Atherosclerotic vertebral artery disease
Chapter
6 Ralf Dittrich and E. Bernd Ringelstein
Introduction
In this chapter we focus on atherosclerotic occlusive
disease of the vertebrobasilar (VB) arteries detectable
by advanced neurovascular ultrasound techniques, but
we will also touch upon steno-occlusive disorders of
the posterior cerebral artery, subclavian artery (SA),
as well as the aortic artery. Even subtle sonographic
abnormalities can indicate life-threatening VB occlu-
sion [1,2]. We will also address nonatherosclerotic dis-
eases of the brain-supplying arteries as far as relevant
for neurovascular ultrasound [3,4].
The clinical dynamics of the stroke syndromes
resulting from posterior circulation occlusive disease
(PCOD) vary widely with a gradual, stepwise or stut-
tered onset or course during hours or days, but also by
a sudden, one-step-only ictus making early prognostic
predictions particularly difficult [4,5]. This underlines
the necessity to clarify the underlying stroke etiology
as rapidly as possible.
From a modern perspective, PCOD, including VB
embolism accounts for 20–30% of all strokes, thus play-
ing a major role for the stroke burden of our aging soci-
eties. PCOD is particularly prominent among Asians
and black populations, mostly due to penetrating small
artery disease [4]. Figure 6.1 shows a diagram of the
posterior circulation addressing the various types of
arteries affected by steno-occlusive atherosclerosis or
embolism.
The most important determinant of outcome of
posterior circulation strokes is the nature of the causa-
tive vascular disease underlying the stroke. Following
acute VB ischemia, 1-month mortalities range from 2%
to over 70% making meaningful predictions based only
on clinical findings impossible. By contrast, the annual
stroke rate in asymptomatic stenosis of the vertebral
Manual of Neurosonology, ed. László Csiba and Claudio Baracchini. Published by Cambridge University Press. © Cambridge
University Press 2016.
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artery (VA) origin (see V0 segment in Table 6.1 later in
this chapter) is as low as 0.4% [6].
As soon as VB ischemic stroke (i.e., posterior fossa
stroke or posterior circulation stroke) has occurred
and posterior cerebral bleeding has been excluded by
computed tomography (CT) or magnetic resonance
imaging (MRI), the first important differentiation of
the underlying pathogenesis is small vessel versus large
vessel disease. While the former as singular stroke
(not as a generalized cerebral disorder) has a relatively
benign prognosis, large artery occlusive disease can
have lethal consequences and requires a rapid diagnos-
tic workup in order to meet therapeutic time windows
in due time (see later in chapter). A firm initial differ-
ential diagnosis is best supported by MRI of the pos-
terior fossa, thalamus and posterior lobes combined
with a thorough arterial ultrasound check. The reason
for this combined approach is as follows: while large
artery disease can directly be visualized at the level of
the arteries themselves by ultrasound and other nonin-
vasive arterial imaging techniques, the affected small
cerebral arteries (Figure 6.1, insert 1A) leading to lacu-
nar infarcts cannot directly be investigated during life
because they are too small in diameter. Cerebral small
vessel disease is inferred indirectly from the lesional
pattern of lacunar infarcts on CT or MRI. It should be
kept in mind, however, that lacunar-like, complete or
partial necrotic lesions of the pons, midbrain or thala-
mus can also be caused by large artery disease like a
transient basilar artery embolus temporarily blocking
deep perforators to the basis pontis or to the thala-
mus (Figure 6.1, insert 5). An unstable atherosclerotic
plaque in the basilar artery can cause a similar type of
lesion before, all of a sudden, it progresses to complete
