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2017 ABC/WIN@ Val d'Isère
Anatomy-Biology-Clinical correlations -Working group in Interventional Neuroradiology
Menu
Various types of vertebral
artery (VA) anomalies in
cases of congenital
atlantoaxial dislocation
(CAAD) have been shown
in posterior and lateral
views.
1. Anatomical consideration of craniocervical junction
2. Pathology of arterial dissections
rt
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Aneurysms and arterial dissections of the
Craniocervical Junction
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3. Imaging modalities and the clinical application
Key words:
Dissections, Internal Elastic Lamina,
Segmental vulnerability,
Lateral spinal artery , Homology
Michihiro TANAKA,M.D., Ph.D.
tio
n
Department of Neurosurgery
Kameda Medical Center
Chiba JAPAN
Anatomic vulnerability associated with kinematics
of craniocervical junction
od
uc
Conflict of Interest Statement
The authors declare that the research was conducted in the absence of any commercial or
financial relationships that could be construed as a potential conflict of interest.
re
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The causes of vertebral artery dissection can be grouped under two main
categories, spontaneous and traumatic.
There have been numerous reports of associated risk factors for vertebral
artery dissection; many of these reports suffer from methodological
weaknesses, such as selection bias. Elevated homocysteine levels, often
due to mutations in the MTHFR gene, appear to increase the risk of
vertebral artery dissection.
ny
Spontaneous
ite
d.
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Other genetic conditions, such as osteogenesis imperfecta type 1, autosomal
dominant polycystic kidney disease and pseudoxanthoma elasticum,
α1 antitrypsin deficiency and hereditary hemochromatosis, but evidence for these
associations is weaker.
pa
ig
Persistent
FIA(first
intersegme
ntal artery)
People with an aneurysm of the aortic root and people with a history of
migraine may be predisposed to vertebral artery dissection.
Atherosclerosis does not appear to increase the risk.
(Kim et al. Thrombosis research 2009)
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Spontaneous cases are considered to be caused by intrinsic factors that weaken
the arterial wall. Only a very small proportion (1–4%) have a clear underlying
connective tissue disorder, such as Ehlers–Danlos syndrome type 4 and more
rarely Marfan's syndrome.
Ehlers-Danlos syndrome type 4, caused by mutations of the COL3A gene, leads
to defective production of the collagen
Marfan's syndrome results from mutations in the FBN1 gene, defective
production of the protein fibrillin-1.
ll
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Salunke et al. Surg Neurol Int. 2014; 5: 82.
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A
Salunke et al. Surg Neurol Int. 2014; 5: 82.
in
a
Salunke et al. Surg Neurol Int. 2014; 5: 82.
M. T. Haneline, A. L. Rosner
Skin Biopsies of 68% of 25 and 55% of 65 CAD Patients Showed Evidence of Irregular
Collagen Fibrils and Fragmentation of Elastic Fibers That Is Thought to Weaken the
Arterial Wall.
These Inherited Connective Tissue Disorders Affect the Skin, Joints, and the Walls of
Blood Vessels. The Incidence of CAD Has Been Reported to Be Higher in Patients With
These Conditions.
Case-Control Studies Point to Recent Infection as a Potential Trigger of CAD, Possibly
Related to Arterial Wall Damage Caused by Proteolytic, Oxidative, or Autoimmune
Defects. Furthermore, the Incidence of CAD Has Been Reported to Be Higher During
Certain Seasons, Which May Be Related to the Higher Incidence of Upper Respiratory
Tract Infections During the Winter.
Especially Apparent in Patients With Total Plasma Levels That Exceed 12 μmol/L. Associated
Arterial Wall Abnormalities May Increase the Artery's Susceptibility to Mechanical Stress.
Affects the ICA More Commonly Than the VA. Present in Up to 23% of ICA Dissection
Patients, Making It the Most Frequently Reported Associated Abnormality. Characterized
by Irregular Segments of Stricture and Dilation in the Vessel.
Focal Degeneration of the Elastic Tissue and Muscle of the Tunica Media, With the
Development of Mucoid Material. There Is a Breakdown of the Collagen, Elastin, and
Smooth Muscle, and an Increase in the Artery's Ground Substance.
Interferes With the Production of Type 1 Collagen. In Some Cases, Collagen Synthesis Is
Decreased, Whereas in Others, Structurally Defective Collagen Is Produced.
May Result in Blood Flow Disturbance Leading to Insufficient Collateral Circulation.
The Atlantal Segment of the VA Is Commonly Anomalous. Arterial Redundancies (eg,
Coils, Kinks, and Loops) and Increased Diameter of the Common Carotid Artery Are
More Common in Patients With ICA Dissection.
Several Studies Have Pointed to Hypertension as a CAD Risk Factor. A Well-Designed
Case-Control Study Reported a Statistically Significant Association in the Subgroup of
VA Dissection Patients, but Not in the Overall CAD Group.
Robust Odds Ratios Have Been Generated in Several Case-Control Studies Pointing to
This Association—7.41 (95% CI 3.11-17.64) in 1 Study.
Has Been Reported in Association With CAD by Several Authors, Although the Frequency
of This Association and the Mechanism Involved Are Unknown.
Why we have to rotate the atlanto-axial joint ?
It is necessary to compensate the blind zone.
Modern life is creating stress and stress.
EE Genotype of the E469K
ICAM-1 Polymorphism83
Methylenetetrahydrofolate
Reductase C677T
Genotype63,65,66,84
α-1-Antitrypsin
Deficiency85-87
Oral Contraceptive
Use60,77,78
Cardiovascular Risk
Factors10,14,61,78,88
re
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There are at least 25 of postulated risk factors.
A Recent Case-Control Study Reported the Presence of Antithyroid Autoimmunity in
31.0% of 29 CAD Patients, Compared With 6.9% of 29 Non-CAD Stroke Patients
(P = .041). There Have Also Been Recent Case Reports of ICA Dissection in Patients
With Graves Disease. Immunologic Mechanisms May Contribute to the Vascular
Damage That Is Thought to Initiate CADs.
The EE Genotype Gives Rise to a Proinflammatory Tendency in Patients That May
Predispose Them to Developing CAD.
Mutation of This Genotype Leads to Elevated Serum Levels of Homocysteine. The Issue
Is Controversial Because Studies Have Not Been in Agreement.
ed
Autosomal Dominant
Polycystic Kidney
Disease79,80
Antithyroid
Autoimmunity81,82
rv
History of Migraine76-78
Researchers Have Theorized That This Deficiency May Lead to a Fragile Vessel Wall That
Is Predisposed to Dissection, but There Is Little Evidence to Support This Relationship. Only
a Few Small Studies Have Reported on This Association, and Their Results Are Conflicting.
Studies That Have Considered This Issue Are in Conflict. Only 1 Small Study Showed
That Current Use of Oral Contraceptives Was Associated With CAD. The Consensus of
Researchers Is That No Good Evidence Exists Supporting This Association.
May Actually Be Protective. Atherosclerotic Changes, Hypercholesterolemia, Advanced
Age, and Diabetes Are Reported to Be Either Not Associated or Significantly Less
Prevalent in CAD Patients.
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Case 1. A 57 year-old-man presented TIA after chiropractic treatment.
20
Chiropractics sometimes gives us, not only the
relaxation, but also the mechanical stress to VA.
rig
CI indicates confidence interval; ICAM-1, intracellular adhesion molecule 1.
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Hypertension14,73-75
se
A
B
Type 1 Osteogenesis
Imperfecta68
Anatomical
Abnormalities12,69-72
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Cystic Medial Necrosis2
s
Fibromuscular
Dysplasia28,67
ht
Hyperhomocysteinemia63-66
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Vascular Type IV EhlersDanlos Syndrome52,57,58
and Marfan Syndrome59
Recent Infection60-62
n
Basis
Connective Tissue
Abnormalities52,56
IN
Risk Factor
tio
Pathophysiological risk factors for CAD
S
em
Table 1
od
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116
3
Pre
Post
Post (High resolution CBCT)
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Case 2. A 58 year-old-man, who had a fall accident, presented with TIA.
in
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Transection of IEL (Internal Elastic Lamina)
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Metal artifact reduction
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High resolution CBCT
Mechanical explanation for the predominance of the right vertebral artery (VA)
dissection during a golf swing.
Note the dislocation of the
both foramen
transversarium
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ing. Eight patients had localized pain at symptom onset. A potenlogic signs and symptoms, treatment, and clinical outcomes. We
ing. Eight patients had localized pain at symptom onset. A potenlogic signs and symptoms, treatment, and clinical outcomes. We
tial source for vasculopathies and cardioembolic stroke was exalso analyzed radiologic findings such as stroke location (anterior
tial source for vasculopathies and cardioembolic stroke was exalso analyzed radiologic findings such as stroke location (anterior
cluded from laboratory and cardiologic studies.
or posterior circulation), side of arterial dissection (right, left, or
cluded from laboratory and cardiologic studies.
or posterior circulation), side of arterial dissection (right, left, or
The location of arterial dissection was confirmed by cerebral
both), and anatomic location of the dissection (extracranial or
The location of arterial dissection was confirmed by cerebral
both), and anatomic location of the dissection (extracranial or
angiography (n ! 11), MR angiography (n ! 2), and Doppler
intracranial). Status at symptom onset was classified as during
angiography (n ! 11), MR angiography (n ! 2), and Doppler
intracranial). Status at symptom onset was classified as during
ultrasound (n ! 1). The imaging studies revealed that 12 patients
swing, after golf exercise, and unknown. Clinical outcome was
ultrasound (n ! 1). The imaging studies revealed that 12 patients
swing, after golf exercise, and unknown. Clinical outcome was
had involvement of the vertebral artery (VA) and 2 patients had
categorized as returned to normal (mRS ! 0 –1), independent
had involvement of the vertebral artery (VA) and 2 patients had
categorized as returned to normal (mRS ! 0 –1), independent
ICA involvement (P ! .008). Nine patients had arterial dissec(mRS ! 2–3), dependent (mRS ! 4 –5), and death (mRS ! 6) at
ICA involvement (P ! .008). Nine patients had arterial dissec(mRS ! 2–3), dependent
(mRS ! 4 –5), and death (mRS ! 6) at
tions on the right side, of which 2 had ICA involvement; 3 had left
discharge.11 Differences between the stroke location, side of distions on the right side, of which 2 had ICA involvement; 3 had left
discharge.11 Differences between the stroke location, side of disside involvement; and 2 had bilateral lesions (P ! .046). There
section, and anatomic location of the dissection were analyzed by
involvement;
and 2 and
had2bilateral
lesions
(P(P!!.046).
section,
location
of thesignificance
dissection were
analyzed
by atside were
2
12 extracranial
intracranial
cases
.008).There
Normal
useand
of anatomic
the
!
test.
