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Table A5.1 Common carotid artery intima-media thickness distribution in a population-based ultrasound analysis: Maximal wall thickness,
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.
combined data from the left and right side. (From Howard et al 1993). Values above the 95th percentile can be considered as pathologic.
Ethnicity Percentile Women Men
Age (years) Age (years)
45 55 65 45 55 65
White 25th 0.47 0.55 0.61 0.52 0.59 0.65
50th
75th 0.61 0.71 0.81 0.70 0.80 0.93
90th 0.68 0.82 0.94 0.80 0.91 1.11
95th 0.73 0.91 1.04 0.89 1.00 1.30
Black 25th 0.51 0.59 0.63 0.53 0.61 0.72
50th 0.58 0.68 0.74 0.62 0.72 0.85
75th 0.65 0.78 0.85 0.72 0.84 1.01
90th 0.73 0.91 1.00 0.83 0.96 1.22
95th 0.81 1.03 1.12 0.90 1.07 1.43
0.54 0.62 0.71 0.60 0.68 0.77
109Arterial Pathology
the left side as on the right (67% versus 33%). Also plaque
thickness was greater on the left side (3.1 ± 1.2 versus 2.9 ±
1.3 mm), whereas grade of stenosis was similar (Selwaness
et al 2014). According to the Mannheim consensus criteria, atherosclerotic plaques are defi ned as follows: Plaque
is a focal structure encroaching into the arterial lumen of
at least 0.5 mm or 50% of the surrounding IMT value, or
demonstrates a thickness >1.5 mm as measured from the
media–adventitia interface to the intima–lumen interface
(Touboul et al 2012). Atherosclerotic plaques usually involve only one segment of the wall circumference; at the
carotid bifurcation they are often found on the posterior
wall. Atherosclerotic plaques can be further characterized
by the following criteria (Figs. A5.6–A5.11):
• Number: Singular, multiple.
• Location: Aff ected vessel, anterior/posterior wall, later-
al or medial wall.
• Extension: Circumscribed, longish.
• Form: Marginal, concentric/circular, eccentric/
semicircular.
• Size: Length in longitudinal section and thickness in
cross-section (in mm).
• Texture: Hyperechoic, isoechoic, hypoechoic, anechoic
(isoechogenicity = intima brightness), homogenous or
heterogeneous pattern, calcifi cations with or without
acoustic shadowing.
• Surface: Regular smooth, irregular with recess/ulcerated.
• Vessel lumen reduction: Grade of stenosis.
• Response of the plaque to contrast agents: Enhancement versus no enhancement.
Because of accessibility to duplex ultrasound and clinical relevance, plaque description focuses mainly on the
CCA and ICA. The vessel walls should be studied in both
planes. Transverse images are mandatory to delineate the
real extension of the plaque (Fig. A5.6 and Fig. A5.7). A
vessel ulcer may be detected in larger lesions (Fig. A5.8).
Plaques of low echogenicity may be diffi cult to detect in
routine B-mode examination, but color-mode imaging
AB
DC
Fig. A5.6 Extracranial duplex. (A–C) B-mode insonation. (A) Longitudinal view of the carotid bifurcation. Large near-wall hype rechoic
plaque (arrowhead) with pronounced acoustic shadowing (arrows).
(B) Cross-sectional view of the CCA: Semicircular eccentric plaque
of largely homogenous isoechogenicity and a smooth surface (arrows). Note the circumscribed anechoic lesion within the plaque
(middle arrow) which might be intraplaque hemorrhage or necrotic core. (C) Longitudinal view of the CCA: Multiple, predominantly
hyperechoic plaques (arrows). (D) Color-mode insonation, longitudinal view of the carotid bifurcation, composite image: Large hypoechoic material (arrow).
uncovers its extent and intraluminal eff ect (Fig. A5.9). A
homogenous hypoechoic plaque may appear similar to a
fresh thrombus (Fig. A5.10). In steno-occlusive disorders
of the CCA and ICA, description of plaque and stenosis
in the external carotid artery (ECA) becomes more relevant. The vertebral arteries (VAs), especially their most
frequently aff ected proximal part, are only rarely acces-
sible for B-mode analysis of plaque composition and even
plaque presence (see also Video
A5.1).
For follow-up studies plaque size can be measured
by recording the longest diameters in diff erent planes.
110 5 Vascular Pathology
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.
A
C
Fig. A5.7 Extracranial duplex. (A) Longitudinal view of the proximal ICA revealing an almost homogeneous hypoechoic near-wall
plaque (arrows). (B) Doppler spectrum analysis revealing a mildly
turbulent fl ow within normal velocities ranges (82/36 cm/s). (C,D)
Cross-sectional color-mode image of the proximal ICA: Circular, almost concentric mixed plaque with hyper- and hypoechoic areas.
Diameter reduction, 55%. Area reduction of the same location, 80%.
