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AB
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
Fig. B25.1 MR FLAIR images, axial plane. (A) Multiple right hemi-
spheric signal abnormalities, consistent with a large basal ganglia
ischemia and anterior and external border zone infarction (arrow).
(B) Internal border zone infarction at the cella media level (arrow) in
addition to partial inhomogeneous territorial MCA infarction. (Courtesy of Dr. Schröter, Radiologische Praxis am Krankenhaus Rüdersdorf, Rüdersdorf, Germany.)
389Clinical Course (1)
Fig. B25.2 DSA, right ICA injection, posteroanterior view. High-
grade right M1-MCA stenosis (arrows). Note the concomitant fi lling
of the fetal-type PCA (single arrow). (Courtesy of Dr. Schröter, Radiologische Praxis am Krankenhaus Rüdersdorf, Rüdersdorf, Germany.)
AB
Fig. B25.3 MR FLAIR image, axial plane. (A) Shrunken ischemic
l e s i o n s i n t h e r i g h t h e m i s p h e r e . E n l a r g e d r i g h t f r o n t a l h o r n , s e c o n d ary to the adjacent ischemic defect. (B) Mildly enlarged ventricles.
Note the residual external anterior border zone infarction (arrow).
left MCA. There were no signs of vasculitis or fi bromuscular
dysplasia (Fig. B25.12, Fig. B25.13, Fig. B25.14).
Clinical Course (1)
The new transient ischemic event was thought to be of
hemodynamic origin. The pathogenesis of the progressive right M1-MCA stenosis was unclear. A cardiac or
artery-to-artery embolism was unlikely. Thrombophilia,
vasculitis, and autoimmune disease had been ruled out.
The young age of the patient, the rapid progression of
the stenosis, and the normal vessel wall fi ndings in the
ICA-L
Fig. B25.4 Extracranial duplex, longitudinal plane. Normal fl ow
s i g n a l i n t h e l e f t I C A ( fl ow velocity 45/21 cm/s). Note a normal pul-
satility index (PI) of 0.84.
e x t r a c r a n i a l c a r o t i d a r t e r i e s a r g u e d a g a i n s t a t h e r o s c l e rotic stenosis despite the presence of multiple vascular
risk factors. Moyamoya disease was discussed but seemed
unlikely because of the rapid progression of vessel disease
and the spared terminal ICA on both sides.
Xenon CT following acetazolamide infusion revealed
diminished cerebrovascular reactivity (CVR) on the
e ff ected side. Because of the rapid progression and
the recurrent symptoms as well as the limited hemodynamic reserve, an extracranial–intracranial superior
temporal artery (STeA)–MCA bypass was performed
and long-term stroke prevention with clopidogrel was
continued.
390 Case 25 Progressive Right M1 Middle Cerebral Artery Occlusion Treated with Extracranial–Intracranial Bypass Surgery
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
ICA-R
Fig. B25.5 Extracranial duplex, longitudinal plane. Normal fl ow
signal in the right ICA (fl ow velocity 49/34 cm/s). Note a normal
PI of 0.76.
M1-MCA-R
M1-MCA-L
Fig. B25.6 TCCS (tr anst emporal appro ach) , left -sided insonati on,
midbrain plane. Mildly increased and turbulent fl ow in the left
M1-MCA (fl ow velocity 181/83 cm/s).
A1-ACA-L
Fig. B25.7 TCCS (t rans tempo ral approach) , right -sid ed in sona tion,
midbrain plane. Severely reduced fl ow without turbulence in the
right M1-MCA over all his length (arrows) (fl ow velocity 17/10).
A1-ACA-R
Fig. B25.9 TCCS (t rans tempo ral approach) , right -sid ed in sona tion,
midbrain plane. Strong fl ow signal in the right A1-ACA, indicating
leptomeningeal collateralization (fl ow velocity: 156/84).
