide adequate visualization of opposite PICA.
Less well appreciated is a curious lack of visualization of the aneurysm
by initial studies in this location; hence the need to repeat arteriography
until one is completely satisfied with the anatomical delineation (46). The
mechanism in this situation is unclear, and may involve the lysis of a clot
extending into the neck of the aneurysm (46). Hudgins et al. (4) and
Salcman et al. (46) reported two patients each whose PICA aneurysms
were missed on initial angiograms. Horiuchi et al. (42) in their study,
reported that the initial angiograms did not show a distal PICA aneurysm
in 5 (21.7%) of 23 patients.
It is also important to determine whether the PICA is reduplicated,
whether the opposite artery is present, whether the PICA territory is
irrigated by another vessel (e.g., the AICA), and whether the posterior
communicating arteries are present and, if so, whether they are
exceptionally large or fetal in nature; all of this information is vital in the
event of a planned or emergency vertebral occlusion (68, 69, 70).
Vasospasm (combined angiographic and clinical) was found in seven out
of 21 patients in the study by Hudgins et al. (4). This incidence of 33% is
essentially the same as that reported for all aneurysms (71). Gacs et al.
(45) reported 4 cases of vasospasm in their series and were of the opinion
43
that spasm of the major arteries was found only after rupture of
aneurysms located on the more proximal segments of the cerebral
arteries. Bleeding of the more distal aneurysms caused no spasm or spasm
only in the neighboring small arteries. These findings may support the
debated role of local, direct, mechanically induced factors elicited by the
aneurysm rupture in the pathogenesis of spasm in SAH.
Figure 10: Lateral view of a digital subtraction angiogram of a patient
with ruptured PICA aneurysm showing a small saccular aneurysm arising
at from the caudal loop of the PICA (tonsilomedullary segment).
44
Figure 11: Lateral view of a digital subtraction angiogram of a patient
with ruptured PICA aneurysm showing a small saccular aneurysm arising
at from the telovelotonsillar segment of PICA.
Aneurysm size is an important factor in determining hemorrhage risks
and treatment options, particularly in those patients presenting with
unruptured lesions. The “safe” size under which hemorrhage is less
probable is most often quoted as less than 10 mm (72, 73). This rule
clearly does not apply to distal PICA aneurysms. Small peripheral
aneurysms arising on the cerebellar arteries probably have thinner walls,
rendering them more prone to hemorrhage (45).
45
The most important angiographic findings of dissecting aneurysms are:
irregular tapering or narrowing of the arterial lumen; intimal flap;
double lumen; false aneurysm; and irregularity of the arterial wall
with a wave-like pattern but no appreciable luminal narrowing. Among
such findings, confirmation of the true lumen and the false lumen is
the true "diagnostic sign."(74) It is very difficult to differentiate
fusiform aneurysms and dissecting aneurysms on the basis of VA
angiography alone.
The individual anatomy of the AICA and the PICA is quite variable.
They generally complement each other and the caliber of these two
vessels is often found to be inversely proportionate to one another. The
AICA-PICA variant is a well-recognized entity in which the AICA
provides blood supply to the distribution of both the AICA and the PICA.
This variant is relatively common seen in nearly 24% of routine vertebral
angiograms. The caudal trunk of AICA supplied the ipsilateral PICA
territory in 22% of cases.
46
Figure 12: Preoperative CT angiogram (A, anteroposterior; B, oblique)
and vertebral angiogram (C, anteroposterior; D, lateral) showing
aneurysm from the tonsillar segment of left AICA-PICA variant. Post
operative angiogram (E, anteroposterior; F, lateral) demonstrating
complete obliteration of the aneurysm after clipping.
Association with AVMs:
In 2.7% to 8.7% of patients with AVM's intracranial aneurysm is a
simultaneous finding (75, 76, 77, 78). On the other hand, based on the
work of Locksley (1) and Suzuki and Onuma (78) only about 0.1%
of patients with aneurysms show simultaneous occurrence of AVM's.
The association of AVM's and aneurysms may be partly explained on
47
the basis of a congenital vascular anomaly and partly by the
presumption that the increased blood flow through the feeding arteries
hemodynamically facilitates aneurysm formation. Because of the rate
of occurrence of aneurysms in the general population (5% in autopsy
cases (79, 80)), some authors believe that the 2.7% to 8.7%
simultaneous occurrence of aneurysm in AVM cases is probably
coincidental (81).
Authors of recent reports have suggested that the incidence of aneurysms
arising in association with AVMs may be as high as 46% (78, 82, 83, 84),
and that the incidence may be greater for infratentorial lesions (85). All
aneurysms associated with AVMs in a large number of series reported in
the literature were located on distal segments of the PICA, which fed the
AVM; a markedly increased incidence when compared with
supratentorial AVMs (82, 84). These aneurysms may not remain stable
and have been shown to be dynamic lesions that evolve over time (37,
86). Aneurysms arising near the nidus have been specifically identified as
potentially carrying an increased risk of hemorrhage (83, 87). Others,
however, report that the risk of hemorrhage is higher for the AVM (88).
48
Treatment
Preoperative management
All patients are begun on oral Nimodipine 60mg 4th hourly upon
admission. Other standard procedures include bed rest in a quiet room,
blood pressure control if necessary, initiation of antiepileptic, analgesic
for headache and occasional use of phenobarbital for sedation.
Emergency ventriculostomy might be required in a patient with
hydrocephalus associated with depressed consciousness.
Surgical treatment
PICA-VA complex aneurysms
Surgery for aneurysms of the PICA-VA complex has traditionally been
carried out at a delay of several days to weeks (46). Yamaura (35) had no
examples operated on within 72 hours of the SAH, and only two
operations were performed at less than 1 week. All of the 21 cases in the
series reported by Hudgins and colleagues (4) were done on a delayed
basis, possibly due to referral pattern at their institution. Salcman et al.
(46) advocate early surgery when feasible, because relatively little
retraction is required for exposure and the structures involved (i.e., the
brainstem and cranial nerves) do not swell appreciably after hemorrhage,
unlike the cerebral hemispheres.
49
The PICA has the most variable course of all the cerebellar arteries,
and its course is the primary determinant of the location of the
aneurysm and of the direction in which the aneurysm is pointing. The
point at which the aneurysm originates determines the surgical approach
and alternatives in aneurysm obliteration (4). Aneurysms at the PICA-
vertebral junction and the initial two segments of the PICA would
best be approached via an elongated suboccipital incision one finger’s
breadth mesial to the mastoid process and 10cm in length (46). Trapping
procedures should not be used on these aneurysms, as blood flow
to vital medullary perforators may be compromised.
The patient is placed in the lateral recumbent "park bench" position. This
approach appears advantageous in PICA-vertebral junction aneurysms
for several reasons (4) : 1) there is a decreased incidence of air embolism
and hypotension, because the head is lower than the heart; 2) less
retraction on the cerebellum (and if necessary, the medulla) is
necessary, as gravity causes them to fall away; and 3) the potential
obstructive effect of the jugular tubercle and foramen magnum can be
minimized by the superior and more lateral angle of this exposure.
A major cause of morbidity in PICA-vertebral aneurysms is the
inadvertent disruption of the rootlets of the ninth through the 12th
cranial nerves. The PICA takes a variable course through these
50
rootlets, frequently looping superiorly so that it touches the anterior
or inferior surface of the facial and/or vestibulocochlear nerve (26).
With the patient in the "park bench" position, the rostral location of
the surgeon allows better visualization of proximal aneurysms in this
area, and minimizes the amount of retraction and dissection necessary
for excellent visualization and clip placement (4).
In most far lateral suboccipital craniectomies, it is not necessary to
remove the posterior lip of the foramen magnum or the arch of C1 (46,
89).
The majority of PICA aneurysms (76%) are located at or below the knee
of the vertebral artery, where it turns forward to run ventral to the brain
stem (4). The PICA arises dorsal or lateral to the aneurysm in almost
every case, with the exception of an occasional PICA posterior and
medial to the neck; hence, a lateral approach results in the vessel being
delineated before dissection of the aneurysm itself (90).
The clip is usually applied with the blades pointing forward, parallel to
the long axis of the VA distal to the PICA-VA junction (46).
51
Figure 13: Illustration demonstrating surgical clipping of a right-sided
VA-PICA junction aneurysm. This can often be accomplished with a
straight clip; however, wide-neck aneurysms often require a straight
fenestrated clip placed down the long axis of the VA, including the PICA
origin in the fenestration as shown.
The extreme tortuosity of the vertebral and PICA arteries may also
occasionally influence the laterality of the operative approach. Drake (25)
described an aneurysm arising from the right vertebral artery distal to
the PICA which was clipped through a left suboccipital craniectomy
because the tortuosity of the vertebral artery caused it to cross the
52
midline. In using the contralateral approach to a PICA aneurysm, the
vertebral artery on the side of the surgery should be traced to its junction
with the ipsilateral PICA without any initial regard for the contralateral
artery; since the origin of the opposite PICA is often at approximately the
same level, retraction of the brainstem can be carried out at this point if
necessary and the contralateral aneurysm identified (46).
Yamaura et al. (91) has correlated the risk of serious morbidity for all
PICA-VA complex aneurysms with a proximity to the midline of less
than 10mm; another unfavourble prognostic factor is a distance of more
than 13mm from the clivus to the aneurysm. In the latter circumstance,
the aneurysm is buried on the ventral aspect of the brainstem and
retraction of the medulla may be required to reach it.
Traditionally, a paramedian suboccipital craniotomy is used (92, 93).
Nevertheless, the closer the lesion is to the foramen magnum, or the
farther away it is toward the midline, the more difficult it is to visualize
adequately all the anatomical details of the region with the standard
approaches without extending the craniotomy at the skull base level. It is
now well known that both the far-lateral approach and the transcondylar
approach are very useful in treating VA–PICA aneurysms. (2,8,89,94).
Different terminologies are used to describe the far-lateral approach
described by Heros (89) to the VA and VBJ regions, depending on the
53
extent of the bone removal. These terms include the lateral suboccipital,
posterior suboccipital, posterolateral, dorsolateral, far-lateral, extreme
lateral, transcondylar, supracondylar, paracondylar, and transcondylar
fossa approach (95, 96, 97, 89, 98). Thorough inferolateral bone removal
in the suboccipital region, accompanied by removal of the posterior arch
of C-1 laterally to the sulcus arteriosus of the vertebral artery, provides
excellent exposure of the vertebral artery throughout its intracranial
course to the vertebrobasilar junction with minimal or no retraction of the
medulla (89).
The patient is placed in the straight lateral position. The head is
maintained with the nose straight ahead (at a 90° angle from the floor)
and with a 30°-angle tilt toward the ipsilateral shoulder. The skin incision
is started at about the level of the top of the ear in a sagittal plane about
three finger-breadths medial to the mastoid. The incision first extends
straight downward toward the mastoid, then curves sharply medially to
the midline, and then goes straight downward to the spinous process of C-
2.
