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Case 11 Secondary Occlusion in Internal Carotid Artery Dissection
186
Degree of Neurosonologic Difficulty: Medium
Fig. B11.5 Extracranial duplex, longitudinal plane. Right ICA with
normal flow signal (flow velocity: 78/26 cm/s).
Fig. B11.7 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Poststenotic flow pattern in the left A1-ACA (flow
velocity: 32/20 cm/s).
Fig. B11.6 TCCS (transtemporal approach), left-sided insonation
midbrain/thalamic plane. Poststenotic flow pattern in the left M1MCA (flow velocity: 31/20 cm/s).
Fig. B11.8 TCCS (transtemporal approach), right-sided insonation
midbrain plane. Normal flow in the right M1-MCA (flow velocity: 94/
46 cm/s).
Fig. B11.9 TCCS (transorbital approach), left-sided insonation. Reversed flow direction in the left OA (flow velocity: 70/40 cm/s).
Fig. B11.10 TCCS (transorbital approach), right-sided insonation.
Normal flow direction in the right OA (flow velocity: 65/20 cm/s).
Final Diagnosis
187
Degree of Neurosonologic Difficulty: Medium
Fig. B11.11 TCCS (transtemporal approach), left-sided insonation,
thalamic plane. Normal flow velocity in the distal left P2-PCA (flow
velocity: 46/28 cm/s).
Fig. B11.13 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Further worsening of the preexisting marked compromised poststenotic flow pattern in the left M1-MCA (flow velocity: 25/14 cm/s). Note the positive oscillation effect caused by mild
oscillation of the left optic bulb (arrows).
Fig. B11.12 Extracranial duplex, longitudinal plane. High-resistance
flow signal with a low and short systolic flow and completely absent
diastolic flow component considered to correspond to distal left ICA
occlusion.
Fig. B11.14 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Similar worsened poststenotic flow pattern in the
left A1-ACA (flow velocity: 25/10 cm/s).
Fig. B11.15 TCCS (transtemporal approach), left-sided insonation,
midbrain/thalamic plane. Increased flow velocity in the left distal P2PCA indicating leptomeningeal collateral flow (flow velocity: 122/
53cm/s).
Fig. B11.16 TCCS (transorbital approach), left-sided insonation.
Further increase of the reversed flow in the left OA (flow velocity:
97/54 cm/s).
Case 11 Secondary Occlusion in Internal Carotid Artery Dissection
188
Degree of Neurosonologic Difficulty: Medium
Fig. B11.17 Schematic drawing of the extra- and intracranial brain-
supplying arteries of the patient in Case 11. Note the left distal ICA
occlusion (circle). Collateral blood flow is via left ECA and retrograde
OA toward the left MCA and ACA aswell as to theright ACA territory.
There is additional leptomeningeal collateralization of the left MCA
territory after secondary occlusion via the left PCA (green arrow).
Fig. B11.18 CTA, curviplanar sagittal ICA reconstruction. Occlusion
of the left ICA in its petrosal part (arrowhead). Note thebeginning of
the dissection in the middle segment of the extracranial ICA (arrows).
Fig. B11.19 MR FLAIR-weighted image, axial plane. Large internal
border zone infarction between the left ACA and MCA territories.
Fig. B11.20 Extracranial duplex, longitudinal plane. Partial reopening with low flow signal in the left ICA similar to the findings on
admission (flow velocity: 30/20 cm/s).
Final Diagnosis
189
Degree of Neurosonologic Difficulty: Medium
Fig. B11.21 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Ameliorated poststenotic flow pattern with increase
of flow velocity in the left M1-MCA (flow velocity: 44/30 cm/s),
similar to the findings of the first examination.
Fig. B11.23 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Normalized flow signal in the left M1-MCA (flow
velocity: 88/43 cm/s).
Fig. B11.22 Extracranial duplex, longitudinal plane.Further normalization of the left ICA flow (flow velocity: 47/24 cm/s).
Fig. B11.24 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Normalized flow signal in the left A1-ACA (flow
velocity: 110/47 cm/s). Note the distinct flow velocity compared to
the left M1-MCA indicating blood supply to both A2-ACAs.
Fig. B11.25 TCCS (transorbital approach), left-sided insonation.