Fig. B25.8 TCCS (tr anst emporal appro ach) , left -sided insonati on,
midbrain plane. Normal fl ow in the left A1-ACA (fl ow velocity
110/68 cm/s).
P2-PCA-L
Fig. B25.10 TCCS (trans temp oral ap proa ch), left-s ided ins onati on,
midbrain plane. Normal fl ow signal in the left proximal P2-PCA
(fl ow velocity 61/25 cm/s).
P2-PCA-R
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
Fig. B25.11 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Increased fl ow in the right proximal P2-
PCA, indicating leptomeningeal collateralization (fl ow velocity
105/57 cm/s).
391Follow-up Neurosonologic Findings (10 Months)
Fig. B25.12 DSA, right ICA injection, posteroanterior view. Near-
oclusion of the right M1-MCA corresponding to the site of stenosis
seen 1 year before in Fig. B25.2 (arrow). Note the residual fl ow signal
in the distal M1-MCA and M2-MCA (arrows). Note also the leptomeningeal collaterals from the ACA and PCA (arrowheads).
Fig. B25.13 DSA, right ICA injection, lateral view. Markedly reduced
contrast fi lling of the right MCA (arrows). There was no circum-
scribed vessel narrowing seen. Note the fetal-type PCA (arrowhead).
Clinical Course (2) and Follow-up
Neuroradiologic Findings
DSA immediately after surgery showed patent collateral
vessels (not shown). Cerebral CT revealed no intracranial
bleeding and no new ischemic brain lesion (not shown).
Three months later the patient presented with a new TIA
aff ecting the contralateral side with sensory disturbances
in the right arm and additional headaches. Cerebral MRI
showed no evidence of new ischemic lesions but revealed
a chronic right frontal subdural hematoma. MR angiography (MRA) was indicative of an occlusion of the right
M1-MCA segment and a mild stenosis of the left M1-MCA
segment (Fig. B25.15). Clopidogrel was stopped and the
hematoma successfully treated by a burr-hole craniotomy. A follow-up CT after surgery was unremarkable.
Fig. B25.14 DSA, left ICA injection, posteroanterior view. In contrast with the TCCS fi ndings there is no visible vessel narrowing of
the left M1-MCA.
Follow-up Neurosonologic Findings
(10 Months)
Extracranial Duplex Sonography
Again, all extracranial signals were normal (not shown).
Transcranial Duplex Sonography
The systolic fl ow velocity of the left M1-MCA segment
remained slightly increased (176 cm/s). Again, mildly
raised fl ow velocities were observed in the right-sid-
ed A1-ACA segment and the main stem of the PCA,
suggestive of leptomeningeal collateral function. No
fl ow was detected within the right M1-MCA segment
in spite of the optimal insonation conditions (low PRF,
392 Case 25 Progressive Right M1 Middle Cerebral Artery Occlusion Treated with Extracranial–Intracranial Bypass Surgery
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
DMCV-R
Fig. B25.15 Small image: MR T2-weighted image, axial plane.
Chronic right frontal subdural hematoma. Large image: 3D TOF-
MRA, coronal maximal intensity projection (MIP). Missing right MCA
signal, suggesting occlusion. Circumscribed signal intensity reduction in the left proximal M1-MCA indicative of stenosis (arrowhead).
Also note the bilateral A1-ACA segment narrowing—a clear diff eren-
tiation between artifact and real stenosis is not possible.
high color gain) through the right-sided trepanation defect. A venous signal was present in the lateral fi ssure
only, corresponding with the deep middle cerebral vein
(Fig. B25.16). A normal fl ow signal was seen in the main
stem of the right STeA. The STeA–MCA bypass could not
be visualized (not shown).
Conclusion
Further progression of the right-sided MCA pathology
now considered as main-stem occlusion with leptomeningeal collateral blood fl ow from the ACA and PCA.
Unchanged mild stenosis of the left proximal M1-MCA
segment. Occlusion of the right STeA–MCA bypass.
