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Fig. B21.17 DSA, right common carotid artery (CCA) injection,
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.
posteroanterior view. Filling of both PCAs (arrowheads) from the
right ICA via the PCoA.
359Discussion
Fig. B21.18 DSA, right ICA injection, lateral view. Retrograde fi lling
of the distal BA (single arrow) and SCA (arrows) via a strong PCoA
(arrowhead).
There are no well-established therapeutic guidelines
for intracranial dissections. Because of the increased
risk of intracranial bleeding, anticoagulation is usually
not performed. In dissecting aneurysms with or without
SAH, anticoagulation is contraindicated. In ischemia of
suspected thromboembolic origin, antiplatelet therapy is
recommended (Schievink 2001). Experience with endovascular therapeutic approaches is rather limited and of
questionable benefi t in BA dissection up to now (Li et al
2015). Interventional strategies such as stent implantation or proximal vessel occlusion in the anterior and posterior circulation have been reported. However, stenting
should be reserved for patients who, despite suffi cient
medical treatment, have episodes of recurrent ischemia
and in whom a hemodynamic etiology is proven (Kim et
al 2015). For further discussion on intracranial stenting,
see also Case 5 and Case 26.
Contrary to previous assumptions, patients with intracranial dissection usually have a good clinical outcome.
As in extracranial dissections, an intramural hematoma
and thrombus formation occurs which subsequently
leads to embolism. This is then followed by a repair phase.
Accordingly, single cases of vascular pathology remission
(e.g., of thrombosis in an associated aneurysm) have been
reported. However, as intracranial vasa vasorum are less
well developed, the repair processes might be less eff ec-
tive (Chen and Caplan 2005). In contrast to extracranial
dissections, which reopen over time in most cases, only
scarce positive data are available for intracranial dissections (Ohkuma et al 2003). A small study in intracranial
VA dissection reported complete vessel restitution in four
of six patients (Kitanaka et al 1994a).
As in extracranial imaging, MRI can be used in the diagnosis of intracranial dissections to visualize the intramural hematoma. Instead of fat-saturated 2D T1-weighted
LR
Fig. B21.19 Schematic of the patient’s extra- and intracranial
brain-supplying arteries. Mid-basilar occlusion (large circle) and left
P1-PCA stenosis (small circle). Collateral blood fl ow toward both
PCAs and into the distal BA via the right PCoA.
axial spin echo images, 3D T1-weighted fast spin echo
sequences with variable fl ip angles (proprietary names
VISTA, SPACE, or CUBE) have been recommended. These
combine comprehensive neck coverage, high spatial resolution, fat saturation, and black-blood eff ect (Edjlali et
al 2013). Distinguishing between a dissecting aneurysm
without SAH and a true aneurysm can be diffi cult. In
these cases, serial follow-up studies may be of help.
In our patient, the unusual onset of headaches several
days prior to stroke and the severe mid-basilar stenosis
comprising an intima fl ap were indicative of an isolated
spontaneous BA dissection. Because of the assumed high
360 Case 21 Mid-basilar Artery Occlusion Due to Intracranial Dissection
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.
embolic risk, and after exclusion of SAH and dissecting
aneurysms, we decided on initial intravenous PTT-guided
heparinization. During this treatment a secondary BA occlusion occurred (for reading on BA occlusion, see Case 8).
A potential explanation for this phenomenon could be an
increase of the intramural hematoma, possibly facilitated
by the anticoagulation. A similar course was observed in
two of our other reported cases with extracranial ICA dissection (see also Case 11 and Case 24).
Angiologic and Anatomic Aspects
In this patient an intracranial dissection was considered
because of the narrowing of the BA in its mid part and the
intimal fl ap seen on DSA imaging. As in extracranial eval-
uation, a confi dent diagnosis may be diffi cult even using
DSA if no intimal fl ap or dissecting aneurysm is seen. MRI
may reveal intramural hematoma or an obvious widening of the lumen, but the smaller vessel sizes may hinder
detection. Multislice CTA is increasingly used for diagnosis (Yoon et al 2007). A strange-looking long segmental
stenosis may indicate a dissection but may also be seen
in atherosclerosis, radiation-induced vasculopathy, partially recanalized embolic occlusions, and FMD without
dissection.
Whenever ischemic stroke or TIA of the posterior circulation is suspected, cerebrovascular imaging should be
performed immediately. The most sensitive technique for
parenchymal imaging of the vertebrobasilar territory is
MRI using diff usion-weighted images. The majority of
patients with posterior circulation infarctions and TIAs
lasting >1 hour present with acute MRI lesions (Kidwell
et al 1999, Linfante et al 2001, Marx et al 2002). Cranial CT
is of limited use for brainstem imaging because of typical
beam-hardening artifacts in the posterior fossa.