Normalized orthograde flow in the left OA (flow velocity: 45/
12 cm/s).
Fig. B11.26 TCCS (transtemporal approach), left-sided insonation,
thalamic plane. Normalized flow signal in the left distal P2-PCA (flow
velocity: 51/27 cm/s).
Case 11 Secondary Occlusion in Internal Carotid Artery Dissection
190
Discussion
Clinical Aspects
Arterial dissections of the brain-supplying arteries are
usually caused by an intimal tear, which allows blood to
enter between the layers of the arterial wall resulting in
intramural hematoma. Sometimes, no tear is present. In
these cases bleeding of the vasa vasorum is thought to be
the cause of the intramural hematoma. Most frequently
the hematoma is found within the medial layer. From there
it may evolve toward the subintimal or subadventitial
compartments. A dissection with accumulation of blood
between the intima and the media is more likely to cause
Degree of Neurosonologic Difficulty: Medium
vessel stenosis or occlusion. A dissection path between the
media and the adventitia may lead to the development of
aneurysms.
Dissections can be divided into spontaneous and trau-
matic (Mokri 1990). The pathogenesis of a spontaneous
dissection is unknown but an increased vessel wall vulnerability seems likely, especially as there is a link to known
connective tissue disorders such as Ehlers–Danlos and
Marfan syndromes and fibromuscular dysplasia. Mild ultrastructural connective tissue alterations have been
found in 68 % of patients with spontaneous dissection
despite the absence of any skin, joint, or skeletal abnormalities (Brandt et al. 1998). These patients may therefore
represent a “vascular” phenotype of an underlying connective tissue disorder. The potential link with common
vascular risk factors such as smoking, hypertension, or oral
contraceptives has not yet been evaluated in larger studies. Atherosclerosis appears to be distinctly uncommon in
these patients.
Spontaneous dissections of the carotid or vertebral ar-
teries occur in only about 2 % of all ischemic strokes. However, they are an important cause of stroke in young and
middle-aged patients. In these age groups spontaneous
dissections account for up to 25 % of cases (Schievink and
Roiter 2005). Spontaneous dissections, however, may be
underdiagnosed in the elderly (Ahl et al. 2004). Extracranial arteries are more frequently affected than intracranial
vessel segments (for further information about intracranial dissections, see Case 21, p. 261, and Case 24, p. 287).
The annual dissection rate in the extracranial ICA (3 per
100 000 per year) is twice as high as in the extracranial VA
(1.5 per 100 000 per year) (Schievink and Roiter 2005) (for
further discussion about VA dissections, see Case 19, p. 245
and Case 26, p. 306).
Patients with traumatic dissection always report an epi-
sode ofhead or neckinjury. The question of whether trivial
trauma may contribute to a cervical dissection is still a
matter of debate. There are reports of dissections in association with Valsalva maneuver, coughing, sneezing, vomiting, defecation, sexual activity, or chiropractic neck manipulation (Dziewas et al. 2003, Reuter et al. 2006). Furthermore, dissections have been reported during physical
exercise such as volleyball, tennis, or even after sudden
turns of the head (Barker et al.1976, Luken et al. 1979). It is
thoughtthatasuddenhyperextensionorrotationofthe
neck may then injure the ICA or VA as a result of mechanical stretching (Hufnagel et al.1999, Schievink 2001). However, there are no reliable statistics to assess the actual risk
of having a dissection due to abrupt movements of the
cervical spine (Brandt and Grond-Ginsbach 2002).
Our patient reported that his symptoms started during
mild exercise in a gym, but he denied any sudden hyperextension or rotation of the neck. However, he had history
of migraine with visual aura a condition which has been
associated with spontaneous cervical artery dissections
and is considered as an independent risk factor. In a hospital-based case–control study migraine was diagnosed in
49 % of patients with spontaneous dissection (Tzourio et al.
2002). Another case–control study including 72 patients
found the incidence of migraine to be 60 % compared with
30 % in the control group of infarcts without a dissection
and 18% in healthy controls (Pezzini et al. 2005). With
regard to gender differences, a study of 696 patients with
dissection, the incidence of migraine in women was 47 %
comparedwith20%inmen(Arnoldetal.2006b).