Clinical Course (3)
A follow-up DSA was performed, which confi rmed
the occlusion of the STeA–MCA bypass as well as the
complete occlusion of the right M1-MCA segment (not
shown). As the patient had now remained stable, no
second bypass operation was planned. Because of the
contralateral transient brain ischemia, progression of
right-sided MCA pathology, and the failure of stroke
prevention with clopidogrel, oral anticoagulation with
phenprocoumon was started. During the clinical and
MRI follow-up over 2 years, no new ischemic event was
reported.
Fig. B25.17 shows a schematic of the patient’s extra-
and intracranial brain-supplying arteries.
Final Diagnosis
Recurrent cerebral ischemia in both MCA territories
caused by a progressive right MCA stenosis with secondary occlusion and stable mild stenosis of the left M1-MCA
Fig. B25.16 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Insonation of the right deep middle cerebral
vein which parallels the course of the M1-MCA. Note the absent
fl ow signal of the right M1-MCA.
RL
Fig. B25.17 Schematic of the patient’s extra- and intracranial
brain-supplying arteries. Right M1-MCA occlusion and left M1-MCA
stenosis (circles). Collateralization of the right MCA territory via
leptomeningeal collaterals from the right ACA and right PCA (red
arrows). Note the right fetal-type PCA.
segment of unknown origin. Secondary occlusion of the
right-sided STeA–MCA bypass.
Discussion
Clinical Aspects
This patient was a 31-year-old woman who had recurrent cerebral ischemia because of bilateral MCA stenosis. The right side demonstrated rapid progression
and subsequent occlusion. The etiology of the stenosis remained unclear, although the patient had a positive vascular risk profi le. However, her young age, the
dynamic progression, and the absence of extracranial
393Discussion
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
atherosclerosis argued against an intracranial atherosclerotic origin. Other vasculopathies were considered
but diagnostic tests for these were negative (for further
reading on nonatherothrombotic stroke in young people,
see also Case 5, Case 6, Case 14, and Case 31). Moyamoya
disease was considered but seemed unlikely because of
the ICA-sparing pattern and of the fast progression of the
disease (for further discussion on moyamoya disease, see
also Case 9).
The rapid progression of vessel narrowing, recurrent ischemia despite medical treatment, and the impaired CVR
diagnosed by acetazolamide xenon CT led to the decision
to perform an EC–IC bypass operation. An impaired CVR
increase is known to increase the risk of ipsilateral annual
stroke recurrence up to 30% (Garett et al 2009). Also, it has
been shown that an EC–IC bypass improves or even normalizes an altered CVR (Anderson et al 1992, Baron et al
1981, Gibbs et al 1987, Hirai et al 2005, Schmiedek et al
1994). Bypass surgery may also ameliorate a previously
diminished CBF. Postsurgical baseline CBF increased significantly, from 595 ± 89 mL/min by 78 ± 43 mL/min, measured with phase-contrast MRI (Neff et al 2004).
EC–IC bypass surgery was introduced in 1967 but has
been controversial since the EC–IC Bypass Study was
published in 1985. This study demonstrated that EC–IC
bypass in patients with symptomatic high-grade ICA,
high-grade MCA stenosis, or occlusion did not yield better results than the best medical treatment (EC/IC Bypass
Study Group 1985). A total of 1,377 patients were included in this trial, of whom 714 were treated medically
and 663 surgically. The technical results of the surgical
interventions were good, as 96% of all bypasses remained
patent. The dominant vascular pathology in the surgical
group was extracranial ICA occlusion in 58.1%, of whom
64% were asymptomatic since the fi rst event. The remain-
ing patients presented with recurrent cerebrovascular
events. A distal extracranial ICA stenosis was present in
15.4% and 14.4% had MCA stenosis and 12.1% MCA occlusion. The observed 30-day surgical mortality and major
stroke morbidity rate was 0.6% and 2.5%, respectively.