However, in addition to imaging of the parenchymal lesions, rapid evaluation of the underlying vascular
p a t h o l o g y i s e s s e n t i a l w h i l e m a k i n g t r e a t m e n t d e c i s i o n s .
This applies to any ischemic stroke of the posterior
circulation and especially if a BA occlusion is suspected.
Early MRI studies using TOF-MRA sequences demonstrated a reasonable high sensitivity and specifi city for
detecting occlusion in the brain-supplying arteries. New
MRI techniques combining 3-T and sensitivity-encoding
methods can increase the spatial resolution of TOF-MRA
even further (Choi et al 2007). Diff erentiation of anatomic
variants, i.e., BA fenestration, from intraluminal pathology may remain diffi cult when relying on MRA alone
(Palazzo et al 2014). In presumed acute BA occlusion,
however, multislice CT angiography (CTA) is the current
method of choice (Bash et al 2005, Klingebiel et al 2002).
DSA nevertheless remains relevant as a diagnostic method, especially whenever therapeutic interventions (e.g.,
intra-arterial thrombolysis, mechanical thrombectomy,
balloon dilatation, or stenting) are being considered,
although it may be inferior to CTA in precisely identifying
a BA near-occlusion (Bash et al 2005) (for discussion on
neuroimaging in intracranial occlusion, see also Case 10).
Little has been published about the relevance of posterior circulation diagnostic ultrasound under emergency
conditions. A study comparing CTA and extracranial continuous-wave Doppler combined with transcranial Dop-
pler (TCD) demonstrated that ultrasound fi ndings were
specifi c but the sensitivity of the method was low (Brandt
et al 1999). The use of extracranial and transcranial duplex ultrasound, however, might lead to diff erent results
and may be particularly valuable in centers with limited
availability of DSA or CTA, for example.
In presumed BA pathology, both extracranial V2-VA
segments should always be studied. If bilateral highresistance fl ow signals characterized by high pulsatility
and low fl ow velocity are present in normal-sized vessels
a relevant distal obstruction is practically evident. However, this is only true in normal-sized VAs as the same
prestenotic pattern can also appear physiologically in VA
hypoplasia (see also Chapter 2, “Extracranial Vertebral
Artery” under “Special Arterial Anatomy and Ultrasound
Anatomy”). Normal extracranial VA ultrasound fi ndings,
on the contrary, cannot rule out distal BA pathology and
therefore require additional transcranial insonation starting with the transforaminal approach. In cases of normal
transforaminal fi ndings in both V4-VA segments and the
proximal BA, a distal BA occlusion is unlikely, although an
occlusive process at the top of the BA could still be present. One has to keep in mind that the mean visible transforaminal length of the BA is ~2 cm, which corresponds to
the proximal two-thirds of the vessel (Iglseder et al 2000,
Pade et al 2011, Schulte-Altedorneburg et al 2000). The
last third is usually not accessible in adults by transforaminal ultrasound. In proximal or mid-basilar BA occlusion
a retrograde distal BA fl ow can be seen and was reported
in fi ve patients with angiographically confi rmed proxi-
mal BA occlusion via a transforaminal access and utilizing
echo contrast agents (Koga et al 2002). A reversed BA signal was also demonstrated in 8 of 12 patients studied by
transforaminal power-motion TCD (Ribo et al 2004) (see
also Case 41). However, careful analysis is required to
avoid confusing the BA with the physiologic AICA signal,
especially when TCD is used.