Statistical
was
considered
wereactivity
12 extracranial
and in
2 intracranial
cases
! .008).
use of
the.05.
!2 test. Statistical significance was considered at
was possible
7 patients, but
the(Pother
casesNormal
revealed 5
P"
activity
was possible
in 7 patients,
but the
other cases
revealed
5
P " .05.
independent
patients
and 1 death
(On-line
Table).
Radiologic
independent
patients
and
1
death
(On-line
Table).
Radiologic
findings (stroke location and dissection focus) of our 7 cases are
RESULTS
(stroke
and dissection focus) of our 7 cases are
RESULTS
Fourteen male patients were examined. The demographic andfindings
shown
in Figlocation
1.
Fourteen
male patients findings
were examined.
The demographic
clinical-radiologic
are provided
in the On-lineand
Table.shown in Fig 1.
clinical-radiologic
are provided
in#the
On-line
The mean agefindings
of the patients
was 46.9
12.8
years, Table.
which was
DISCUSSION
The mean
agethan
of the
was 46.9
# 12.8
years, which
younger
thatpatients
of the general
stroke
population.
Seven was
patientsDISCUSSION
Our study illustrates that arterial dissection from golf-related
younger
that of the general
population.
Seven patients
studywas
illustrates
thattoarterial
dissection
golf-related
werethan
right-handed.
Of the 7stroke
patients,
2 were professional
golfersOurstroke
more likely
be on the
right sidefrom
and predominantly
were with
right-handed.
Ofof
theexperience,
7 patients,and
2 were
professional
golferswerestroke
wasextracranial
more likelyvertebrobasilar
to be on the right
side This
and predominantly
15–17 years
the remaining
patients
in the
system.
preference may be
with 15–17
years
of experience,
and experience
the remaining
were 7in the
extracranial
vertebrobasilar
system. This
preference
may besysamateur
players
with playing
for patients
approximately
explained
by the
anatomic vulnerability
of the
vertebrobasilar
amateur
players
with
playing
experience
for
approximately
7
explained
by
the
anatomic
vulnerability
of
the
vertebrobasilar
sysyears (range, 0.1–30 years). None of the patients had a history of
tem and the biomechanics of the golf swing.
years hypertension,
(range, 0.1–30diabetes,
years). None
of the patients
had aSymptom
history ofonsettem andRecent
the biomechanics
of thedifferences
golf swing.in spontaneous vertebral
or autoimmune
disorder.
studies on ethnic
hypertension,
orgolf
autoimmune
onset(n ! Recent
studies onhave
ethnic
differences
in spontaneous
vertebral
occurred diabetes,
during the
swing (n !disorder.
9), at an Symptom
unknown time
artery dissection
shown
that intracranial
dissection
is more
occurred
during
swing(n(n!!2).
9),Twelve
at an unknown
(n !
artery
dissection
shown that
intracranial
dissection
is more 7
3), or
after the
golfgolf
playing
patients time
had posterior
common
thanhave
extracranial
dissection
in East
Asian populations.
7
3), orcirculation
after golf symptoms
playing (n such
! 2).asTwelve
had and
posterior
than extracranial
dissection
in artery
East Asian
populations.
vertigo,patients
nystagmus,
body tilt-common
Our study
of golf-related
vertebral
dissection
shows that
circulation symptoms such as vertigo, nystagmus, and body tiltOur study of golf-related vertebral artery dissection shows that
Choi M et al. AJNR 2014;35:323-326
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Choi Feb 2014 www.ajnr.org
Choi Feb 2014 www.ajnr.org
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NeuroformR 4×30mm
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Authentic bow does not compromise the vertebral artery.
20
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Nine dissections were found on the right side, 3 on the left side,
and 2 were bilateral (P =.046).
FIG 1. Radiologic findings (stroke location, dissection focus, and follow-up) of our 7 cases. Five cases had right-sided involvement: 3 patients
FIG 1. Radiologic findings (stroke location, dissection focus, and follow-up) of our 7 cases. Five cases had right-sided involvement: 3 patients
(cases 1–3) with extracranial vertebral artery, 1 with intracranial VA (case 4), and 1 with extracranial carotid artery (case 5). One patient (case 6) had
(casesa1–3)
extracranial
vertebral
artery,
VA (case 4),VA
and
1 with extracranial
carotid
artery (case
5). One patient
6) Dotted
had
leftwith
extracranial
VA and
1 patient
(case1 with
7) hadintracranial
bilateral intracranial
involvement.
Black
indicate
the dissection
focus (case
or foci.
Choi
M
etarrows
al.indicate
AJNR
a left rectangles
extracranialindicate
VA andfollow-up
1 patient (case
7) of
haddissection
bilateral intracranial
VA involvement.
Black
arrows
the 2014;35:323-326
dissection focus or foci. Dotted
images
focus or foci.
rectangles indicate follow-up images of dissection focus or foci.
re
Case 3. A 37 year-old-woman wanted to make her car parking in proper position.
After few minutes, she presented with severe dizziness, vertigo and right hand
ataxia.
IN
There are many stress in modern society…
Lustrin ES et al. Pediatric cervical spine: Normal anatomy, variants, and trauma.
Radiographics 2003; 23:539-60.
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Golf can be a risk factor for VA dissections.
Functional anatomy of craniocervical junction
ASA and anterior medullary perforators from the union of
Interventional Neuroradiology 14: 49-58, 2008
vertebro-basilar artery.
www.centauro.it
Vascular Microanatomy
of the Pontomedullary Junction,
Posterior Inferior Cerebellar Arteries,
and the Lateral Spinal Arteries
PH. MERCIER, G. BRASSIER**, H-D FOURNIER, J. PICQUET, X. PAPON,
P. LASJAUNIAS*
Laboratoire d’Anatomie, Faculté de Médecine, Angers cédex, France
* Département de Neuroradiologie, avenue du Gal Leclerc, Hôpital Bicêtre, le Kremlin, France
** Université de Rennes 1, Rennes, France
Key words: medulla oblongata, posterior inferior cerebellar artery (PICA), perforating arteries, lateral spinal artery
Summary
This study of 25 brains at the pontomedullary
junction defined the different possible origins of
the perforating arteries and lateral spinal arteries in relation to the posterior inferior cerebellar
arteries (PICAs).
- If the PICA emerges from the common
trunk of the AICA-PICA coming from the basi-
teries arise 1,4,5,7-10,12-17. From these arteries also
emerge the lateral spinal arteries responsible
for the vascularization of the posterior surface
of the medulla oblongata 6,11.
This region is increasingly solicited in interventional neuroradiological procedures for embolization or arterial aneurysm, dissections, arteriovenous malformations, dural fistula or repair of an occlusive disease. The procedures
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AICA
ASA
an
pe terio
rfo r m
rat
ors edu
lla
ry
tio
n
Right lateral view showing the caudal
loop of the PICA. No perforating arteries
emerge from the vertebral artery under
the PICA’s emergence.
Mercier P. et al. INR 2008
ev
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rt
PICA
se
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ed
ite
d.
AICA
AICA
PICA
in
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Pair of ASAs originate from both fenestrated trunk.
ASA and anterior medullary perforators
originating from the VA distal to the
orifice of PICA.
Rt.perforators originating relatively lower
part of V4 portion that is at least 10mm
apart from the union.
Mercier P. et al. INR 2008
rt
an
pe terio
rfo r m
rat
ASA
ors edu
lla
ll
r
ig
ASA and anterior
medullary perforators
pa
ht
s
is
re
pr
PICA
oh
ib
-A
ny
re
pr
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uc
Fig.12
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Anatomical variation:
Results from 12056 cases of MRA (2004∼2006)
1. Basilar trunk fenestration: 156 (1.29%)
2. Anterior communicating artery fenestration: 91(0.75%)
is
3. Persistent primitive trigeminal artery :82 (0.68%)
rt
4. Accessorius or duplication of middle cerebral artery: 69 (0.57%)
pa
5. Azygos A2: 28(0.23%)
in
6. Primitive dorsal ophthalmic artery: 6 (0.05%)
ev
en
7. Middle cerebral artery (M1) fenestration: 4 (0.04%)
8. Infraoptic course of anterior cerebral artery: 3 (0.025%)
tio
n
9. Persistent hypoglossal artery 7 (0.06)
od
uc
www.centauro.it
Interventional Neuroradiology 11 (Suppl 1): 000-000, 2005
www.centauro.it
Interventional Neuroradiology 11: 000-000, 2005
Neuroradiological Analysis of 23 Cases
of Basilar Artery Fenestration Based
on 2280 Cases of MR Angiographies
pr
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www.centauro.it
B
Interventional Neuroradiology 11: 000-000, 2005
B
-A
ny
A
M. TANAKA, Y. KIKUCHI*, T .OUCHI*
A
Interventional Neuroradiology 11: 000-000, 2005
Key words: basilar artery, fenestration, MR angiography
C
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Triple fenestrations of basilar trunk
in
D
Double fenestrations of basilar trunk
D
C
C
Tanaka M.et al. Interventional neuroradiology 2006
n
S
em
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tration studied by magnetic resonance (MR)
angiography are rare 2.The purpose of this study
Basilar artery (BA) fenestrations are the most is to report the incidence of BA fenestration defrequently observed variant of the cerebral arter- lineating its configurations and to investigate
ies. We examined the magnetic resonance (MR) the associated other vascular disease based on
angiographic incidence, location, characteristic large series of cranial MR angiography.
configuration of BA fenestration and associated
vascular disease.
Material
and locating
Methods
Figure
1 Type
I: fenestration
proximaltotoAICA,
AICA,
Type
II: bilateral
symmetrically
originating
from the fenFigure
1 Type
I: fenestration
locating proximal
Type
II: bilateral
AICAAICA
symmetrically
originating
from the fenFrom April 2004 to September 2004, a total of estrated
estrated
trunk,
Type
unilateralAICA
AICA originating
one
sideside
of the
trunk, trunk,
Type IV:
fenestration
locating distal
trunk,
Type
III:III:
unilateral
originating
one
of fenestrated
the fenestrated
Type
IV: fenestration
locating distal
to AICA.
