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Case 21 Mid-basilar Artery Occlusion
266
Degree of Neurosonologic Difficulty: High
Fig. B21.19 DSA, right ICA injection, lateral view. Retrograde filling
of the distal BA (single arrow) and SCA (arrows) via a strong PCoA
(arrowhead).
Discussion
Clinical Aspects
Here we describe a 33-year-old woman who sustained
multiple infarcts within the posterior circulation. A spontaneous BA dissection was assumed, leading to secondary
BA occlusion and causing artery-to-artery embolic events.
There are no detailed epidemiological data on the incidence and prevalence of intracranial dissections. An intracranial dissection is a rare cause of stroke and, compared with extracranial dissections, there are few supplementary data on them. Single casereports and smaller case
series, at least in vertebral dissection, suggest that predominantly younger patients (between 30 and 50 years)
and more males than females are affected (Bassetti et al.
1994, Caplan 1988). The underlying mechanism of extraand intracranial dissection is similar. After an intimal tear,
blood can enter the wall of the artery leading to vessel wall
hematoma. However, as intracranial arteries have smaller
medial and adventitial layers and lack an external elastic
lamina, intracranial arteries develop aneurysms relatively
more frequently, and carry a subsequent risk of SAH
(O’Connell et al. 1985). An autopsy study revealed in dissection-induced SAH in 79 % of cases a vessel lesion between the medial and adventitial layer (Yamaura and Ono
1994).A dissection and hematoma between the intima and
media, will however, lead to a reduction in the vessel lumen.
Fig. B21.20 Schematic drawing of the extra- and intracranial brain
supplying arteries of the patient in Case 21. Mid-basilar occlusion
(large circle) and left P1-PCA stenosis (small circle). Collateral blood
flow toward both PCAs and into the distal BA via the right PCoA.
The anterior circulation is more frequently affected in
children and young adults, whereas the posterior circulation is generally more involved in adults (Schievink et al.
1994b). Within the anterior circulation, dissections are
most frequently found in the intracranial ICA. Approximately 100 cases have been reported in the English literature so far. The most frequent location is the supraclinoid
C1/C2-ICA segment, from which the dissection often extends into the proximal MCA and ACA (Chaves et al. 2002).
Isolated MCA and ACA dissections may also occur. Until
2005 only 23 patients with MCA dissection had been reported (Lin et al. 2005) (for further discussion on MCA
dissection, see also Case 24, p. 287). In ACA dissection,
ischemic stroke is often related to A2-ACA segment involvement and SAH to A1-ACA involvement (Ohkuma et
al. 2003). In the posterior circulation, dissections most
frequently occur in the V4-VA segment, close to the PICA
origin. An extension into the BA might also be seen while
singular BA dissections are extremely rare (Alexander et al.
1979).
The causes of intracranial dissections are not clearly
established. Mechanical injuries such as within the extracranial system seem far less likely, as intracranial arteries
arelessmobileandarenotadherenttobone.Otherpotential explanations are the presence of an arteriopathy
that may lead to vessel wall instability. For instance, Ehler–Danlos syndrome and FMD are associated with spontaneous dissections, however, with clear preference of the
extracranial arteries (Schievink et al. 1994a, Schievink
Discussion
267
2001). Similar to extracranial dissection, migraine is a
common finding in intracranial spontaneous dissection.
Clinical presentation of extra- and intracranial dissections is different. In intracranial dissections, unilateral severe headaches are almost always present. Furthermore,
the interval between dissection and the manifestation of
clinical symptoms tends to be shorter (Zweifler et al.
2004). Often, the extent of the neurologic deficit fluctuates
within the first 2 weeks, which has been attributed to
hypoperfusion induced by vessel lumen reduction (Hart
and Easton 1983). In posterior circulation dissection large
or multiple posterior circulation strokes may occur (Caplan et al. 1988).
There are no well-established therapeutic guidelines for
intracranial dissections. Because of the raised 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 and regular MRI
controls are recommended (Schievink 2001). Experience
with endovascular therapeutic approaches is rather limited and mainly restricted to treatment of extracranial
dissections. Interventional strategies such as stent implantation should be reserved for patients who, despite suffi-
cient medical treatment, have episodes of recurrent ischemia and in whom a hemodynamic etiology is suspected
(for further discussion on intracranial stenting, see also
Case 5, p.149 and Case 26, p. 306).