If the BA cannot be visualized transforaminally or if
there are confl icting fi ndings, axial transtemporal inson-
ation may be of help. This enables assessment of fl ow in
both P1-PCA segments and in the top of the BA. A visible
BA head and normal fl ow signals in one or both P1-PCAs
almost defi nitively rules out BA occlusion. In mid- basilar
occlusion, a retrograde fl ow may be found in the top of the
BA and in at least one of the P1-PCA segments, together
with a fl ow in one or both PCoAs toward the BA. If an
insuffi cient transtemporal bone window hinders inson-
ation, echo contrast agents can be used. Contrast administration increases the vessel detection rate of the P1-PCA
segment from 35% to 75% and of the BA head from 62%
to 91%, in patients with ischemia of the posterior circulation (Stolz et al 2002b). If only the P2- or P3-PCA
segments are visible—which is the case in almost all patients even with insuffi cient temporal bone windows—
simultaneous digital tapping of the dominant V3-VA at
the atlas loop and the ipsilateral ICA at the submandibular level will help to clarify the fl ow pathways. A clearly
positive oscillation eff ect during atlas loop tapping argues
in favor of a blood supply to the PCA via the BA, which is a
strong argument against occlusion within the BA. A more
pronounced eff ect during ICA tapping argues in favor of
a relevant BA fl ow obstacle but may also be observed in
361Discussion
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 presence of a fetal-type PCA. Finally, the BA may be
insonated in its middle and distal segments using the posterior coronal insonation plane, which might help to further
clarify the vascular situation (for further reading, see also
Chapter 2, “Distal Basilar Artery” under “Special Arterial
Anatomy and Ultrasound Anatomy;” for ultrasound fi nd-
ings in BA occlusion, see also Chapter 5, “BA Occlusion”
under “Intracranial Pathology”). The combination of the
aforementioned direct and indirect signs using modern
ultrasound systems leads in fact to a high diagnostic certainty, achievable even in the acute stroke patient. The
use of echo contrast agents further improves the evaluation of the posterior circulation.
Several of the signs discussed above were present in
our patient with a mid-basilar occlusion. Both extra- and
intracranial VAs demonstrated high-resistance fl ow sig-
nals despite the presence of normal vessel diameters. The
mid and distal parts of the BA were not visible on transforaminal insonation, even after intravenous echo contrast
administration. Finally, transtemporal insonation yielded
a retrograde distal BA fl ow signal.
Ultrasonography of the posterior circulation, particularly if done under time constraints, requires good
technical equipment and an expert sonographer. A study
reported positive experiences with a diagnostic protocol
including transcranial color-coded duplex sonography
(TCCS) as the fi rst step in most of the patients with pre-
sumed BA occlusion. CTA and/or subsequent DSA were
performed only if the intracranial segments of the pos-
terior circulation were inaccessible by TCCS or if fi ndings
were unclear (Kermer et al 2006).
As in the anterior circulation (e.g., in MCA occlusion), a
particular benefi t of ultrasound is the opportunity to gain
insights into the temporal dynamics, such as recanalization kinetics, which might help to assess prognosis or even
infl uence subsequent therapeutic steps (see also Case 10).
Apart from its use for diagnostic purposes, ultrasound
has also been shown to have a therapeutic potential not
only in embolic occlusive disorders of the anterior circulation but also in BA occlusion. One study included 20
patients with BA occlusion <12 hours. Beside systemic rtPA treat ment the p atien ts we re inso nated v ia th e tra nsforaminal approach using a diagnostic 2-MHz transducer
over 2 hours, and three boluses of an echo contrast agent
were given. Complete recanalization was observed at
1 hour in 10% of cases, at 6 hours in 35%, and in 24 hours
in 50%, rates which are higher than published data for
thrombolysis alone (Pagola et al 2007). At 3 months, the
reported mortality was 35% compared with 50% in those
with systemic thrombolysis and 55% in those with intra-arterial thrombolysis (Lindsberg and Mattle 2006).
Each center will develop its own diagnostic protocols. In
large institutions where all imaging modalities are available, CTA will probably be the fi rst diagnostic tool. However,
24-hour CTA and DSA are not yet widely available, so TCCS
ultrasound systems in the hands of a well-trained sonographer may have an important role as a screening tool or
even in assumed BA pathology in the acute phase.
362
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 22
Right Mid-part M1 Middle Cerebral Artery Occlusion with
Prominent Early Temporal Branch and Patent Foramen Ovale
Clinical Presentation
A 41-year-old woman was admitted to the emergency
d e p a r t m e n t w i t h a c u t e w e a k n e s s o f h e r l e f t a r m a n d l e g .
The symptoms had commenced 1 hour prior to presentation
while she had been walking. No headaches were reported.
The patient had no vascular risk factors except that she
experienced about two migraine attacks with visual aura
per month. On neurologic examination, the woman had
left-sided supranuclear facial palsy, gaze deviation to the
right side, and marked left sensorimotor hemiparesis
( N a t i o n a l I n s t i t u t e o f H e a l t h S t r o k e S c a l e [ N I H S S ] s c o r e : 1 2 ) .