In spontaneous ICA dissection, pain most commonly
occurs in the form of headaches and facial or neck pain.
Pain is the presenting complaint in about 60 % of cases and
occurs during the course of the disease in about 75 % of
patients. As a sole manifestation pain may appear in up to
4.5 %. Unilateral pain is more frequent then bilateral pain
and headache in ICA dissection may be confounded with a
migraine attack. Interestingly, our patient with a known
history of migraine did not experience dissection-related
headaches.
Horner syndrome is considered to be a typical clinical
feature and was also present in our patient. Overall, however, it has only been observed in 40 % of cases with ICA
dissection. Isolated Horner syndrome may be seen in
about 10 % of cases. Cranial nerve palsies, mostly affecting
nerves IX–XII, are found in up to 16% of patients (Baumgartner and Bogousslavsky 2005).
Cerebral or retinal ischemia occurs in about 75 % of
spontaneous ICA dissection. In an analysis of 145 symptomatic patients, Baumgartner found ischemic stroke to be
the most common manifestation affecting 80 % of cases,
followed by cerebral transient ischemic attack (TIA) in
15%. Amaurosis fugax was present in 1 % of cases and a
retinal infarct occurred in 5 % of patients (Baumgartner et
al 2001). Retinal TIAs like in our patient with reduced
vision can be caused by embolism, such as in the typical
amaurosis fugax, or may be of hemodynamic origin due to
a diminished blood flow toward the optic nerve. The incidence of a hemodynamic-related visual impairment
might be underestimated, as they do not cause a typical
transient monocular blindness (Biousse et al. 1998).
In the majority of cases neuroimaging reveals territorial
MCA infarctions, which suggest arterial embolism as the
main cause of stroke in ICA dissection. In a study of 130
patients with brain infarction after ICA dissection, only one
Discussion
191
patient had an ACA infarction; all others had territorial
MCA infarcts. In 5 % of patients, additional border zone
infarctions (BZIs) were observed. In this study, BZI alone
did not occur (Benninger et al. 2004). Other studies reported an incidence of BZI of up to 16 % (Steinke et al. 1996).
In contrast, hemodynamic BZIs in patients with atherosclerotic symptomatic high-grade ICA stenoses or occlusionshavebeenobservedinapproximately50%ofcases
(Szabo et al. 2001). This difference may in part be explained by better and more effective collateral pathways
in the younger dissection population (for further discussion on border zone infarction, see Chapter 4, “Arterial
Ischemia,” p. 64, and Case 30, p. 338).
There is no evidence-based recommendation for the
therapeuticmanagement of cervical arterydissection. Currently the most frequently used treatment is an initial PTTguided anticoagulation with intravenous heparin, aiming
to prevent secondary embolism, followed by oral anticoagulation for 3–6 months. In a retrospective study no
difference was observed between oral anticoagulants
and aspirin in secondary prevention of ischemia in patients with ICA dissection (Engelter et al. 2000). A recently
published prospective observational study showed a nonsignificant trend toward better risk control with regard to
recurrent TIA, stroke, or death in patients treated with oral
anticoagulants (8.3 %) compared with aspirin (12.4%) (Beletsky et al. 2003). Anticoagulation, however, may lead to
secondary increase of the intramural hematoma, which
might cause progression of stenosis or even secondary
vessel occlusion. A study comprising 20 patients with ICA
stenosis caused by dissection, reported a delayed occlusion in 5 patients (25%) during heparin therapy. These
patients had much higher PTT values than those without
delayed occlusion, indicating the importance of diligent
PTTcontrol (Dreier et al. 2004). Our patient, asone of them,
was the only one who clinically deteriorated because of his
particularly unfavorable collateral pathways. A similar rate
of secondary vessel occlusion (29 %) was recently reported
(Dittrich et al. 2006). A large clinical trial to assess the role
of anticoagulants and aspirin in secondary stroke prevention is warranted (Engelter et al. 2007). Current treatment
should, as far as possible, be tailored to the condition of the
individual patient. As arterial embolism seems to be the
greatest risk in the acute stage, initial PTT-guided heparin
treatment should be attempted. Assessment of the CW and
the collateral function should be part of the initial examination. In cases with impaired collaterals, aspirin and
blood pressure stabilization may be preferred treatment
options. Systemic recombinant tissue plasminogen activator (rt-PA) thrombolysis in stroke caused by extracranial
dissection is probably safe. In a small study of 11 thrombolyzed patients with ICA dissection there were no deaths
and only one patient had symptomatic hemorrhage. Four
patients had an excellent outcome (Derex et al. 2000). In a
second report of 33 patients with ICA dissection no local
worsening, such as the formation of aneurysms or vessel
rupture, was observed. A modified Rankin Scale ≤ 2was
observed in 52 % of cases (Georgiadis et al. 2005). On the
base of these data, it seems therefore reasonable to perform thrombolysis in patients with signs of cerebral ischemia independently of the cause of arterial embolism.