Contrary to previous assumptions, patients with intracranial dissection usually demonstrate a good clinical outcome. It has been postulated that, as in extracranial dissections, an intramural hematoma and thrombus formation leading to embolism occurs, which is then followed by
a reparation 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 reparation processes might be less effective (Chen and Caplan 2005). In
contrast to the extracranial dissections, which recanalize
in the majority of cases over time, only scare 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. In VA dissection, positive findings in five consecutive cases were reported (Kitanaka et al. 1994b). Distinguishing between a dissecting aneurysm without SAH
and a true aneurysm can be difficult. In these cases, serial
follow-up studies may be of help.
In our patient, the unusual onset of headaches several
days prior to stroke as well as the severe mid-basilar
stenosis comprising an intima flap were indicative of an
isolated spontaneous BA dissection. Because of the assumed high 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. A potential explanation for
this phenomenon could be an increase in the intramural
hematoma, possibly facilitated by the anticoagulation. A
similar course was observed in two other of our reported
cases with extracranial ICA dissection (see also Case 11,
p.183, and Case 24, p. 287).
Angiologic and Anatomic Aspects
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 diffusion-weighted images. The majority of patients with posterior circulation infarctions and TIAs lasting greater than 1 hour present with acute MRI lesions
(Linfante et al. 2001, Kidwell et al. 1999, Marx et al. 2002).
Cranial computed tomography (CCT) is less suitable for
brain stem imaging because of frequent artifacts in the
base of the skull.
However, in addition to imaging of the parenchymal
lesions, rapid evaluation of the underlying vascular pathology is essential while making treatment decisions
whenever ischemic stroke of the posterior circulation occurs and especially if a BA occlusion is suspected. Early MRI
studies using TOF MRA sequences demonstrated a reasonable high sensitivity and specificity for detection of occlusion in the brain-supplying arteries. New MRI techniques
combining 3 T and sensitivity encoding methods can even
further increase the spatial resolution of TOF MRA (Choi et
al. 2007). In presumed acute BA occlusion however, multislice computed tomographic angiography (CTA) is, if available, the current method of choice (Bashet al. 2005, Brandt
et al. 1999, Klingebiel et al. 2002). DSA will nevertheless
remain relevant as a diagnostic method, especially whenever therapeutic interventions (e. g., intraarterial thrombolysis, intraarterial balloon dilatation, or stenting) are
being considered. Compared with CTA it may, however,
be inferior in exactly identifying a BA near occlusion (Bash
et al. 2005) (for discussion on neuroimaging in intracranial
occlusion,seealsoCase10,p.176).
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 Doppler (TCD) demonstrated that ultrasound findings were
specific but the sensitivity of the method was low (Brandt
et al. 1999). The use of extra- and transcranial duplex
ultrasound, however, might lead to different results and
may even be of special value, for example, in centers with
limited availability of DSA or CTA.
In presumed BA pathology, both extracranial V2-VA segments should always be studied. If bilateral high resistance
flow signals characterized by high pulsatility and low flow
velocity are present in normal-sized vessels a relevant
distal obstruction is practically evident. However, this is
Degree of Neurosonologic Difficulty: High
Case 21 Mid-basilar Artery Occlusion
268
only true in normal-sized VAs as the same prestenotic
pattern can also physiologically appear in VA hypoplasia
(see also Chapter 2, “Extracranial Arterial Anatomy,” p.13).
Normal extracranial VA ultrasound findings, on the contrary, cannot rule out distal BA pathology and therefore
require additional transcranial insonation starting with
the transforaminal approach. In cases of normal transforaminalfindingsinbothV4-VAsegmentsandtheproximal
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 approximately 2 cm, which corresponds
to the proximal two-thirds of the vessel (Iglseder et al.
Degree of Neurosonologic Difficulty: High
2000, Pade et al. 2007a, Schulte-Altedorneburg et al.