Initial Neuroradiologic Findings
Emergency unenhanced cranial CT revealed mild early
signs of infarction comprising less than one-third of the
right middle cerebral artery (MCA) territory and a dense
media sign. Perfusion CT showed a pronounced perfusion defi cit within the right hemisphere. CT angiography
(CTA) depicted a right proximal M1-MCA occlusion. On
the basis of these fi ndings and after considering exclu-
sion criteria, intravenous thrombolysis with recombinant
tissue plasminogen activator (IV rt-PA) was performed
(Fig. B22.1, Fig. B22.2, Fig. B22.3).
Suspected Diagnosis
Right M1-MCA occlusion of unknown origin.
Questions to Answer by Ultrasound
Techniques
spectrum analysis of the right ICA showed a discrete
increase in pulsatility and a mildly reduced fl ow velocity
when compared with the left side (fl ow velocity: right ICA
54/22 cm/s, PI = 1.0; left ICA 67/32 cm/s, PI = 0.8). Normal
fi ndings were seen in the other extracranial vessels.
Transcranial Duplex Sonography
Color-mode imaging revealed a discontinuous image
of the presumed right M1-MCA segment only. Doppler spectrum analysis showed reduced fl ow velocity
in the right proximal M1-MCA segment (fl ow velocity
60/30 cm/s). The middle M1-MCA segment signal was absent. However, signals from the distal M1-MCA segment
at a depth of 40 mm demonstrated a fl ow pattern simi-
lar to the proximal segment. The right A1 segment of the
anterior cerebral artery (ACA) revealed a mildly increased
fl ow velocity with a high diastolic fl ow component (fl ow
velocity 159/77 cm/s). A lower fl ow velocity was seen in
the left A1-ACA segment (fl ow velocity 125/53 cm/s). The
right posterior cerebral artery (PCA) showed higher fl ow
velocities in the P2-PCA segment compared with the left
P2-PCA segment (fl ow velocity: right, 87/30 cm/s; left,
50/20 cm/s) (Figs. B22.6–B22.12; see also Video
B22.1).
Conclusion
Reopening of the right M1-MCA segment after thrombolysis but indirect signs of relevant distal fl ow
occlusion at the M2-MCA level corresponding to TIBI
(Thrombolysis In Brain Ischemia) grade 3 and COGIF
(Consensus on Grading Intracranial Flow obstruction)
grade 3. Leptomeningeal collateralization via the right
ACA and PCA.
• Was there recanalization of the right MCA after intravenous thrombolysis?
• Was there evidence of an embolic source in the internal
carotid artery (ICA), such as atherosclerotic vessel wall
changes or dissection?
Initial Neurosonologic Findings (Day 1)
Extracranial Duplex Sonography
There was no evidence of atherosclerotic vascular
changes or dissection (Fig. B22.4 and Fig. B22.5). Doppler
Clinical Course (1)
Despite thrombolysis, the patient did not improve clinically.
Follow-up cranial CT 1 day later showed subcortical infarction, predominantly in the right putamen and a persisting
hyperdense media sign (Fig. B22.13). Transesophageal
echocardiography (TEE) revealed a patent foramen ovale
(PFO) with spontaneous right-to-left shunt but no atrial
septum aneurysm. Deep vein thrombosis could have been
a potential source for such a paradoxical embolic event but
no signs were found by duplex ultrasound, and blood tests
excluded thrombophilia.
363Neurosonologic Findings (Day 10)
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. B22.1 Unenhanced cranial CT, axial plane. Left: Hyperdense
media sign on the right side indicating proximal M1-MCA occlusion
(arrow). Right: Note the hypoattenuation of the right putamen
(circle) and loss of cortical ribbon in the right MCA territory.
CBF
AB C
Fig. B22.3 Perfusion CT, rCBF, rCBV, and mean transit time (MTT)
maps axial planes: cerebral blood fl ow/volume (CBF/CBV) mismatch
indicating tissue at risk within the right MCA territory. (A) Decreased
CBF (arrows). (B) Mildly reduced CBV. (C) Delayed MTT.
CBV MTT
Fig. B22.2 CTA, coronal maximal intensity projection (MIP). Proximal occlusion of the right M1-MCA segment (single arrow). The
faint signal beneath the presumed M1-MCA segment was afterwards interpreted as an early temporal branch (short arrows). Note
also the strong signals of the sylvian MCA branches (large arrows).
ICA-R
Fig. B22.4 Extracranial duplex, longitudinal plane. Mildly reduced
fl ow and increased pulsatility in the right ICA (fl ow velocity
54/22 cm/s, PI = 1.0).
Questions to Answer by Ultrasound
Techniques
• Was there secondary reocclusion after systemic
t h r o m b o l y s i s ?