Patients
2280 cranial MR angiographies were performed to AICA.
April
2004
and September
2004,
a longitudinal
at our institution. Twenty-three BA fenestrations otherBetween
across the midline.
During
the second
the basilar artery. When
the paired
across
the midline.
During
second neural
the arteries
basilar fail
artery.
When
the paired
stage
of development,
five
weeks’the
gestation,
to fuse,
fenestration
maylongitudinal
octotal
of
2280atfive
cranial
MR
angiographies
were
(1.0%) were detected on MRA. There were 13 other
stage
of development,
weeks’
arteries
fuse, of
fenestration
fusion
of the channelsatgradually
startsgestation,
to form curneural
anywhere
alongfail
the to
course
the basilar may ocof the channelsat
gradually
starts to form cur
anywhere
alongconthe course of the basilar
performed
our institution.
These
2280
males and ten females in this group and mean fusion
age was 57.6 years old. Three cases of these fen- secutive patients consisted from 1013 females
3
estration group are suffered with atherothrombic and 1267 males.
The mean age of the patients at the time of
infarction in the territory of vertebro-basilar sysA 57y/o
female examination
with rt.hemifacial
spasm
was 61.8 ± 14.5
(mean ± standard
tem. Seven of 23 cases (30%)
were associated
with intracranial aneurysm. Of those four cases, deviation) years (range 0-95 years). In this series, there
403 cases ofspasm
asymptomatic
pa- years,
located
anterior suffered
circulation. from
The aneurysms
patient,were
who
hasat been
rt. were
hemifacial
for 10
Of those three cases, the aneurysms were associ- tients for brain check including screening studpresented
increasing
frequency
and deterioration
of the
MRA
ies, 523 cases presented
with spasm.
headache but
no and
atedlocating
with
BA
fenestration.
Since
saccular
aneurFigure 1 Type I: fenestration
proximal
to AICA,
Type II: bilateral AICA
symmetrically
originating from
the fenestrated trunk, Type III: unilateral AICA originating one side of the fenestrated trunk, Type IV: fenestration locating distal
remarkable neuroradiological
abnormality,
365
ysms are reported torevealed
arise frequently
at BA
fen-aneurysm
to AICA.
CT angiography
that
this
is originating
from proximal
estration, knowledge and recognition of fenestra- cases with vertigo and/or tinnitus without neuother part
across the tion
midline.
During
the second
theimportant
basilar artery. When
the
paired
longitudinal
of
the
fenestration
of
lower
basilar
trunk,
and
it's
complex
aneurysm
roradiological
findings
and
859
cases
diagnosed
are
useful
and
in
the
interpretastage of development, at five weeks’ gestation, neural arteries fail to fuse, fenestration may ocFigure 1 Type
I: fenestration
locating
proximal
to AICA,
Type
II:cur
bilateral
AICA along
symmetrically
originating
the fenfusion
of the channels
starts
to form
anywhere
the course
of thefrom
basilar
as a stroke including asymptomatic lacuna intiongradually
of cerebral
MR
angiography.
estrated trunk, Type
III: unilateral AICA originating one
side of thethe
fenestrated
trunk, Type IV: fenestration locating
distal
invaginates
into
brainstem
where
is adjacent to the rt.REZ of CN Ⅶto AICA.
farction.
rt
ht
s
Summary
Case Illustration :
-W
IN
od
uc
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“Das Arteriensystem der Japaner”
pr
Ⅷ complex.
Introduction
3
re
C
other across the midline. During the second the basilar artery. When the paired longitudinal
stage of development, at five weeks’ gestation, neural arteries fail to fuse, fenestration may ocThestarts
incidence
fusion of the channels gradually
to form of
curbasilar
anywhere artery
along the(BA)
course fenestraof the basilar
3
MRI and Radiological Findings
All patients were studied with two of 1.5 Tesla units (SIEMENS, Magnetome VISION and
GE,Excite) and one of 1.0 Tesla unit (SIE-
1
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Lower BA trunk saccular aneurysm associated with Type I
fenestration invaginating into the REZ of CN VII-VII th complex.
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tion was reported to be 0.6~1.7 % based on angiography 1,2,3,4. However, reports of BA fenes-
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Department of Neurosurgery and Radiology*, Kameda Medical Center; Chiba, Japan
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2. Pathology of arterial dissections
3. Imaging modalities and the clinical application
PICA
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1. Anatomical consideration of craniocervical junction
AICA
-A
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Menu
AICA
Ic. Pontine Perforation Zone
re
The pontine perforation zone encompasses the
ht
rig
ll
A
in
ar
.
S
A double lumen is formed when a
subintimal hemorrhage ruptures back into
the arterial lumen distally.
-W
ration sites on the basal surface of the medulla. One
such array, the medial medullary group is evident
the midline
extendingPerforation
from the foramen
caecum
Id.inBasal
Medullary
Zone
20
17
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A
B
C
caudally (see Fig 124B-C). The caudal limit of this
Denuded
specimens
revealed
arrays
of perfogroup is
not apparent
and itrich
clearly
continues
to
ration
siteslevels
on theinbasal
the medulla.
spinal
the surface
anterior ofmedian
fissure.One
As
such
array,intheFigs
medial
medullary
group isthe
evident
shown
138A-C
and 139A-C
two
Fig 138A-C Regular penetrating arteries arising from the most
in the
midline
extending
fromlaterally
the foramen
caecum
pyramids
must
be
retracted
to
expose
two
distal vertebral arteries (beyond the anterior spinal arteries) or
caudally
Fig 124B-C).
caudal limit
of this
parallel(see
paramedian
rows The
of perforation
sites,
the
most proximal basilar artery and entering the brain in the
is not
apparent
and itrostrally
clearly atcontinues
to
neighborhood of the foramen caecum. A Injected specimen. Bgroup
largest
of which
are located
the foramen
Schematic drawing.
caecum.
become progressively
smaller
spinal
levelsThe
in sites
the anterior
median fissure.
As
CSeveral
Formalin-fixed
brain
after
the
reflexion
of
the
vertebrostudies have shown that pain is typically
the in
firstFigs
symptom
associated
with CAD,
caudally.
shown
138A-C
and 139A-C
the two
basilar
arteries.
Perforators
from
basilar
artery
(arrows).
Fig 138A-C
penetrating
arteries
arisinginvolving
from the most
andRegular
a recent
descriptive
study
245 CAD patients reported that 8% of them
pyramids
must
be
retracted
laterally
to
expose
two
distal vertebral
arterieswith
(beyond
theor
anterior
presented
head
neckspinal
pain arteries)
as theiroronly
symptom.
parallel
paramedian rows of perforation sites, the
most proximal basilar artery and entering the brain in the
neighborhood of the foramen caecum. A Injected specimen. B largest of which are located rostrally at the foramen
Schematic drawing.
caecum. The sites become progressively smaller
C Formalin-fixed brain after the reflexion of the vertebrocaudally.
basilar arteries. Perforators from basilar artery (arrows).
Several studies have shown that pain is typically the first symptom
associated with CAD, and a recent descriptive study involving 245 CAD
patients reported that 8% of them presented with head or neck pain as
their only symptom.
em
Cervical artery dissection typically
involves an initial tear in the artery
lining. It may cause the layers to
separate from each other forming
a subintimal dissection.
IN
may beperforation
appreciated zone
near the
midline of the
Thesites
pontine
encompasses
the
ponssurface
on its basal
surface.
small,
basal
of the
pons.Although
Here, generally
in the surface
the sites
of this amedial
pontine
group are
denuded
specimens,
linear array
of perforation
present and are
sitesconsistently
may be appreciated
nearnotthesignificantly
midline ofinfluthe
enced
their surface.
distribution
by thegenerally
often deviated
pons
on itsinbasal
Although
small,
basilar
artery. pontine
Additionalgroup
perforation
the course
sites ofofthethis
medial
are
sites are seen scattered more laterally over the pons
consistently present and are not significantly influand brachium pontis to form a lateral pontine group
enced
in
their
distribution
by
the
often
deviated
(see Fig 124B-C). In latex injected specimens small
course
of
the
basilar
artery.
Additional
perforation
branches from the undersurface of the basilar artery
siteswere
are seen
seen to
scattered
laterally
thewhile
pons
enter themore
medial
pontineover
group
andbranches
brachiumofpontis
to form acerebellar
lateral pontine
group
the superior
and anterior
(seeinferior
Fig 124B-C).
In latex
injected
small
cere-bellar
arteries
were specimens
seen to enter
the
branches
from
the
undersurface
of the basilar artery
scattered
sites
noted
more laterally.
were seen to enter the medial pontine group while
branches of the superior cerebellar and anterior
inferior
cere-bellar
arteriesPerforation
were seen to
enter the
Id. Basal
Medullary
Zone
scattered
sites
noted more
laterally.
Denuded
specimens
revealed
rich arrays of perfo-
s
surface of the pons. Here, in the surface
Ic.basal
Pontine
Perforation Zone
denuded specimens, a linear array of perforation
ve
n
Post@6month
MRA 3D TOF
ev
en
155
Pre
tio
I. Basal Perforation Zones
I. Basal Perforation Zones
Post
→ Cure of hemifacial spasm
completely
IN
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Pre
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IntraaneurysmalflowcondiAon
Subintimal dissection with
thrombus formation.
SAH
Right VA
Autopsy on Day 8
No
Proximal clipping on Day 1
SAH
Left VA
Autopsy on Day 12
No
SAH
Left VA
Autopsy on Day 14
Day 2
No
SAH
Left VA
Autopsy on Day 14
Day 7
No
SAH
Right VA
Autopsy on Day 15
Day 0
No
SAH
Right ICA
Autopsy on Day 17
Day 9 –11, 5 times
No
SAH
Left A2–A3
Surgery on Day 19
No
SAH
Left SCA
Emboli may detach from a primary
thrombus and travel distally to obstruct
Surgery
on Day 23
Nobrain.
progressively
smaller vessels in the
SAH
Right VA
Autopsy on Day 35
ct A
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e
Proximal clipping on Day 1
pr
oh
ib
it e
d.