The recommended 3–6 month period of oral anticoagulation is partly based on follow-up studies by Doppler and
duplex ultrasound showing recanalization within this
timeframe in most cases. During the recanalization process, oral anticoagulation might prevent downstream arterial embolism, but this assumption is not evidence
based. After its discontinuation, secondary prophylaxis
with platelet inhibitors is sometimes recommended on
an empirical basis. This might be particularly useful if the
dissection led to the formation of persistent extracranial
aneurysm (see also Case 26, p. 306).
Recanalization after ICA dissection, as in our patient, is a
frequent finding. In the case of an initial stenosis restitution occurs in about 70 %, most often completely. In vessel
occlusions at least a partial recanalization will take place in
about 90 % of cases. The process can start immediately and
may be completed within the first weeks (Steinke et al.
1994). Continuing vessel restitution beyond a period of 3
months is unlikely. Dissecting aneurysms (also called
pseudoaneurysms) may be found in 13–49 % of ICA dissections. They have been reported to persist in 46 %, to
disappear in 36 %, and to decrease in size in 18 % during an
observation period of several years. Aneurysm enlargement has not been described. The general prognosis is
good and stenting or prolonged oral anticoagulation is
not recommended (Guillon et al. 1999, Touzé et al. 2001).
The clinical long-term outcome is good independent of
recanalization or persistence of occlusion. The annual
stroke rate for the ipsilateral carotid territory was found
to be 0.3 % in reopened vessels and 0.7 % in permanent
occluded vessels (Kremer et al. 2003). The risk of a recurrent dissection in a patient without a family history or
connective tissue disorder is low, at about 1 % per year
(Schievink and Roiter 2005).
Angiologic and Anatomic Aspects
Ultrasound near the carotid bifurcation yields information
about the vessel lumen as well as mural and intramural
structures. However, the most common sites of ICA dissection, in contrast with atherosclerotic lesions, are at the
midcervical region of the ICA or near the base of the skull.
The intramural hematoma usually starts further downstream and dissecting aneurysms may involve any segment along the affected artery. Therefore, direct morphologic signs can rarely be detected with duplex ultrasound.
A digital subtraction angiography (DSA) study in patients
with ICA dissection demonstrated stenoses in 50 % of cases,
vessel occlusion in 30 % of cases, and vessel dilatation or
dissecting aneurysms in the remaining group (Pelkonen et
al. 2003). Other authors using DSA, CTA, and MRA found
occlusion rates of up to 51 % (Dziewas et al. 2003).
Degree of Neurosonologic Difficulty: Medium
Case 11 Secondary Occlusion in Internal Carotid Artery Dissection
192
High-grade stenoses are a frequent finding. When performing duplex sonography care should be taken in cases
with long segment stenosis and near occlusions as intrastenotic flow velocity might be normal or even reduced.
Furthermore, embolic occlusions of distal vessel segments
may result in reduced flow velocities. However, none of
the above findings are pathognomonic for a dissection.