• What was the magnitude of the cardiac right-to-left
shunting based on neurosonologic testing?
in contrast with the contralateral side the vessel seemed
to turn down toward the base of the skull. This segment
was therefore thought to be an early prominent temporal
branch of the M1-MCA and not the M1-MCA segment itself, of which occlusion had initially been suspected. Unchanged, mildly increased fl ow velocities were seen in the
right-sided A1-ACA and P2-PCA segments. In addition, a
right-sided fetal-type PCA was found (not shown).
Neurosonologic Findings (Day 10)
PFO Testing
Transcranial Duplex Sonography
The reduced fl ow velocity persisted in the proximal MCA
(fl ow velocity 66/31 cm/s). Again, there was impaired signal
continuity in the mid M1-MCA segment despite the visualization of the lateral fi ssure and the assumed M1-MCA and,
At rest, three high-intensity transient signals were observed in the simultaneously insonated proximal MCAs
after antecubital injection of ultrasound contrast agent
(Echovist). Sixteen further such signals were seen after a
controlled Valsalva maneuver (Fig. B22.14).
364 Case 22 Right Mid-part M1 Middle Cerebral Artery Occlusion with Prominent Early Temporal Branch and Patent Foramen Ovale
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-L
Fig. B22.5 Extracranial duplex, longitudinal plane. Normal fl ow in
the left ICA (fl ow velocity 67/32 cm/s, PI = 0.8).
M1-MCA-R
M1-MCA-R
Fig. B22.6 TCCS (t rans tempo ral approach) , right -sid ed in sona tion,
midbrain plane. Reduced fl ow velocity but otherwise normal fl ow
signal in projection of the right proximal M1-MCA at a depth of
53 mm (fl ow velocity 60/30 cm/s). Note that there is poor color
imaging throughout the total length of the M1-MCA and a fl ow gap
in its mid part (arrows).
M1-MCA-L
Fig. B22.7 TCCS (t rans tempo ral approach) , right -sid ed in sona tion,
midbrain plane. Distal artery at a depth of 40 mm initially considered to be the right distal M1-MCA revealing a reduced velocity
(fl ow velocity 45/21 cm/s).
Conclusion
Right-sided mid-part M1-MCA occlusion. A patent early
temporal M1-MCA branch was confused with the main
stem in the initial ultrasound examination. Marked leptomeningeal collateralization via ACA and PCA. Small
spontaneous right-to-left shunt and moderate right-toleft shunt during Valsalva maneuver in correlation with
the echocardiographic fi ndings.
Neuroradiologic Findings (Day 11)
Cerebral MRI revealed hemorrhagic transformation in
the area of infarction and mild local swelling. The infarct area itself extended to the right insula and temporal
lobe. Time-of-fl ight MR angiography (TOF-MRA) showed
a right proximal M1-MCA occlusion. No temporal MCA
Fig. B22.8 TCCS (tr anst emporal appro ach) , left -sided insonati on,
midbrain plane. Normal fl ow in the left M1-MCA (fl ow velocity
133/52 cm/s).
branch was visualized (Fig. B22.15 and Fig. B22.16).
Digital subtraction angiography (DSA) was performed
on the same day to resolve the confl icting evaluations. It
confi rmed the presence of a mid-part M1-MCA occlusion,
a prominent temporal MCA branch, and leptomeningeal
collaterals from the ACA and PCA as well as the fetal-type
PCA (Fig. B22.17, Fig. B22.18, Fig. B22.19).
Fig. B22.19 shows a schematic of the patient’s extra-
and intracranial brain-supplying arteries.
Clinical Course (2)
Paradoxical embolism was suspected as a potential cause
of stroke on the basis of the PFO. As a diff erential diag-
nosis, an in-situ thrombus was also considered because
of the persisting M1-MCA occlusion after 11 days of
stroke, which seems long for typical cardiac embolism,
365Final Diagnosis
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.
A1-ACA-R
Fig. B22.9 TCCS (t rans tempo ral approach) , right -sid ed in sona tion,
midbrain plane. Mildly increased fl ow velocity with high diastolic
fl ow component in the right A1-ACA indicating leptomeningeal collateral fl ow (fl ow velocity 159/77cm/s).
P2-PCA-R
A1-ACA-L
Fig. B22.10 TCCS (trans temp oral ap proa ch), left-s ided ins onati on,
midbrain plane. Normal fi ndings in the left A1-ACA (fl ow velocity
125/53 cm/s).
