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Vertebral artery
Stenosis Hypoplasia
Chapter 5 · Extracranial Cerebral Arteries
344
5 Intrastenotic-to-prestenotic PSV ratio: not meaningful
due to completely dierent hemodynamic situation in
the subclavian artery.
In view of these diculties, an exception is made here and
the intrastenotic-to-poststenotic PSV ratio is accepted for
stenosis grading (see nomogram in . Fig. 1.48). High- grade
stenosis is diagnosed when there is a marked increase in PSV
(>160cm/s; see . Fig.5.88 (Atlas)).
. Fig. 5.39 Diagrams of Doppler waveforms illustrating normal and
5
abnormal ndings in the vertebral arteries (7 Sect. 5.4.2). The rst
drawing presents normal waveforms from the right and left vertebral
arteries. The second drawing illustrates the situation when the left vertebral artery is stenosed. The postocclusive waveform is characterized
by a delayed systolic upstroke, decreased peak systolic velocity (PSV),
and a relatively large diastolic component. The third drawing shows
one hypoplastic and one hyperplastic vertebral artery. The waveform
from the hypoplastic artery diers from a poststenotic waveform in
that diastolic velocity is decreased as well (Modied according to
Widder 1995)
More distal vertebral artery stenosis (involving the prevertebral V1 segment or intertransverse V2 portion) is rare,
and luminal narrowing of these segments is virtually always
due to dissection or inammatory vascular disease.
5.6.2.2 Occlusion
A vertebral artery can become occluded if it is aected by progressive atherosclerosis or atherosclerosis extending from the
subclavian artery. ese occlusions are limited to the prevertebral portion (V0 and V1 segments), and since collateralization
via the spinal arteries and contralateral vertebral artery is good,
they are typically detected incidentally and rarely cause brain
stem infarction. Occlusion of the proximal vertebral artery is
diagnosed by the absence of ow signals from these segments
aer scan parameters have been adjusted to slow ow. A Doppler waveform recorded distal to an occluded vertebral artery
segment reects the complex hemodynamic situation arising
from variable collateralization but will typically show signs of
abnormal ow (reduced or otherwise altered pulsatility) (see
. Fig. 5.90 (Atlas)). While contrast-enhanced ultrasound
(CEUS) usually allows good dierentiation of an occluded vertebral artery from a patent or relled artery, dierentiation
from a very hypoplastic vertebral artery (which is notoriously
dicult to identify) can pose a problem. is applies especially
if the occlusion extends to the intertransverse portion (V2 and
V3 segments); however, this portion will only be involved if
occlusion is due to dissection. Intracranial occlusion downstream of the origins of the rst intracranial branches leads to
a markedly higher pulsatility in the upstream segment and
slower diastolic blood ow. Higher pulsatility (or even to-andfro ow) may point to basilar artery occlusion.
its origin from the subclavian artery (A.S). The hypoplastic artery has a
diameter of 1.3mm with a peak systolic velocity (PSV) of 45cm/s and
relatively pulsatile ow in the waveform. The vertebral vein (V) is seen
along the artery, and there is aliasing in the left half of the image. b The
diameter of the contralateral vertebral artery shows a compensatory
increase to 5.2mm with a PSV of 80cm/s
. Fig. 5.40 a Severe hypoplasia of the vertebral artery (A.VERT) at
5.6.2.3 Dissection
Dissection of the vertebral artery may occur aer trauma or
spontaneously and aects the intertransverse portion (V2
segment). Even a very long dissection will typically spare the
rst few centimeters of the artery. CEUS can help in visualizing the true and false lumen. A diagnostic problem may
arise if there is long dissection with thrombosis of the false
lumen, which may be mistaken for a hypoplastic vertebral
artery. In case of dissection, an eccentric tubular structure of
low echogenicity, oen taking a spiral-like course, is visualized along a long portion of the patent vertebral artery lumen
(depiction of ow by color duplex). e dierential diagnosis
includes vasculitis, which is a rare condition causing circumferential arterial wall thickening.
Vertebral artery in
In
Thyrocervical trunk
vical
5.6 · Ultrasound Criteria, Measurement Parameters, andDiagnostic Role
345
5
5.6.2.4 Subclavian Steal Syndrome
e vertebral artery system is of special signicance in the
subclavian steal syndrome. Proximal stenosis or occlusion of
the subclavian artery diverts blood away from the basilar territory when the ipsilateral arm is used. Clinically, the steal
phenomenon is characterized by symptoms of intermittent
brain stem and cerebellar ischemia including dizziness,
ataxia, and drop attacks. Flow reversal in the ipsilateral vertebral artery is typically triggered by exercise but can also occur
at rest. In this situation, blood is supplied to the aected arm
by other cerebral arteries, in particular the contralateral vertebral artery.
e subclavian steal syndrome is diagnosed by the demonstration of reversed ow in the vertebral artery at rest or
upon provoked hyperemia in the ipsilateral arm (see
. Figs.5.91, 5.92, and 5.93 (all Atlas)).
e severity of the subclavian steal syndrome varies with
the extent of the occlusive process in the subclavian artery
and the role of the vertebral artery in collateral ow to the
arm. e increasing signicance of the ipsilateral vertebral
artery as a collateral is reected in the Doppler waveform,
which shows changes ranging from increasing systolic deceleration, to to-and-fro ow with retrograde systolic ow and
antegrade diastolic ow (incomplete steal), to complete retrograde ow (complete steal) (. Fig.5.41).