Pre- and poststenotic vessel segments will show the familiar pre-and poststenotic flow patterns on which, for example, the presumed diagnosis of a distal ICA dissection may
be based. A systematic ultrasound analysis of hemodynamic parameters in 70 patients with known distal ICA
dissection revealed the following findings: a right to left
difference in common carotid artery (CCA) resistance in-
Degree of Neurosonologic Difficulty: Medium
dex of >10 % in 85.7 %, an > 30 % ipsilateral CCA flow reduction in 78.6 %, an ipsilateral biphasic (“staccato”)ICAflow
indicative of distal occlusion in 45.7 %, an increased distal
ICA flow velocity (defined as an ipsilateral ICA/CCA and
ipsilateral ICA/contralateral ICA systolic flow velocity >1.5)
in 8 %, and a retrograde OA flow in 38 % of cases. Direct
morphologic abnormalities, considered to be dissection
specific, were: a tapering occlusion in 11.4%, a double lumen in 7.1 %, and a localized ectasia distal of the carotid
sinus with concomitant eccentric narrowing suggestive of
intramural hematoma in 21.4% of cases. A hypoechogenic
or anechogenic intraluminal formation alone was not considered to be a specific finding, as it could also correspond
to a mural thrombus or an anechogenic plaque. Combining
direct and indirect signs, the sensitivity and specificity
were 90 % and 60 %, respectively, (Alecu et al. 2007).
Another study including 181 patients with 200 spontaneous ICA dissections assessed the extracranial as well as
intracranial hemodynamics. Pathological extracranial/intracranial ultrasound results in 145 patients with and 55
patients without cerebral and/or retinal ischemia were
present in 95 %/30 % and 71 %/4 %, respectively. An extracranial ICA stenosis > 80 % or an occlusion was found in
83 %/40 % of patients with and without ischemia (Baumgartner et al. 2001). Compared with DSA and/or MRA, a
combined application of extracranial and intracranial hemodynamic ultrasound parameters in patients with presumed ICA dissection yielded a diagnostic sensitivity, specificity, and positive and negative predictive values of 96 %,
94 %, 92 %, and 97 %, respectively (Benninger et al. 2006).
In summary, duplex ultrasound of the brain-supplying
arteries plays an important part in the initial investigation
as well as follow-up of patients with ICA dissection revealing abnormalities in more than 90 % of cases, mostly of
hemodynamic character. A combination of extra- and
transcranial color-coded duplex sonography provides the
greatest diagnostic yield. A combination of unilateral highgrade stenosis, absence of atherosclerosis (seen in 80–90 %
of dissections), and the young age of the affected patient
make the diagnosis of a ICA dissection very likely. However, if atherosclerosis is present, ultrasound carries the
risk of overlooking a dissection and presuming an atherosclerotic stenosis instead. It is worth mentioning that the
incidence of > 80 % ICA stenosis or occlusion is only 40 % in
patients without cerebral ischemia compared with 83 % in
those who had a stroke (Baumgartner et al. 2001). This
implies that further neuroradiological diagnostics must be
performed in patients with clinically suspected dissection,
even if ultrasound findings are normal.
Conventional angiography has long been the gold standard in the diagnosis of arterial dissections, since it can
show the arterial lumen and allows extensive characterization of carotid and vertebral arteries. The most common
findinginICAdissectionisthesmoothorirregulartapered
midcervical stenosis or occlusion. A dissection may be
assumed only if a rat-tail-shaped or flamelike occlusion
is present. Pathognomonic features such as an intima flap
or a double lumen are rarely detected. Pelkonen and coworkers (2003) found that most of their patients had
irregular stenoses (47 %), followed by occlusions (29 %),
dissecting aneurysms (17 %), or irregular dilatations (5 %).
A double lumen was observed in only 1 % (Pelkonen et al.
2003). The main problem of catheter angiography is its
invasiveness. In high-risk populations it carries a 4 % risk of
causing a permanent neurologic deficit (for further discussion, see Case 24, p. 287). Today,DSA has to be regarded
as a second-line method, not only because of the above
limitations but also because alternative and less invasive
methods yielding similar or even greater diagnostic accuracies are available.
MRI in combination with vascular ultrasound is now
mostly replacing conventional angiography in the diagnosis and follow-up of dissections of the carotid and vertebral
arteries. In particular, the option of directly visualizing the
intramural hematoma on cross-sectional images renders
MRI a very useful technique in presumptive vessel dissection. A direct demonstration of the widened vessel lumen
and the intramural hematoma succeeds in a large number
of patients. Blood-sensitive MRI, especially T1- with or
without fat suppression and T2-weighted sequences allow
detection of the intravascular hematoma about day three
as a distinct signal increase which subsequently fades up
to 2 months after acute dissection (Paciaroni et al. 2005).