P2-PCA-L
Fig. B22.11 TCCS (transtemporal approach), right-sided insonation, thalamic plane. Right distal P2-PCA with mildly raised fl ow
velocities in comparison with the contralateral side indicating leptomeningeal collateral fl ow (fl ow velocity 87/30 cm/s).
p a r t i c u l a r l y f o l l o w i n g s y s t e m i c t h r o m b o l y s i s . H o w e v er, the defi nitive etiology remained unclear. The patient
was referred to a neurologic rehabilitation unit. After
3 months, no further clinical events had occurred during
anticoagulation therapy but the neurologic defi cit had de-
creased. At this time an endovascular device occlusion of
the PFO was performed without our involvement. Longterm stroke prevention was switched to antiplatelet therapy with aspirin. The patient was then lost to follow-up.
Final Diagnosis
Large ischemic stroke in the right MCA territory caused
by a right mid-part M1-MCA occlusion. Suspected cardiac
embolism due to the presence of a PFO. Collateralization
via a patent early temporal MCA branch originating proximal to the occlusion as well as via leptomeningeal pathways from the ACA and PCA.
Fig. B22.12 TCCS, (tr anst emporal approa ch), le ft-s ided in sona tion, midbrain plane. Normal fl ow in the left P2-PCA (fl ow velocity
50/20 cm/s).
Fig. B22.13 Unenhanced follow-up cranial CT (1 day later), axial
plane. Left: Persisting hyperdense media sign (arrow). Right:
Demarcation of a large putaminal infarction.
366 Case 22 Right Mid-part M1 Middle Cerebral Artery Occlusion with Prominent Early Temporal Branch and Patent Foramen Ovale
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. B22.14 Foramen ovale test: Bilateral M1MCA TCD monitoring. High-intensity transient
signals (arrows) in both MCAs (left > right) appearing during Valsalva maneuver, indicative of
Valsalva
right-to-left shunting.
Fig. B22.15 Left: MR T2-weighted image, axial plane (day 11).
Hemorrhagic transformation of the infarction with mild local
e d e m a . C o m p a r e d w i t h t h e e a r l i e r C T , i n f a r c t s i z e h a s i n c r e a s e d ,
now also partially aff ecting the right insula and temporal lobe.
Right: 3D TOF-MRA, coronal MIP. Proximal M1-MCA occlusion
( a r r o w ) . T h e e a r l y t e m p o r a l b r a n c h a s w e l l a s t h e s y l v i a n M C A
branches is not visualized. Note the large bright artifact caused by
hemorrhagic transformation of the infarction.
Discussion
Clinical Aspects
Here we discuss a 41-year-old woman with right MCA
infarction caused by a mid-part M1-MCA occlusion. Collateralization occurred in part via an early temporal MCA
branch, which proved diffi cult to assess not only by ultra-
sound but also by MRA and CTA. Considering the acute
treatment for stroke and systemic thrombolysis in this
patient, we draw attention to the extended discussion in
Case 10. A cardiac embolic event seemed to be the most
likely etiology because of the PFO and the spontaneous
Fig. B22.16 DSA, left ICA injection, posteroanterior view. Normal
fi lling of intracranial arteries. Note the straight course of the M1MCA as expected in a young patient without arterial hypertension
as well as a small proximal and a more prominent distal temporal
MCA branch (arrowheads).
cardiac right-to-left shunt. Another potential risk factor
was migraine with aura.
The association between PFO and cryptogenic stroke is
well established. Anatomically, a PFO is in most cases an
insignifi cant connection between the right and the left cir-
culation at the atrial level. It can be diagnosed directly in
vivo by TEE if spontaneous or Valsalva-induced shunting
of microbubbles is seen after injection of an ultrasound
contrast agent. It may also be seen during conventional
catheter examination. Its prevalence decreases with increasing age. In an autopsy study of 965 patients the prevalence ranged from 34% in the 1–29-year-old population
to 20% in subjects >80 years of age (Hagen et al 1984).
367Discussion
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. B22.17 DSA, right ICA injection (early arterial phase), posteroanterior view. Mid-part M1-MCA occlusion (single arrow). Note
the prominent early temporal MCA branch (arrows). Contrast fi lling
of the PCA, indicating a fetal-type PCA (arrowhead).
S i m i l a r r e s u l t s w e r e r e p o r t e d u s i n g T E E , y i e l d i n g a p r e v alence of 25.6% in subjects with a mean age of 45 years
(Meissner et al 1999). The shunt volume of the PFO may
decrease over time and the PFO may even disappear, especially in patients after cryptogenic stroke (Tanislav et al
2010). Peak exercise before Valsalva strain may, however,
lead to reoccurrence (Reichenberger et al 2013).