AB
B
D
A
C
Fig. A5.8 Extracranial duplex. (A) Color-mode image, longitudinal
plane. (B) Simultaneous Doppler spectrum analysis. Proximal carotid
artery stenosis with a fl ow velocity of 211/48 cm/s. (C) B-mode im-
age demonstrating a mild hyperechoic plaque. Note the anechoic
round structure (arrow) within the plaque, which might be overlooked if the gain is not carefully adjusted. (D) Same area in colormode imaging with reduced PRF. Note that the anechoic structure
is now delineated as a plaque ulcer comprising blood fl ow with low
fl ow velocities (arrow).
AB
B
D
DC
Fig. A5.9 Extracranial duplex, longitudinal view of the carotid bifurcation. (A) B-mode image with optimal gain setting revealing a
homogeneous mild hypoechoic near-wall plaque. (B) Color-mode
image helps to delineate the real size of the plaque or stenosis. (C)
Low gain leads to underestimation or overlooking of plaque. (D)
High gain leads to a loss of B-mode details in the surrounding tissue, but delineation of the plaque remains good.
As well as the fi nding of plaque progression, plaque re-
gression can also be observed under medical therapy. A
large study in 4,378 ultrasound-assessed patients even
reported a change in the number of patients with observed plaque regression from 25% before initiation of
an intensifi ed medical treatment, to 50% of patients after
initiation of treatment (Spence and Hackam 2010). The
authors concluded, “treating arteries without measuring plaque would be like treating hypertension without
measuring blood pressure” and recommended validation
of the fi ndings in a randomized clinical trial.
Fig. A5.10 Extracranial duplex, fresh thrombus in the proximal ICA
caused by a distal ICA occlusion. (A) Color-mode, cross-sectional
view showing an eccentric hypo- to isoechoic structure resembling
thrombotic material (arrows) with incomplete fi lling of the vessel
lumen. Note the color signal in the ECA (arrowhead). (B) B-mode,
longitudinal view delineates a complete fi lling of the proximal ICA
(arrows) by the fresh thrombus.
In our laboratories we measure the diameter of a
plaque in relation to the vessel in the cross-sectional
plane. Starting up with a local diameter reduction of 30%
we grade a local stenosis in 10% steps up to a stenosis of
50% (Fig. A5.11). A diameter reduction below 30% is not
reported as “stenosis” but described as severe atherosclerotic macroangiopathy.
Area measurements are an additional tool for assessing a
lumen reduction. This approach may become of greater relevance as high-resolution CT angiography (CTA) also allows
diameter and area measurements for comparison. Both
methods, however, are hindered by severe calcifi cations. In
111Arterial Pathology
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.
stenoses, the sonographer should note if the distal end
is detectable as it may have implications for the vascular
surgeon. If shadows caused by calcifi ed plaque impede
the assessment, this should also be noted. Homogenous
hypo echoic plaques are sometimes diffi cult to detect and
require optimal gain adjustments and the use of color-mode
imaging. In young patients without visible calcifi cations it
may be impossible to distinguish a dissection with wall hematoma from a large plaque of low echogenicity. In these
cases transverse planes should be studied. An enlargement
of the total vessel circumference indicates a dissection.
Atherosclerotic vessel wall changes in the brainsupplying arteries show a specifi c distribution pattern.
According to a four-vessel catheter angiographic analysis
of 3,788 patients in the chronic phase after cerebral ischemia performed in the 1960s, stenoses are most frequently found at the extracranial ICA origin followed by
the VA origin, the subclavian artery (SA), and the intracranial ICA whereas vessel occlusions may be found at slightly diff erent locations (Fig. A5.12). Note that the number
of intracranial stenoses may be an underestimate as no
subtraction technique was applied.
Like IMT enlargement, carotid plaques are associated
with several vascular risk factors and are strong predictors of stroke, death, or myocardial infarction even after
adjustment for classic risk factors such as hypertension,
smoking, and cholesterol levels (Silvestrini et al 2013,
Spence 2006).
A large number of studies have tried to identify “highrisk” (vulnerable/complicated) plaques by using morphologic ultrasound criteria. Calcium as a sign of regressive
plaque modulation seems to lower the risk. In contrast,
heterogeneous echogenicity and ulcerated plaques, i.e.,
with an irregular surface and/or ulceration, are postulated
to be less stable and more likely to cause embolic ischemic
events. Also, hypoechoic plaques seem to be more likely
to become symptomatic than hyperechoic plaques (Lal et
al 2002, 2006, Sabetai et al 2000). More recently, plaque
analy sis by means of contrast-enhanced (ce) ultrasound
has been introduced. The observable ultrasound perfusion characteristics seem to correlate well with histological fi ndings of plaque neovascularization (Li et al 2014).
The latter is more frequently seen in symptomatic patients with carotid artery stenosis (Xiong et al 2009). Histopathology fi ndings such as fi brous cap confi guration,
necrotic core, or intraplaque hemorrhage are beginning
to be investigated by ultrasound but are currently not
satisfactorily accessible (Funaki et al 2011) (for further
details, see Case 1 and Video
A5.2).