Fatal and nonfatal strokes occurred signifi cantly more
often and earlier in the surgery group. When perioperative strokes were included, surgery led to a 14% increase
in relative risk of fatal and nonfatal stroke. In particular,
patients with recurrent ischemic events and MCA stenosis revealed less favorable clinical outcomes. Functional
outcome comparison between both groups after a mean
observation period of 3.5 and 3.8 years was similar, however: 31% in the surgical arm and 29% in the medical arm.
Subsequently, EC–IC bypass surgery was largely abandoned and only a few specialized centers still have the
expertise to perform this type of operation.
A comprehensive review in 2010 confi rmed the results
of the EC–IC Bypass Surgery trial (Fluri et al 2010). An
analysis of data from 21 studies including a total of 2,591
patients indicated that the operation did not yield benefi ts
in terms of the outcome parameters (stroke, death, and
functional independence). The Japanese EC–IC Trial (JET)
recruited patients with impaired cerebral hemodynamics assessed by acetazolamide single photon emission CT
(SPECT) assessment and randomized patients into a surgical and a medical/conservative group. However, the trial
failed to demonstrate a benefi t in surgically treated pa-
tients in terms of the primary outcomes of death from all
causes and any stroke (Ogasawara and Ogawa 2006).
The American Carotid Occlusion Surgery Study (COSS)
did not show superiority of EC–IC treatment in patients
with ICA occlusion. Patients were included if hemodynamic impairment was present, measured by a PETderived increased oxygen extraction fraction (OEF). The
increased OEF allows metabolism to be maintained if CBF is
decreased, before cerebral ischemia develops. All patients
in the COSS study had a symptomatic carotid occlusion
with ischemic stroke or TIA within the last 120 days prior to inclusion. Patient characteristics, antithrombotic
therapy, and risk factors were similar in both treatment
arms. Following an interim analysis of 195 patients, the
trial had to be stopped for futility. Although interventions
were performed successfully and OEF values improved
after surgery, the clinical outcome did not diff er between
both groups. The combined risk of perioperative stroke,
death, and following ipsilateral stroke after 2 years was
21% in the bypass group and 22.7% in the medically treated group. The 30-day risk of ipsilateral stroke was 14.4%
and 2%, respectively (Powers et al 2011).
The following points have to be considered as explanations for the above negative fi ndings. In the medically
treated group, the primary endpoint risk was 22.7% for
2 years rather than the calculated 40% that had been assumed on the basis of the available data (Derdeyn et al
2000, Grubb et al 1998). A similar phenomenon was
observed in the SAMMPRIS trial, where conventionally treated patients performed considerably better than
expected. Better medical control of vascular risk factors
and the use of statins, which are postulated to improve
CVR and to improve collateral function, have been considered as the underlying explanation (Forteza et al 2012,
Ovbiagele et al 2007). Corresponding to this hypothesis,
patients in the COSS study showed very good treatment
compliance concerning the antithrombotic therapy (94%),
68% had good LDL cholesterol control, and 46% had follow-up blood pressure levels <130 mm Hg. Another factor
possibly contributing to the negative COSS result could be
patient selection, which was based on PET-determined
OEF alterations in the aff ected hemisphere. Criticisms
are that this parameter does not reliably identify a hemodynamic compromise and that the technique does not
consider the regional aspects of hypoperfusion (Bang
et al 2008a, Carlson et al 2011). Also, it remains unclear
whether the OEF was really a suitable inclusion criterion,
as it has rarely been used for CVR assessment and never
formally compared with well-established methods such
as ultrasound-derived vasomotor reactivity testing.
Known postoperative complications of EC–IC bypass
surgery other than ischemia are subdural hygroma and
hematoma, epidural hematoma, seizures, and meningitis.