However, in the hyperacute stage the hematoma is often
missed and the imaging might need to be repeated. Morphologically the hematoma may appear crescent shaped,
but it could be oval or circumferential (as seen in Case 20,
p. 251). A recent intraluminal thrombus may mimic wall
hematoma but often reveals a varying signal intensity,
especially of an intraluminal thrombus, may vary depending on its specific components (Schwaighofer et al.1990). A
crescent-shaped formation with homogeneously increased signal intensity is highly suggestive for dissection
but not specific while an additional thickening and widening of the external vessel lumen is confirmatory of dissection. If additionally performed, the flow-sensitive TOF
MRAisabletoshowflowreduction,forexample,dueto
a sub-basal extracranial stenosis in form of a reduced
intracranial ICA signal intensity. In-plane flow due to the
tortuous anatomical course of the ICA as well as turbulent
Discussion
193
flow may impair the image quality, e. g., lead to an overestimation of the degree of stenosis or to a false diagnosis
of a false occlusion. In the subacute stage a high-intensity
signal of the intraluminal clot may mimic intactblood flow.
Despite these restrictions, a sensitivity of 95 % and specificity of 99 % were reported for the detection of ICA dissection when TOF MRA was compared with DSA (Levy et al.
1994). The diagnostic yield, for example to detect dissecting aneurysms, might further be improved if contrastenhanced MRA is performed (Touzé etal.2001).Because
of its better spatial resolution and better visualization of
lumen narrowing, vessel occlusion, and dissecting aneurysm, contrast-enhanced MRA should be performed whenever MRI is used for diagnosis of presumed dissection.
Helical CT-angiography is a contrast-enhanced technique that sensitively depicts the characteristic imaging
appearance of a tapering vessel following dissection but
cannot directly visualize intramural hematoma, due to a
limited soft tissue contrast. It needs careful interpretation
withinthebaseoftheskullbecauseofthefrequentartifacts caused by the bony structures surrounding the ICA. A
critical evaluation of the source images might help to
evaluate the vessel continuity and integrity.Results similar
to those of MR techniques have been reported for the
detection and follow-up of ICA dissections (Leclerc et al.
1996). Because of the short investigation time, multislice
CTA is, if available, currently the first-line modality in
presumed cervicocerebral vascular pathology, especially
in stroke patients. This technique providescomprehensive
and high-resolution vesselassessment, superior to current
MRA modes. Like MRI, the CTA technique allows visualization of the frequently seen enlarged external vessel
diameter of the dissected vessels. An initial small study
comparing CTA and MRI/TOF MRA demonstrated CTA
superiority as it depicted all seven dissections, of which
two were missed by the MRI technique. In the same series,
CTA identified a dissecting aneurysm, missed by MRI (Elijovich et al. 2006). A new CT development is the recently
introduced CTA digital subtraction technique, which might
even help to overcome the above-mentioned problems of
vessel delineation in close proximity to the skull base
(Sakamoto et al. 2006).
Degree of Neurosonologic Difficulty: Medium
194
Case 12
Bilateral Proximal Extracranial Internal Carotid Artery Occlusion and
High-grade V1 Vertebral Artery Stenosis
Clinical Presentation
A 47-year-old man presented with a stepwise deterioration of a right-sided sensorimotor hemisyndrome that had
developed over the preceding weeks. His wife also reported transient episodes of speech disturbance and behavioral change over the same period. The patient had no
vascular risk factors except for pronounced nicotine misuse. Two weeks before his initial symptoms, he complainedof right-sided neckpain following atraffic accident
with a questionable whiplash injury that was treated by a
single session of chiropractic manipulation. Neurological
examination on admission revealed a right-sided mild
brachiofacial hemiparesis and Broca aphasia. Horner syndrome was not present (National Institutes of Health
Stroke Scale [NIHSS] score 4).
Initial Neuroradiologic Findings
Unenhanced cranial computed tomography (CT) demonstrated a cortical/subcortical territorial infarction in the
left anterior middle cerebral artery (MCA) territory. Magnetic resonance imaging (MRI) revealed additional hemodynamic infarctions; one large left-sided internal border
zone infarction and one small right frontal external border
zone infarction between the anterior cerebral artery (ACA)
and MCA territories (Figs. B12.1–B12.3).