Plaques of intracranial vessels cannot be visualized by
ultrasound. An unenhanced CCT scan can be suggestive
of relevant atherosclerosis, as calcifi ed plaques will delin-
eate the aff ected vessel segments. Appropriate contrast
AB
DC
Fig. A5.11 Extracranial duplex, B-mode, cross-sectional view of
the ICA with diff erent grades of local stenosis (lumen reduction)
by eccentric plaques in the CCA. (A) Atherosclerotic plaque without
considerable lumen reduction. (B) Atherosclerotic plaque with 30%
vessel diameter reduction. (C) Atherosclerotic plaque with 40% vessel diameter reduction. (D) Atherosclerotic plaque with 50% vessel
diameter reduction.
A3.5 3.2
2.8
5.5
2.6 2.6
6.7
4.9
18.4
8.3
4.2
7.7
4.13.2 B
3.3
6.0
6.6
3.8
9.18.0
34.133.8
4.83.2
22.3
12.4
1.2
1.5
0.7
2.8
8.6
8.5
4.0
0.8
0.6
2.2
2.11.5 1.7
0.8
Fig. A5.12 Distribution pattern of stenosis
>50% (A) and vessel occlusion (B), assessed by
conventional angiography in patients in the
chronic phase following cerebral ischemia.
1.4
Preferential sites are indicated in yellow, fol-
1.7
lowed by turquoise (adapted from Hass et al
1.0
1968).
9.29.0
3.2
8.7
8.5
2.21.0
5.7
2.5
112 5 Vascular Pathology
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.
AB C
DE
Fig. A5.13 Unenhanced CCT scans, axial plane. Arrows indicate calcifi cations. (A,B) Distinct VA calcifi cation. Note the bet-
ter delineation of calcium formation in the conventional setting.
However, if diff erentiation of calcifi cation from bony structures is
diffi cult, visualization using the bone window settings may be help-
ful. (C) Calcifi cations of all vertebrobasilar segments. (D) Distinct
bilateral carotid siphon calcifi cations in the bone window setting.
(E) Rare fi nding of MCA calcifi cations.
window settings are essential when reading the CT scan,
as vessel calcifi cations appear exaggerated in the typical
window setting for brain parenchyma. Intracranial plaques
are highly prevalent in the elderly general population. In
a study population of 2,500 participants with a mean age
of 70 years, they were found in over 80% of cases (Bos et
al 2012). Usually they are present in the carotid siphon,
followed by the VA and BA. In the MCA, ACA, and PCA calcifi cations are rarely seen (Fig. A5.13). Carotid siphon cal-
cifi cations are correlated with advanced atherosclerosis of
the carotid bulb and severe carotid siphon calcifi cation is
correlated with stroke (Bos et al 2014, Fisher et al 1965b).
Calcifi cation of the vertebrobasilar arteries is more often
found in patients with stroke history (Pikija et al 2014). In
acute vessel occlusion, a fresh embolus can also be depicted by noncontrast CT, e.g., in proximal M1-MCA occlusion
in the form of a positive MCA sign, in M2-MCA occlusion as
a so-called “dot sign” (Fig. A5.14). However, in the diff er-
ential diagnosis between a thrombus/embolus or a calcifi -
cation clear diff erentiation may be diffi cult.
CT is particularly suitable for analyzing extracranial calcifi cations and other vessel wall pathologies of the
brain-supplying arteries. Since the introduction of multislice CT in 1999 high-resolution plaque assessment has
become available and even small ulcerations can be seen
as pits fi lled by contrast medium. CTA-determined mean
soft plaque thickness (assessed in the source data images)
seems to be a useful marker for symptomatic ICA plaques
and is also correlated with intraplaque hemorrhage (Gupta et al 2015a, 2015c). Conventional CTA, however, is less
meaningful in the analysis of plaque composition or surface description in noncalcifi ed plaques if compared with
histopathologic fi ndings (Denzel et al 2005, Oliver et al
1999, Saba et al 2007). Dual-source CT, allowing removal of hard plaque by using diff erent tube voltages, seems
more promising for plaque defi nition. Surface irregu-
larity or ulceration was more frequently detected with
d u a l - s o u r c e C T A t h a n w i t h T O F - M R A a n d d i g i t a l s u b -
Fig. A5.14 Unenhanced CCT, axial plane, parenchymal contrast
settings. Left: Positive right-sided “media sign” resembling a fresh
M1-MCA clot which extends into the M2 segments (arrow). Right:
Right-sided positive “dot sign” (arrow) indicating cross-sectional
imaging of embolic M2-MCA branch occlusion.
traction angiography (DSA) (Lv et al 2014). Cone beam
CTA has recently been reported to provide high spatial
resolution images of plaque morphology that might give
additional information on intracranial atherosclerosis
compared to DSA (Safain et al 2014).
As with duplex sonography, the behavior after contrast
agent administration may help to detect unstable plaques
and stenoses. In one study analyzing symptomatic and
asymptomatic carotid stenoses the presence of carotid
wall enhancement was higher in symptomatic stenoses
whereas the presence of either calcifi ed plaque or no wall
enhancement was more often observed in asymptomatic
patients (Romero et al 2013).