Other unwanted events may occur which do not necessarily increase the morbidity: for example, a secondary
bypass occlusion, occurring in ~5–10% of cases, or a secondary MCA occlusion in cases where high-grade MCA
stenosis was the indication for the bypass operation. Our
patient had both complications. Although the underlying reason is unclear, the bypass occlusion may have
been facilitated by the cessation of antiplatelet therapy
394 Case 25 Progressive Right M1 Middle Cerebral Artery Occlusion Treated with Extracranial–Intracranial Bypass Surgery
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
at the time of surgery for the subdural hematoma. Two
explanations are possible for the MCA occlusion during
follow-up. The occlusion might have been caused by a
bypass-induced reduced perfusion pressure at the site of
the stenosis. This mechanism had already been considered to be one of the reasons for the poor outcome in the
MCA stenosis patients in the EC–IC bypass study. Alternatively, in our case the MCA occlusion might also have
been the natural course of the primary vascular disease.
In summary, considering the complication rates of
the operation on one hand and the low complication and
event rates in the medically treated patients on the other
hand, a routine recommendation for EC–IC bypass surgery
cannot be given on the basis of the currently available
data. For further reading on EC–IC bypass surgery, see
also Case 9 and Case 28).
Angiologic and Anatomic Aspects
The initial ultrasound fi nding in the right-sided M1-MCA
segment was interpreted as a near-occlusion. This was
based on the coexistence of a long-segmented M1-MCA
color-mode signal and the low fl ow pattern with a fl ow
velocity of 17/10 cm/s. In contrast with the well-defi ned
near-occlusions in the extracranial ICA, there are no clear
recommendations regarding the intracranial circulation.
Similar to the fl ow dynamics in extracranial ICA, it can
be assumed that fl ow velocity increases up to a diameter
reduction of ~80% only. A further increase will then lead
to a breakdown of perfusion pressure, subsequent reduction of fl ow and fl ow velocity, and fi nally vessel occlusion.
R e d u c e d fl ow velocities may, according to the physics of
fl ow, also be found in less severe long- segmented stenoses.
This might be an alternative explanation of the transcranial color-coded duplex sonography (TCCS) fi nding in our
patient (for further discussion on near- occlusion of the
MCA see also Case 30; for further discussion on nearocclusion of the extracranial ICA see also Case 15).
The evaluation of the contralateral, clinically symptomatic, left-sided M1-MCA segment by diff erent
techniques yielded ambiguous results. Ultrasound analysis demonstrated a mild turbulence and a mildly raised
non-angle-corrected fl ow velocity of 183/83 cm/s, in-
terpreted as a low-grade stenosis which could not be
confi rmed by DSA. On follow-up TCCS again, M1-MCA
stenosis was diagnosed and was then further supported
by time-of-fl ight (TOF)-MRA fi ndings. M1-MCA systol-
ic fl ow velocities between 155 cm/s and 220 cm/s have
been reported to correlate well with stenoses <50% diagnosed by DSA, with sensitivity, specifi city, and positive
and negative predictive values of 94%, 100%, 95%, and
100%, respectively (Baumgartner et al 1999). The mean
value of M1-MCA stenosis in this study measured by DSA
was 36.8%. The question therefore arises whether DSA is
sensitive enough to detect low-grade intracranial stenoses in all instances. As a mild stenosis might be eccentric in location, it might not be appropriately visualized in
standard posteroanterior and lateral projections. In addition, superior sensitivity for CTA in posterior circulation
steno-occlusive disease as compared with DSA has been
reported when low fl ow was present (Bash et al 2005).
Ultrasound and TOF-MRA are both fl ow-sensitive meth-
ods. Ultrasound fl ow velocities are directly related to the
square of the vessel diameter and are therefore particularly sensitive for low-grade stenoses. TOF-MRA regularly
overrates the grade of stenosis and therefore often cannot
be used for stenosis graduation; however, it is helpful as
a screening method. Its major limitation is the inability to confi dently distinguish a real low-grade stenosis
from the frequently observed artifacts suggesting vessel
narrowing. Yet, when using 3-T scanning, 3D TOF-MRA
performed comparably to CTA for extracranial vessel
a s s e s s m e n t o f E C – I C b y p a s s e s i n m o y a m o y a p a t i e n t s , a n d
was even superior for the intracranial vessel segment (Q.