If stroke is related to a PFO a paradoxical embolism
from the venous system into the cerebral circulation is
hypothesized. However, venous thrombi are found in
only ~10% of patients with PFO and cerebral ischemia
(Lethen et al 1997). Other hypotheses are that the PFO
itself is the source of embolism as it has a tunnel-like
structure with a low net fl ow which might subsequently
lead to thrombus formation. In addition, patients with
PFO more often have atrial arrhythmias, which in turn
might lead to intra-atrial thrombus formation (Berthet
et al 2000). Several case–control studies have shown
a high prevalence of PFO in cryptogenic stroke. In patients <40 years of age it has been seen in 40% of cases
compared with 15% of controls (Webster et al 1988). An
identical prevalence was observed in a patient group
<55 years of age compared to 10% in controls. In this
study, patients with no identifi able cause of stroke had
an even higher prevalence (54%), whereas only 21% of
patients with a determined etiology had this condition (Lechat et al 1988). Medium to large PFOs (≥2 mm)
were more frequently found among cryptogenic strokes
and showed larger infarcts on imaging (Jung et al 2013,
Steiner et al 1998).
This observation is supported by TCD emboli detection
studies, which found an association between large PFOs
and increased rates of spontaneous microembolic signals
(Telman et al 2008, Kobayashi et al 2009). Other studies,
Fig. B22.18 DSA, right ICA injection (late arterial phase), posteroanterior view. Leptomeningeal collateralization of the MCA
territory via ACA (arrows) and early temporal MCA branch (arrow).
RL
Fig. B22.19 Schematic of the patient’s extra- and intracranial
brain-supplying arteries. Mid-part M1-MCA occlusion on the right
side (circle). Collateralization of the MCA territory via an early temporal MCA branch as well as leptomeningeal collaterals from the
right ACA and right PCA via the right fetal-type PCA.
however, demonstrated that there was no relation between shunt volume and infarct size and that the incidence of large shunts in presumed PFO-related stroke was
not increased (Akhondi et al 2010, Wessler et al 2014).
A recent meta-analysis of 14 studies including 4,251
p a t i e n t s c o n c l u d e d t h a t P F O s i z e d o e s n o t c o r r e l a t e w i t h
the risk of recurrent stroke. Interestingly, no increased
risk for recurrent stroke or TIA in stroke patients with
PFO was found compared to stroke patients without PFO
(Katsanos et al 2014b).
368 Case 22 Right Mid-part M1 Middle Cerebral Artery Occlusion with Prominent Early Temporal Branch and Patent Foramen Ovale
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.
Besides PFO, an atrial septal aneurysm (ASA) has also
been linked with stroke. ASA is a localized saccular deformity, generally at the level of the oval fossa. In contrast
to PFO, diff erent defi nitions of ASA have been used. Some
authors have defi ned an atrial septum extension ≥11 mm
beyond the plane of the atrial septum into either the right
or left atrium or both as an ASA (Mas et al 2001). Others used a ≥10 mm extension into the left or right atrium
(Homma et al 2002) or a ≥15 mm extension into one or
both atria as cut-off values (Bonati et al 2006). The cur-
rent guidelines of the American Heart Association defi ne
an ASA as a ≥10 mm excursion in the septum (Furie et al
2011). An extension <10 mm is therefore considered as a
hypermobile septum.
The prevalence of ASA is far lower than that of PFO.
The population-based Stroke Prevention Assessment
of Risk in a Community (SPARC) study, which analyzed
581 subjects aged ≥45 years, found an ASA in 2.2% subjects (Meissner et al 1999). Autopsy analysis revealed a
prevalence of 1% for ASA (Hagen et al 1984). In subjects
with ASA, a concomitant PFO is found in about one-third
of cases (Mügge et al 1995). In patients with cryptogenic
stroke aged 18 to 55 years an ASA may be present in up to
10% of patients, while up to 19% of patients with PFO have
an ASA in addition (Mas et al 2001). ASAs vary in size and,
like PFOs, their infl uence on stroke risk is controversial.
In one study, patients with PFO and an ASA extending
>10 mm in one or both directions were found to have an
increased stroke risk (Cabanes et al 1993). Another study
demonstrated that PFO is an independent risk factor for
cryptogenic stroke in the age group >55 years, with an
increasing association in patients with an additionally diagnosed ASA (Handke et al 2007).