The craniectomy extends from the junction of the transverse and sigmoid
sinuses superolaterally to just beyond the midline through the foramen
magnum inferiorly in a teardrop fashion with the wider opening
superolaterally. The arch of C-1 is removed from just beyond the midline
54
in the opposite side to the sulcus arteriosus underlying the vertebral
artery. Removing the arch of C-1 allows an approach from a more
inferior direction, below the cerebellar tonsil, without having to retract
the cerebellar hemisphere medially (89). The most important aspect of
this exposure is a very radical removal of bone in the area of the foramen
magnum going laterally as far as the condylar fossa, just posterior to the
occipital condyle and just above and behind where the vertebral artery
enters the dura (89). This extreme lateral removal of bone in the area of
the foramen magnum is the key to being able to approach the front of the
brain stem from an inferolateral angle with minimal or no brain-stem
retraction.
Aneurysms at a more distal PICA origin are usually approached in the
space between the 11th cranial nerve and the ninth and 10th cranial
nerves. The vertebrobasilar junction can usually be approached from
inferolaterally, still working between the 11th cranial nerve inferiorly and
the ninth and 10th cranial nerves superiorly, and following the vertebral
artery distally with the line of vision essentially in the same direction of
the artery.
When using lateral approaches, the jugular tubercle and the occipital
condyle are confronted as obstacles. The former constitutes a greater
problem in VA–PICA aneurysm surgery (98).
55
Bertalanffy and Seeger (99) have described their transcondylar approach
for treating lesions in the lower clivus and the anterior portion of the
craniocervical junction. Their approach is very useful for treating lesions
located in the anterior portion of the foramen magnum. In the
transcondylar approach, the essential step is a partial resection of the
occipital condyle and lateral atlantal mass.
The transcondylar fossa (supracondylar transjugular tubercle) approach
described by Matsushima et al. (98) is an anatomically refined version of
the far-lateral approach described by Heros. In the transcondylar fossa
approach, the condylar fossa and the posterior portion of the jugular
tubercle are extradurally removed up to the hypoglossal canal by using
the posterior condylar canal and the emissary vein as anatomical
landmarks without injuring the atlantooccipital joint. The occipital
condyle is kept intact. The transcondylar fossa approach provides an
entire view of the cerebellomedullary cistern including the VA, the
anterior and lateral medullary segments of the PICA, the cisternal portion
of the ninth, 10th, 11th, and 12th cranial nerves, and the lateral recess in
the cerebellomedullary fissure.
56
Distal PICA aneurysms
Because of the high incidence of bleeding when these aneurysms are
small, distal PICA aneurysms should be obliterated in almost all instances
whenever they are encountered (36).
Patients presenting with hemorrhage (real or suspected), in whom an
aneurysm is the only pathological condition identified, should be treated
urgently and not in a delayed fashion. Those patients presenting with
hemorrhage who harbor both an aneurysm and an AVM should also be
treated promptly. In this situation, the aneurysm is often the source of
bleeding, and the natural history of such lesions if untreated appears
much worse over a shorter interval than that of the AVM as a separate
entity (87, 100). A decision whether to treat the AVM at the same
hospitalization should be made, depending on the individual
characteristics of the AVM itself, particularly its size, location, and the
method chosen to obliterate the aneurysm.
The ideal treatment of a truly saccular lesion is clipping or endovascular
obliteration of the aneurysm neck with preservation of the lumen of the
PICA. A different strategy must be considered, however, whenever the
underlying cause of the lesion might represent a dissection (in which case
any residual vessel wall may be weakened and allow reformation of the
aneurysm) or when a seemingly saccular lesion cannot be clipped without
57
parent vessel occlusion. In such cases, aneurysm location relative to the
origin of brainstem perforating vessels becomes the most crucial factor
when choosing a treatment option.
A surgical–anatomical classification schema (36), based on whether the
vessel lacks perforating vessels to the brainstem, is useful in deciding
whether the PICA can be potentially sacrificed at that point without
producing major functional impairment risks. If the PICA is sacrificed,
leptomeningeal communications with the superior cerebellar artery and
the AICA are usually sufficient to protect against functionally significant
cerebellar infarctions (37).
Direct inspection of the affected segment during open surgery provides
several significant advantages compared with endovascular therapy,
particularly in cases of proximal lesions (36). Direct visualization of the
affected arterial segment allows for better decisions regarding the need to
sacrifice or spare the parent vessel. Clips placed obliquely across the
PICA can be quite focally and accurately applied to spare the patency of
perforating vessels, whereas a longer segment of the PICA is often
sacrificed whenever the artery is obliterated by endovascular means.
Surgery is also preferable whenever a significant hematoma needs to be
evacuated, when a coexistent AVM is identified that can be
simultaneously removed with a low risk (particularly when the bleeding
58
source is unclear), or when PICA preservation must be maintained (for
example, if the aneurysm is found in a proximal location or if there is a
dominant PICA with a very small AICA) (36).
For those lesions treated surgically, a combination of midline and lateral
suboccipital skull base approaches are useful, depending on the segment
of the PICA that is affected, the need for PICA reconstruction, and the
presence and location of an associated AVM.
For proximal lesions, a far-lateral suboccipital–transcondylar approach
provides sufficient proximal PICA exposure to ensure adequate
visualization and working room to apply temporary or permanent clips
and to perform direct anastomosis if required.
For aneurysms arising within transitional or distal segments, a bilateral
midline suboccipital craniotomy is usually sufficient, with additional
bone removal ipsilateral to the aneurysm or AVM and tonsillar
mobilization as needed.
For those aneurysms located beneath the tonsil, where mobilization of
this structure may be associated with a risk of premature rupture, subpial
tonsilar resection may be a preferred technique for exposure.
If an aneurysm, particularly a dissecting one, involves predominantly a
side-wall blow out, the apparently healthy residual portion of the vessel is
59
often weak and aneurysm reformation can easily occur. For such lesions
in which PICA flow must be maintained, aneurysm ablation can be
achieved and the patency of the PICA lumen can be preserved by
stacking a row of fenestrated clips (36).
Whenever the safety of leaving a patent PICA is questioned, sacrifice of
the vessel should be seriously considered. In such circumstances,
excision of the aneurysm and arterial reconstitution, performed either by
direct end-to-end anastomosis or insertion of an interposed arterial graft
(most commonly taken from the OA) may be possible options. When
direct reconstruction is not possible, a clip placed on the PICA proximal
to the aneurysm (including the rupture site) combined with a PICA–PICA
or OA– PICA anastomosis are applicable solutions (36).
60
Figure 14: Drawings depicting surgical strategies used to treat
“unclippable” distal PICA aneurysms. A: Fusiform distal PICA
aneurysm. B: Clip reconstruction achieved using stacked fenestrated
clips. C: Aneurysm resection and direct reanastomosis. D: Aneurysm
resection and interposed graft. E: Proximal ligation (flow reversal) and
distal bypass. F: Aneurysm trapping and distal bypass: G: Aneurysm
trapping and PICA–PICA anastomosis.
61
AIM OF THE STUDY
The aim of this study was to retrospectively study the PICA aneurysms
treated surgically at our institute and to know the outcome of treatment.
62
MATERIALS AND METHODS
All patients who were surgically treated at the Department of
Neurosurgery, Sree Chitra Tirunal Institute for Medical Sciences and
Technology, Thiruvananthapuram, with the diagnosis of PICA aneurysm
had their charts retrospectively reviewed for the period of January 1991
to June 2011.
Data were collected concerning patient age, sex, time interval between
date of ictus to date of admission, clinical symptoms and signs at the time
of ictus and at presentation, WFNS grade, computerized tomography
features including presence of subarachnoid hemorrhage [SAH],
intraventricular hemorrhage [IVH], intracerebellar hemorrhage [ICeH],
infarcts and hydrocephalus, angiographic features including aneurysm
characteristics (location on PICA, type and size), existence of multiple
aneurysms, timing of surgery, surgical approach and procedure, and
postoperative neurological complications.
Patient’s condition and outcome (Glasgow Outcome Scale [GOS]) were
evaluated at the time of discharge and at 6 and 12 months after discharge.
The clinical outcomes were categorized according to the Glasgow
Outcome Scale as favorable (good recovery and moderate disability) or
unfavorable (severe disability, vegetative state, or dead).
63
RESULTS
Demographics:
During the study period between January, 1991 and June, 2011, twenty
eight patients with PICA aneurysms were treated surgically and formed
the basis for this series. The results of all the 28 patients are summarized
in Table 1. There were 21 females (75%) and 7 males (25%), with female
to male ratio of 3:1. The average age of the patients was 45.22 years, with
a range of 25 to 68 years. The mean time from ictus to referral was 12.82
days, with a range of 2 to 93 days.
Clinical characteristics:
Headache was present in all the patients (100%), altered sensorium was
present in 28.57% (n=8), and neck stiffness was present in 50% (n=14).
Four patients (14.28%) presented with cerebellar signs. Two patients
(7.14%) presented with lower cranial nerve palsy. Two patients (7.14%)
had a lateral rectus restriction, both on the side of the aneurysm. None of
the patients presented with limb weakness. WFNS grade was grade I in
85.71% patients (n=18), grade II in 14.28% patients (n=3). There were no
patients with a WFNS grade III or above. Six patients had a history of
hypertension and two patients had a history of chronic smoking.