basilar artery thrombosis (Figure 6.1, insert 6). It is
therefore reasonable to investigate the large arteries of
87
 Chapter 6: Atherosclerotic vertebral artery disease
1A 1B 2A 2B
1 4,5,6
2
3
6 5 4 3
Figure 6.1 Most frequent types of vertebrobasilar (VB) occlusive
disease. Insets: (1a) Cerebral small vessel disease of pontine
perforator by atherolipohyalinosis (inset: cross section of the
lesion). (1B) Atheroma of the basilar artery occluding a penetrating
small artery mimicking small vessel disease (so-called branch
occlusion). (2A,B) Severe atheromatous stenosis/occlusion of major
basilar branch (e.g., anterior cerebellar artery) by atherothrombosis
(A) or embolism (B). (3) Predilection site of distal vertebral artery
atherothrombosis in the V4 segment. Thrombotic occlusion
simultaneously causing blockage of penetrating small arteries to
the medulla oblongata. (4) Diffuse severe atheromatosis of the
VB artery, finally leading to complete basilar artery thrombosis in
insert (6). (5) Cardiac embolus sticking in the mid basilar artery with
unpredictable consequences (e.g., VB transient ischemic attack
due to rapid lysis, or causing locked-in syndrome due to complete
transsectional pontine necrosis).
the VB system also in patients who present with lacu-
nar syndromes either clinically, or morphologically
on MRI.
Twenty percent of the cerebral blood volume
is channeled into the VB distribution leading to
the little-known fact that approximately 20% of
aorto-cardiac cerebral emboli enter the VB pathway.
By reviewing various stroke registries, Caplan [4] came
to the conclusion that about 20–30% of all ischemic
VB strokes are cardioembolic (in the wider sense of
aorto-cardioembolic etiology) with a present trend to
even higher proportions due to improved cardiac diag-
nostics, but also due to the worldwide atrial fibrillation
epidemic [7,8].
Presumably, intra-arterial VB embolism aris-
88
ing from occlusions or high-grade stenosis of the
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extracranial VAs (i.e., the above-described V0–V3 seg-
ments) is still underestimated due to lack of systematic
and longitudinal ultrasound studies on this particular
type of disease combined with microembolus detec-
tion [9,10,11].
Short overview of existing
non-ultrasound imaging techniques
The correct allocation of stroke symptoms to the VB
circulation (i.e., to PCOD), has been revolutionized by
modern imaging techniques, in particular by means
of both magnetic resonance brain imaging (MRI) of
the posterior fossa and systematic neurosonology of
the brain supplying neck arteries, and large intracra-
nial arteries with color-coded duplex scanning and
transcranial Doppler [12,13], as well as improved car-
diac imaging and rhythm monitoring. Invasive digital
subtraction angiography (DSA) and completely non-
invasive CT and MRI arteriograms added consider-
ably to our present understanding of VB occlusive
disease [14].
Particularly in the posterior circulation, ischemic
strokes vary widely in their severity, ranging from
mild, transient lacunar strokes to devastating strokes
(because of the infarcts’ strategic localization like
thalamic infarcts) or even to life-threatening, huge
pontocerebellar infarctions due to basilar artery
thrombosis with up to 70% mortality [15].
Focused questions
• Why is VB occlusive disease clinically so
important for investigation?
• What is the specific role of neurovascular
ultrasound among the spectrum of presently
available diagnostic tools?
• Which other imaging techniques are important for
the VB system?
• Which steps of the ultrasound investigation
are particularly useful and help to improve the
management of the patient?
• Is there a role of VB ultrasound for the patient’s
follow-up?
Anatomy
For better anatomical orientation, and because of
the specific and different prognostic and therapeutic
impact of VB occlusive disease, the following nine