OBJECTIVE: This was a pathological study to investigate the healing process for
cerebral dissecting aneurysms presenting with subarachnoid hemorrhage
(SAH).
is
pa
rt
Trapping " aneurysm resection on
Day 19
METHODS: Thirteen dissecting aneurysms that presented with SAH were
obtained from 13 patients. Nine aneurysms arose from the vertebral artery, two
arose from the anterior cerebral artery, one arose from the internal carotid artery,
and one arose from the superior cerebellar artery. Eight aneurysm specimens
were collected during autopsy and five were resected during surgery (trapping
with or without bypass). The period between the onset of SAH and the time of
specimen collection ranged from 6 hours to 35 days. All 13 aneurysms were
pathologically examined with immunohistochemical staining, with a focus on the
chronological healing process after SAH.
RESULTS: All dissecting aneurysms were generated with sudden
widespread disruption of the internal elastic lamina and media.
The healing process occurred with neointimal proliferation. The
neointima, consisting mainly of newly synthesized smooth muscle cells and
collagen fibers, extended from the disrupted ends of the media proper forward to
the ruptured portion.
Day 14
ev
en
in
Trapping " aneurysm resection "
STA-SCA bypass on Day 23
No
Subadventitial dissection occurs when blood penetrates
through the tunica media into the subadventitial plane.
FIGURE 1. Patient 6, a 67-year-old
male. The left VA
dissecting aneurysm
Onset
Location
Collection method
Rebleeding
Surgery
presented
with
SAH,
wason treated with
1
60/M
SAH
Left VA
Surgery on Day 0
Day
0
Trapping
" aneurysm
resection
Day 0
proximal
clipping
on Day 1, and was
2
48/M
SAH
Left VA
Surgery on Day 0
Day 0
Trapping " aneurysm resection on
Day 0
collected
during
autopsy
on Day 12.
3
52/M
SAH
Left A2
Surgery on Day 1
No
Trapping " aneurysm resection "
A3-A3 bypass on Day 1
A, photomicrograph
demonstrating siurysms were4 generated
with Autopsy
sudden
51/M
SAH
Left VA
on Day 2
No
No
lent
repair
of the area of IEL disrup5
50/M
SAHlamina
Right VA (IEL)
Autopsy onand
Day 8
No
Proximal clipping on Day 1
n of the internal
elastic
6
67/M
SAH
Left VA
Autopsy on Day 12
No
Proximal clipping
on Day 1
tion.
Localized
thickening
of the neoind IELMdid
not
reconnect
in
any
of
the
56/M
SAH
Left VA
Autopsy on Day 14
Day 2
IZUTANI ET 7AL.
tima canNo
be observed (*). Arrows,
8
SAH
Left arteries,
VA
Autopsy on Day
14
Day 7
No
. Interestingly,
in43/F several
the
disrupted
9
41/M
SAH
Right VA
Autopsy on Day 15
Day
0
No ends of the IEL (elastica van
IEL, which did
not
develop
an Autopsy
arterial
10
70/F
SAH
Right ICA
on Day 17
Day 9 –11, 5 times
No
Gieson stain;
original magnification,
11
59/M
SAH
Left A2–A3
Surgery on Day 19
No
Trapping " aneurysm resection on
ly covered with neointima (Fig. 1A).
19
!40). B,Dayphotomicrograph
of the an12
34/F
SAH
Left SCA
Surgery on Day 23
No
Trapping " aneurysm resection "
eurysm STA-SCA
at the
ruptured
portion. Arbypass
on Day 23
13
49/M
SAH
Right VA
Autopsy on Day 35
Day 14
No
rows, disrupted
ends of the IEL. Arrowheads, disrupted ends of the
ges
FIGURE 1. Patient
6, a 67-year-old
adventitia
(elastica van Gieson stain;
RESULTS
male. The left VA dissecting
aneurysm
Mizutani
T. Neurosurgery 2004
presented with SAH, was treated with
sms (Cases 1 and 2) that were resected
original magnification, !12.5).
proximal clipping on Day 1, and was
RESULTS
Age (yr)/
sex
FIGURE 1. Patient 6, a 67-yearold male. The left VA dissecting
aneurysm presented with SAH,
was treated with proximal
clipping on Day 1, and was
collected during autopsy on Day
12. A, photomicrograph
demonstrating silent repair of the
area of IEL disruption. Localized
thickening of the neointima
can be observed (*).
Arrows, disrupted ends of the IEL
(elastica van Gieson stain;
original magnification, 40).
ET AL.
MIZUTANI
ET AL.
A 41-year-old male. The right VA dissecting aneurysm presented
with SAH, was treated conservatively, and was collected during
autopsy on Day 15.
A 41-year-old male. The right VA dissecting aneurysm presented with
SAH, was treated conservatively, and was collected during autopsy on
Day 15.
B, high-magnification
view of the slice
Arrow, neointima,
consisting mainly of
smooth muscle cells and
collagen fibers
(azan stain; original
magnification, 100).
rt
Mizutani T. Neurosurgery 2004
Mizutani T. Neurosurgery 2004
in
a
aches, SAH, and cerebral infarction. Therefore, specimens of
cerebral dissecting aneurysms collected at different times after
genesis eloquently demonstrate chronological changes. These
changes may represent the healing process after the genesis of
od
uc
pr
-A
ed
rv
se
Mizutani T. Neurosurgery. 45(2):253, 1999
Mizutani T. Neurosurgery. 45(2):253, 1999
ht
.
Mizutani T. Neurosurgery. 45(2):253, 1999
A
B
C
-W
IN
S
em
in
ar
.
A
ll
rig
wall (Fig. 2A). The ruptured portion was covered only with
DISCUSSION
thrombus and appeared very fragile (Fig. 2D). In the superior
wall (Fig. 2A). The ruptured portion was covered only with
DISCUSSION
Saccular aneurysms may have a permanent
risk of bleeding.
cerebellar artery aneurysm (Case 13), which was resected durthrombus and appeared very fragile (Fig. 2D). In the superior
It seems that the healing mechanism is not sufficiently effecing surgery (trapping and resection) on Day 23, the neointima
Saccular aneurysms may have a permanent risk of bleeding.
cerebellar artery aneurysm (Case 13), which was resected durtive, possibly because of the aneurysm structure. We are curcompletely covered the vascular wall (Fig. 3A), with endotheIt seems that the healing mechanism is not sufficiently effecing surgery (trapping and resection) on Day 23, the neointima
rently unable to ascertain the age of saccular cerebral aneulium covering the entire surface of the neointima. However,
tive, possibly because of the aneurysm structure. We are curcompletely covered the vascular wall (Fig. 3A), with
endotherysms,
because they usually present no symptoms at the time
the neointima was broken in some of the slices (Fig. 3B),
rentlymay
unable
to ascertain
thefrom
age of
saccular cerebral aneucovering
entire
of the neointima.
However,
of development.
They
gradually
enlarge
arterial
suggesting that lium
this new
layerthe
was
not surface
strong enough
to
rysms,
because
they
usuallydissecting
present no
symptoms at the time
the neointima
in some
of 14)
the slices
(Fig. 3B),which
bifurcations,
lack IEL
(15). In
contrast,
aneusustain the hemodynamic
stress. was
One broken
VA aneurysm
(Case
of
development.
They widespread
may gradually
enlarge from arterial
thatexhibited
this newrebleeding
layer wasonnot
enough
to
rysms
are usually
generated
with sudden
disrupthat was treated suggesting
conservatively,
Daystrong
bifurcations,
which
(15).
In contrast,
dissecting
aneu- the site
sustainduring
the hemodynamic
VA4A)
aneurysm
Dissection
aneurysm.
focal IEL
narrowing
(arrow)
of
the right vertebral
artery indicating
tion (Case
of the14)
IEL (6,
14).
Thiswith
type
of lack
cerebral
arterial
trunk
14, and was collected
autopsy on stress.
Day 35One
(Fig.
of
intimal
disruption,
and
a
distal
dilatation
(arrowheads).
are usually
generated
sudden
thatextending
was treated
conservatively,
exhibited
rebleeding
on Day
aneurysm
should rysms
be classified
as Type
1 (acutewith
cerebral
dis-widespread disrupexhibited neointima
from
the media proper
but not
tion
the IEL
(6,
14).
This type
of clascerebral
arterial
trunk
and was
collected
during
on Daysecting
35 (Fig.
4A)
b | of
Photomicrograph
(10×
magnification;
hematoxylin
and eosin stain)
demonstrates
complete
aneurysms),
according
to our
clinicopathological
yet covering the14,
ruptured
portion,
which
was autopsy
still covered
disruption of the intima and media, and a dissection plane (thrombus) that propagated
should
be classified
as Type
exhibited
neointima extending
from
the media proper
but not
sification
(7), andaneurysm
should
be
from
Type1 3(acute cerebral diswith thrombus (Fig.
4B). Endothelium
covered the
neointima
superficial to
the distinguished
media.
aneurysms),
according
ourofclinicopathological
clasyetthecovering
ruptured
portion,
which was (chronic
still covered
enlargingsecting
dissecting
aneurysms)
(4). The to
time
genbut did not cover
residualthe
thrombus.
Along
the luminal
c | Photomicrograph (10× magnification; Movat's pentachrome stain) demonstrates an intact
sification
(7),lamina
and
should
be the
distinguished
from Type 3
with thrombus
(Fig. 4B). Endothelium
covered the
internal
elastic
(arrows)
from
site of intimal disruption.
margin of the thrombus,
the accumulation
of macrophages
esisneointima
of acute dissecting
aneurysms
can
be away
clearly
determined
Type 4 aneurysm
(saccular
aneurysm8,orablister
like aneurysm
arising
(chronic
enlarging
dissecting
aneurysms)
(4).
The
time
of
genbut
did
not
cover
the
residual
thrombus.
Along
the
luminal
FIGURE
5. Patient
43-year-old
female.
Thefrom
dissecting aneurysm
ariswas observed (Fig. 4C), suggesting active phagocytosis. In
on the basis of clinicalAbbreviations:
presentation,
including
preceding headM, media;
T, thrombus.
arterial trunk). The Type 4 aneurysm arises from the portion of minimally
theintimal
left VAthickening.
presented The
with
SAH, was conservativelyaneurysms
treated, and in which
margin
the thrombus,
the
accumulation
macrophages
esis of acute
dissecting
aneurysms
can beofclearly determined
disrupteding
IEL from
without
dome comprises fragile
Genesis
and healing
of cerebral
dissecting
aneurysms.
the of
media
and
IEL complex
had
com- of
aches,
SAH, and cerebral
infarction.