Unlike CCT, MRI is unable to depict plaque calcifi cation.
However, high-resolution MR—using blood-suppressed T1-,
T2-, and proton density-weighted fast spin echo, gradient
echo, and time-of-fl ight sequences—is able to visualize
carotid plaque components such as hemorrhages, the necrotizing core, and fi brous components in vitro and in vivo
(Makris et al 2015, Millon et al 2013, Puppini et al 2006).
Using 3D T1-weighted MRI of carotid plaques with histopathologic validation sensitivity and specifi city of 100% was
reported for discriminating vulnerable from stable plaques
(Narumi et al 2015). Gadolinium enhancement was also
detected in vulnerable plaques as has been shown after
histologic analysis of surgical specimens after carotid endarterectomy (Millon et al 2012). A new approach for the
detection of lipid-rich necrotic plaque cores is the diff u-
sion-prepared turbo-spin-echo (DP-TSE) technique which
allows plaque analysis with high spatial resolution (Xie
et al 2014). The use of MRI techniques may be particularly valuable in the determination of high-risk plaques, for
i n s t a n c e i n p a t i e n t s w i t h h i g h - g r a d e a s y m p t o m a t i c c a r o t i d
stenosis (Crouse 2006, Gupta et al 2013, Nighoghossian et al
2005, Saam et al 2006) or in patients in whom CTA cannot
be performed because of a renal insuffi ciency, often seen in
vascular patients.
113Arterial Pathology
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.
AB
C D
Fig. A5.15 MRI, axial plane. (A,B) Enlarged T2-weighted image.
(A) Normal fl ow void in both A1-ACA and M1-MCA segments.
(B) MCA stenosis causing a reduced fl ow void within the right M1-
MCA segment (arrow). (C) MRI, axial plane. Enlarged T2-weight-
ed image: Absent fl ow void within the left M1-MCA segment in
M1 occlusion (arrow). (D) Corresponding 3D TOF-MRA with absent
M1-MCA signal (arrow).
Despite advances in the description of extracranial carotid plaques, the current spatial resolution of MRI
prevents a detailed plaque evaluation of intracranial
s t e n o s e s . H e r e , h i g h - r e s o l u t i o n M R I w i t h a n d w i t h o u t
gadolinium administration using at least 3–7 T potentially allows the graduation of stenosis, the assessment
of plaque presence, and composition of intracranial wall
pathologies similar to the extracranial brain-supplying
arteries (Bodle et al 2013, Degnan et al 2012, Majidi et al
2013, Swartz et al 2009). Noncontrast sequences, in particular T2-weighted images, however, permit the assessment of vessel patency by analysis of the intravascular
fl ow void (Fig. A5.15). We strongly recommend that if a
CT scan or MRI has been performed before the ultrasound
examination, the available information about vessel wall
pathology should be taken into consideration.
Arterial Stiff ness
Arterial stiff ness is a relatively new biomarker which has
recently gained attention, in particular within an epidemiological context of early vascular risk assessment (Bruno
et al 2014, Laurent et al 2012, Tomiyama and Yamashina
2010). Besides the measures of IMT, arterial stiff ness seems
to be an additional and even earlier observable parameter,
related not only to general cardiovascular morbidity but
also to cerebral microangiopathy and impaired cognitive
brain function (Singer et al 2014). The analysis principle
is based on the assessment of arterial distensibility, i.e.,
the Windkessel function (for further reading also see also
Chapter 3, “Analysis of Cerebral Blood Flow”) which is defi ned by the elastic properties of the arterial vessel walls.
These elastic properties decrease with age and are related
to an individual’s systemic blood pressure. B-mode ultrasound makes it possible to measure vessel wall movements
and to analyze their extent and temporal pattern, resulting
A
Fig. A5.16 Extracranial duplex ultrasound, B-mode imaging of
the common carotid artery, longitudinal plane. (A,B) Automated
measurements of local arterial stiff ness in form of mean arterial
distensibility in two diff erent patients. Note the excellent pulse
curve reproduction (blue), derived from the moving vessel walls
in the ultrasound images. (A) High mean CCA distensibility of
531 ± 37 μm compared with (B) showing a reduced distensibility
value of 367 ± 30 μm. Note the correspondingly diff erent ampli-
tudes between both pulse curves.
B
in typical pulse wave curves (Fig. A5.16). Comparison of
time delay between pulse waves assessed in the carotid artery and in the femoral artery is then used to calculate the
pulse wave velocity (PWV = distance/transit time) which is
currently considered to be the “gold standard” for arterial
stiff ness assessments. Reference values derived from more
than 16,000 subjects have been published (Mattace-Raso
et al 2010) and can be used to identify individuals with an
increased cardiovascular risk. A variety of systems for routine assessment of arterial stiff ness are available. However,
newly emerging techniques such as ultrafast ultrasound
imaging, which even makes it possible to assess a local
pulse wave velocity, may further simplify this diagnostic
approach (Messas et al 2013; see also Chapter 1, “Ultrafast
Imaging” under “Imaging Modalities, Parameters, and Settings”). Attempts to evaluate arterial stiff ness in relation to
medical therapy have been made by analyzing the eff ect of
diff erent antihypertensive medications in coronary artery
disease. However, high-class evidence for treatment guidance is still lacking (Liao and Farmer 2014).