arterial segments should be considered individually
and investigated separately: (1) V0 (0 = zero) segment
of the VA (i.e., the origin [mouth] of the VA normally
arising from the SA) (2) the V1 segment of the VA
extending from its origin downstream to its entrance
into the transverse processes of the vertebral column
(mostly at C6), (3) the V2 segment of the VA extending
throughout the bony canal of the transverse processes
C6 to C2, (4) the V3 segment extending from beyond
the atlas to the foramen magnum and dura, and (5) V4
extending from the dura up to the conjunction with
the companion VA to form the (6) basilar artery. The
proximal and distal parts of the basilar artery should
also be considered separately. The same holds true for
(7) the P1 and P2 segments of the posterior cerebral
artery (each of them separated from one another by
the origin of the posterior communicating artery).
(8) The proximal SA and the brachiocephalic trunk
are brain-supplying vessels reaching from the aortic
arch to the origin of the VA, or right common carotid
artery, respectively [16], whereas (9) the distal SA is
a limb-supplying, high resistance vessel. By means of
a subclavian steal mechanism, however, it may cause
abnormal cerebral hemodynamics within the VB
distribution.
Basic imaging tips
Table 6.1 lists the above-listed arterial segments of the
VB system and the nature of the disease most probably
affecting them, as well as preferable ultrasound tech-
niques for interrogation.
Steps of ultrasound investigation to
approach vertebrobasilar occlusive
disease
V0/V1 segment
With continuous-wave (CW) Doppler probes, all seg-
ments of the VA can be insonated, a clear-cut advan-
tage of this simple technique during initial screening.
For the VA’s origin, a 4-MHz probe is feasible. The
patient is lying in a supine position with his/her head
straight and the neck extended. The anatomical land-
mark is the proximal part of the SA with its charac-
teristic triphasic flow pattern. After identifying this
artery proximally, the probe should be moved slowly
along the anterior lower neck within the supraclavicu-
lar fossa in a distal and posterior direction. There is a
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Chapter 6: Atherosclerotic vertebral artery disease
change of the flow form from a triphasic waveform to
a sharp rise in flow velocity during systole and grad-
ual tapering of continuous forward flow throughout
diastole. This is the characteristic waveform of the VA
due to the low resistance vascular bed of the hindbrain
[17]. For the unequivocal identification of the VA it is
helpful to rhythmically compress it behind the mas-
toid at the level of the V3 segment. This manipulation
leads to a short repetitive modulation of the diastolic
flow and allows a correct identification of the VA. The
origin of the VA could be found in approximately
65–85% of patients [18,19]. Color-coded duplex
sonography may facilitate the insonation of the verte-
bral origin. Particularly on the right side, it is easy to
visualize its origin with a linear 7–15-MHz probe. In
obese patients with a short neck, a 5–8-MHz sectorial
probe could be superior. With the ongoing develop-
ment of color-coded duplex sonography instruments,
we recommend using this technique.
Specific findings at the V0/V1 segment
The normal mean blood flow velocity at the origin of
the VA is 64 cm/s (range 30–100 cm/s) [20]. However,
these velocities can differ considerably due to frequent
asymmetries in the VA diameter in approximately 73%
of normal individuals [21].
Pragmatically, a low-grade stenosis (<50%)
at the origin of the VA can be diagnosed by means
of a peak systolic velocity (PSV) at its origin of
≥85 cm/s. Additional criteria are the ratio of the PSV
at the origin/PSV at the V2 segment of ≥1.3, and the
end-diastolic velocity at the origin being ≥27 cm/s.
For a medium-grade stenosis of 50–69%, a PSV at the
origin of ≥140 cm/s is characteristic. Additional crite-
ria are a ratio of the PSV at the origin/PSV at the V2 of
≥2.1, and an end-diastolic velocity at the origin being
≥35 cm/s. For the diagnosis of a high-grade stenosis
(with 70–99% lumen narrowing), a PSV at the VA’s
origin of ≥210 cm/s is mandatory. This diagnosis is
supported by ancillary criteria (like an PSV origin/
PSV V2 ratio of ≥4.0, and an end-diastolic velocity at
the origin of ≥50 cm/s [22,23]). In our experience, the
peak systolic velocity is the most robust criterion. In
case of VA occlusion, the diagnosis is more difficult
due to the anatomical vicinity of the inferior thyroid
artery and the frequent development of cervical col-
lateral pathways mimicking a normal anatomy. The
absence of a flow signal has to be interpreted with
caution. 89
 Chapter 6: Atherosclerotic vertebral artery disease