64
Case Age/ Sex
Presentation WFNS grade
CT findings
Side Site (segment)
Form Associated malformation
Surgery (approach/ procedure)
ETV/ VPS
Outcome (GOS)
1 41/M HA 1 SAH, IVH R 1(origin) Saccular none MS / clipping No 5
2 61/F HA, V 2 SAH, IVH, HCP
R 1(origin) Saccular none LS / clipping No 5
3 65/F HA, V - IVH L 1(origin) Saccular ACom aneurysm
LS / clipping No 5
4 49/F HA, LCN, CE - InCeH L 3 Saccular none LS / clipping No 5
5 52/F HA, V 1 SAH, IVH R 1(origin) Saccular none LS / clipping No 5
6 38/M HA, V, CE 1 SAH, IVH L 2 Saccular none LS / clipping No 5
7 38/F HA - IVH L 4 Saccular none MS / clipping No 5
8 45/M HA, V 1 SAH R 1(origin) Saccular none LS / clipping No 5
9 44/M HA, V 1 SAH, IVH L 4 Saccular none LS / clipping No 5
10 58/M HA, V 2 SAH, IVH, HCP
R 1(origin) Saccular Right SCA & MCA aneurysm
LS / clipping No 3
11 25/F HA, V 1 SAH, IVH R 1 Saccular none LS / clipping No 5
12 28/F HA, V 1 SAH, IVH, HCP
L 2 Saccular none LS / clipping No 5
13 56/M HA, V, LCN 1 SAH, IVH, HCP
L 1(origin) Saccular none LS / clipping No 5
14 35/F HA, CE 1 SAH, IVH R 4 Saccular none MS / clipping No 4
15 44/F HA, V 1 SAH, IVH R 1(origin) Saccular none LS / clipping Yes 1
16 66/F HA, V 1 SAH, IVH R 4 Saccular none MS / clipping No 5
17 35/F HA, V 1 SAH, IVH, HCP
L 1(origin) Saccular none LS / clipping No 5
18 38/F HA, V - IVH L 1(origin) Saccular none LS / clipping No 5
19 62/F HA 1 SAH,HCP L 1(origin) Saccular none LS / clipping No 5
20 34/F HA - InCeH L 4 Saccular none MS / clipping No 5
21 35/F HA, V, CE, LR
2 SAH, IVH, HCP
L 2 Fusi-saccular
none MS / aneurysmorraphy + wrapping
Yes 5
65
Table 1: Clinical data of 28 patients with PICA aneurysms
ACoM, anterior communicating artery; CE, cerebellar signs; ETV, endoscopic third ventriculostomy; GOS, Glasgow outcome scale (at discharge); HA, headache; HCP, hydrocephalus; IVH, intraventricular hemorrhage; L, left; LCN, lower cranial nerve dysfunction; LR, lateral rectus paresis; LS, lateral suboccipital approach; MCA, middle cerebral artery; MS, midline or paramedian suboccipital approach; R, right; SAH, subarachnoid hemorrhage; SCA, superior cerebellar artery; V, vomiting; VPS, ventriculoperitoneal shunt, #: AICA-PICA variant aneurysm
Symptoms and signs Number of patients (percent) Headache 28 (100%) Neck stiffness 14 (50%) Altered sensorium 8 (28.57%) Lateral rectus paresis 2 (7.14%) Glossopharyngeal & vagal palsy 2 (7.14%) Cerebellar signs 4 (14.28%)
Table 2: Presenting symptoms and signs
22 49/F HA, V 1 SAH,HCP InCeH,
L 1 Saccular none LS / aneurysmorraphy
Yes 5
23 45/F HA, V 1 SAH, IVH, HCP
L 1(origin) Fusi-saccular
none LS / aneurysmorraphy
No 5
24 68/F HA, V - IVH, HCP R 4 # Saccular none MS / clipping No 2
25 42/M HA 1 SAH, IVH L 1(origin) Saccular none LS / clipping No 5
26 63/F HA, V 1 SAH, IVH L 3 # Saccular none LS / clipping No 5
27 33/F HA, V - IVH, HCP L 3 Saccular none MS / clipping No 5
28 62/F HA, V 1 SAH, IVH R 1(origin) Saccular none LS / clipping No 5
66
Figure 15: Pie chart showing the skewed sex ratio of PICA aneurysms in
this study
Computerized tomography features:
All the patients who presented with acute symptoms consistent with SAH
underwent CT scanning within 24 to 48 hours after the ictus. In most of
the cases patients were referred to us after imaging from local hospitals
and there was a delay in patient referral. On examining their CT scans,
SAH was present in 75% (n=21) patients. Intraventricular hemorrhage
was evident in 82.14% (n=23) of the patients. Five patients (17.85%)
presented only with IVH. Intracerebellar hemorrhage (10.71%) was
observed in the vermis of 1 patient and in the hemisphere of 2 others.
25%
75%
Sex ratioMale Female
67
Twenty six patients (92.85%) had a Fisher (101) grade of 4 and two
patients (7.1%) had a Fisher grade of 3. Eighteen (64.28%) patients
demonstrated SAH with extension into the ventricular system. Isolated
IVH without cisternal SAH was seen with proximal PICA aneurysms in
10.52% (n=2), though it was more evident following rupture of distal
PICA aneurysms, 33.33% (n=3). Early hydrocephalus was present in
39.28% (n=11) of which 7.14% (n=2) of patients required an external
ventricular drain prior to surgery. Only one patient (3.57%) had a
cerebellar infarct.
Features on CT Number PercentSubarachnoid hemorrhage (SAH) 21 75% Intraventricular hemorrhage (IVH) 23 82.14% Intracerebellar hemorrhage (ICeH) 3 10.71% Isolated IVH without SAH 5 17.85% Hydrocephalus (HCP) 11 39.28% Infarct 1 3.57%
Table 3: Computerized tomography features
Angiographic features:
Four-vessel cerebral angiography was done in all the patients. In 26
(92.85%) patients the angiogram revealed the aneurysm while in the
remaining 2 patients, a second angiogram repeated after 2 weeks detected
the aneurysm.
68
Fifty percent (n=14) patients had aneurysms located at the PICA origin.
Rest of the aneurysms were located along the PICA, with 7.14% (n=2)
arising from the anterior medullary segment, 10.71% (n=3) from the
lateral medullary segment, 10.71% (n=3) from the tonsillomedullary
segment, 21.42% (n=6) from the telovelotonsillar segment and none from
the cortical segment. Nineteen aneurysms (67.85%) were located on the
proximal segment of PICA and 32.14% (n=9) were located on the distal
segment. We had two cases of distal AICA-PICA variant aneurysms, one
arising from the telovelotonsillar segment and the other from the
tonsillomedullary segment.
Location of aneurysm Number Percent VA-PICA junction 14 50% Anterior medullary segment 2 7.14% Lateral medullary segment 3 10.71% Tonsillo-medullary segment 3 10.71% Telovelotonsillar segment 6 21.42% Cortical segment 0 0% Right side 11 39.28% Left side 17 60.71%
Table 4: Location of PICA aneurysms on angiography
Among the treated aneurysms 26 (92.85%) were saccular in shape and 2
(7.14%) were fusi-saccular arising from the PICA proper. Of the 28 PICA
aneurysms, 23 (82.14%) were small (<1.5cm) in size, 4 (14.28%) were
69
large (1.5 – 2.5cm) and one (3.57%) was a giant aneurysm (>2.5cm). Of
the 28 PICA aneurysms 39.28% (n=11) were located on the right and
60.71% (n=17) on the left. 89.28% (n = 25) of the patients treated had
only one aneurysm, whereas 7.14% (n = 2) had multiple aneurysms.
Associated vascular anomalies were noted in two cases. One had an
aneurysm arising from the ACom artery and the other patient had two
aneurysms, one arising from the ipsilateral SCA and the other from
MCA. Angiographic evidence of vasospasm was not found in any patient.
Preoperative care:
All patients were begun on oral Nimodipine 60mg 4th hourly upon arrival
at our institution. Other standard procedures consisted of bed rest in a
quiet room, blood pressure control if necessary, initiation of antiepileptic
(phenytoin), paracetamol for headache and occasional use of
phenobarbital for sedation. No patient had recurrent hemorrhage after
arrival at our institution.
Surgical procedure:
Of the 28 ruptured aneurysms, none were treated within 48 hours of
hemorrhage, 35.71% (n=10) were treated within 2 to 5 days, and 64.28%
(n=18) were treated after a time period longer than 5 days. The reason for
late treatment was generally delayed referral. No patient had recurrent
70
hemorrhage upon arrival at our institution. All proximal aneurysm
clippings were performed using a lateral, suboccipital approach and those
in the distal segments were approached using a midline/ paramedian
approach. Twenty five aneurysms (89.28%) were directly clipped without
any intraoperative complications. One patient (Patient no: 21) had a large
fusi-saccular aneurysm from the lateral medullary segment that was
partially thrombosed and calcified. Aneurysmorrhaphy was done with
prolene suture and wrapped with muscle tissue. In 2 patients (patient no:
22 and 23) in view of poor aneurysm configuration for clipping,
aneurysmorrhaphy was done with multiple clips. None of the cases
required parent vessel occlusion or bypass procedure. Intraoperative
temporary arterial occlusion was performed depending on the surgeon
and the extent of aneurysm dissection. It never exceeded 3 minutes
without at least a 5 minute period of reperfusion. There was no
intraoperative complication of aneurysm rupture. Estimated blood loss
was 500ml or less for all procedures.
Two patients had multiple aneurysms. The patient who had an anterior
communicating artery aneurysm (Patient no.3) underwent pterional
craniotomy and clipping of the aneurysm during the same admission. The
post-operative period was uneventful. The patient who had a right
superior cerebellar artery and middle cerebral artery aneurysms (Patient
71
no.10) had a poor outcome after surgical clipping of PICA aneurysm that
had bled. The patient developed transient lower cranial nerve palsy and
required tracheostomy. He was discharged to a local hospice for nursing
care and was lost to follow-up.
Complications and outcomes:
Six of the patients (21.42%) developed new postoperative neurological
deficits representing neurological complications. Three (10.71%) patients
developed vocal cord paralysis, two of them requiring tracheostomy; one
being transient in nature. Three (10.71%) patients underwent CSF
diversion in the form of a ventriculoperitoneal shunt or endoscopic third
ventriculostomy for persisting radiographic hydrocephalus. Three
(10.71%) developed postoperative gait ataxia which improved in one
patient but persisted to a mild degree in 2 patients at 1 year follow-up.
Postoperative CT image in both these patients revealed a small ipsilateral
cerebellar infarct without any mass effect. One patient (3.5%) died
during hospitalization, and no patient subsequently hemorrhaged. The
mean duration of hospital stay was 18.53 days (range 9 to 101 days). 25
patients were discharged home, 2 were transferred to a rehabilitation
facility and 1 died in the hospital.
When analyzed according to aneurysm size, 21.73% (n = 5) of the
patients with lesions less than 1.5 cm in diameter developed at least one
72
new postoperative neurological complication each, whereas 25% (n = 1)
of the patients with aneurysms that were 1.5 to 2.5 cm in diameter did so,
and the one patient with aneurysm that was larger than 2.5 cm in diameter
did not develop any new deficits. The patients with distal aneurysms had
a 33.3% (n = 3) incidence of ataxia after surgery.
A check conventional angiogram / CT angiogram after surgery was
performed in 16 (57.14%) patients depending on the surgeon’s
preference. None of the angiograms revealed any residual aneurysm.
Patient’s status at discharge and at follow up was recorded using the
Glasgow Outcome Scale (GOS, Table 5). GOS scores were determined at
the time of discharge for 100% of the patients (n=28), at 6 months after
discharge for 25 patients (89.28%) and at 1-year after discharge from the
hospital for 20 patients (71.42%). At 6 months follow-up, 24 (85.71%)
patients were independent (GOS score of 4 or 5) and had a favourable
outcome and at 1 year after discharge, 20 (71.4%) patients who continued
to be on regular visits were independent. The reduction in percent at 6
months and at 1 year was because of a reduction in the number of patients
available for follow up.