2000). The last third is usually not accessible by transforaminal ultrasound. In proximal BA occlusion a retrograde distal BA flow may be observed. Koga and coworkers
(2002) analyzed patients with angiographically confirmed
BA occlusion with transforaminal echo contrast-enhanced
ultrasound. They found a retrograde BA flow in five patients with proximal or mid-basilar occlusion, whereas
this was not the case in two patients with distal BA occlusion. A reversed BA signal, indicating a preserved collateral
flow was also demonstrated in eight in 12 patients studied
by transforaminal power-motion TCD (Ribo et al. 2004).
However, careful analysis is required to avoid confusing
the BA with the physiologic AICA signal, especially when
TCD is used.
IftheBAcannotbevisualizedbytheaboveapproachorif
conflicting findings are present, axial transtemporal insonation is added. This allows analysis of flow in both P1-PCA
segment and the top of the BA. A visible BA head and
normal flow signals in one or both P1-PCAs definitively
ruled out BA occlusion. In mid-basilar occlusion, retrograde flow can be found in the top of the BA and at least
one of the P1-PCA segment together with a flow in one or
both PCoAs towards the BA. If an insufficient transtemporal bone window hinders insonation, an intravenous echocontrast agent 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 P2- or P3-PCA segments are visible—
which is the case in almost all patients, even with insuffi-
cient temporal bone windows—simultaneous oscillation
of the dominant V3-VA at the atlas loop and the ipsilateral
ICA at the submandibular level will help to clarify the flow
pathways. A clearly positive oscillation effect during atlas
loop oscillation argues in favor of a blood supply to the PCA
via the BA which is a strong argument against a flow
obstruction within the BA. A more pronounced effect during ICA oscillation argues in favour of a relevant BA flow
obstacle but may also be observed in 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 detailed information, see also Chapter 2, “Intracranial Arterial Anatomy,” p.15). The combination of direct and indirect signs results in the high diagnostic certainty achievable with modern ultrasound systems, even in the acute stroke patient. The use of echocontrast agents further improves the evaluation of the
posterior circulation.
In our patient with a mid-basilar occlusion, several of
the above discussed signs were present: Both extra- and
intracranial VAs demonstratedhigh resistance flow signals
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 flow signal.
Use of ultrasound for the posterior circulation, particularly if performed under time constraints, requires good
technical equipment and an expert sonographer. It has to
be kept in mind that these criteria also apply to any of the
other angiologic techniques. As in the anterior circulation
(e. g., in MCA occlusion), a particular benefit of ultrasound
is the opportunity to gain insights into the temporal dynamics, such as recanalization kinetics, which might help
to asses prognosis or even influence subsequent therapeutic steps (see also Case 10, p.176). Apart from its use for
diagnostic purposes, ultrasound has recently also shown
to have a therapeutic potential not only in embolic occlusive disorders of the anterior circulation but also in BA
occlusion. A first study included 20 patients with BA occlusion <12 hours. Beside systemic rt-PA treatment the
patient were isonated via the transforaminal approach
using a diagnostic 2 MHz transducer over 2 hours and 3
boluses of an echo-contrast agents were given. Complete
recanalization was observed at 1 hour in 10 %, at 6 hours in
35 %and in 24 hours in 50 % of cases, rates which are higher
compared with published data if thrombolysis was used
alone (Pagola 2007). At 3 months, the reported mortality
was35%whichislessthaninpatientswithsystemic(50%)
or intraarterial thrombolysis (55 %) (Lindsberg and Mattle
2006).
Recently, a study reported early positive experiences
with a diagnostic protocol including transcranial colorcoded sonography (TCCS) as the first step in most of the
patients with presumed BA occlusion. CTA and/or subsequent DSA were performed only if the intracranial segments of the posterior circulation were inaccessible by
TCCS or if findings were unclear (Kermer et al. 2006).
Each center has to develop its own diagnostic protocols.
In large institutions, where all imaging modalities are
available, CTA will probably be the first diagnostic tool.
However, 24-hour CTA and DSA are not yet widely available, Therefore, modern TCCS ultrasound systems, in the
hands of a well-trained sonographer, if present, may gain
an important role, at least as a screening tool.
Case 22
M1 Middle Cerebral Artery Occlusion with Prominent
Early Temporal Branch
269
Clinical Presentation
A 41-year-old woman was admitted to our emergency
room with acute weakness of her left arm and leg. 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 migraines with visual aura per
month. On neurologic examination, the patient had leftsided supranuclear facial palsy, gaze deviation to the right
side, and marked left sensorimotor hemiparesis (National
Institute of Health Stroke Scale [NIHSS] score 12).