Table 6.1 Posterior circulation disease: site, frequency, and type

Arterial segment Frequency Most probable Typical vascular Ultrasound Preferred probe
of affection pathogenesis complication technique to use
V0 Frequent Atherosclerotic Thromboembolism CWD CWD 4 MHz
Origin of VA (atherothrombotic) hardly CCDS Linear probe
hemodynamic 6–12 MHz
Sectoral probe 5–8
MHz
V1 Rare Dissection Thromboembolism CWD Linear probe 6–12
Free proximal segment CCDS MHz
V2 Rare Dissection Thromboembolic CCDS Linear probe 6–12
Bony canal of cervical rarely mechanical rarely hemodynamic (complete US MHz
column compression shadow at level
sometimes of transverse
traumatic processes)
V3 Very rare Dissection Thromboembolism CWD CWD 4 MHz
Atlas loop of VA rarely arteritis (rarely CCDS Linear probe
Reaching to foramen hemodynamic) 6–12 MHz
ovale Sectoral probe 5–8
MHz
V4 Frequent Atherothrombotic Thromboembolic TCD TCD 2 MHz
intradural part of distal occlusion TC-CCDS TC-CCDS 2–3 MHz
VA thromboembolism
Basilar artery (BA) Frequent Atherothrombotic Any of the above TCD TCD 2 MHz
– proximal embolic TC-CCDS TC-CCDS 2–3 MHz
(caudal) rarely arteritis
– distal (oral)
Posterior cerebral artery Frequent Embolic more Occlusion and TCD TCD 2 MHz
– P1 (proxymal) frequent than peripheral embolism TC-CCDS TC-CCDS 2–3 MHz
– P2 (distal) atherosclerotic by atherothrombosis
rarely arteritis
Subclavian artery Frequent Atherosclerosis Strong marker CWD CWD 4 MHz
– proximal lesion of CAD CCDS Sectoral probe 5–8
– distal if prox.: SC steal MHz
mechanism
Persistent primitive Very rare Developmental Prawn to TCD TCD 2 MHz
trigeminal artery anomaly cardiogenic TC-CCDS TC-CCDS 2–3 MHz
embolism
(otherwise
unknown)
CAD = coronary artery disease; CCDS = color-coded duplex scanning; CWD = continuous-wave Doppler; SC = subclavian;
TC = transcranial; TCD = transcranial Doppler; US = ultrasound; VA = vertebral artery.

V2 segment segments (or more) of the V2 segment of the VA are

For the investigation of the V2 segment of the VA,
color-coded duplex sonography with a 7–15-MHz
linear ultrasound probe is superior to CW Doppler
sonography alone because it allows the unequivocal
identification of the vascular bed of the VA as such. The
90 acoustic shadows from the transverse processes of the
vertebrae will appear as a helpful landmark because the
directly located between these processes [24].
Specific findings at the V2 segment
In the V2 segment, the normal peak systolic flow ranges
from19 to 98 (mean 56) cm/sec [18]. A focal increase
to >100 cm/s is indicative of a significant stenosis [25].
However, an atherosclerotic stenosis in the V2 segment

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 Chapter 6: Atherosclerotic vertebral artery disease

Figure 6.2 Color-coded duplex

sonography with a sectoral probe.
Stenosis of the vertebral artery in the V0
segment with a peak systolic velocity of
300 cm/s. The subclavian artery is visible
on the right side.

Figure 6.3 Dissection of the VA with

an intramural hematoma, B-mode
investigation with a linear ultrasound
probe. The red lines show the course of
the arterial lumen and the arrows mark
the intramural hematoma.

is very rare, as opposed to dissections of the VA typi-
cally occurring in the V2/V3 segment [26].
Occlusions of the VA in the V2 segment are char-
acterized by the absence of flow during color-coded
duplex sonography, or by a high-resistance flow pat-
tern proximal to the occlusion [27]. With color-coded
duplex sonography it is possible to visualize the
V2 segment in up to 100% [22], therefore this is the
method of choice. However, its positive predictive
value is limited because VA hypoplasia can also lead to
a high-resistance waveform [28,29]. An indirect sign
for a proximal VA stenosis is the decreased poststenotic
pulsatility. In combination with the direct visualiza- 91
tion of the V2 segment during color-coded duplex, this