Therefore,
specimens
collected
during autopsy on Day 14. The photomicrograph of the rupFIGURE
6. Genesis(Fig.
and healing
of cerebral dissecting
adventitia orwas
connective
tissue.
was
observed
4C),
suggesting
active
phagocytosis.
In
on
the basis of
clinicalatpresentation,
including
preceding
Krings
T. et al. Nature
reviews. headNeurology 2011
pletely separated
from
the adventitia
(Cases
7, 8, and
13), aneurysms.
cerebral2004
dissecting
aneurysms
collected
different times
after
Mizutani
T.
Neurosurgery
tured portion of the aneurysm demonstrates that the ruptured portion was
aneurysms
in which
andthe
IELinicomplex
had eloquently
comaches,
SAH, and
cerebral infarction.
Therefore, specimens of
neointima formation
was minimal
eventhe
14 media
days after
genesis
demonstrate
chronological
changes. These
still covered with dense thrombus. Neointima formation was not observed
8, andmay
13),represent
cerebral
aneurysms
collected
tial SAH (Fig. 5).pletely separated from the adventitia (Cases 7,changes
the dissecting
healing process
after the
genesisatofdifferent times after
(azan stain; original magnification, !20).
neointima formation was minimal even 14 days after the inigenesis eloquently demonstrate chronological changes. These
©
www.neurosurgery-online.com
M
17
ve
n
rently unable to ascertain the age of saccular cerebral aneuneointima. However,
rysms, because they usually present no symptoms at the time
the slices (Fig. 3B),
of development. They may gradually enlarge from arterial
ot strong enough to
344 | VOLUME 54 | NUMBER 2 | FEBRUARY 2004
bifurcations, which lack IEL (15). In contrast, dissecting aneuaneurysm (Case 14)
rysms are usually generated with sudden widespread disrupd rebleeding on Day
tion of the IEL (6, 14). This type of cerebral arterial trunk
on Day 35 (Fig. 4A)
aneurysm should be classified as Type 1 (acute cerebral dismedia proper but not
secting aneurysms), according to our clinicopathological clasch was still covered
sification
(7), (dolichoectatic
and should be
distinguished
from Type 3
vered the neointima Type
3 aneurysm
dissecting
aneurysm).
Type 3enlarging
aneurysmdissecting
has a fragmented
IEL with
thickening.
(chronic
aneurysms)
(4). intimal
The time
of gens. Along the luminal The
Multiple
occur inaneurysms
the thickened
(Slices
A and B).
ion of macrophages
esis ofdissections
acute dissecting
canintima
be clearly
determined
is formed
in and
around the dissected
(Slices
A-C).
ive phagocytosis. In Thrombus
on the basis
of clinical
presentation,
includingintima
preceding
head-
Type 1 aneurysm (classic dissecting aneurysm).
A. At the peripheral portion of the aneurysm, the continuity of the IEL is preserved
IZUTANI
ET AL
and the pseudolumen
is detected.
B. Widespread disruption of the IEL is observed at the midportion of the aneurysm
re
VOLUME 54 | NUMBER 2 | FEBRUARY 2004 | 343
FIGURE 2. Patient 9, a 41-year-old male. The right VA dissecting aneurysm
mainly of smooth muscle cells and collagen fibers (azan stain; original magniA-D correspond
the slices !100). C, the same slice as in A, stained for collagen Type I (collagen
presented with SAH, was treated conservatively, and wasSlices
collected
during with fication,
shownThe
in b.right
Widespread
disruption aneurysm
of
FIGURE 2. Patient 9, a 41-year-old male.
VA dissecting
mainly of smooth muscle cells and collagen fibers (azan stain; original magniautopsy on Day 15. A, photomicrograph of an axial slice the
of the
aneurysm.
Type
IEL is
shown in Slices A-C.
P, I stain; original magnification, !100). Arrow, neointima, including
presented with SAH, was treated conservatively,
and was collected
during
fication, !100). C, the same slice as in A, stained for collagen Type I (collagen
pseudolumen.
Arrows, disrupted ends of the media and IEL complex. The neointima
extended
abundant collagen Type I fibers,
with
the media
proper. D, photomiTypecompared
2 aneurysm
(segmental
ectasia).
autopsy on Day 15. A, photomicrograph of an axial slice of the aneurysm.
Type Slice
I stain;
original
magnification,
!100). Arrow, neointima, including
A, normalportion,
artery, shows
from the disrupted ends of the media (azan stain; original magnification,
!20). from the
crograph of an axial slice of the ruptured
whichintact
wasIEL.
still covered with
Slice
E was
obtained
Arrows,
disrupted
ends
of
the
media
and
IEL
complex.
The
neointima
extended
abundant
collagen
Type
I
fibers,
compared
with
the media (Slice
proper.
D, with
photomiThe Type
2 aneurysm
has
stretched
B)
or fragmented
C) IEL
adaptive
B, high-magnification view of the slice in A. Arrow, neointima,
fragile thrombus (arrow) (azan
stain;
original magnification,(Slice
!20).
oppositeconsisting
normal vertebral artery.
intimal
thickening.
from the disrupted ends of the media (azan stain; original magnification, !20).
crograph of an axial slice of the ruptured portion, which was still covered with
The luminal surface of the intimal thickening is smooth. Thrombus formation does not
B, high-magnification view of the slice in A. Arrow, neointima, consisting
fragileoccur
thrombus
(arrow)
(azan
stain;
original
magnification,
!20).
in Type 2 aneurysms.
s
©
20
17
magnification, 20).
wall (Fig. 2A). The ruptured portion was covered only with
DISCUSSION
thrombus and appeared very fragile (Fig. 2D). In the superior
Saccular aneurysms may have a permanent risk of bleeding.
cerebellar artery aneurysm (Case 13), which was resected durIt seems that the healing mechanism is not sufficiently effecing surgery (trapping and resection) on Day 23, the neointima
tive, possibly because of the aneurysm structure. We are curcompletely covered the vascular wall (Fig. 3A), with endotherently unable to ascertain the age of saccular cerebral aneulium covering the entire surface of the neointima. However,
rysms, because they usually present no symptoms at the time
the neointima was broken in some of the slices (Fig. 3B),
t VA dissecting
aneurysm
of smooth
cells and
collagentofibersof
(azan
stain; original
magnidevelopment.
They
may gradually enlarge from arterial
suggesting
that thismainly
new layer
wasmuscle
not strong
enough
which
lack IEL (15). In contrast, dissecting aneusustain the
hemodynamic
stress.
One
aneurysm
and was collected
during
fication,
!100).
C,VA
the same
slice as(Case
in A,14)
stainedbifurcations,
for collagen Type
I (collagen
rysms are
usually including
generated with sudden widespread disruptreated conservatively,
rebleeding on !100).
Day Arrow,
al slice ofthat
the was
aneurysm.
Type I stain;exhibited
original magnification,
neointima,
tion
of the
IELD,(6,photomi14). This type of cerebral arterial trunk
14, and
was collected
duringcollagen
autopsy
onI Day
(Fig. 4A)
x. The neointima
extended
abundant
Type
fibers,35compared
with the
media
proper.
be classified
as Type 1 (acute cerebral disexhibited!20).
neointima crograph
extending
theslice
media
proper
but not
ginal magnification,
of from
an axial
of the
ruptured
portion, aneurysm
which was should
still covered
with
secting aneurysms),
yet covering
portion, (arrow)
which was
covered
ow, neointima,
consistingthe ruptured
fragile thrombus
(azanstill
stain;
original magnification,
!20). according to our clinicopathological classification (7), and should be distinguished from Type 3
with thrombus (Fig. 4B). Endothelium covered the neointima
(chronic enlarging dissecting aneurysms) (4). The time of genbut did not cover the residual thrombus. Along the luminal
margin of the thrombus, the accumulation of macrophages
esis of acute dissecting aneurysms can be clearly determined
s covered
only with
DISCUSSION
was observed (Fig. 4C), suggesting active phagocytosis.
In
on the basis of clinical presentation, including preceding head2D). In aneurysms
the superior
in which the media and IEL complex had comaches, SAH, and cerebral infarction. Therefore, specimens of
Saccular
aneurysms
may
have
a
permanent
risk of bleeding.
ch was resected
durpletely separated from the adventitia (Cases 7, 8, and 13),
cerebral dissecting
aneurysms collected at different times after
seems
thateven
the 14
healing
mechanism
isgenesis
not sufficiently
effecDay 23, the
neointima
neointima
formationItwas
minimal
days after
the inieloquently demonstrate
chronological changes. These
tial SAH
(Fig. 5).
may We
represent
the healing process after the genesis of
tive, possibly because of the aneurysmchanges
structure.
are curg. 3A), with
endothe-
tio
n
synthesized tissue did not entirely cover the ruptured vascular
20
B
A
the appearance of macrophages and neointima, was not de-
FIGURE 2. Patient 9, a 41-year-old male. The right VA dissecting aneurysm D, photomicrograph
mainly of smooth muscle cells
(azan stain; original magniof and
ancollagen
axialfibers
slice
presented with SAH, was treated conservatively, and was collected during
fication, !100). C, the same slice as in A, stained for collagen Type I (collagen
of the
ruptured portion,
which
wasArrow, neointima, including
autopsy on Day
15. A, photomicrograph of an axial slice of the aneurysm.
Type I stain; original
!100). 2004
NEUROSURGERY
VOLUME magnification,
54 | NUMBER 2 | FEBRUARY
| 343
covered
with
fragile
thrombus
Arrows, disrupted ends of the media and IEL complex. The neointima extended still abundant
collagen
Type
I fibers, compared
with the media proper. D, photomifrom the disrupted ends of the media (azan stain; original magnification, !20). (arrow)
crograph
of an axial
slice oforiginal
the ruptured portion, which was still covered with
(azan
stain;
B, high-magnification view of the slice in A. Arrow, neointima, consisting
fragile thrombus (arrow) (azan stain; original magnification, !20).
Mizutani T. Neurosurgery 2004
re
S
em
IN
Left vertebral arteriogram showing a Type
1 aneurysm.
Stenotic portion indicated by an arrow
corresponds with Slice D in b.
b, postmortem photographs of the
aneurysm arising from the left vertebral
artery.
c, photomicrographs of the serial axial
slices of the aneurysm (Slices A-D)
(elastica van Gieson; original
magnification, x4).