When the outcome was analyzed according to the location of the
aneurysm, 17 proximal PICA aneurysms (89.4%) had a favourable
outcome (GOS score of 5 or 4); whereas 2 proximal PICA aneurysms
73
(10.52%) had an unfavourable outcome (GOS of 3, 2 or 1). Seven distal
segment aneurysms (77.77%) had a favourable outcome (GOS score of 5
or 4); whereas 2 distal PICA aneurysms (22.22%) had an unfavourable
outcome (GOS of 3, 2 or 1).
Score
Outcome
1 Dead
2 Vegetative state
3 Severe disability; able to follow commands/unable to live independently
4 Moderate disability; able to live independently, unable to return to work or school
5 Good recovery; able to return to work or school
Table 5: Glasgow Outcome Scale, scale for measurement of outcome after brain injury (102) Glasgow outcome scale score Number (%) 5 24 (85.71%) 4 1 (3.57%) 3 1 (3.57%) 2 1 (3.57%) 1 1 (3.57%)
Table 6: Glasgow outcome scale score for 28 patients who underwent surgical treatment for PICA aneurysms
74
Figure 16: Surgical outcome for 28 patients with ruptured PICA aneurysms, favourable outcome (GOS of 5 or 4), unfavourable outcome (GOS 3, 2 or 1)
0
5
10
15
20
25
30
Favourable unfavourable
Outcome
75
DISCUSSION
DEMOGRAPHICS:
Between January, 1991 and June, 2011, 28 cases of PICA-vertebral
and distal PICA aneurysms were operated upon in the Neurosurgery
Department at SCTIMST.
There was a striking female predominance (75%, n=21). Several other
series of PICA aneurysms demonstrate a similar female predisposition (4,
42, 2, 44, 45, 46, 8), while the series by Dimsdale and Logue (103) and
Lewis et al. (36) show an equal male to female ratio. Only the series of
Hammon and Kempe (104) shows a male predominance, a skew not
unexpected from their predominantly military population at Walter
Reed General Hospital, USA.
In our study the average age of these patients was 45.22 years, with a
range of 25 to 68 years. The mean age of patients who present with PICA
aneurysms is younger than those with aneurysms at other locations.
Horiuchi et al. (42) reported a mean age of 62 years in their study of
distal PICA aneurysms. Hudgins et al (4) reported a mean age of 52
years. Lewis et al. (36) reported a mean age of 51 years. In a report by
Dernbach and colleagues (105), the mean age was slightly lower at 44.7
76
years but with a similar sex distribution. The Hammon and Kempe series
(104) differs in that the average age of patients with PICA aneurysms is
33 years, and probably reflects their specialized referral base.
CLINICAL CHARACTERISTICS:
The mean time from ictus to referral was 12.82 days in our study. This
delay in referral skews our series toward patients who did relatively well
after their initial hemorrhage, and prevents any conclusions regarding the
natural history and preoperative mortality rate associated with such
lesions.
All patients presented with aneurysmal rupture. The most common
presentation in our series, as well as in others (4,42,2,44,45,46,8,9,47,36)
was headaches, decreased level of consciousness, and meningismus
without focal deficits. All patients presented with classic SAH symptoms:
sudden severe headache (usually occipital). This was followed by an
altered level of consciousness, in 8 cases. Five patients also had neck
pain. Thirteen patients had neck stiffness. Six patients had papilledema.
Twenty patients exhibited no focal abnormalities during the initial
evaluation. The remaining patients exhibited some focal neurological
deficits.
77
Four patients in our series presented with cerebellar signs, predominantly
gait ataxia, attributable to unilateral cerebellar dysfunction caused by the
pressure effect of the aneurysm or the intracerebellar hemorrhage.
Although Laine (48) described a syndrome of localizing value for
ruptured vertebral and PICA aneurysms, this was not confirmed in our
series. However, in most cases, the symptoms of aneurysms at this
location are related to subarachnoid hemorrhage. Altough focal
neurological deficits are rare (40), these aneurysms can present as
bilateral abducent palsy, hemiparesis and truncal ataxia and this has been
described earlier (49, 20, 50). Even when these aneurysms reach giant
proportions, the clinical characteristics are quite variable, and these
lesions have been reported to present as posterior fossa tumor (51),
foramen magnum syndrome (50), obstructive hydrocephalus (52), and
cerebellopontine angle syndrome (53). Early evacuation of blood from
the ruptured aneurysm at this location prevents severe neurological
impairment (54). It is known that giant aneurysms of the distal PICA
are often present in patients with symptoms of extra or intra-axial
posterior fossa tumors or fourth ventricular tumors
(105,50,106,107,51).
The arachnoid trabeculae of the cisterna magna are coarse, and the only
structure surrounding the PICA is the network of caudal cranial nerves on
78
the lateral medullary segment. In the event of aneurysm rupture, blood
can penetrate the ventricles without difficulty, allowing massive
bleeding and rebleeding (9).
Like patients who rebled from aneurysms at other sites, those with
ruptured distal PICA aneurysms display progressive disturbance of
consciousness. Also, with distal PICA aneurysm, respiratory
insufficiency is more likely to develop, and to be fatal, as a result
of rebleeding. Awareness of the higher risk of rebleeding with distal
PICA aneurysms is an important factor in their management (9).
However, no patient in our series presented with a rebleed or
hemorrhaged during the time interval between admission and surgery.
Patients presenting with SAH (n = 21) were stratified according to the
WFNS grading scheme (108). Without adjusting for other medical
illnesses, 85.71% (n=18) of the patients presented with WFNS grade 1,
14.28% (n=3) with grade 2 and none with grade 3 or above. Horiuchi et
al. (42) reported that poor preoperative grade adversely affected the
outcome of patients with distal PICA aneurysms.
PATTERNS OF HEMORRHAGE:
The hemorrhage patterns shown on CT scans are generally specific to the
PICA segment from which the aneurysm arises. Blood in the fourth
79
ventricle without blood in the suprasellar, prepontine, and/or
circumesencephalic cisterns is said to be the typical CT appearance of
bleeding secondary to PICA-VA aneurysms (4). Some distal PICA
aneurysms present with only cerebellar or fourth ventricular hemorrhages
(55). Rupture of proximal PICA aneurysms is evidenced by presence of
clots within the ipsilateral basal cisterns, with or without extension into
the fourth ventricle. In our series, SAH was present in 75% (n=21)
patients, IVH was present in 82.14% (n=23) patients, intraparenchymal
hemorrhage was seen in 10.71% (n=3) patients. Eighteen (64.28%)
patients demonstrated SAH with extension into the ventricular system.
Isolated IVH without cisternal SAH is uncommonly seen with proximal
PICA aneurysms (10.52% (n=2) in our series) though more evident
following rupture of distal PICA aneurysms (33.33% (n=3) in our series)
(4, 56, 55, 57). Hydrocephalus was present in 39.28% (n=11) patients,
which was less compared to other series (56). Aneurysms arising from the
tonsillomedullary segment are known to hemorrhage into the fourth
ventricle alone.
Rupture of aneurysms along the cortical or telovelotonsillar
segment may cause an intracerebellar hematoma that secondarily extends
into the ventricular system. Identification of any small focal peri-fourth
ventricular clot should alert the clinician to this possibility. In our series
80
intracerebellar hematoma was seen in 3 patients (10.71%) of which one
was due to a giant aneurysm from the proximal segment (Patient no.22).
Kallmes et al. (56) described the patterns of hemorrhage in 44
cases of angiographicaly confirmed ruptured PICA aneurysms. Posterior
fossa SAH was present in 95% of cases. Isolated posterior fossa SAH was
present in 30% of cases, but in no case was isolated supratentorial SAH
present. Supratentorial SAH was present in 70% of cases. Intraventricular
hemorrhage (IVH) with or without associated SAH was seen in 95% of
cases, whereas isolated IVH was seen in 5% of cases. Hydrocephalus was
present in 95% of cases. Both IVH and hydrocephalus were present in
93% of cases. Other authors also have noted high frequencies of IVH
associated with ruptured PICA aneurysms. Sadato et al. (58) detected
IVH in 13 (100%) of 13 cases of ruptured PICA aneurysms and Andoh et
al. (47) found IVH in 83% of cases.
Therefore, a patient presenting with neither hydrocephalus nor IVH
would be highly unlikely to harbor a ruptured PICA aneurysm. The
presence of SAH along the convexity would further diminish the
likelihood of a ruptured PICA aneurysm. When encountering a pattern of
SAH highly atypical of ruptured PICA aneurysms, difficult vertebral
artery catheterizations might be deferred in the acute setting. Conversely,
encountering a pattern highly typical for ruptured PICA aneurysms would
81
mandate careful evaluation of the vertebral arteries, even if other
aneurysms had already been angiographically documented (56).
The high frequency of IVH in ruptured PICA aneurysms may
result from the close association between the PICA and the foramina of
Luschka and Magendie, with retrograde flow of extravasated blood into
the fourth ventricle (58, 65). It is likely that the higher frequency of
hydrocephalus associated with PICA aneurysms compared with other
aneurysms is related to the high frequency of IVH in ruptured PICA
aneurysms (56).
Early CT literature suggested that extensive supratentorial SAH
was unusual with ruptured posterior fossa aneurysms. More recent
literature has noted extensive supratentorial SAH in as many as 50% of
ruptured posterior fossa aneurysms (58). Kallmes et al. (56) reported that
supratentorial SAH was present in 70% of cases.
Angiographic features:
Although arteriography of the dominant vertebral artery reveals the
aneurysm, the necessity for direct visualization of each VA and its PICA
has been repeatedly stressed by many authors. One should not depend on
washout down the contralateral VA to provide adequate visualization of
opposite PICA. Less well appreciated is a curious lack of visualization of
82
the aneurysm by initial studies in this location; hence the need to repeat
arteriography until one is completely satisfied with the anatomical
delineation (46). The mechanism in this situation is unclear, and may
involve the lysis of a clot extending into the neck of the aneurysm (46).
Two of the aneurysms in our series were invisible on the original study
despite a complete absence of vasospasm. Hudgins et al. (4), Salcman et
al. (46) also reported two patients each whose PICA aneurysms were
missed on initial angiograms. Horiuchi et al. (42) in their study, reported
that the initial angiograms did not show a distal PICA aneurysm in 5
(21.7%) of 23 patients.
It is also important to determine whether the PICA is reduplicated,
whether the opposite artery is present, whether the PICA territory is
irrigated by another vessel (e.g., the AICA), and whether the posterior
communicating arteries are present and, if so, whether they are
exceptionally large or fetal in nature; all of this information is vital in the
event of a planned or emergency vertebral occlusion (68, 69, 70).
We did not find any case with evidence of vasospasm in our series.
Vasospasm (combined angiographic and clinical) was found in seven out
of 21 patients in the study by Hudgins et al. (4). This incidence of 33% is
essentially the same as that reported for all aneurysms (71). Gacs et al.