Suspected Diagnosis
Multiple recurrent territorial and hemodynamic cerebral
ischemia in the left and right carotid artery territory.
Initial Neurosonologic Findings
Extracranial Duplex Sonography
B-mode sonography revealed only mild atherosclerosis.
Both common carotid arteries (CCAs) had a high-resistance flow signal with an increased pulsatility. Anechogenic material was present in the left internal carotid
artery (ICA), but no flow signal was seen directly above
the carotid bifurcation. The right ICA was also occluded
1 cm above the carotid bifurcation. Both external carotid
arteries (ECAs) showed normal flow signals without indirect signs of intracranial collateralization. Assessment of
the left vertebral artery (VA) demonstrated an increased
flow velocity and turbulence in the V0/V1-VA segmentand
a poststenotic flow pattern in the V2-VA segment. Normal
flow signals were seen in the V1-VA and V2-VA segment of
the right side. VA diameter of the V2-VA segment was
5.5 mm on the left side and 3.9 mm on the right side
(Figs. B12.4–B12.12).
Transcranial Duplex Sonography
A poststenotic flow pattern was observed in both MCAs.
Slight manual oscillation of the right VA at the atlas loop
led to positive oscillation effects in both MCAs. Blood flow
in both ACAs was orthograde and also showed a poststenotic flow pattern. Flow velocity in the P1 segment of the
posterior cerebral artery (PCA) on both sides was increased. Both posterior communicating arteries (PCoAs)
revealed biphasic turbulent signals indicating collateral
flow from the posterior to the anterior circulation. No
flow signals could be detected in either of the ophthalmic
arteries (OAs) (Figs. B12.13–B12.20).
Questions to Answer by Ultrasound Techniques
• Was there evidence of ahigh-grade stenosis or occlusion
of the brain-supplying arteries?
• If so, was it a result of atherosclerosis or dissection?
• What was the pattern of collateral blood flow?
Conclusion
BilateralproximalextracranialICAocclusion.High-grade
stenosis at the V0/V1-VA segment of the dominant left VA.
Intracranial collateral blood flow towards both MCA and
ACA territories via both PCoAs.
Clinical Course
195
Conventional Angiography
Digital subtraction angiography (DSA) confirmed bilateral
occlusion of the extracranial ICA and left high-grade proximal VA stenosis. Prominent collateral blood flow for the
anterior circulation via the PCoA on both sides was seen.
No signs of dissection or fibromuscular dysplasia could be
observed (Figs. B12.21–B12.26).
Figure B12.27 shows a schematic drawing of the extra- and
intracranial brain-supplying arteries of the patient.
Clinical Course
The etiology of the bilateral ICA occlusion remained unclear (24-hour electrocardiogram, echocardiography, coagulation studies, and vasculitis parameters normal), but
eventually atherosclerosis was suspected. A
photon emission computed tomography (SPECT) scan during acetazolamide administration to assess the risk of
further hemodynamically induced ischemic events demonstrated a preserved cerebrovascularreactivity (CVR) (for
further discussion, see Chapter 3, “Parameters of Cerebral
99 m
Tc sin gle
Degree of Neurosonologic Difficulty: Medium
Fig. B12.1 Unenhanced CCT, axial plane. Hypodensity in the cort-
ical/subcortical area of the left anterior MCA territory, indicating
territorial MCA ischemia (arrowhead).
Fig. B12.3 MR T2-weighted image, axial plane. Intact signal void of
the BA, but absent signal void in projection of both ICAs (arrows).
which is a strong indicator for severe ICA pathology
Fig. B12.2 MR T2-weighted image, axial plane. Multiple signal abnormalities within both hemispheres. Left-sided known anterior
territorial MCA infarction and assumed large internal border zone
infarction (arrows). In addition, right-sided small anterior external
border zone infarction (arrowhead).
Fig. B12.4 Extracranialduplex, longitudinal plane. Left CCA Doppler
spectrum with increased pulsatility (flow velocity: 41/11 cm/s).