Treat men t strate gies aft er cry ptoge nic s tro ke an d sep tal abnormalities are controversial. An early large study
indicated that aspirin alone is suffi cient to prevent recur-
rence in cryptogenic stroke with PFO but not with a combined septal pathology. Analyzing 581 aspirin-treated
stroke patients aged 18–55 years (216 with PFO, 10 with
ASA alone, 51 with both conditions, 304 without septal
abnormalities) over 4 years, the annual risk of recurrence
was 0.6% in the PFO group, 3.8% if an ASA was additionally
present, 1.1% if no septal abnormalities were seen, and 0%
if only an ASA was present (Mas et al 2001). The increased
risk in combined ASA and PFO was underlined by a higher
rate of silent infarctions compared with PFO alone (Bonati
et al 2006). In some countries long-term oral anticoagulation or interventional closure was therefore recommended instead of aspirin. Diff erent conclusions were
drawn from the PICSS trial (PFO in Cryptogenic Stroke
Study) which compared the 2-year outcomes in 630 patients with PFO and stroke (265 of them with cryptogenic
stroke) who were randomized to either aspirin or warfarin. No signifi cant superiority of warfarin over aspirin
was seen (16.5% versus 13.2%), which was also independent of the presence and the size of the PFO, or the association with an ASA (Homma et al 2002).
Three further randomized trials comparing interventional PFO closure with antithrombotic treatment in patients after ischemic stroke have so far been published
(Carroll et al 2013, Furlan et al 2012, Meier et al 2013). The
CLOSURE I and PCA studies recruited patients with TIA or
stroke, the RESPECT study included patients after stroke
only. The decision between platelet inhibitor therapy and
oral anticoagulation in the medically treated groups was
left to the treating physician. None of the three studies
could in fact demonstrate signifi cant superiority of the
interventional PFO closure. The annual stroke risk in the
medical treatment group ranged from 0.6% to 1.5%, which
was lower than initially expected. The calculated number
of cases for all the above trials was based on an assumed
stroke risk of 3–4%, which turned out to be twice as high
as was eventually observed in the conventionally treated
patients. A subgroup analysis in the RESPECT trial yielded
a statistically signifi cant advantage for PFO closure in pa-
tients with ASA or a large shunt, but the CLOSURE I and the
PCA trial could not reproduce this fi nding. The periproce-
dural complication rate in the interventionally treated
groups ranged from 0% to 4.2%. In the CLOSURE I trials,
atrial fi brillation occurred in 5.7% of patients with an in-
serted device and in 0.7% of the medically treated patients.
On the basis of the available data, several rather
contradictory meta-analyses have been published (Kitsios
et al 2012) as they range from “clear benefi t from PFO
closure” (Khan et al 2013), to doubting superiority of
closure (Spencer et al 2014) and even to “increased stroke
risk” for patients with PFO closure (Udell et al 2014).
From the above discussion, we can currently summarize as follows: Young patients after cryptogenic stroke
who have a PFO without ASA should be treated with
platelet inhibition unless any other indication for anticoagulation is found. So far there is no convincing data
available which could prove superiority of oral anticoagulation over platelet inhibition in the above condition. Only
if other factors are present—such as clear evidence for a
paradoxical embolism (with triggering Valsalva maneuver and concomitant deep venous thrombosis), anamnestic hints of spontaneous thromboses in the past, a family
history of thromboses or a thrombophilia—then anticoagulation should be considered, at least temporarily. PFO
closure cannot currently be recommended and can only
be considered in selected individual cases.
With increasing age, the rate of cryptogenic strokes
decreases as the underlying stroke mechanism can more
often be identifi ed. However, valid data on the actual
stroke risk of PFO in the elderly population does not exist.
Percutaneous PFO closure is successful in 98% of cases
(Windecker et al 2000). Intervention-related severe complications such as death, a life-threatening bleed, embolic
events, or cardiac tamponades have been reported in 1.5%
of patients. Less relevant side eff ects such as arrhythmi-
as, device arm fracture, device embolization, and device
thrombosis were reported in 7.9% of cases (Homma and
Sacco 2005).
In our present case of cryptogenic stroke in a young
patient, a PFO without accompanying ASA was present.
A cardiac embolus or paradoxical embolic event seemed
possible but could not be proven. The fi nal decision to
close the PFO was a result of an extended ambulatory
cardiologic consultation with the patient and was fi nal-
ly performed at the request of the patient herself. From
a neurologic point of view, there was no indication for
interventional PFO closure. Postinterventional follow-up
information has not been available to us.
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