C
-W
collected during autopsy on Day 12.
A, photomicrograph demonstrating silent repair of the area of IEL disruption. Localized thickening of the neointima can be observed (*). Arrows,
disrupted ends of the IEL (elastica van
Gieson stain; original magnification,
!40). B, photomicrograph of the aneurysm at the ruptured portion. Arrows, disrupted ends of the IEL. Arrowheads, disrupted ends of the
adventitia (elastica van Gieson stain;
original magnification, !12.5).
ny
General Findings
pping and resection)
on
Day with0,sudden
fresh
All dissecting aneurysms
were generated
widespread disruption of the internal elastic lamina (IEL) and
media. The disrupted
IEL did a
not small
reconnect in any
of the
e ruptured portion,
with
number
aneurysm specimens. Interestingly, in several arteries, the
tected
1B).
In one VA aneurysm (Case 9) that was treated
wall of the disrupted IEL, which did not develop an arterial
slice(Fig.
as in A,
stained
mulated around
the thrombus. Macro-C, the same
dissection, was silently covered with neointima (Fig. 1A).
for collagen Type I (collagen Type
and collected during autopsy on Day 14, neorved. In two VA aneurysms (Cases 5 andI stain; conservatively
original magnification,
Changes
with parent Chronological
artery
clipping on Day 1 and100). intima, consisting mainly of newly synthesized smooth musIn two VA aneurysms (Cases 1 and 2) that were resected
Arrow, neointima, including
(trapping and resection) on Day 0, fresh
clecollagen
cells Type
andI fibers,
collagen fibers, began to extend from the media
psy on Dayduring
8 surgery
and
Day
thrombus
covered the
ruptured12,
portion,respectively,
with a small number
abundant
tected (Fig. 1B). In one VA aneurysm (Case 9) that was treated
of neutrophils accumulated around the thrombus. Macrocompared
the
media
proper.
conservatively
and with
collected
during
autopsy
on ruptured
Day 14, neophages were not observed.accumulation
In two VA aneurysms (Cases 5 and
proper
to
the
portion (Fig. 2, A–C). However, the
including neutrophil
and
intima,
consisting
mainly
of
newly
synthesized
smooth mus6) that were treated with parent artery clipping on Day 1 and
cle cells and collagen fibers, began to extend from the media
autopsy on Day 8 and Day 12, respectively,
acrophagescollected
andduring
neointima,
was not detissue
not entirely cover the ruptured vascular
proper to thesynthesized
ruptured portion (Fig. 2, A–C).
However,did
the
the healing process, including neutrophil accumulation and
L complex had comCases 7, 8, and 13),
14 days after the ini-
pa
Arrows, disrupted ends of the media and IEL complex.
The neointima extended from the disrupted ends of the
media (azan stain; original magnification, 20).
in
ll
r
Arrows, disrupted ends of the IEL.
Arowheads, disrupted ends of the
adventitia (elastica van Gieson stain;
original magnification, 12.5).
ev
en
ig
B, photomicrograph of the aneurysm
at the ruptured portion.
SAH, subarachnoid hemorrhage; VA, vertebral artery; ICA, internal carotid artery; SCA, superior cerebellar artery; STA, superficial temporal artery.
r.
A
a
is
ht
s
re
pr
se
rv
ed
-A
ny
re
Patient
no.
pr
TABLE 1. Clinical summarya
MIZUTANI
ite
d.
CEREBRAL DISSECTING ANEURYSMS
CONCLUSION: It is assumed that the healing process, with neointimal
proliferation, begins after 1 week and may not be complete even after 1 month,
depending on the extent of the wall injury.
Mizutani T. Neurosurgery 2004
Perrone, R. D. et al. Vascular complications in autosomal
dominant polycystic kidney disease, Nat. Rev. Nephrol. 2015
oh
ib
FOR
tunica adventitia outward, producing a pseudoaneurysm.
od
uc
HEALING PROCESS
tio
n
morrhage; VA, vertebral artery; ICA, internal carotid artery; SCA, superior cerebellar artery; STA, superficial temporal
artery.
Blood accumulating
between these layers deforms the
9. Rhoton AL Jr. The foramen magnum. Neurosurgery 47, S155 - S193, 2000
ct A
io ll
r
n
i
g
in
ev h
pa
01
en t
rt
7
i
n
©
is
pr
se AB
o
rv
C
h
ed
-W
ib
i
t
I
e
-A
N
d
S
ny
em
in
re
ar
i
p
n
.A
r
o
io
l
d
l
n
rig
u
c
e
10. Sato K, Endo T, Niizuma K, Fujimura M, Inoue T, Shimizu H, Tominaga T. Concurrent dural and
perimedullary arteriovenous fistulas at the craniocervical junction: case series with special
reference to angioarchitecture. J Neurosurg 118, 451-459, 2013
Segmental susceptibility to dissection
http://neuroangio.org/
od
uc
tio
n
ev
en
in
pa
rt
is
pr
oh
ib
it e
d.
Segmental susceptibility to dissection
J. gabrieli et al.
J. gabrieli et al.
ny
re
pr
Segmental susceptibility to dissection
Sato K,et al Concurrent dural and perimedullary
arteriovenous fistulas at the craniocervical junction .
J Neurosurg 118, 451-459, 2013
http://neuroangio.org/
3. Imaging modalities and the clinical application
pr
rt
pa
in
n
tio
od
uc
cal junction affected
and usually
originatesstagnating
from thecontrast
vertebral
ar- e: Posttreatment
As demonstrated
by this
theprojection
codominant
by the recumbent
media.
left vertebral artery
DSA case,
in lateral
showingLSA
the
tery. It is considered
to be theof result
of the embryological
cranially
directed
supply
theand
PICA
mayflow
be toward
supplied
complete occlusion
the aneurysm,
a mild spasm at the origin
of the bulbar
artery to
(black
arrow),
reversed
the by
1
dominance of
a posterior
artery.
the ASA
through the anastomotic
network ofMR
theimage
coronary
glue
cast throughradiculopial
small anastomotic
branches (dotted white arrows).
F: Postembolization
axial diffusion-weighted
(3 T)
The PICAshowing
usually
arises from
dominance
of aoblongata
sinThis
codominant
ASAwith
supply
could
be either
hyperintensity
of the
the left
dorsal medulla
is vessels.
seen (dotted
white
arrow), consistent
an acute
ischemic
stroke.a
gle pial vessel at the level of the hypoglossal nerve. Howprimitive variant or the result of a postdevelopmental ocever, several variations have been reported in the literaclusion of a proatlantal feeder followed by hypertrophy
ture,
notably a cranialdiscussion,
anterior inferior
cerebellar
artery wasof the drome
existingwith
coronary
network;
thenor
latter
seems more
multidisciplinary
endovascular
treatment
neither
diplopia
nystagmus
swallowing
(AICA)–PICA
variant
caudal
proatlantal
C-1 and
C-2
likely difficulty
to explainrelated
the features
observed
in ournerve
case palsy,
(Fig. hoarseconsidered to
be theormost
suitable
treatment
option.
to a left
ninth cranial
originsUnder
characterized
dominance
segmental
the collateral circulation often develops from
general by
anesthesia,
viaofanearby
6-F guiding
catheter3). Indeed,
ness arterial
and severe
hiccups,
ipsilateral
reduction
of pain and
levels; such cases are usually associated with a hypertroembryonic
systems,
but acquired
vascular
patterns
segment
of
the
left
positioned
at
the
distal
aspect
of
the
V
temperature
sensation
of
the
face,
and
contralateral
loss
2 hypoglossal
phic bulbar perforator arising at the usual
do not reproduce embryonic stages.1 In this case, a postvertebral
artery, n-butyl cyanoacrylate (Glubran 2, GEMdevelopmental
of pain and
temperature
sensation
the multiple
body. DiffusionThe PICA is related to the lateral spinal artery (LSA)
vessels involved may vascularize eloquent regions of the
arrangement
is more
likelyof
since
segmental
level.
as much as the posterior radiculomedullary arteries are rebrainstem and the treatment consists of a selective vascuSrl) diluted
at 30%
Lipiodol
was selectively
weighted
images
confirmed
the presence
of a left bulirregular
tortuousMR
feeders
point
to the overuse
of the adult
While
dominance
is in
certainly
the(Guerbet)
most common
analated to the posterior spinal artery, and this relationship is
lar sacrifice. It is a common opinion that such selective
delivered
through
a
4 flow-dependent microcatheter (1.2-F
bar
stroke
(Fig.
1F).
The
patient
was
subsequently
referred
confirmed by the fact that in most instances (73%) an LSA
segmental occlusion is usually well tolerated, even if pernetwork rather than the persistence and development of
tomical form, up to 2% of cases may exhibit an unusual
is visible originating from the PICA itself. Thus, if the
forators arise next to or from the trapped segment; neverMagic, Baltalso
Extrusion).
DistalPICA
navigation
obtainedembryonic
for functional
and
speech
reeducation.
characcodominance,
called a double
origin,3was
vessels that
usually
regress.
Nevertheless, this
PICA proximal to the restiform body (junction of the LSA
theless, the risk is present and should be balanced with the
withbythe
help of segments
a 0.007-inch
microtheguidewire
(Hybrid,configuration
and PICA) fails to develop or sufficiently enlarge, usuexpected benefits.