(45) reported 4 cases of vasospasm in their series and were of the opinion
83
that spasm of the major arteries was found only after rupture of
aneurysms located on the more proximal segments of the cerebral
arteries. Bleeding of the more distal aneurysms caused no spasm or spasm
only in the neighboring small arteries. These findings may support the
debated role of local, direct, mechanically induced factors elicited by the
aneurysm rupture in the pathogenesis of spasm in SAH.
In our series 39.28% (n=11) of the aneurysms were located on the right
and 60.71% (n=17) on the left. This finding may be related to the fact that
the left vertebral artery is the dominant or larger artery (69). The left
dominance of the
aneurysm may be caused by more hemodynamic stress than on the right
side.
Aneurysm characteristics:
In our series, 23 aneurysms were small in size, 4 were large and one was
a giant aneurysm. This is consistent with Drake's observation (25) that
most of these aneurysms are less than 1.25 cm or greater than 2.5 cm. We
did not, however, see the large percentage of giant aneurysms
reported by Drake (25,109) (six of 50 aneurysms) and Kempe (110)
(fifteen of 48 aneurysms). Even when these aneurysms reach giant
proportions, the clinical characteristics are quite variable, and these
84
lesions have been reported to present as posterior fossa tumor (51),
foramen magnum syndrome (50), obstructive hydrocephalus, (52) and
cerebellopontine angle syndrome(53). Aneurysm size is an important
factor in determining hemorrhage risks and treatment options, particularly
in those patients presenting with unruptured lesions. The “safe” size
under which hemorrhage is less probable is most often quoted as less than
10 mm (72, 73). This rule clearly does not apply to distal PICA
aneurysms. Small peripheral aneurysms arising on the cerebellar arteries
probably have thinner walls, rendering them more prone to hemorrhage
(45).
In this study aneurysms are defined as saccular (26 cases) or fusisaccular
(2 cases), a decision based on the appearance of the lesion’s luminal
shape on arteriography and modified by surgical findings. Most fusiform
lesions represent dissecting arteries, although the classic arteriographic
features of pearl-and-string sign (15), a double lumen (74), linear defects,
and focal outpouching (14, 111) are difficult to demonstrate when
encountered in small vessels (for example, those on the peripheral PICA).
Although the finding of small peripheral aneurysms should prompt
consideration of infectious causes, no such lesions were encountered in
our series and are rarely described in the literature (112).
85
Surgical treatment, complications and outcome:
In this series, 14 cases of VA-PICA aneurysms, 3 cases of proximal
segment aneurysms and 3 cases of distal segment aneurysms were treated
with a lateral suboccipital approach. Midline suboccipital approach was
used in 6 cases of distal segment aneurysms, one case of proximal
segment aneurysm, and one case of aneurysm arising at VA-PICA
junction.
The point at which the aneurysm originates determines the surgical
approach and alternatives in aneurysm obliteration. Aneurysms at the
PICA-vertebral junction and the initial two segments of the PICA
would best be approached via a lateral suboccipital approach to afford
the best visualization of their necks. Trapping procedures should not
be used on these aneurysms, as blood flow to vital medullary
perforators may be compromised. Aneurysms from the first two
segments of the PICA are best approached via a lateral exposure, but
those arising from the distal three segments, posterior to the brain stem,
are better handled through a bilateral (midline) suboccipital
craniectomy. The extreme tortuosity of the vertebral and PICA arteries
may also occasionally influence the laterality of the operative approach.
Although clipping across the aneurysmal neck is preferable, trapping
may be utilized in those lesions arising from or distal to the
86
telovelotonsillar segment, as no further brain-stem perforators arise
beyond this point.
Only 21.42% (n=6) of the patients had new postoperative neurological
deficits, of which the majority recovered within 6 months. Nevertheless
7.14% (n=2) had persistent problems in the form of mild gait ataxia at 1
year after discharge. In our series postoperative morbidity was more
related to hydrocephalus than lower cranial nerve dysfunction. Of the
series that discuss perioperative morbidity, the incidence of transient and
permanent lower cranial nerve deficits ranges from 20% to 66%.
Favourable outcome (GOS of 5 or 4, good recovery or moderate
disability, respectively) was seen in 25 (89.28%) of the patients.
Unfavourable outcome (GOS of 3, 2 or 1, severe disability, vegetative
state, or dead respectively) was seen in 3 (10.71%) patients. A correlation
between the severity of the WFNS grades at the time of admission with
the GOS scores at the time of discharge could not be demonstrated
because of the small numbers and patient referral from local hospitals
after improvement in the neurological status.
Three patients had poor results. One of these patients (Patient no. 10) had
a small cerebellar infarct in the post-operative scan and transient lower
cranial palsy necessitating tracheostomy. He developed ventilator
associated pneumonia that was managed aggressively with intravenous
87
broad-spectrum antibiotics and chest physiotherapy. He was discharged
to a local hospice after closing the tracheostomy, for general nursing care.
The second patient (Patient no 24), operated for a distal AICA-PICA
variant aneurysm was stable in the immediate postoperative period but
gradually deteriorated from the second day onwards. She developed
hemodynamic instability and irregular respiration, suggesting medullary
dysfunction. This was further complicated by neurogenic pulmonary
edema and fulminant meningitis. The patient underwent tracheostomy
and was kept on prolonged ventilator support. Serial postoperative CT
scans were normal. A postoperative vertebral angiogram was not done in
view of her poor neurological status and unstable hemodynamic
parameters. She had a stormy postoperative course and at the time of
discharge to another nursing care centre she was in a vegetative state.
Both the above mentioned patients never returned for follow-up visits.
The third patient (Patient no.15) underwent a ventriculoperitoneal shunt
for persistent hydrocephalus 2 days after clipping of PICA aneurysm. A
week after surgery she complained of chest pain following which she had
a cardiac arrest and could not be resuscitated. This was the only mortality
in our series that could not be directly attributable to the primary
pathology or its management.
88
The experience of Charles G Drake and S J Peerless with 1767
vertebrobasilar artery aneurysms is the largest till date (92). Out of these
176 aneurysms were located at the VA-PICA junction (150) or on the
PICA (26). Twenty two of these aneurysms were giant (>25mm) in size.
Majority of the giant aneurysms had mass effect only, with various
degrees of bulbar paresis and ataxia, often with mild hemiparesis,
hemisensory loss, and limb dysmetria. VIth nerve palsy was the most
frequent preoperative cranial nerve dysfunction. In 75%, it recovered
completely. In 221 patients with vertebral or PICA aneurysms, more than
one-fifth of the patients had IX–X nerve deficits after surgery; two-thirds
of them were transient, but in follow-up, four patients had severe
dysphagia requiring prolonged tracheostomy. Intraoperative aneurysm
rupture (7%) was rare but dangerous: of 16 patients, 4 died and 1 was
severely disabled. They categorized outcomes as excellent, good, poor
and dead. Patients with good Hunt and Hess grades at the time of
admission had better overall outcome than patients who were in poor
neurological status. 94% of the patients with small aneurysms had good
results.
Yasargil (93) described 15 PICA aneurysms, 10 of which were at the
vessel origin. No specifics relating to outcome were provided aside from
noting that 14 patients had good outcomes and 1 had a fair outcome.
89
R. J. Hudgins, et al. (4) in their experience with 21 surgically treated
PICA aneurysms. Forty-three percent were Hunt and Hess Grade I, 38%
were Grade II, and 19% were Grade III. Patients presenting with higher
grades had a greater incidence of adverse outcomes. Sixty-six percent of
Grade I patients were normal at the time of discharge, whereas only 25%
of Grade II and 50% of Grade III patients were without deficits. The
overall results included a 14% incidence of hydrocephalus, 14%
hemiparesis (10% postoperative hemiparesis), 33% dysarthria, 5%
dysphagia, 5% Wallenberg's syndrome, and 10% death. They divided
results into four categories: 1) good, able to return to full previous
activities; 2) fair, minor neurological deficits which slightly modified life-
style (such as functionally significant dysarthria, decreased palatal
excursion); 3) poor, disabling neurological deficits; and 4) death. In terms
of outcome, 62% of the patients returned to all previous activities, 19%
had minor new deficits that modified their previous lifestyles, 9.5% had
disabling deficits, and 9.5% died. This study, however, did not provide
specifics in terms of resolution of various symptoms during the
convalescent period.
Gacs et al. (45) reported their series of 16 peripheral aneurysms of
cerebellar arteries, out of which 8 had aneurysms of the PICA. They
noted vasospasm in the basilar and the vertebral arteries in 4 cases (all
90
had a PICA aneurysm). Among the patients with PICA aneurysms,
outcome was excellent in 4 (50%), good in 2 (25%), poor in one and one
patient died.
Yamaura (35) reported 90 PICA aneurysms, 77 of which involved the
PICA origin. No specific data were provided concerning morbidity and
mortality, except the statement that three patients developed Cranial
Nerve VI palsy and eight patients developed Cranial Nerve IX and X
palsies. The authors' long-term results were truly remarkable. All lower
cranial nerve deficits improved in days to weeks, except in one patient,
who had a persistent hoarse voice after surgery.
Salcman et al. (46) studied 22 PICA aneurysms, 18 of which were at the
PICA origin, 4 were on the distal PICA. Out of these 17 were treated by
them. Three patients did not undergo surgery. Eighteen percent were
Hunt and Hess Grade I, 23.5% were Grade II, 41% were Grade III, 12%
were Grade IV and one was Grade V. Perioperative morbidity was seen
in 7% of the patients. They categorized outcomes as independent,
dependent and dead. Outcome included 64.7% patients who were
independent, 11.7% patients who were dependent and 23.5% were dead.
Their immediate perioperative morbidity and management mortality may
reflect the fact that the majority of their patients had aneurysms in Hunt
91
and Hess Grades 3 and 4, a factor associated with higher morbidity and
mortality independent of the location of the aneurysm (113).
Yamamoto et al. (44) reported that the outcome for surgically treated
patients is generally favorable. In 42 (91 %) of the 46 surgical cases they
reviewed, the outcomes were good or excellent and only four patients
(9%) died.
Bertanalffy et al. (2) studied 27 patients with VA-PICA complex
aneurysms. Twenty-two patients in this series suffered from a
subarachnoid hemorrhage (SAH). Of these, two patients were admitted in
Hunt and Hess (H&H) grade I, two patients in grade II, 11 patients in
grade III, four patients in grade IV, and three individuals in grade V.
Aneurysms of the VA and the proximal PICA were approached via a
transcondylar (n=11) or lateral suboccipital route (n=3), while aneurysms
originating from the distal PICA were exposed via a paramedian
suboccipital craniotomy (n=7). Four of the patients treated surgically
required a permanent shunting due to a posthemorrhagic hydrocephalus.