Dissection
Ultrasound as well as DSA, CTA, and MRI can be used in
diagnosis and follow-up of patients with isolated dissections of the extracranial brain-supplying arteries in
the ICA (Fig. A5.17, Fig. A5.18, Fig. A5.19, Fig. A5.20,
Fig. A5.21) and vertebral arteries (Fig. A5.22 and
Fig. A5.23; see also Videos
in patients with dissections of the CCA continuing from
lesions of the aortic arch (Fig. A5.24; see also Videos
A5.5 and A5.6). Clear ultrasound signs of dissection are
a large-vessel occlusion without atherothrombotic wall
pathology, a cone-shaped occlusion, and a vessel wall
hematoma with an anechoic or hypoechoic appearance. The latter leads to an obvious widening of the
A5.3 and A5.4), as well as
114 5 Vascular Pathology
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All rights reserved. Usage subject to terms and conditions of license.
A
Fig. A5.17 ICA dissection. (A) DSA, left CCA injection, lateral view:
Proximal occlusion of the ICA caused by a dissection. Note the typical cone-shaped or “fl ame-like” occlusion (arrow). (B,C) Duplex
ultrasound, longitudinal plane. (B) B-mode image demonstrating
the cone-shaped vessel narrowing (arrows). (C) Color-mode image
demonstrates absent fl ow in the distal ICA (arrows). Note that no
clear wall hematoma is visible in this case.
A
B
C
AB
Fig. A5.18 ICA dissection. (A) Contrast-enhanced 3D MRA, coronal
MIP in acute dissecting ICA occlusion 3 days after symptoms onset (arrow). (B) MR T1-weighted fat-suppressed image, axial plane
corresponding to the white dotted line in A showing a moderate
hyperintense vessel wall hematoma signal because of the recent
bleeding. The typical bright signal may appear days later. A fresh
intraluminal thrombus may mimic a wall hematoma. The marked
widening of the external vessel lumen (maximal 7.9 mm; arrowheads) is, however, confi rmatory of dissection in case of doubt.
Note the normal diameter of 4.5 mm in the unaff ected ICA (arrows)
with normal fl ow void indicating undisturbed fl ow.
B
Fig. A5.19 ICA dissection. (A) MR T1-weighted fat-suppressed
image, axial plane showing subacute ICA dissection. The vessel
wall hematoma appears brighter surrounding a patent lumen
but the vessel diameter is clearly widened (arrowheads) in
comparison to the normal contralateral diameter and flow void
(arrows). (B) Color-mode image of the mid ICA, axial plane,
c o r r e s p o n d i n g t o t h e M R i m a g e . A f i r s t l o o k m a y s u g g e s t n o r mal vessel appearance, but on a second look the eccentric
h o m o g e n o u s h y p o e c h o i c w a l l h e m a t o m a b e c o m e s o b v i o u s ( C).
(C) Inner circle: residual lumen, hardly affected; outer circle: delineation of widened outer vessel circumference.
C
vessel which can be best seen if it occurs in the V3-VA
segment at the atlas arch. If the dissection is in a more
distal location the widening of the ICA may be missed.
Other ultrasound fi ndings are irregular vessel mem-
brane with double lumen (Alecu et al 2007, Bartels
and Flügel 1996, Lu et al2000, Touboul et al 1988). As
well as occlusion, a dissection may also cause stenosis.
Dissections usually aff ect longer vessel segments and
are mostly found in extracranial locations. In contrast
to atherosclerotic vessel wall alterations, extra cranial
ICA dissections are located distally near the base of the
skull, which often limits their visualization by duplex
sonography.
However, on rare occasions, dissections may also
o c c u r o r e x t e n d i n t r a c r a n i a l l y . T h e s i t e o f d i s s e c tion should be determined according to its beginning. Intrastenotic fl ow velocities are often lower than
expected in vessel dissections if compared with short
segment stenoses of atherosclerotic origin. A dissecting
aneurysm may also be detected if accessible by ultrasound (Fig. A5.25). In the chronic phase after vessel recanalization a collapse-like appearance of the ICA may
be observed. Flow analysis then shows that the main
fl ow is into the ophthalmic artery (OA). In such a case
the ipsilateral anterior circulation is perfused via one
or both communicating arteries (Fig. A5.26). For a more
detailed discussion, see Case 11, Case 18, and Case 19.