Initial Neuroradiologic Findings
Emergency unenhanced cranial computed tomography
(CCT) 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 deficit within the right
hemisphere. Computed tomographic angiography (CTA)
depicted a right proximal M1-MCA occlusion. On the basis
of these findings and after considering exclusion criteria,
intravenous thrombolysis with recombinant tissue plasminogen activator (rt-PA) was performed (Figs. B22.1–
B22.3).
Suspected Diagnosis
Right M1-MCA occlusion of unknown origin.
Questions to Answer by Ultrasound Techniques
• Was there recanalization of the right MCA after intravenous thrombolysis?
• Was there evidence of an embolic source in the 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 (Figs. B22.4, B22.5). Doppler spectrum analysis of the right ICA showed a discrete increase in pulsatility and a mildly reduced flow signal when compared
with the left side (flow velocity: right ICA 54/22 cm/s; left
ICA 67/32 cm/s). Normal findings 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 flow velocity in a vessel
considered to represent the right proximal M1-MCA segment (flow 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 flow pattern similar to the proximal segment.
The right A1-ACA segment revealed a mildly increased
flow velocity with a high diastolic flow component (flow
velocity: 159/77 cm/s). The left A1-ACA segment was normal (flow velocity: 67/32 cm/s). The right PCA showed
higher flow velocities in the P2-PCA segment compared
with the left P2-PCA segment (flow velocity: right: 87/
30 cm/s, left: 50/20 cm/s) (Figs. B22.6–B22.12).
Conclusion
ReopeningoftherightM1-MCAsegmentafterthrombolysis but indirect signs of relevant distal flow occlusion at
the M2-MCA level corresponding to Thrombolysis In Brain
Ischemia (TIBI) grade 3. Partial leptomeningeal collateralization via the right anterior cerebral artery (ACA) and
posterior cerebral artery (PCA).
Clinical Course (1)
Despite thrombolysis, the patient did not improve clinically. Follow-up CCT 1 day later showed subcortical infarction, predominantly in the right putamen and a persisting
hyperdense media sign (Fig. B22.13). Transesophageal
echocardiography revealed a persistent foramen ovale
Case 22 M1 Middle Cerebral Artery Occlusion with Prominent Early Temporal Branch
270
(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 embolicevent but
no typical signs were found by duplex ultrasound, and
blood tests excluded thrombophilia.
Questions to Answer by Ultrasound Techniques
• Was there secondary reocclusion after systemic thrombolysis?
• What was the magnitude of the cardiac right-to-left
Degree of Neurosonologic Difficulty: High
shunting based on neurosonologic testing?
Neurosonologic Findings (Day 10)
Transcranial Duplex Sonography
The reduced flow velocity persisted in the proximal MCA
(flow velocity 66/31cm/s). Again, there was impaired signal continuity in the mid M1-MCA segment and, 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 segmentitself
of which occlusion had initially been suspected. Unchanged mildly increased flow 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).
PFO Testing
At rest, three high-intensity transient signals were observed in the simultaneously insonated proximal MCAs
after antecubital Echovist injection. Sixteen further such
signals were seen after performing a controlled Valsalva
maneuver (Fig. B22.14).
Conclusion
Right-sided mid M1-MCA occlusion. Patent early temporal
MCA branch which was confused with the M1-MCA segment in the initial ultrasound examination. Leptomeningeal collateralization via the ACA and PCA. Small spontaneous right-to-left shunt and moderate right-to-left shunt
during Valsalva maneuver in correlation with the echocardiographic findings.
Neuroradiologic Findings (Day 11)
Cerebral magnetic resonance imaging (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-flight (TOF) magnetic resonance angiography (MRA) showed a right proximal M1-MCA occlusion but no temporal MCA branch was
detected (Figs. B22.15, B22.16). DSA wasperformed on the
same day to resolve the conflicting evaluations. It confirmed the presence of a mid M1-MCA occlusion, a prominent temporal MCA branch, the leptomeningeal collateralsfromtheACAandPCAaswellasthefetal-typePCA
(Figs. B22.17–B22.19).
Fig. B22.1 Unenhanced CCT, 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.