Chen et al 2014). Comparing TCD, TOF-MRA, and DSA
the highest correlation was seen in TCD and MRA when
analyzing MCA stenoses (Röther et al 1994). Six stenoses
diagnosed by TCD and MRA were not demonstrated by
DSA in this study. It therefore seems that there is a risk of
overlooking low-grade MCA stenoses with routine DSA,
especially in standard biplanar imaging.
During follow-up, our patient developed a total
M1-MCA occlusion, demonstrated by the absent arterial
signal. Diff erentiating near-occlusion might be diffi cult,
but in our case occlusion was beyond doubt. The skull
bone defects resulting from the bypass operation yielded
optimal transtemporal insonation conditions, permitting
an excellent view of the lateral fi ssure where the main
stem of the MCA is located. Instead of the MCA, only a
low fl ow signal away from the probe and attributable to
the deep middle cerebral vein was detected. Visualization
of accompanying veins in cases of absent arterial fl ow sig-
nals may also be used in other locations as a diagnostic
aid to confi rm occlusion: for example, the vertebral vein
may be visible in extracranial vertebral artery (VA) occlusion and the basal vein of Rosenthal in cases of intracranial PCA occlusion (see also Chapter 5, “PCA Occlusion”
under “Intracranial Pathology,” and Case 39).
Main-stem MCA occlusions may lead to fl ow reduction
in the extracranial ICA in the form of a reduced fl ow ve-
locity and mildly increased pulsatility. This was not the
case in our patient because of the presence of an ipsilateral fetal-type PCA. In this constellation the ICA supplies
the ACA and PCA, both also working as collateral vessels
supplying the MCA territory, which explains why the
fl ow signal of the extracranial ICA was not altered. As a
fetal-type PCA is present in ~10–15% of subjects, such a
constellation can be regarded as an exception. In most
cases, reduced fl ow velocity and mildly increased pulsa-
tility in the extracranial ICA is highly indicative of a distal
obstruction of the proximal MCA or distal ICA (see also
Fig. A5.98). In our patient, TCCS could not visualize the
posterior communicating artery (PCoA) directly. Because
of the normal fl
, a prominent P
er
ow pattern of the extracranial ICA, howev-
CoA was assumed to be present, which
was later confi rmed by DSA. In case of doubt, the tap test
can be used to verify a fetal-type PCA (for further details
about the tap test, see also Chapter 2, “Posterior Communicating Artery” under “Special Arterial Anatomy and
Ultrasound Anatomy”).
Finally, ultrasound bypass evaluation should be
discussed. We recommend fi rst gently palpating the
proximal STeA and following the vessel course toward
the trepanation defect. Using TCCS, the main stem of
395Discussion
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
the STeA and the bypass can then be insonated directly. In patients with extracranial ICA occlusion and a
well-functioning bypass, the M2-MCA branches and
even the M1-MCA segment itself may show a retrograde
fl ow. On brief STeA compression, fl ow decreases or even
ceases completely. A less patent bypass may lead only
to partial, peripheral retrograde MCA blood fl ow while
the M1-MCA segment continues to have compromised
antegrade fl ow (Umemura et al 2002). A well-operating
bypass can also be recognized by a raised fl ow velocity
and reduced pulsatility within the STeA (Arakawa et al
2003, Inoue and Fujimoto 2005).