Follow-up
at 4 months
revealed
a general improvement
terized
2 separate
supplying
PICA proper.
somehow
completes
the aforementioned
ally the LSA becomes the dominant/codominant channel
Alternatively, selective exclusion of the aneurysm(s)
Balt
Extrusion)
to reach
the farthest
position. Glue
This
condition,
often
underreported,
is associated
with injec-schemewith
and,residual
to our deficit;
knowledge,
has not
been previously
the main
complaint
concerned body
and is supplied either cranially by an anastomotic channel
plus a vascular PICA-PICA bypass distal to the origin of
from the AICA or caudally from a segmental branch origthe aneurysm to protect the medulla via retrograde flow
tion aneurysm
was satisfactory,
resulting
in due
complete
exclusion ofreported
higher
prevalence,
possibly
to a regional
in and
the literature.
pain
temperature sensation. The patient was unable to
inating from the extraspinal longitudinal arteries (most
in case of feeder sacrifice has previously been reported
3
the bleeding
sourcedisorganization.
with neither proximal
nor distal mi- Unfortunately,
vascular
developmental
still a challenge,
since
the to procommonly the vertebral artery). Interestingly, the location
at least once. In our case, this option did not seem to add
continue histreatment
previousisoccupation
and was
referred
sufficient benefit since the ASA-PICA network already
of the PICA’s origin seems not only to be related to the
gration
of the
liquid to
embolic
agentspinal
(Fig. artery
1D). Control
The
PICA
is related
the lateral
(LSA) angi-vesselsfessional
involved rehabilitation;
may vascularize
regions
of the
hiseloquent
modified
Rankin
Scale score
constitutes a natural bypass, as demonstrated by the postLSA but also to affect the origin of the ventral spinal aroperative patency of all vessels including a retrograde flow
tery.
as much
as the
posterior
radiculomedullary
arteries
areexcept
re- forbrainstem
and the treatment
consists
ography
revealed
patency
of all regional
vessels
at discharge
was evaluated
at of
2. a selective vascuIndeed, the well-known scheme proposed by Lasjautoward the glue cast. A distal bypass nevertheless could
lated
the posterior
spinal artery,
and retrograde
this relationship
thetoembolized
segment
and mild
flow istowardlar sacrifice. It is a common opinion that such selective
nias et al. allows the theoretical possibility for the ASA
have a hemodynamic impact reducing the flow through
also to be the origin or co-origin of the PICA, just as the
the proximal network and the shear stress on the wall of
confirmed
the(Fig.
fact that
segmental occlusion is usually well tolerated, even if perthe gluebycast
1E).in most instances (73%) an LSA
basilar artery regularly gives origin to the AICA.
its arteries.
1
Discussion
Thus, aif left
the Wal-forators
is visible
originating from
the evaluation
PICA itself.showed
arise next to or from the trapped segment;7 neverPostprocedure
clinical
J neurosurg April 1, 2016
3
PICA
proximal
to the restiform
body (junction
the LSA syn-theless, the
riskPICA
is present
and should
be balanced
the
lenberg
syndrome
characterized
by leftofHorner’s
The
is a highly
variable
artery atwith
the craniocervi4
J
neurosurg
April
1,
2016
5
and PICA) fails to develop or sufficiently enlarge, usuexpected benefits.
ally2 the LSA
becomes
the
dominant/codominant channel
Alternatively, selective exclusion of the aneurysm(s)
J neurosurg
April
1, 2016
the
and is supplied either cranially by an anastomotic channel
plus a vascular PICA-PICA bypass distal to the origin of
m and
brain ste
the
from the AICA or caudally from a segmental branch origto
the aneurysm
to
protect
the
medulla
via
retrograde
flow
High resolution CBCT
g arteries
Mercier
P. et longitudinal
al. INR 2008
rforatin
inating from
the extraspinal
arteries (most
in case of feeder sacrifice has previously been reported
3C Pe
Fig 7.2
.
commonly the vertebral artery). Interestingly, the location
at least once.6 In our case, this option did not seem to add
callosum
corpus
sufficient benefit since the ASA-PICA network already
of the PICA’s origin seems not only to be related to the
and the
n stem
to the brai
constitutes a natural bypass, as demonstrated by the postLSA but also to affect the origin of the ventral spinal ararteries
ting
fora
C Per
operative patency of all vessels including a retrograde flow
tery.5
Fig 7.23 osum.
call
corpus
Indeed, the well-known scheme proposed by Lasjautoward the glue cast. A distal bypass nevertheless could
nias et al.2 allows the theoretical possibility for the ASA
have a hemodynamic impact reducing the flow through
also to be the origin or co-origin of the PICA, just as the
the proximal network and the shear stress on the wall of
basilar artery regularly gives origin to the AICA.
its arteries.
1
A
ev
en
325
Fig. 2. left: Illustration summarizing
lationthe anatomical configuration observed in our case. right: DSA fusion image obtained by
ircu
overlap
of 2 separate
injections Vascuat the level of the ASA and of the bulbar artery. The PICA is supplied by the
Microcsuperselective
1. Lasjaunias P, BerensteintheA,
terBrugge
KG:
Clinical
rebral
LSACe
(double
arrowheads) fed by the ASA (double arrows) through the hypertrophic coronary vessels (dotted arrow) and by the
of the
lar Anatomyaniand
Variations.
bulbar artery Berlin:
(arrow), whichSpringer,
harbors a small2001
aneurysm (arrowhead). Only partial filling of the aneurysm is visible. Mild retrograde
zation
Org
opacificationH,
of theterBrugge
vertebral artery (asterisk)
is observed.
color online only.
2. Lasjaunias P, Vallee B, Person
K, Chiu
M: Figure is available inDisclosures
The lateral spinal artery of the upper cervical spinal cord.
cal junction and usually originates from the vertebral arAs demonstrated
by reports
this case, that
the codominant
LSA
Dr. Sourour
he is a consultant
and proctor for CoviAnatomy, normal tery.
variations,
andtoangiographic
aspects.
J
It is considered
be the result of the
embryological
cranially
directed
supply the PICA may be supplied by
dien
andtoStryker.
dominance1985
of a posterior radiculopial artery.1
the ASA through the anastomotic network of the coronary
Neurosurg 63:235–241,
The PICA usually arises from the dominance of a sinvessels. This codominant ASA supply could be either a
3. Lesley WS, Rajabgle
MH,
Case
RS:
Double
origin
of
the
postepial vessel at the level of the hypoglossal nerve. Howprimitive
variant orcontributions
the result of a postdevelopmental ocauthor
rior inferior cerebellar
artery:
association
intracranial
ever, several
variations
have beenwith
reported
in the literaclusion of a proatlantal feeder followed by hypertrophy
ture, notably
a cranial anterior
artery
of the Conception
existing coronaryand
network;
the latter
seems more
design:
Gabrieli.
Acquisition of data: Sourour.
aneurysm on catheter
angiography.
AJR inferior
Am Jcerebellar
Roentgenol
(AICA)–PICA variant or caudal proatlantal C-1 and C-2
likely to explain the features observed in our case (Fig.
Analysis
and circulation
interpretation
of data:
189:893–897, 2007
origins characterized by dominance of nearby segmental
3). Indeed,
the collateral
often develops
fromGabrieli, Clarençon. Critically
revising
article:vascular
all authors.
suchMatsushima
cases are usuallyT,associated
hypertroembryonic
arterial
systems,the
but acquired
patterns Reviewed submitted version
4. Lister JR, Rhotonlevels;
AL Jr,
Peace with
DA:a Micro1
In this case, a postphic bulbar perforator arising at the usual hypoglossal
do not of
reproduce
embryonicall
stages.
manuscript:
authors.
surgical anatomy segmental
of the posterior
inferior cerebellar artery.
developmental arrangement is more likely since multiple
level.
irregular
tortuous
feeders
point
to
the
overuse
of
the
adult
While
dominance
is
certainly
the
most
common
anaNeurosurgery 10:170–199, 1982 4
networkcorrespondence
rather than the persistence and development of
tomical form, up to 2% of cases may exhibit an unusual
5. Mercier P, Brassier
G, Fournier
D, Hentati
Pasco-Papon
codominance,
also called
a double N,
PICA
origin,3 characembryonic vessels that usually regress. Nevertheless, this
terized by 2 separate
supplying
completes
the aforementioned
A, Papon X: Predictibility
of the segments
cervical
origintheofPICA
theproper.
ante- configuration
Josephsomehow
Gabrieli,
Department
of Neuroradiology, Pitié-Salpêtrière
This condition, often underreported, is associated with
scheme and, to our knowledge, has not been previously
rior spinal artery. higher
Interv
Neuroradiol 3:283–288, 1997
Hospital, 47 Bd de l’Hôpital, Paris 75013, France. email: joseph.
aneurysm prevalence, possibly due to a regional
reported in the literature.
3
6. Mortazavi MM, Frerich
JM, Sekhardisorganization.
LN: Multiple
aneurysms
[email protected].
vascular developmental
Unfortunately,
treatment is still a challenge, since the
pr
shown. D: Glue cast after glue injection under blank road map. The removed microcatheter tip (black arrowhead) and excluded
s p. 396
Reference
aneurysm (white arrowhead) are seen. Note that also the faded white area is part of the glue cast since also the roadmap was
references
re
-W
C
B
Fig. 1. a: Pretreatment left vertebral artery DSA in lateral projection showing the bulbar artery origin (single black arrow), the ASA
origin (double black arrows), the aneurysm at the posterior medullary segment (white arrowhead), and the junction between the
andIllustration
the PICA summarizing
proper (whitethe
arrow).
b: Superselective
injection at
the ASA
arrows).
A hypertrophic
vasoFig.LSA
2. left:
anatomical
configuration observed
in the
our origin
case. of
right:
DSA(double
fusion image
obtained
by
the overlap
2 separate
superselective
injectionsvessels
at the level
of the
ASAarrow),
and of LSA
the bulbar
artery.
PICA is supplied
by thejunction (white
coronaoforiginates
from
the ASA. Coronary
(dotted
black
(double
blackThe
arrowheads),
LSA-PICA
LSA arrow).
(double arrowheads)
fed by injection
the ASA (double
the hypertrophic
(dotted
arrow)
and by was
the not possible;
c: Superselective
distally arrows)
into thethrough
bulbar artery
just beforecoronary
the gluevessels
injection,
further
navigation
bulbar
artery
(arrow),
which harbors
small aneurysm
partial filling of
the aneurysm
is visible.