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 Chapter 6: Atherosclerotic vertebral artery disease
criterion achieved a 71% sensitivity and 99% specificity
for the detection of >70% proximal VA stenosis [30].
The diameter of the VAs is mostly different on either
side. A diameter of <2.5 mm has been defined to rep-
resent hypoplasia and seems to be an independent risk
factor for VA atherothrombosis and VB stroke [31].
V3 segment
With the 4-Mhz CW Doppler probe, the V3 segment
can be insonated reliably. Placed behind the mastoid
and directed toward the contralateral eye, the typical
VA waveform will be identified in either direction due
to the tortuous course of the artery in this segment (the
so-called atlas loop). Again, color-coded duplex sonog-
raphy with a sectorial probe, or a >7.5-MHz linear
probe, or a 2–4-MHz phased array transducer facilitates
the artery’s identification. The appearance of the VA in
this location is comparable to the handle of a coffee cup.
In the proximal part of the atlas loop, the direction of
the blood flow is toward the probe, whereas in the distal
part blood is flowing in the opposite direction.
Specific findings at the V3 segment
In the V3 segment, atherosclerosis is nearly never
92 found. If this segment is stenosed at all, a VA dissec-
tion is the most frequent cause of stenosis or occlusion
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Figure 6.4 Alternating flow in the V3
segment of the VA due to proximal VA
occlusion at the V4 level. The red lines
mark the vascular bed of the VA.
(26,32). There is no clear cut-off value of the peak sys-
tolic velocity to define a V3 stenosis, but a significant
difference of the flow on the right compared to the
left in the absence of hypoplasia is indicative of a sig-
nificant stenosis. The bending or looping course of the
artery makes an angularly corrected measurement of
the flow velocity difficult or even impossible. Therefore
the afferent and efferent part of the artery should be
investigated separately.
Most frequently, indirect signs of a proximal or dis-
tal atherosclerotic VA steno-occlusion can be demon-
strated. An example is the alternating flow in the V3
segment due to a proximal occlusion, or a preocclusive
signal due to a distal VA occlusion.
V4 segment and basilar artery
The intracranial (better to say “intradural”) V4 seg-
ment can best be assessed by means of a pulsed-wave
2-MHz probe. Either in the supine position with slight
contralateral rotation or upright position, the investiga-
tion should start in a paramedian position of the probe
at the upper part of the neck through the suboccipital
transforaminal window. After identification of the VA
at a depth of 60–66 mm, the probe should slowly be
shifted along the medial and cephalad direction aiming
at the bridge of the nose. The origin of the basilar artery

will be hit at a depth of 75–80 mm, or above [12]. The
advantage of the color-coded duplex sonography with
a 2–4-MHz phased-array transducer is the direct visu-
alization of both the V4 segments and the basilar artery.
The blood flow direction is away from the probe, and
the junction of both V4 segments forming the origin of
the basilar artery looks like an inverted “y.”
Specific findings at the V4 segment and the
basilar artery
The intracranial VA and the basilar artery are predi-
lection sites for atherosclerosis [33]. The normal peak
systolic velocity is <100 cm/s, a stenosis can be diag-
nosed with a flow velocity of ≥120 cm/s (correspond-
ing to >3-kHz frequency shift). Increased pulsatility
in the proximal VA is an indirect sign, but this is only
indicative as long as the artery has a normal diameter
and no proximal stenosis [34]. A focal increase of the
peak systolic velocity is, however, also indicative of a
stenosis (see Figures 6.6 and 6.7). Additional echocon-
trast agent can be very useful for a confident diagnosis,
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Chapter 6: Atherosclerotic vertebral artery disease
Figure 6.5 High-resistance preocclusive
signal in the V3 segment due to a distal
V4 occlusion. The white lines mark the
arterial course of the VA and the Doppler
signals show the typical sharp small
systole without any diastolic signal.
since enhancement of the arteries allows for superior
visualization of the VA [35]. Whenever a basilar artery
steno-occlusive disease, or a high-grade V4 stenosis
should quickly be ruled out, contrast agents should be
used for a swift and more accurate diagnosis.
Subclavian steal phenomenon
The subclavian steal phenomenon is caused by a stenosis
of the SA proximal to the VA origin leading to a transsten-
otic pressure drop and delay of the pulse wave traveling
cephalad. The degree of the stenosis of the SA correlates
with the downstream flow changes in the VA best seen
in the V2 segment. An SA stenosis of about 50% leads
to an early systolic deceleration of the VA flow followed
by a rounded systolic peak. This phenomenon is prob-
ably caused by the Venturi effect at the ostium of the VA
[29,36]. An SA stenosis of >80% leads to an incomplete
steal with a bidirectional VA wave form (Figure 6.8).
A complete steal with a retrograde flow in the corre-
sponding VA is found in patients with very high-grade 93
stenosis or occlusion of the proximal SA.
 Chapter 6: Atherosclerotic vertebral artery disease
A Figure 6.6 Low-grade stenosis
The clinical impact of the subclavian steal phe-
nomenon is a matter of debate and has probably been
overestimated in the past. Only rarely is a steal phe-
nomenon associated with hemodynamically caused
ischemic brainstem symptoms [37,38,39]. This is why
the steal phenomenon should strictly be separated
from the subclavian steal syndrome which is rare and
is defined by clinical VB ischemic signs and symptoms.
Dissections of the vertebrobasilar
circulation
Dissections are the third most frequent type of occlu-
sive disease in the VB system. They are frequently, but
not always, associated with a throbbing ache in the pos-
94
terior or lateral anterior neck. They come along with a
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of the basilar artery with on-site
peak systolic velocity of <100 cm/s.
The focal increase of the flow
velocity is indicative of the stenosis.
(A) Prestenotic 45 cm/s flow in the
basilar artery at a depth of 84 mm.
(B) Focal increase of the peak systolic
velocity by about 50% up to 80 cm/s at
an insonation depth of 94 mm.
very high risk of arterio-arterial embolism into the basi-
lar distribution. Color-coded duplex sonography (but
also CW Doppler or transcranial Doppler sonography)
can help to quickly differentiate this type of lesion by its
typical location different from atherothrombosis [40].
Dissections preferably affect those arterial segments not,
or less, damaged by atherosclerosis like the V2 or V3 seg-
ment (see earlier section). Additionally, the diagnosis is
highly suggested by several typical features of the lesion
itself seen within the ultrasound image (Figure 6.3).
Vertebrobasilar arteritis
Another rare but clinically important differential
diagnosis is arteritis. The etiological background can
be manifold like infectious arteritis of the intracranial
VB artery (syphilis, borreliosis, herpes zoster, tropical
 Chapter 6: Atherosclerotic vertebral artery disease