Most relevant, however, is the resulting blood
v o l u m e fl ow as a direct marker of CBF. The question
of how much blood can be contributed via the bypass
is, for example, defi ned by the size of the donor and
r e c i p i e n t v e s s e l s a s w e l l a s b y t h e d e g r e e o f t h e a c t u a l
h e m o d y n a m i c i m p a i r m e n t . K e e p i n g t h i s i n m i n d , d o n o r
and recipient vess els should have a diameter of at least
1 mm. A phase-contrast MRI study reported volume
fl ow levels of 84 ± 32 mL/min (range 14–177 mL/min)
within the bypasses analyzed (Neff et al 2004). Assuming
a mean volume fl ow of 150–200 mL/min carried by the
MCA in healthy individuals, a bypass may therefore be
able to provide the necessary volume fl ow of the total
MCA territory. This goal is probably rarely achieved. However, providing even 50% of the MCA territory blood fl ow
r e q u i r e m e n t s m i g h t b e s u ffi cient for clinical stabilization
if additional leptomeningeal collateral fl ow is present.
Ultrasound measurements of the STeA blood volume fl ow
in bypass patients have not yet been reported.
The CTA technique does not permit direct volume
fl ow measurements but may clearly visualize the
i n t e g r i t y a n d c a l i b e r ( s e e a l s o Fig. 9.19), as well as
p o t e n t i a l s t e n o s e s o f t h e b y p a s s ( T e k s a m e t a l 2 0 0 4 ) . I n
addition, CT perfusion may be performed to assess the
p a r e n c h y m a l p e r f u s i o n s t a t u s a s t h e p r i m a r y t h e r a p e u tic target of bypass surgery.
396
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
Case 26
Extracranial Left Vertebral Artery Dissecting Aneurysm
Following Basilar Artery Stenting
Clinical Presentation
A 58-year-old man was admitted to a district general
hospital with right-sided sensorimotor hemisyndrome
and dysarthria. Several weeks earlier he had complained
of transient vertigo and a gait disorder. The patient had
known vascular risk factors of arterial hypertension, hypercholesterolemia, and diabetes mellitus. On admission
he presented fl uctuating symptoms with a moderate pro-
portional hemiparesis, hemihypesthesia on the right side,
and dysarthria (National Institute of Health Stroke Scale
[NIHSS] score: 7).
Initial Neuroradiologic Findings
The initial cerebral CT scan showed hypodensities in
both cerebellar hemispheres and a small hypodense area
in the right pons consistent with subacute infarction
(Fig. B26.1). Diff usion-weighted MRI revealed acute left
paramedian pontine ischemia (Fig. B26.2) MR angiography (MRA) was not performed.
Suspected Diagnosis
Recurrent ischemia in the vertebrobasilar artery territory suspicious of basilar artery (BA) pathology (plaque,
stenosis, or thrombosis).
Conventional Angiography
Digital subtraction angiography (DSA) demonstrated a
high-grade stenosis in the middle segment of the BA. The
vertebral and carotid arteries were normal (Fig. B26.3).
new ischemic lesions (Fig. B26.4). Secondary stroke prevention was commenced with aspirin and clopidogrel and
the patient was referred to a rehabilitation center. By this
stage there had still not been any neurosonologic examination.
Two we ek s a ft er th e s ten ti ng , t he pat ie nt ha d a
t r a n s i e n t i s c h e m i c a t t a c k ( T I A ) w i t h d o u b l e v i s i o n
and a left-sided hemiparesis that lasted a few hours.
F u r t h e r m o r e , t h e r e s i d u a l r i g h t - s i d e d h e m i p a r e s i s a n d
the dysarthria mildly worsened. The patient was then
admitted to our department for the fi rst time.
Questions to Answer by Ultrasound
Techniques
• Was there restenosis or occlusion of the stented BA?
• Was there evidence of an embolic source in the verte-
brobasilar system?