Mild retrograde
only
partial
opacification
of theaaneurysm
is seen(arrowhead).
on DSA dueOnly
to intrasaccular
recumbent
stagnating
contrast
media. Bulbar artery
opacification
of thearrow),
vertebral
artery (asterisk)
is observed.LSA-PICA
Figure is available
color arrow),
online only.
origin (black
aneurysm
(white arrowhead),
junctionin(white
and microcatheter tip (black arrowhead) are
Key words:
Dissections, Internal Elastic Lamina,
Segmental vulnerability,
Lateral spinal artery , Homology
on inter-PICA communicating collaterals: case report on a
rare entity. Cureus 6:e181, 2014
7. Pasco A, Thouveny F, Papon X, Tanguy JY, Mercier P,
Caron-Poitreau C, et al: Ruptured aneurysm on a double origin of the posterior inferior cerebellar artery: a pathological
entity in an anatomical variation. Report of two cases and
review of the literature. J Neurosurg 96:127–131, 2002
This case highlights a particular anatomical arrangement, its associated aneurysmal lesion, and once again7
stresses the importance of the medullary perforating vessels, especially in cases of variations of the PICA origin.
ny
In vivo microneuroangiography
IN
7
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5
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is
ht
s
ig
Fig. 3. Schematic of the developmental pathways allowed at the craniocervical junction, depicted in the style shown in Lasjaunias
p. 396 63:235–241, 1985. left: A hypothetical insult (X) at the level of a low PICA origin. right: Postdevelopmental
eten
al.:
ceJsNeurosurg
Referhypertrophy
of the ASA (double arrows), vasocorona (arrowhead), and bulbar artery (arrow). VERT = vertebral artery. Figure is
available in color online only.
ll
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r.
A
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Autoradiogram
oh
ib
2. Pathology of arterial dissections
325
lation
crocircu
rebral Mi
the Ce
anterior spinal and bulbar artery supply to the pica
ation of
Organiz
Mizutani K. et al. BJR Case Rep 2016;2:
106
3
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.
J neurosurg April 1, 2016
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Anatomical consideration of craniocervical junction
ite
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anterior spinal and bulbar artery supply to the pica
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Sato K1.
Case 4
A 76 year-old-man presented with sudden onset of
headache and loss of consciousness.
H&H grade 2, WFNS grade 2, Fisher group 3
completely block the retrograde flow from the
contralateral VA, trapping will be most effective
to prevent rebleeding.27) However, it was reported
that higher incidence of ischemic complication was
observed in trapping than proximal occlusion. 26)
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1. Vertebral artery
VA is the most frequently affected site in IAD.
In the nationwide study of IAD in Japan, 82% of
IAD is located in VA.3) There are several treatment
strategies for VA dissection; proximal occlusion,
tio
n
Type 4
Arimura K. et
al. Neurologia
medico-chirurgica
2016
Neurol
Med Chir (Tokyo)
56, September, 2016
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Pre
Semi jail technique with Headway 21, LVIS 4.5×23mm,
Target Nano 1.5mm×2cm, Deltaplush 1.5mm×2cm
Post
He could return to his home @15th post onset.
mRS 0
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Fig. 1 Treatment strategies for vertebral artery dissecting aneurysms. An: aneurysm, EC-IC: extracranial-intracranial.
in
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A
High resolution cone beam CT
K. Arimura et al.
treatment. Mizutani demonstrated that most IAD
causing SAH bled within a few days after onset
of dissection indicated by preceding headache.15)
Since it was reported that serial angiographic
change was seen in 88.2% of unruptured vertebral
artery (VA) dissection and it may be amenable for
surgical treatment,16) a follow-up angiography should
be recommended during the early stage (within
approximately 3 weeks after onset).16,17) Moreover,
another paper reported that unruptured VA dissection had bled 4 months after onset.18) Consequently,
even unruptured IAD should be followed carefully
at least a few months by neuroimaging, and surgical
treatment may be considered if the formation or
enlargement of the aneurysmal dilatation has been
confirmed.
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Onset
Onset
Surgical Strategy @1week
1. Vertebral artery
VA is the most frequently affected site in IAD.
In the nationwide study of IAD in Japan, 82% of
IAD is located in VA.3) There are several treatment
strategies for VA dissection; proximal occlusion,
trapping (surgical or endovascular) with or without
extracranial-intracranial (EC-IC)
bypass,(coronal)
clipping or
VasoCT
wrapping of the aneurysm sac,19,20) stent-assisted
coil embolization of the aneurysm sac,21) and stent
monotherapy including the use of flow diverters22,23)
(Fig. 1). Therapeutic safety and efficacy of endovascular and surgical treatment have not been tested in
a randomized trial. Recently, endovascular (internal)
trapping is undertaken more frequently than surgical
treatment for ruptured intracranial VA dissection.24)
Although internal trapping is effective to avoid
rebleeding and less invasive, postoperative medullary infarctions remains unresolved.25)
Recent nationwide study of vertebrobasilar artery
Highthat
resolution
dissections in Japan demonstrated
craniotomy
accounted for 20% of all intervention
(including
CBCT
surgical and endovascular treatment), and trap@3the
weeks
ping was
most frequent (62.5%) procedures in
the craniotomy.26) Since proximal occlusion cannot
completely block the retrograde flow from the
contralateral VA, trapping will be most effective
to prevent rebleeding.27) However, it was reported
that higher incidence of ischemic complication was
observed in trapping than proximal occlusion. 26)
17
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Type 1 Classic dissection
20
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em
Case 5.
A 37 year-old-man presented with suboccipial and nuchal pain.
Fig. 1 Treatment strategies for vertebral artery dissecting aneurysms. An: aneurysm, EC-IC: extracranial-intracranial.
Arimura K. et
al. Neurologia
medico-chirurgica
2016
Neurol
Med Chir (Tokyo)
56, September, 2016
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uc
Pre
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ite
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trapping (surgical or endovascular) with or without
extracranial-intracranial (EC-IC) bypass, clipping or
wrapping of the aneurysm sac,19,20) stent-assisted
coil embolization of the aneurysm sac,21) and stent
monotherapy including the use of flow diverters22,23)
(Fig. 1). Therapeutic safety and efficacy of endovascular and surgical treatment have not been tested in
a randomized trial. Recently, endovascular (internal)
trapping is undertaken more frequently than surgical
treatment for ruptured intracranial VA dissection.24)
Although internal trapping is effective to avoid
rebleeding and less invasive, postoperative medullary infarctions remains unresolved.25)
Recent nationwide study of vertebrobasilar artery
dissections in Japan demonstrated that craniotomy
accounted for 20% of all intervention (including
surgical and endovascular treatment), and trapping was the most frequent (62.5%) procedures in
the craniotomy.26) Since proximal occlusion cannot
completely block the retrograde flow from the
contralateral VA, trapping will be most effective
to prevent rebleeding.27) However, it was reported
that higher incidence of ischemic complication was
observed in trapping than proximal occlusion. 26)
CT on admission
-W
IN
od
uc
tio
n
S
em
in
a
r.
A
Surgical Strategy
1. Vertebral artery
VA is the most frequently affected site in IAD.
In the nationwide study of IAD in Japan, 82% of
IAD is located in VA.3) There are several treatment
strategies for VA dissection; proximal occlusion,
ny
K. Arimura et al.
treatment. Mizutani demonstrated that most IAD
causing SAH bled within a few days after onset
of dissection indicated by preceding headache.15)
Since it was reported that serial angiographic
change was seen in 88.2% of unruptured vertebral
artery (VA) dissection and it may be amenable for
surgical treatment,16) a follow-up angiography should
be recommended during the early stage (within
approximately 3 weeks after onset).16,17) Moreover,
another paper reported that unruptured VA dissection had bled 4 months after onset.18) Consequently,
even unruptured IAD should be followed carefully
at least a few months by neuroimaging, and surgical
treatment may be considered if the formation or
enlargement of the aneurysmal dilatation has been
confirmed.
ev
en
518
ny
B
re
C
pr
AICA
ed
20
17
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-A
A
PICA
ht
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ar
.
A
mRS 0@30day post op.
17
©
A
B
C
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IN
S
em
Case 6.
A 60 y/o female has presented her nuchal and occipital
headache for a couple of days.
She consulted a neurologist in regional hospital, but was not
diagnosed as a SAH.
Afterwards, she presented with more severe headache and
vomiting.
An emergency CT showed a massive SAH mainly distributed at
the level of cerebello-medullary and prepontine cistern.
20
ve
n
Arimura K. et
al. Neurologia
medico-chirurgica
2016
Neurol
Med Chir (Tokyo)
56, September, 2016
s
Rt.PICA extracranial origin, Lt.PICA-AICA
Fig. 1 Treatment strategies for vertebral artery dissecting aneurysms. An: aneurysm, EC-IC: extracranial-intracranial.
re
se
rv
PICA
CT on admission (H&K grade IV,WFNS grade 4)
CT on admission H&K grade IV
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Final View
pa
rt
is
Lt.PICA
Rt.PICA
ev
en
in
Rt.VA
ASA
tio
n
Rt.V4 trunk is indeed hypoplastic
but bilateral PICA originate symmetrically. →ASA and
145
medullary perforators come from symmetrically.
Lateral
2794488
pr
is
pa
rt
Although left VA is hypoplastic, dominant ASA
and anterior medullary perforators are
originating from left side.
Note the dominancy of PICA
Frontal
Mercier P. et al. INR 2008
Left VAG （post embolization）
ev
en
in
When something is small, it doesn’t have to mean
that it is not important.
in
a
r.
A
ll
r
ig
ht
s
re
Rt.AICA-PICA
The Galerie de paléontologie et d'anatomie comparée in Paris
2010/11/29
@1 year post Op.
s
mRS 0
rig
ht
2010/10/02
H&H grade IV
Infratentorial arterial system
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20
17
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Cortical territory of cerebellar hemisphere
A
ll
Summary
em
in
ar
.
1. There are two major factors as the susceptibility to dissection
of VA.
・Kinetic motion factor at the level of atlantoaxial joint.
・Anatomical fragility of the intracranial V4 portion and PICA
-W
IN
S
corresponding to the vasa corona as the homology of lateral
spinal artery.
C
2. Functional vascular anatomy is the key to indicate the proper
management and decision making.
A
©
3. Sophisticated imaging technologies (e.g.high resolution
CBCT) can provide in vivo microneuroangiography.
17
More you see in detail,
more you are fascinated.
B
→ Anatomical disposition is the message to predict the
important perforators.
20
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Frontal
Thank you…

第22回 流体科学におけるバイオ・医療に関する講演会

International Journal of Computer Theory and Engineering

Uterine Fibroid Embolisation (UFE)*

2세대 약물 용출 관상동맥 스텐트 삽입 후 급성 심근 경색으로 병발한

An unusual variation of vertebral artery

NUMERICAL SIMULATIONS OF ARTERIES WITH AN ADAPTIVE

Sonazoid 造影超音波を用いた肝臓の組織進展度診断

Saccular Aneurysm of the External Jugular Vein: A Case Report

《鈍的脳血管損傷（とくに頚椎損傷にともなう椎骨動脈損傷）について