Fig. B22.2 CTA, coronal MIP. Proximal occlusion of the right M1MCA 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).
Final Diagnosis
271
Figure B22.20 showsa schematicdrawing of the extra- and
intracranial brain-supplying arteries of the patient.
Clinical Course (2)
Paradoxical embolism was suspected as a potential cause
of stroke on the basis of the persistent foramen ovale. As a
differential diagnosis, 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, particularly following systemic thrombolysis.
However, the definitive etiology remained unclear. The
patient was referred to a neurologic rehabilitation unit.
After 3 months, no further clinical events had occurred
during anticoagulation therapy whereas the neurologic
deficit had reduced. At this time an endovascular device
occlusion of the PFO was performed without our involvement. Long-term 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 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.
Degree of Neurosonologic Difficulty: High
Fig. B22.3 Perfusion CT,rCBF, rCBV and MTT maps axial planes: CBF/
CBV mismatch indicating tissue at risk within the right MCA-territory. A Decreased cerebral blood flow (CBF) (arrows). B Mildly reduced cerebral blood volume (CBV). C Delayed MTT.
Fig. B22.5 Extracranial duplex, longitudinal plane. Normal flow in
the left ICA (flow velocity: 67/32 cm/s).
Fig. B22.4 Extracranial duplex, longitudinal plane. Mildly reduced
flow and increased pulsatility in the right ICA (flow velocity: 54/
22 cm/s).
Fig. B22.6 TCCS (transtemporal approach), right-sided insonation,
midbrain plane. Reduced flow velocity but otherwise normal flow
signal in projection of the right proximal M1-MCA at a depth of
53 mm (flow velocity: 60/30 cm/s). Note that there is poor color
imaging throughout the total length of the M1-MCA.
Case 22 M1 Middle Cerebral Artery Occlusion with Prominent Early Temporal Branch
272
Degree of Neurosonologic Difficulty: High
Fig. B22.7 TCCS (transtemporal approach), right-sided insonation,
midbrain plane. Distal artery at a depth of 40 mm initially considered
to be the right distal M1-MCA revealing a reduced velocity (flow
velocity: 45/21 cm/s).
Fig. B22.9 TCCS (transtemporal approach), right-sided insonation,
midbrain plane. Mildlyincreased flow velocity with highdiastolic flow
componentintherightA1-ACA(flowvelocity:159/77cm/s).
Fig. B22.8 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Normal flow in the lef t M1-MCA (flow velocity:
133/52 cm/s).
Fig. B22.10 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Normal findings in the left A1-ACA (flow velocity:
125/53 cm/s).
Fig. B22.11 TCCS (transtemporalapproach), right-sided insonation,
thalamic plane. Right distal P2-PCA with mildly raised flow velocities
in comparison with the contralateral side (flow velocity: 87/30 cm/s).
Fig. B22.12 TCCS, (transtemporal approach), left-sided insonation,
midbrain plane. Normal flow in the lef t P2-PCA (flow velocity: 50/
20 cm/s).
Final Diagnosis
Fig. B22.13 Unenhanced follow-up CCT (1 day later), axial plane.
Left: Persisting hyperdense media sign (arrow). Right: Demarcation
of a large putaminal infarction.
Fig. B22.14 Foramen ovale test: Bilateral M1MCA TCD monitoring. High-intensity transient
signals(arrows)inbothMCAs(left>right)
appearing during Valsalva maneuver indicative
of right-to-left shunting.
273
Degree of Neurosonologic Difficulty: High
Fig. B22.15 MR T2-weighted image, axial plane (day 11). Hemor-
rhagic transformation of the infarction with mild local oedema.
Compared with the earlier CT, infarct size has increased, now also
partially affecting the right insula and temporal lobe.
Case 22 M1 Middle Cerebral Artery Occlusion with Prominent Early Temporal Branch
274
Degree of Neurosonologic Difficulty: High
Fig. B22.16 3D TOF MRA, coronal MIP. Proximal M1-MCA occlusion
(arrow). The early temporal branch as well as the sylvian MCA
branches are not visualized. Note the large artifact caused by hemorrhagic transformation.