Figure 6.7 Subsequent confirmation

of the low-grade BA stenosis on
conventional angiography.

Figure 6.8 Bidirectional flow in the V2

segment of the VA due to a left-sided
proximal >80% subclavian stenosis.

fungi), rarely granulomatous angiitis of the central

nervous system, or other rare entities with specific
Other types of vertebrobasilar occlusive
ultrasound findings like Takayasu disease (pulseless disease
syndrome) [41], Moya-Moya disease or Moya-Moya If multiple stenotic lesions can be detected in vari-
syndrome, and also arteritis temporalis (Horton’s arte- ous VB segments, recent subarachnoid hemorrhage 95
ritis, giant cell arteritis [41–47]). with vasospasm should be considered. The explosive
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 Chapter 6: Atherosclerotic vertebral artery disease
headache may pass unnoticed because of initial coma,
particular in people who live on their own when later
found helpless in their homes. The same holds true for
bacterial meningitis and for ergot alkaloid intoxication
and drug abuse (“speed”).
Mechanical (“rotational”) obstruction of one VA
is frequent and physiological, but very rarely symp-
tomatic because this requires (near) occlusion of the
companion VA (so-called bow hunter’s syndrome).
In the VB system, the ultrasound is both difficult
and suitable for a solid vascular diagnosis and progno-
sis [48]. On the one hand, the anatomy limits the ultra-
sound accessibility to short arterial segments only, but
on the other hand the VB system is quite resistant to
critical flow drops as long as systemic blood pressure is
in a normal range [49].
Recent progress and future directions
An important, relatively new approach is microembo-
lus (MES) detection. In a recent study on 140 patients
with posterior circulation ischemia, the detection of
MES was associated with severe intracranial VB ste-
nosis and embolic infarction [11]. However, the probe
position and insonation through the suboccipital bone
window is fragile and not suitable for clinical routine.
96 Another approach was blood flow volume meas-
urement to detect patients prone to VB ischemia. On
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Figure 6.9 The duplex scan of the
temporal superficial artery shows an
echolucent thickening of the arterial wall
around the red-colored blood flow. This
finding is indicative and characteristic for
a temporal arteritis.
an individual basis, however, this technique could
not deliver diagnostically useful information, and its
application remained restricted to cohort studies so far
[50–54].
Automated embolus detection with self-adjusting
probes is a new technical field with major potential to
significantly improve ultrasound-based VB diagnos-
tics in the future. This relies mainly on the incorpora-
tion of modern robotics into this field.
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