Two patients developed a complete dorsolateral medullary syndrome due
to a partial occlusion of the PICA following prolonged intraoperative
temporary clipping of this vessel. Two patients had a transient sixth
cranial nerve palsy, two patients who had developed aspiration
pneumonia required prolonged ventilation. Two of the patients treated
92
with surgery died postoperatively due to massive vasospasm.
Endovascular therapy was used in three patients who could not be treated
surgically. Twenty two (81.48%) patients had an excellent outcome, and
two (7.4%) patients had a fair outcome. These authors emphasize that
removal of the arch of C1 and partial drilling of the occipital condyle
provide an optimal view for proximal PICA aneurysms and minimize the
potential for injury to lower cranial nerves and perforating arteries in this
area. Their results are more promising with transient lower cranial nerve
palsies in only two patients (29%), neither of whom required
tracheostomy (0%), and CSF leak requiring a second operation in one
patient (14%).
Horowitz et al. (8) reported their surgical results for 38 patients with
PICA aneurysms. Their study clearly indicated that these lesions were not
benign and that overall outcome was good, with 91% of the patients
evaluated at 6 months after discharge being independent. Although 66%
of the patients had new postoperative neurological deficits, the vast
majority achieved significant recoveries. Nevertheless, 37% had
persistent problems at 1 year after discharge. 74% of the patients had a
GOS score of 1 or 2 at the time of discharge, 91% at 6 months after
surgery and 89% at 1 year after surgery. Higher GOS scores at the time of
discharge and at 6 and 12 months after discharge seemed to be associated
93
with the presence of hydrocephalus and clinical vasospasm. Because of
the relatively small number of lesions within this study, they could detect
no firm correlations between Fisher grade and outcome. The severity of
the Hunt and Hess grades at the time of admission seemed to correlate
with the GOS scores at the time of discharge and at 6 months after
discharge, although statistical significance could not be demonstrated
because of small numbers and incomplete follow-up. Their opinion was
that by removing the ring of C1 and working more along the axis of the
brain stem with the operative side down in a caudal-to-rostral direction,
PICA aneurysms could be approached from the ventral side of the nerves,
thus reducing the need for excessive cranial nerve manipulation.
Lee et al. (114) described 14 PICA aneurysms, 10 of which were located
at the vessel origin. Outcomes for all 14 lesions were listed and included
29% vasospasm, 14% hydrocephalus, 14% dysphagia, and 7% vocal cord
paralysis requiring a tracheostomy. Of those patients presenting with
Hunt and Hess Grade I, all returned to full activity. Of those patients
presenting with Hunt and Hess Grade II, 66% returned to full activity and
33% died. Thirty-three percent of Hunt and Hess Grade III patients
returned to full activity, whereas 33% had poor outcomes and 33% died.
All Grade IV patients returned to full activity.
94
S. B. Lewis, et al. (36) analyzed 20 consecutive patients with 22
aneurysms of the peripheral PICA. Sixty percent of the patients (12 of 20)
experienced some consequences of their disease and/or complications
during the course of their treatment, including hydrocephalus requiring
shunt placement (nine cases), ataxia (five cases), dysphagia (two cases),
pneumonia (two cases), hyponatremia (two cases), meningitis (one case),
repeated hemorrhage before treatment (one case), and Terson syndrome
(one case). Eighty percent of patients (16 in all) were functionally
independent (excellent, good, or fair) at the time of discharge from the
hospital. At the last follow-up examination, an excellent or good outcome
had been achieved in 17 (85%) of 20. Two patients had poor long-term
results and one patient died. Only one patient experienced a true lower
cranial nerve paresis related to surgical intervention. The distal nature of
aneurysms encountered in this series placed the majority of distal PICA
lesions superficial to the lower cranial nerves.
Horiuchi et al. (42) reported a series of 24 patients with 27 distal PICA
aneurysms. They found that unfavorable outcome was significantly
associated with the preoperative World Federation of Neurosurgical
Societies grade and the presence of obstructive hydrocephalus. They
further concluded that surgical outcome of PICA aneurysms located at the
proximal side of the PICA origin, especially the vertebral artery-PICA
95
bifurcation, tends to be unfavorable compared with the distal PICA
aneurysm because of the deep, narrow operative fields, perforating
arteries to the brainstem, and the cranial nerves. In addition, size of the
aneurysm and Fisher group usually will have an impact on prognosis. The
most common site of the aneurysms was at the telovelotonsillar segment
(29.6%).
D’Ambrosio et al. (97) reported the clinical outcomes obtained via a far
lateral suboccipital approach in 20 consecutive proximal PICA
aneurysms. The far lateral suboccipital approach achieved adequate
exposure in all cases. There were no intraoperative complications or
intraoperative aneurysm ruptures. Two (10%) patients developed vocal
cord paralysis as a result of surgery, with only 1 (5%) requiring
temporary tracheostomy. There were three cases of CSF leakage
requiring wound revision, with one subsequent wound infection. Fourteen
patients (70%) had radiographic hydrocephalus, for which 8 (40%)
required external ventricular drain placement. Only 1 patient required a
permanent CSF diverting procedure in the form of a ventriculoperitoneal
shunt. One patient required tracheostomy and percutaneous endoscopic
gastrostomy for medical reasons unrelated to surgery. At 3 months of
follow-up, 93% of the subarachnoid hemorrhage patients achieved a
Glasgow Outcome Scale score of 1 to 2. At 12 months of follow-up, 92%
96
achieved a Glasgow Outcome Scale score of 1 to 2. These authors
conclude that the far lateral suboccipital approach incorporating the
removal of the posterior arch of C1 can provide the added space
necessary to clip these lesions without undue manipulation of the lower
cranial nerves.
Al-khayat et al. (115) studied 52 patients to identify factors predicting
postperative lower cranial nerve palsy (LCNP) among patients
undergoing surgery for VA-PICA aneurysms. Postoperative LCNP
occurred in 25 patients (48.1%) with VA-PICA aneurysms. Of the factors
investigated, the use of temporary or total occlusion was associated with
increased incidence of postoperative LCNP. Nosocomial pneumonia
occurred only in patients with moderate to severe LCNP. Postoperative
LCNP resolved completely within 3 months in 12 patients (48%) and
within 6 months in 19 patients (76%).
97
CONCLUSIONS
PICA aneurysms, by virtue of their relative rarity, strategic location and
complex anatomy pose unique diagnostic and technical challenges.
In treating patients with suspected SAH whose CT imaging is normal,
special attention should be given to the fourth ventricle and the possibility
of VA-PICA aneurysms.
Angiography should be performed with separate injections of each
vertebral artery. Occasionally, these aneurysms may be missed on the
initial study and therefore the study has to be repeated again after an
interval of at least 2 weeks. As compared with aneurysms at other sites,
PICA-VA lesions are frequently missed on the initial study and, on rare
occasions, must be looked for in extracranial locations.
Surgical planning must take into account the location of the aneurysm,
the presence of any anatomical variations of the parent vessel and the
need for an anastomosis or bypass procedure. Preoperative planning for
large PICA-VA aneurysms should include a contingency plan for
possible trapping or vertebral ligation. In this regard, preoperative test
occlusions of the vertebral artery with an intravascular balloon are
helpful.
98
Although clipping across the aneurysmal neck is preferable, trapping
may be utilized in those lesions arising from or distal to the
telovelotonsillar segment, as no further brain-stem perforators arise
beyond this point. A thorough search for brainstem perforators is
essential prior to trapping though it has been claimed to be safe for
aneurysms arising distal to the choroidal point.
The use of a far lateral approach without condylar resection provides
sufficient space for aneurysm dissection without significant manipulation
of the lower cranial nerves, and avoids the increased morbidity associated
with condylar resection. Maintaining a caudal-rostral trajectory beneath
the cranial nerves rather than through them has significantly decreased
postoperative lower cranial nerve dysfunction that used to be the major
cause of morbidity.
Majority of PICA aneurysm patients have an excellent outcome after
surgical treatment and their presence should not deter the surgeon from
clipping them. Good results may be achieved in patients with PICA
aneurysms by tailoring the therapeutic strategy with consideration for the
condition of the patient, the arterial and aneurysmal morphology.
99
REFERENCES
1. Locksley HB: Report on the Cooperative Study of Intracranial Aneurysms and Subarachnoid Hemorrhage. Section V, Part I. Natural history of subarachnoid hemorrhage, intracranial aneurysms, and arteriovenous malformations. Based on 6368 cases in the Cooperative Study. J Neurosurg 25:219-239, 1966.
2. Bertalanffy H, Sure U, Petermeyer M, Becker R and Gilsbach JM, Management of Aneurysms of the Vertebral Artery-Posterior Inferior Cerebellar Artery Complex, Neurol Med Chir Suppl (Tokyo) 38, 93-103, 1998.
3. Rhoton AL Jr, Jackson FE, Gleave J, et al: Congenital and traumatic intracranial aneurysms. CIBA Clin Symp 29(4):2-40, 1977.
4. Hudgins RJ, Day AL, Quisling RG, Rhoton AL Jr, Sypert GW, Garcia-Bengochea F: Aneurysms of the posterior inferior cerebellar artery: A clinical and anatomical analysis. J Neurosurg 58:381-387, 1983.
5. Weir B: Aneurysms affecting the Nervous System. Baltimore, Williams & Wilkins, 1987, pp 489-491.
6. McDonald CA, Korb M: Intracranial aneurysms. Arch Neurol Psychiatry 42:298-328, 1939.
7. Pia HW: Classification of vetrebro-basilar aneurysms. Acta Neurochir (Wien) 47:3-30, 1979.
8. HorowitzM, Kopitnik T, Landreneau F, Krummerman J, Batjer HH, Thomas G, Samson DS: Posteroinferior cerebellar artery aneurysms: Surgical results of 38 patients. Neurosurgery 43:1026–1032, 1998.
9. Ishikawa T, Suzuki A, Yasui N: Distal posterior inferior cerebellar aneurysms: Report of 12 cases. Neurol Med Chir (Tokyo) 30:100–108, 1990.
10. Nishino A, Sakurai Y, Satoh H, Niizuma H, Kayama T, Ogawa A, Ohtoh T: Aneurysms of the distal posterior inferior cerebellar
100
artery: The report of 10 cases [in Japanese]. No Shinkei Geka 19:925–932, 1991.
11. Rothman SLG, Azar-Kia b, Kier EL, Schechter MM, Allen WE III: The angiography of posterior inferior cerebellar artery aneurysms. Neuroradiology 6:1-7, 1973.