Fibromuscular Dysplasia (FMD)
The brain-supplying arterial segments which are most
frequently aff ected by FMD, i.e., the distal segments of
the extracranial ICA and VA, are not readily accessible
by duplex ultrasound (see Fig. A5.1). FMD is therefore
rather diagnosed by DSA, CTA, or ce-MRA. However, if
proximal vessel segments are aff ected, the irregular ar-
terial vessel walls may also be visualized by duplex ultrasound (Fig. A5.27). There is an overlap between FMD
and vessel dissection, as patients with FMD are prone
to dissecting lesions. For a more detailed discussion of
FMD, see Case 13.
115Arterial Pathology
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.
A
Fig. A5.20 ICA dissection. (A) Contrast-enhanced 3D MRA, coronal MIP in dissecting ICA stenosis after partial recanalization
6 weeks after symptoms onset (arrows). (B) MR T1-weighted
fat-suppressed image, axial plane corresponding to the white
dotted line in A showing vessel wall hematoma now revealing
the typical crescent sign with an eccentric hyperintense rim indicating hematoma transformation. (C) Color-mode image of
the midpart ICA, axial plane, corresponding to the MR image
showing the almost hypoechoic and homogenous eccentric wall
hematoma (arrows).
AB
B
C
AB
1
2
Fig. A5.21 ICA dissection. (A) Contrast-enhanced 3D MRA, coronal
MIP in dissecting ICA stenosis after partial recanalization 6 weeks
after onset of symptoms. The white dotted line indicates the assumed widening of the outer wall due to intramural hematoma.
(B) Color-mode image of the midpart ICA, longitudinal insonation
plane. Corresponding to the MR image a large hypoechoic hematoma is detected. The fi ne hyperechoic line, indicated by the arrows
corresponds to the outer vessel wall (arrows). 1 indicates the normal vessel diameter of 4.5 mm, 2 indicates that the outer diameter
has almost doubled.
CD
Fig. A5.22 VA d issec tio n at the atlas ar ch ( V3) . (A) Color-mode image, longitudinal view demonstrating a normal diameter (4.0 mm),
vessel wall, and color signal of the proximal V2-VA. (B) Longitudinal
color-mode image at the atlas arch (V3) showing an enlarged vessel
diameter (8.2 mm) and a remaining perfused lumen of 2.1 mm.
(C) T1-weighted MRI, fat-suppressed image, axial plane showing
the wall hematoma (arrow). (D) Doppler spectrum analysis with
turbulent fl ow and raised intrastenotic fl ow velocity of 199/91 cm/s.
Vasculitis/Arteritis
Ultrasound, CTA, and MRI may be used to diagnose vasculitis of large- and medium-sized arteries and DSA of
all types including small-vessel arteritis. Conditions accessible to duplex ultrasound are intracranially the primary intracranial arteritis and extracranially Takayasu’s
arteritis and the giant cell arteritis (Fig. A5.1, Fig. A5.28,
Fig. A5.29). For a more detailed discussion of giant cell
arteritis, see Case 16; for Takayasu’s arteritis, see Case 23.
Fig. A5.23 VA di sse cti on at th e at las ar ch (V3 ). Left: T1 weighted
MRI, fat-suppressed image, coronal plane showing the wall hematoma (arrow). Right: Color-mode image, longitudinal view with initial hypoechoic enlarged vessel wall (top and middle). Complete
normalization after 2 months (bottom).
Carotidynia and Carotid Artery Vasospasm
Carotidynia is a rare clinical diagnosis. Patients report
mild to moderate neck pain with point-tenderness over
the anterolateral aspects of the neck, without history of
trauma. The pain responds quickly to steroids or nonsteroidal anti-infl ammatory drugs (NSAIDs). Duplex
sonography reveals hypoechoic wall thickening of the
carotid bulb in the region of tenderness leading to a mild
lumen narrowing and an outward extension of the ves-
116 5 Vascular Pathology
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AB
C
Fig. A5.24 Aortic arch dissection DeBakey type I, extending into
the CCA. Duplex ultrasound. (A) Cross-sectional image of the CCA.
Top: B-mode image revealing a hyperechoic membrane within the
vessel lumen. Bottom: Color-mode image demonstrates fl ow in
both lumina. (B,C) Longitudinal color-mode image and simultaneous Doppler spectrum analysis of the CCA. (B) Sample volume within the true lumen with antegrade unidirectional fl ow. (C) Sample
volume within the false lumen with bidirectional fl ow.
A
B
C
V2
C5C4
Fig. A5.25 V1-VA segment dissection before entering the fi rst
transverse process at C6. Left: Ce-MRA, coronal MIP showing a
dissecting aneurysm (white circle). Top : Ce-MRA, coronal MIP, 90°
counterclockwise rotated to correspond with the ultrasound image.
Bottom: Du plex s onography, B- mode co mpound im age: N ormal V1-
VA dia met er at th e mid par t seg men t ( d1 = 3. 9 mm) , d iam eter w idening of the distal V1-VA before entering the C6 transverse process
(d2 = 6.5 mm), corresponding color-mode image above demonstrating extended fi lling of a dissecting aneurysm, normal distal V2-VA
diameter between transverse processes C4 and C5 (d3 = 4.1 mm).