Initial Neurosonologic Findings (Day 1)
Extracranial Duplex Sonography
B-mode imaging of the carotid arteries showed moderate atherosclerotic vascular changes, more pronounced
in the carotid bifurcation. Doppler spectrum analysis
demonstrated normal fi ndings. The left VA showed a
marked increase in caliber in the V2-VA segment at the
vertebral level between C5 and C6 with a maximal diameter of 10.5 mm in B-mode and color-mode imaging. The
diameter of the V1-VA segment was 5.5 mm. A constant
diameter ranging from 4.3 mm to 4.5 mm was seen in all
segments of the right VA. The Doppler spectrum analysis demonstrated normal fl ow signals in the left middle
and distal V2-VA segment as well as in the right V2-VA
segment (Figs. B26.5–B26.10, see also Video
B26.1).
Clinical Course (1)
In view of the remitting clinical symptoms, and the lesions on MRI, interventional percutaneous transluminal
angioplasty of the BA followed by stent implantation was
performed via the left vertebral artery (VA). This was
technically and clinically successful and a follow-up CT
scan showed a patent BA without evidence of bleeding or
Transcranial Duplex Sonography
Transtemporal insonation yielded normal fi ndings in
the anterior (ACA), middle (MCA), and posterior (PCA)
c e r e b r a l a r t e r i e s o n b o t h s i d e s . T r a n s f o r a m i n a l i n s o n a t i o n
demonstrated normal fl ow signals in the BA and the
intracranial segment of both VA (not shown).
Conclusion
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
Suspected left VA dissection with formation of a dissecting aneurysm in the proximal V2-VA segment at the
C5/C6 level. There were no signs of detectable restenosis
in the stented BA.
Cranial CT and CT Angiography (Day 1)
Cranial CT confi rmed the known cerebellar and pontine in-
farctions. In addition, a new paramedian pontine infarct of
moderate size was seen on the right side adjoining the BA
stent (Fig. B26.11). CT angiography (CTA) confi rmed the wid-
ening of the left V2-VA segment between C5 and C6 which
was diagnosed as a VA dissecting aneurysm (Fig. B26.12).
Clinical Course (2)
The VA dissection was thought to be of iatrogenic origin,
generated during the initial DSA with BA stent implantation.
The recent pontine infarction was attributed to a stent-related secondary occlusion of a perforating artery. An embolic event, potentially originating from the aneurysm, could
not be excluded but seemed unlikely because of the infarct
location. Nonetheless, oral anticoagulation with phenprocoumon was started and the patient was again referred to a
rehabilitation center. He was then lost to follow-up.
397Final Diagnosis
Fig. B26.1 Unenhanced cranial CT, axial plane. Hypodensities in
the right cerebellar hemisphere and a small right-sided hypodense
area within the pons suggestive of non-acute stroke (arrows). Note
the enlarged BA (arrowhead).
Final Diagnosis
Primary left-sided pontine infarction and old right-sided
pontine and cerebellar infarctions caused by BA stenosis
of assumed atherosclerotic origin. Secondary right-sided
pontine infarction after successful BA stenting, probably
induced by secondary occlusion of a pontine perforator
artery within the stented region or by artery-to-artery
embolism from left V2-VA dissecting aneurysm.
Fig. B26.2 MRI, apparent diff usion coeffi cient (ADC) map, axial
plane. Acute left-sided paramedian pontine ischemia (arrow).
398 Case 26 Extracranial Left Vertebral Artery Dissecting Aneurysm Following Basilar Artery Stenting
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
Fig. B26.3 DSA, left VA injection, posteroanterior view. High-grade
stenosis in the middle segment of the BA (arrow).
V1-VA-L
Fig. B26.5 Extracranial duplex, longitudinal plane (B-mode). Left
V1-VA diameter 5.5 mm.
Fig. B26.4 Intracranial CTA, 3D reconstruction showing BA after
stenting (arrows).
V2-VA-L
Fig. B26.6 Extracranial duplex, longitudinal plane (B-mode): Left
V2-VA dilatation between the transverse processes of C5 and C6
(encircled by arrows) with a diameter of 10.5 mm (white dotted
line) suggestive of dissecting aneurysm.
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