Fig. B22.18 DSA, right ICA injection (early arterial phase), posteroanterior view. Mid M1-MCA occlusion (single arrow). Note the prominent early temporal MCA branch (arrows). Contrast filling of the
PCA, indicating a fetal-type PCA (arrowhead).
Fig. B22.17 DSA, left ICA injection, posteroanterior view. Normal
filling of intracranial arteries. Note the straight course of the M1MCAaswellasasmallearlytemporalMCAbranch(arrowhead).
Fig. B22.19 DSA, right ICA injection (late arterial phase), posteroanterior view. Leptomeningeal collateralization of the MCA territory
via PCA and ACA (arrows).
Discussion
Clinical Aspects
Here we discuss a 41-year-old woman with right MCA
infarction caused by a mid M1-MCA occlusion. Collateralization occurred in part via an early temporal MCA branch,
which proved difficult to assess not only byultrasound 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 (p. 176). A
cardiac embolic event seemed to be the most likely etiology because of the persistent foramen ovale (PFO) and the
spontaneous cardiac right-to-left shunt. Another potential
risk factor was migraine with aura.
The association between persistent foramen ovale and
cryptogenic stroke is well established. A PFO is in most
cases a nonsignificant connection between the right and
the left circulation at the atrial level. It can directly be
diagnosed in vivo by transesophageal echocardiography
(TEE) if spontaneous or Valsalva-induced shunting of microbubbles after injection of an echo-contrast agent is
present. However, 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 over 80 years of age (Hagen et al.
1984). Similar results were reported using TEE, yielding a
prevalence of 25.6 % in subjects with a mean age of 45
years (Meissner et al. 1999). The postulated stroke mechanism in PFO is paradoxic embolism from the venous
system into the cerebral circulation. However, venous
thrombi are only found in about 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 flow which
might subsequently lead to thrombus formation. In addition, patients with PFO more often have atrial arrhythmias,
which in turnmight lead tointraatrial thrombus formation
(Berthet et al. 2000). Several case–control studies have
shown a high prevalence of PFO in cryptogenic stroke.
Forty percent of a patient group < 40 years had this condition compared with 15 % of controls (Webster et al.
1988). An identical prevalence was observed in a patient
group < 55 years compared with 10 % in controls. In this
study, patients with no identifiable cause of stroke had an
even higher prevalence of 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 (Steiner et al. 1998).
Besides PFO, an atrial septal aneurysma (ASA) has also
been linked with stroke.Its prevalence is farlower than for
PFO. The population-based Stroke Prevention Assessment
of Risk in a Community (SPARC) study,which analyzed 581
subjects aged 45 years or older, found an ASA in 2.2% and a
PFO in 25.6 % subjects (Meissner et al. 1999). Autopsy
Discussion
Fig. B22.20 Schematic drawing of the extra- and intracranial brainsupplying arteries of the patient in Case 22. Mid 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.
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 cryptogenic stroke, as analyzed in a patient group aged 18–55
years,theprevalenceofASAisincreasedandmaybeas
high as 10%, whereas 19% of patients with PFO from the
above study had an additional ASA (Mas et al. 2001). ASAs
vary in size, which may influence the associated stroke
risk. Cabanes and coworkers (1993) showed that patients
with PFO and an ASA extending less than 10 mm into one
or both directions had no increased risk of stroke, while
those with PFO and an ASA > 10 mm in size had an increased risk. Interestingly, the presence or absence of an
ASA has been differently defined in various studies. Mas
and coworkers (2001) used an atrial septum extension
≥ 11 mm beyond the plane of the atrial septum into either
the right or left atrium or both as a diagnostic criterion
(Mas et al. 2001). Other authors used a ≥ 10 m m ex tension
into the left or right atrium (Homma and Sacco 2002) or a
≥ 15 mm extension into one or both atria (Bonati et al.
2006) as cut-off values.
A variety of concepts have been discussed regarding
treatment strategy after stroke in patients with PFO. Mas
and coworkers (2001) analyzed 581 patients aged 18–55
years after cryptogenic stroke. Of these, 216 did have a PFO,
10 had an ASA alone, 51 presented with both conditions,
and304hadnoseptalabnormalities.Allgroupswere
treated with 300 mg aspirin and stroke recurrence was
analyzed over a 4-year follow-up period. The annual risk
275
Degree of Neurosonologic Difficulty: High