AB
C6
C
V1
Fig. A5.26 ICA dissection. (A) Contrast-enhanced 3D MRA, coronal
MIP in dissecting ICA stenosis after partial recanalization one year
after symptoms onset. The ICA reveals no wall irregularities but
the diameter of 2.8 mm is still lower than normal (arrowheads).
(B) Extracranial duplex, color-mode image, and Doppler spectrum
of the ICA origin, longitudinal insonation plane. Note the low velocity and mildly increased pulsatility (fl ow velocity 52/14 cm/s,
PI = 1.4). (C) TCCS, transorbital approach, color-mode image, and
Doppler spectrum of the ipsilateral ophthalmic artery (OA) revealing
comparable fl ow parameters (fl ow velocity 33/10 cm/s, PI = 1.3). In
the presence of a patent intracranial collateral fl ow through one or
both communicating arteries the ICA may be responsible for the OA
fl ow only, i.e., become an “extended OA,” also termed “OA-like ICA.”
sel wall. Regression or normalization is the usual fi nding
in follow-up examination after several weeks (Arning
2005, Schaumberg et al 2011). MRI corresponds with
duplex sonography describing a hyperintense lesion in
the distal CCA and carotid bifurcation. Gadolinium administration usually leads to an enhancement surrounding the carotid bifurcation without presence of stenosis
Fig. A5.27 Fibromuscular dysplasia: (A) Contrast-enhanced 3D
MRA, coronal MIP revealing marked elongations and caliber irregularities in the ICA (arrows) and even more in the VA (arrowheads).
(B,C) Extracranial duplex, longitudinal color-mode image of the ICA
showing proximal (B) and midpart (C) segmental narrowing and
dilation without raised fl ow velocity (spectrum not shown).
(Burton et al 2000). Also in MRI the fi ndings normalize
over time (Fig. A5.30 and Fig. A5.31). The underlying
pathology remains unclear (Taniguchi et al 2008): A
variant of vasculitis has been suggested. Dissection has
to be excluded and therefore MRI is mandatory. In all
image modalities the alterations may resemble a plaque
(Woo et al 2008). Knowledge of this rare and distinct
117Arterial Pathology
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AB
CD
Fig. A5.28 Ta ka ya su ’s a rt e ri ti s. D up l ex u lt ra so un d o f th e CC A .
11-MHz linear probe. (A,B) Cross-sectional plane. (A) B-mode im-
age: Homogenous, isoechoic to mildly hyperechoic circular vessel
wall thickening. (B) Color-mode image: Color fi lling of the remain-
ing arterial vessel lumen. (C) Doppler spectrum analysis of the affected CCA. (D) Color-mode, longitudinal plane of the same vessel
segment.
A
B
C
Fig. A5.29 Duplex ultrasound of the superfi cial temporal artery.
22-MHz linear probe. Left (A–C): Normal individual. Right (D–F):
Giant cell arteritis. (A) Cross-sectional B-mode image: Isoechoic unremarkable vessel wall. (D) Cross-sectional B-mode image:
Hypoechoic and enlarged vessel appearance. (B) Cross-sectional
color-mode image. Normal vessel wall appearance. (E) Cross-sectional color-mode image. Large circular hypoechoic wall thickening
in form of a typical halo sign. (C) Longitudinal color-mode image.
Isoechoic B-mode aspect of the vessel bordering tissue. (F) Longitudinal color-mode image. Hypoechoic wall thickening over the total
visible vessel length.
D
E
F
Fig. A5.30 Carotidynia. Images of a patient with typical subacute
neck pains. Top: B-mode image longitudinal (left) and transverse
plane (right). Note the mildly hypo-/isoechoic structure in the carotid bifurcation starting in the distal CCA and visible in both planes
which might be mistaken for a homogenous atheroma (arrows).
Right: Same patient with remitted symptoms after 2 weeks of
treatment with nonsteroid analgesics. Note a mild residual structure on the transverse plane only (arrow).
self-limiting syndrome is important and can avoid unnecessary and invasive procedures.
Another rare but distinct entity is recurrent extracranial carotid artery vasospasm. Since the fi rst descrip-
tion by Lieberman et al (1984) only a few patients,
some of them migraine suff erers, have been reported.
The fi rst patient diagnosed by duplex ultrasound pre-
sented in 1998. She was a 32-year-old woman suff er-
ing from cerebral ischemia due to recurrent stenoses of
Fig. A5.31 Carotidynia. MRI and ce-MRA of the same patient on the
day of the fi rst ultrasound examination. Top l eft : Circular but eccen-
tric hyperintense wall thickening (yellow circle). Bottom left: Homogenous contrast enhancement after gadolinium administration
(yellow circle). Middle: Ce-MRA, rotated coronal MIP. Mild proximal
ICA irregularities (arrows) indicate extraluminal location the pathology. Right: Ce-MRA, rotated coronal MIP. MRA revealing normaliza-
tion after 3 months (arrowhead) with only a mild residual vessel wall
thickening and without contrast enhancement (not shown).
the ICA ~4 cm distal to its origin (Arning et al 1998). In
2006 two further patients were reported, clinically also
suff ering from manifest stroke (Janzarik et al 2006).