12. Drake CG: The surgical treatment of vertebral-basilar aneurysms. Clin Neurosurg 16: 114-169, 1969.
13. Rhoton AL Jr: Anatomy of saccular aneurysms. Surg Neurol 14: 59-66, 1980.
14. Waga S, Fujimoto K, Morooka Y: Dissecting aneurysm of the vertebral artery. Surg Neurol 10:237-239, 1978.
15. Yonas H, Agamanolis D, Takaoka Y,White R J: Dissecting intracranial aneurysms. Surg Neurol 8:407-415, 1977.
16. Cruveilhier J: Anatomie Pathologique de Corps Humain. Paris: JB Bailli~re, 1829-1835, Vol 2. Cited in Schwartz HG: Arterial aneurysm of the posterior fossa. J Neurosurg 5:312-316, 1948.
17. Fernet (1864) Bull Soc Anat Paris 39:495. (Reference unverified) 18. Rizzoli HV, Hayes G J: Congenital berry aneurysm of the
posterior fossa. Case report with successful operative excision. J Neurosurg 10:550-55 l, 1953.
19. Schwartz HG: Arterial aneurysm of the posterior fossa. J Neurosurg 5:312-316, 1948.
20. Hook O, Norlen G, Guzman J: Saccular aneurysms of the vertebral-basilar arterial system. Acta neurol Scand 39:271-304, 1963.
21. Richardson AE: The natural history of patients with intracranial aneurysms after rupture. Prog Brain Res 30:269-273, 1968.
22. Uihlein A, Hughes RA: The surgical treatment of intracranial vestigial aneurysms. Surg Clin North Am 35:1071-1083, 1955.
23. DeSaussure RL, Hunter SE, Robertson JT: Saccular aneurysms of the posterior fossa. J Neurosurg 15: 385-391, 1958.
24. Rand RW, Jannetta PJ: Micro-neurosurgery for aneurysms of the vertebral-basilar artery system. J Neurosurg 27:330-335, 1967.
25. Drake CG: Treatment of aneurysms of the posterior cranial fossa. Prog Neurol Surg 9:122-194, 1978.
101
26. Lister JR, Rhoton AL Jr, Matsushima T, Peace DA: Microsurgical anatomy of the posterior inferior cerebellar artery. Neurosurgery 10:170-199, 1982.
27. Rhoton AL Jr., The Cerebellar Arteries, Neurosurgery, Vol. 47, No. 3, September 2000 Supplement, S29-S68.
28. Warwick R, Williams PL: Gray’s Anatomy, 35th British Ed. Philadelphia, WB Saunders, 1973, pp 643-644.
29. Greitz T. Sjogren SE: The posterior inferior cerebellar artery, Acta Radiol [Diagn] (Stockh) 1:284-297. 1963.
30. Krayenbuhl HA, Yasargil MG: Cerebral Angiography, London, Butterworth and Co, 1968, pp 66-74.
31. Salamon G, Huang YP: Radiologic Anatomy of the Brain, Berlin, Springer-Verlag, 1976, pp 305-306.
32. Margolis MT, Newton TH: The posterior inferior cerebellar artery, in Newton TH, Potts DG (eds): Radiology of the Skull and Brain, Angiography, Vol 2, Book 2. St Louis, CV Mosby, 1974, pp 1710-1774.
33. Sunderland S: Neurovascular relations and anomalies at the base of the brain. J Neurol Neurosurg Psychiatry 2:243–257, 1948.
34. Katsuta T, Rhoton AL Jr, Matsushima T: The jugular foramen: Microsurgical anatomy and operative approaches. Neurosurgery 41:149–202, 1997.
35. Yamaura A: Diagnosis and treatment of vertebral aneurysms. J Neurosurg 69:345-349, 1988.
36. Lewis SB, Chang DJ, Peace DA, Lafrentz PJ, Day AL: Distal posterior inferior cerebellar artery aneurysms: clinical features and management. J Neurosurg. 97(4):756-766, 2002.
37. Azzam CJ: Growth of multiple peripheral high flow aneurysms of the posterior inferior cerebellar artery associated with a cerebellar arteriovenous malformation. Neurosurgery 21:934–939, 1987.
38. Miyasaka K, Wolpert SM, Prager RJ: The association of cerebral aneurysms, infundibula, and intracranial arteriovenous malformations. Stroke 13:196–203, 1982.
102
39. Ostergaard JR: Association of intracranial aneurysm and arteriovenous malformation in childhood. Neurosurgery 14:358–362, 1984.
40. Nishizaki T, Tamaki N, Nishida Y, Fujita K, Matsumoto S: Aneurysms of the distal posterior inferior cerebellar artery: Experience with three cases and review of the literature. Neurosurgery 16: 829- 832, 1985.
41. Padget DH: Development of cranial arteries in human embryo. ContribEmbryol 32:205–262, 1948.
42. Horiuchi T, Tanaka Y, Hongo K, Nitta J, Kusano Y, Kobayashi S, Characteristics of distal posteroinferior cerebellar artery aneurysms, Neurosurgery 53:589-596, 2003.
43. Stehbens WE: The pathology of intracranial arterial aneurysms and their complications, in Fox JL (ed): Intracranial Aneurysms. New York: Springer-Verlag, 1983, Vol 1, pp 272-357.
44. Yamamoto I, Tsugane R, Ohya M, Sato O, Ogura K, Hara M: Peripheral aneurysms of the posterior inferior cerebellar artery. Neurosurgery 15:839-845, 1984.
45. Gacs R, Viñuela F, Fox AJ, Drake CG: Peripheral aneurysms of the cerebellar arteries: Review of 16 cases. J Neurosurg 58:63-68, 1983.
46. Salcman M, Rigamonti D, Numaguchi Y, Sadato N: Aneurysms of the posterior inferior cerebellar artery-vertebral artery complex: Variations on a theme. Neurosurgery 27:12-21, 1990.
47. Andoh T, Shirakami S, Nakashima T, Nishimura Y, Sakai N, Yamada H, Ohkuma A, Tanabe Y, Funakoshi T: Clinical analysis of a series of vertebral aneurysm cases. Neurosurgery 31:987-993, 1992.
48. Laine E: Arterial vertebro-basilar aneurysms. Prog Brain Res 30:323-346, 1968.
49. Dumas S, Shults WT (1982) Abducens paresis. A rare presenting sign of posterior inferior cerebellar artery aneurysm. J Clin Neuroophthalmol 2:55–60.
50. Judice D, Connolly ES: Foramen magnum syndrome caused by a giant aneurysm of the posterior inferior cerebral artery. Case report. J Neurosurg 48: 639- 641, 1978.
103
51. Jane JA: A large aneurysm of the posterior inferior cerebellar artery in a l-year-old child. J Neurosurg 18:245-247, 1961.
52. Alexander E Jr, Davis CH Jr, Pikula L: Aneurysm of the posterior inferior cerebellar artery filling the fourth ventricle. J Neurosurg 24:99-101, 1966.
53. Bull J: Massive aneurysms at the base of the brain. Brain 92:535-579, 1969.
54. Pasqualin A, Pian RD, Scienza R, Licata C: Posterior inferior cerebellar artery aneurysm in the fourth ventricle: Acute surgical treatment. Surg Neurol 16: 448-451, 1981.
55. Yeh HS, Tomsick TA, Tew JM Jr (1985) Intraventricular hemorrhage due to aneurysms of the distal posterior inferior cerebellar artery. Report of three cases. J Neurosurg 62:772–775.
56. Kallmes DF, Lanzino G, Dix JE, Dion JE, Do H, Woodcock RJ, Kassell NF (1997) Patterns of hemorrhage with ruptured posterior inferior cerebellar artery aneurysms: CT findings in 44 cases. AJR 169:1169–1171.
57. Urbach H, Meyer B, Cedzich C, Solymosi L (1995) Posterior inferior cerebellar artery aneurysm in the fourth ventricle. Neuroradiology 37:267–269.
58. Sadato N. Numaguchi Y. Rigamonti D. Salcnian M. Gellad FE. Kishikawa T. Bleeding patterns in ruptured posterior fossa aneurysms: a CT study. J Comput Assist Tomogr 1991 : 15:612-6I7.
59. Findlay JM, Wong JH: Clinical aspects of intraventricular hemorrhage, in Welch KMA, Caplan LR, Reis DL, et al (eds): Primer on Cerebrovascular Diseases. San Diego: Academic Press, 1997, pp 437–445.
60. Voelker JL, Kaufman HH: Clinical aspects of intracerebral hemorrhage, in Welch KMA, Caplan LR, Reis DL, et al (eds): Primer on Cerebrovascular Diseases. San Diego: Academic Press, 1997, pp 432–436.
61. Little JR, Blomquist GA Jr, Ethier R: Intraventricular hemorrhage in adults. Surg Neurol 8:143-149, 1977.
62. Ojemann RG, Heros RC: Spontaneous brain hemorrhage. Stroke 14:468-475, 1983.
104
63. Pia HW: The diagnosis and treatment of intraventricular haemorrhages. Prog Brain Res 30"463-470, 1968.
64. Mericle RA, Reig AS, Burry MV, et al. Endovascular surgery for proximal posterior inferior cerebellar artery aneurysms: an analysis of Glasgow Outcome Score by Hunt-Hess grades. Neurosurgery 2006; 58:619-25.
65. West GCH. Forbes WSC. Intraventricular blood without parenchymal clot following spontaneous subarachnoid hemorrhage. Neuroradiologv 1985:27:254-258.
66. Beyerl BD, Heros RC: Multiple peripheral aneurysms of the posterior inferior cerebellar artery. Neurosurgery 19:285–289, 1986.
67. Madsen JR, Heros RC: Giant peripheral aneurysm of the posterior inferior cerebellar artery treated with excision and end-to-end anastomosis. SurgNeurol 30:140–143, 1988.
68. Yamada K, Hayakawa T, Ushio Y, et al: Therapeutic occlusion of the vertebral artery for unclippable vertebral aneurysm: relationship between site of occlusion and clinical outcome. Neurosurgery 15:834-838, 1984.
69. Krayenbuhl H, Yasargil MG: Variationen der A. Vertebralis, Basilaris und ihrere Aste, in Die Vaskularen Erkrankungen in Gebiet der Arteria Vertebralis und Arteria Basilaris. Stuttgart, Thieme Verlag, p 39,1957.
70. Pelz DM, Vinuela F, Fox AJ, Drake CG: Vertebrobasilar occlusion therapy of giant aneurysms: Significance of angiographic morphology of the posterior communicating arteries. J Neurosurg 60:560-565, 1984.
71. Mohan J: The neurosurgeon's view, in Boullin DJ (ed): Cerebral Vasospasm. New York: John Wiley and Sons, 1980, pp 15-35.
72. International Study of Unruptured Intracranial Aneurysms Investigators: Unruptured intracranial aneurysms—risk of rupture and risks of surgical intervention. N Engl J Med 339:1725–1733, 1998.
73. Wiebers DO, Whisnant JP, Sundt TM Jr, et al: The significance of unruptured intracranial saccular aneurysms. J Neurosurg 66:23–29, 1987.
105
74. Kunze S, Schiefer W: Angiographic demonstration of a dissecting aneurysm of the middle cerebral artery. Neuroradiology 2: 201–206, 1971.