Extracranial vasospasms as a cause of stroke might be
considered in patients with recurring ischemic events
and distal ICA stenosis without signs of dissection.
Treatment with NSAIDs and/or calcium channel blockers seemed the best option to reduce the frequency of
vasospasms.
118 5 Vascular Pathology
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ECA
Fig. A5.32 Extracranial duplex, cross-sectional view. (A) B-mode
image: ICA fi lled with mildly hyperechoic material, leading to an
eccentric lumen narrowing. (B) Color-mode image: Confi rmation of
the suspected stenosis. (C) Diameter measurements: D
(green bar), D
(D) Area measurements: A
= 10.1 mm2 (red circle), resulting in an 81% stenosis.
sis
ICA
= 3.4 (red bar), resulting in a 62% stenosis.
stenosis
BA
DC
total
= 52.4 mm2 (green circle), D
total
= 9 mm
steno-
Stenoses and Occlusions
In general all segments of the extracranial and the relevant parts of the intracranial brain-supplying arteries can
be assessed by duplex ultrasound, provided the insonation conditions are good. The extent and order of ultrasound investigation should always be oriented according
to the clinical picture and other relevant clinical data such
as age, vascular risk factors, concomitant circumstances
of the cerebral ischemia, and suspected etiology, based
on a radiologically documented stroke pattern if this is
available before ultrasound examination. For instance, in
a Caucasian who has suff ered an embolic ischemia in the
MCA territory, a proximal ICA stenosis should be considered fi rst, which can be assessed adequately by duplex
ultrasound. If no relevant pathology is found, the distal
extracranial ICA, the intracranial ICA in all its accessible
segments, as well as the MCA in its M1 and M2 segments
must be studied. In an Asian patient, a lesion in the MCA
has to be considered fi rst. In case of a cerebellar ischemia,
the question of a VA stenosis at its origin should be the
primary focus. If not found, a more distal VA stenoocclusive process, typically in the intracranial VA or BA,
has to be looked for. In the case of PCA territory ischemia,
the total visible length of the PCA has to be examined. A
single-vessel pathology might be the cause of the recent
ischemia but ipsilateral (tandem stenosis) or contralateral
steno-occlusive lesions may also present a challenge to
the interpretation of otherwise simple fi ndings.
80
60
40
Area (% stenosis)
20
0
020406080
Diameter (% stenosis)
Fig. A5.33 Calculated relationship of stenosis grade using the diameter and area method. Blue line: Relation in axisymmetric vessel narrowing. A 30% diameter stenosis is equivalent to a ~50%
area stenosis, and a 70% diameter stenosis is equivalent to a
~90% area stenosis. Red line: More linear relation between diameter and area stenosis in severely asymmetric plaque formation and
vessel narrowing.
brain-supplying arteries. For exact assessment of a stenosis all available criteria should be considered. The
proximal extracranial ICA is not only the most commonly
aff ected site (at least in Caucasians), but can also be used
to explain the main principles of ultrasonography in vessel disorders. The following remarks are mainly based on
studies of the extracranial ICA.
Direct Morphologic Assessment
Extracranial duplex ultrasound is able to visualize the arterial vessel lumen near and at the carotid bifurcation, the
formation of intraluminal and vessel-narrowing plaques,
or even complete vessel fi lling, e.g., with thrombotic ma-
terial. As the thrombotic material can be hypoechoic, analysis should always be performed using the combination of
B-mode and color-mode ultrasound. The latter considerably facilitates the detection of the residual perfused lumen
and helps to avoid overlooking, for example, a fresh, hypoechoic, or small fl oating thrombus. Care should be taken
to adjust pulse repetition frequency (PRF) and color gain
to prevent color overlapping beyond the perfused lumen.
Plaque calcifi cation, which may lead to pronounced acous-
tic shadowing, is a limitation for direct morphologic ultrasound assessment. This phenomenon may be observed in
up to 7% of patients (Polak et al 1989). Geometric lumen
reduction on B-mode and color-coded fl ow imaging can be
assessed in two ways: by calculating the reduction in the
cross-sectional diameter or the cross-sectional area.
Ultrasound Criteria of Stenoses
Within the extracranial brain-supplying arteries, duplex
ultrasound permits the morphologic analysis of the
a ff ected vessel segment. Direct (velocity within the ste-
nosis) and indirect hemodynamic eff ects of stenoses
(pre- and poststenotic velocities and waveform abnormalities) may be assessed in all extra- and intracranial
Diameter: Diameter assessments can be performed in
a longitudinal plane, such as with DSA. Color-mode imaging facilitates the recognition of echolucent material
and its use is therefore mandatory in addition to B-mode
imaging. Because of oversteering artifacts this method is
usually used in local ICA or CCA stenoses of ~50% and less.
Care should be taken that the anterior and posterior walls
are simultaneously visible. Measurements are performed
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