75. Cronqvist S, Troupp H: Intracranial arteriovenous malformation and arterial aneurysm in the same patient. Acta Neurol Stand 42:307-316. 1966.
76. Paterson JH, McKissock W: A clinical survey of intracranial angiomas with special reference to their mode of progression and surgical treatment: a report of 110 cases. Brain 79:233-266, 1956.
77. Perret G, Nishioka H: Report on the Cooperative Study of Intracranial Aneurysms and Subarachnoid Hemorrhage. Section VI. Arteriovenous malformations. An analysis of 545 cases of cranio-cerebral arteriovenous malformations and fistulae reported to the Cooperative Study. J Neurosurg 25:467-490, 1966.
78. Suzuki J, OnumaT: Intracranial aneurysms associated with arteriovenous malformations, in Suzuki J (ed): Cerebral Aneurysms. Tokyo: Neuron, 1979, pp 714-722.
79. Chason JL, Hindman WM: Berry aneurysms of the circle of Willis. Results of a planned autopsy study. Neurology 8:41-44, 1958.
80. Stehbens WE: Pathology of the Cerebral Blood Vessels. St Louis: CV Mosby, 1972, p 354.
81. Suzuki J, Ohara H: Origin, rupture and growth of cerebral aneurysms: a clinico-pathological study, in Pia HW, Langmaid C, Zierski J (eds): Cerebral Aneurysms. Advances in Diagnosis and Therapy. Berlin/Heidelberg/New York: Springer-Verlag, 1979, pp 28-40.
82. Kaptain GJ, Lanzino G, Do HM, et al: Posterior inferior cerebellar artery aneurysms associated with posterior fossa arteriovenous malformation: report of five cases and literature review. Surg Neurol 51:146–152, 1999.
83. Miller EM, Newton TH: Extra-axial posterior fossa lesions simulating intra-axial lesions on computed tomography. Radiology 127:675–679, 1978. (94)
106
84. Westphal M, Grzyska U: Clinical signficance of pedicle aneurysms on feeding vessels, especially those located in infratentorial arteriovenous malformations. J Neurosurg 92:995–1001, 2000.
85. Hlavin ML, Takaoka Y, Smith AS: A “PICA communicating artery” aneurysm: case report. Neurosurgery 29:926–929, 1991.
86. Uranishi R, Ochiai C, Tejima T, et al: [A distal posterior inferior cerebellar artery aneurysm in the fourth ventricle: a case report.] No Shinkei Geka 22:1035–1038, 1994 (Jpn).
87. Perata HJ, Tomsick TA, Tew JM Jr: Feeding artery pedicle aneurysms: association with parenchymal hemorrhage and arteriovenous malformation in the brain. J Neurosurg 80:631–634, 1994.
88. Redekop G, TerBrugge K, Montanera W, et al: Arterial aneurysms associated with cerebral arteriovenous malformations: classification, incidence, and risk of hemorrhage. J Neurosurg 89:539–546, 1998. (99)
89. Heros RC: Lateral suboccipital approach for vertebral and vertebrobasilar artery lesions. J Neurosurg 64:559–562, 1986.
90. Drake CG: The treatment of aneurysms of the posterior circulation. Clin Neurosurg 26:96-144, 1979.
91. Yamaura A, Ise H, Makino H: Radiometric study on posterior inferior cerebellar aneurysms with special reference to accessibility by the lateral suboccipital approach. Neurol Med Chir (Tokyo) 21; 721-723, 1981.
92. Drake CG, Peerless SJ, Hernesniemi JA: Surgery of Vertebrobasilar Aneurysms: London, Ontario Experience on 1767 Patients. Vienna: Springer-Verlag, 1995.
93. Yasargil MG: Vertebrobasilar aneurysms, in Yasargil MG (ed): Microneurosurgery: Clinical Considerations, Surgery of the Intracranial Aneurysms and Results. Stuttgart: Georg Thieme, 1984, vol II, pp 290–294.
94. Matsushima T, Tashima T, Sayama T, et al: [Clipping of a midline VA–PICA aneurysm through transcondylar approach: location of the aneurysm and surgical approach.] Surg Cereb Stroke 27:59–63, 1999 (Jpn).
107
95. Babu RP, Sekhar LN, Wright DC: Extreme lateral transcondylar approach: Technical improvements and lessons learned. J Neurosurg 81:49–59, 1994.
96. Bertalanffy H, Gilsbach JM, Mayfrank L, et al: Planning and surgical strategies for early management of vertebral artery and vertebrobasilar junction aneurysms. Acta Neurochir (Wein) 134:60–65, 1995.
97. D’Ambrosio AL, Kreiter KT, Bush CA, et al: Far lateral suboccipital approach for the treatment of proximal posteroinferior cerebellar artery aneurysms: surgical results and long-term outcome. Neurosurgery 55:39–50, 2004.
98. Matsushima T, Matsukado K, Natori Y, et al: Surgery on a saccular vertebral artery-posterior inferior cerebellar artery aneurysm via the transcondylar fossa (supracondylar transjugular tubercle) approach or the transcondylar approach: surgical results and indications for using two different lateral skull base approaches. J Neurosurg 95:268–274, 2001.
99. Bertalanffy H, Seeger W: The dorsolateral, suboccipital, transcondylar approach to the lower clivus and anterior portion of the craniocervical junction. Neurosurgery 29:815–821, 1991.
100. Meisel HJ, Mansmann U, Alvarez H, et al: Cerebral arteriovenous malformations and associated aneurysms: analysis of 305 cases from a series of 662 patients. Neurosurgery 46:793–802, 2000.
101. Fisher C, Kistler J, Davis J (1980). "Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning". Neurosurgery 6 (1): 1–9.
102. Jennett B, Bond M. “Assessment of outcome after severe brain damage.” Lancet 1975 Mar 1:1(7905):480-4.
103. Dimsdale H, Logue V: Ruptured posterior fossa aneurysms and their surgical treatment. J Neurol Neurosurg Psychiatry 22:202-217, 1959.
104. Hammon WM, Kempe LG: The posterior fossa approach to aneurysms of the vertebral and basilar arteries. J Neurosurg 37:339-347, 1972.
108
105. Dernbach PD, Cila CA, Little JR: Giant and multiple aneurysms of the distal posterior inferior cerebellar artery. Neurosurgery 22: 309-312, 1988.
106. Miller EM, Newton TH: Extra-axial posterior fossa lesions simulating intra-axial lesions on computed tomography. Radiology 127: 675-679, 1978.
107. Yoshii Y, Maki Y, Egashira T: Giant aneurysm of the distal portion of the posterior inferior cerebellar artery. Eur Neurol 18: 382-386, 1979.
108. Teasdale GM, Drake CG, Hunt W, Kassell N, Sano K, Pertuiset B, De Villiers JC. A universal subarachnoid hemorrhage scale: report of a committee of the World Federation of Neurosurgical Societies. J Neurol Neurosurg Psychiatry. 1988 Nov:51(11):1457.
109. Peerless SJ, Drake CG: Management of aneurysms of the posterior circulation, in Youmans JR (ed): Neurological Surgery. Philadelphia, W.B. Saunders Co., 1990, ed 4, vol 3, pp 1764-1806.
110. Kempe LG (1979) Aneurysms of the vertebral artery, in Pia HW, Langmaid C, Zierski J (eds): Cerebral Aneurysms. Advances in Diagnosis and Therapy. Berlin/Heidelberg/New York: Springer-Verlag,pp 119-120.
111. Yamaura A, Isobe K, Karasudani H, et al: Dissecting aneurysms of the posterior inferior cerebellar artery. Neurosurgery 28:894–898, 1991.
112. Kurino M, Kuratsu J, Yamaguchi T, et al: Mycotic aneurysm accompanied by aspergillotic granuloma: a case report. Surg Neurol 42:160–164, 1994.
113. Sundt TM, Kobayashi S, Fode NC, Whisnant JF: Results and complications of surgical management of 809 intracranial aneurysms in 722 cases related and unrelated to grade of the patient, type of aneurysm, and timing of surgery. J Neurosurg 56: 753-765, 1982.
114. Lee KS, Gower DJ, Branch CL, Kelly DL, McWhorter JM, Bell WO: Surgical repair of aneurysms of the posterior inferior cerebellar artery: A clinical series. Surg Neurol 31:85-91, 1989.
115. Hisham Al-khayat, Haitham Al-Khayat, Joseph Beshay, David Manner, Jonathan White, Duke S. Samson: Vertebral artery-
109
posteroinferior cerebellar artery aneurysms: Clinical and lower cranial nerve outcomes in 52 patients, Neurosurgery 56:2-11, 2005.
110
PROFORMA
1. Name
2. Hospital number
3. Age/Sex
4. Date of ictus
5. Date of admission
6. Date of surgery
7. Date of discharge
8. Symptoms - Sudden onset headache / vomiting / LOC / others
9. History of hypertension / diabetes / chronic smoking
10. GCS, WFNS grade
11. Signs - Neck stiffness / Fundus / Lower cranial nerves / Other
cranial nerves / Cerebellar signs / motor weakness / others
12. CT Features – SAH location / intraventricular hemorrhage /
parenhymal hemorrhage / hydrocephalus / infarct / Fisher grade /
others
13. Pre-op EVD / ventilation / rebleed
14. DSA – location of aneurysm / type / size /evidence of rupture or
spasm / others
15. At surgery – approach / procedure / others
16. Post-op GCS, whether ventilated post-op (reason)
111
17. Post-op CT head / post-op check angiogram
18. Post-op complications – cranial nerve palsy / weakness / cerebellar
signs / respiratory / others
19. Glasgow outcome scale score at discharge / at 3 months follow-up
/ at 6 months follow-up / at 1 year follow-up / at last follow-up
112
ABBREVIATIONS
ACoM - anterior communicating artery
AICA – anterior inferior cerebellar artery
AVM – arteriovenous malformation
BA – basilar artery
CT – computerized tomography
CE - cerebellar signs
CSF – cerebrospinal fluid
DSA – digital subtraction angiogram
ETV - endoscopic third ventriculostomy
EVD – external ventricular drain
GCS – Glasgow coma scale
GOS - Glasgow outcome scale
HA – headache
HCP – hydrocephalus
ICeH - intracerebellar hemorrhage
IVH - intraventricular hemorrhage
LS - lateral suboccipital approach
LR - lateral rectus
LOC – loss of consciousness
LCN - lower cranial nerve
MCA - middle cerebral artery
113
MS - midline or paramedian suboccipital approach
PICA - posterior inferior cerebellar artery
SAH – subarachnoid hemorrhage
SCA - superior cerebellar artery
VPS - ventriculoperitoneal shunt
VA – vertebral artery
V - vomiting
WFNS – World Federation of Neurosurgeons
Top Related