In the most common situation, known as vertebrovertebral crossover, a steal eect chiey occurs in the contralateral
vertebral artery as the feeding vessel and chiey manifests as
an increase in diastolic ow in response to a provocative
maneuver (. Figs. 5.42 and 5.93 (Atlas)). Other collateral
pathways include the thyrocervical trunk, chest wall vessels,
and cervical vessels supplying so tissue. e better the
collateral circulation, the less severe the steal eect in the
ipsilateral vertebral artery and the less severe the patient’s
symptoms.
e
provocative test for eliciting a steal eect in patients
with less collateral ow through the vertebral artery is performed by applying an upper arm cu inated to over
200mmHg for 3–5min to induce ischemia in the ipsilateral
arm. Subsequent deation will lead to a postischemic
increase in ow velocity in the arm arteries, resulting in an
increase of the steal eect in the vertebral artery. is is
reected in the waveform by an increase in retrograde ow
or even complete ow reversal despite a predominance of
antegrade ow at rest.
Duplex ultrasound is the method of choice for evaluat-
ing patients with subclavian occlusion and symptoms of subclavian steal. It enables detailed evaluation of the steal eect
in the vertebral artery and dierentiation of the stages of
the presence of
normal subclavian
artery
Normal waveform
of vertebral artery
. Fig. 5.41 Changes in the Doppler waveform from the ipsilateral
vertebral artery in subclavian artery occlusion with subclavian steal.
Depending on collateralization and the hemodynamic role of the
vertebral artery as a collateral pathway, changes already occurring
without provocative maneuvers may include systolic deceleration,
to-and-fro ow, and retrograde ow (in patients with marked vertebrovertebral crossover). Provocation may elicit more severe changes in
the postischemic phase, e.g., an increase in the retrograde ow component or transition from systolic deceleration to retrograde ow (see
. Figs.5.91, 5.92, and 5.93 (Atlas))
Vertebral artery – increasing subclavian stenosis/occlusion
– increasing collateral flow through vertebral
artery
Systolic deceleration
Early
To-and-fro flow
Incomplete
subclavian steal effect
Retrograde flow
Complete
Right subclavian
artery
ternal thoracic artery
. Fig. 5.42 Diagram of the course of the vertebral arteries and
blood ow direction (arrows) in occlusion of the left subclavian artery
(marked in black). Flow in the ipsilateral vertebral artery is reversed.
Other collateral pathways are the internal thoracic artery, thyrocervical
trunk, and costocervical trunk (Modied according to Heberer and van
Dongen 1993)
Vertebral artery
Costocer
trunk
346
Chapter 5 · Extracranial Cerebral Arteries
p
intra
< p
dia
p
intra
= p
dia
p
intra
> p
dia
5.8 Rare (Nonatherosclerotic) Vascular
Diseases oftheCarotid Territory
5.8.1 Dissection
Arterial dissection is the spontaneous or traumatic separation of the arterial wall layers caused by blood surging in
through a tear in the intima. Alternatively, blood leaking
from the vasa vasorum can enter the vessel wall; in this case
there is no communication with the lumen. e extravasated
5
. Fig. 5.43 Eects of increasing intracranial pressure on pulsatility in
the extracranial cerebral arteries. The diagrams of the Doppler waveforms from left to right reect the decreasing diastolic component
(P
=diastolic blood pressure) with increasing intracranial pressure
dia
(P
) (According to Widder 1995)
intra
blood elevates the intima, resulting in the creation of a false
lumen alongside the true arterial lumen. If blood dissects
between the media and adventitia, the latter is elevated, giving rise to a pseudoaneurysm. A blind-ending false lumen
becomes thrombosed and compresses the true lumen, causing high-grade stenosis or occlusion in severe cases. When
there is a second tear at the distal end, the blood can re-enter
incomplete steal. However, occlusion of the subclavian artery,
just as of the carotid artery, may have no therapeutic relevance in patients without neurologic symptoms or clinical
complaints.
the true lumen and ow through both lumina.
Dissection may cause various complications with manifestations ranging from headache to hemisymptoms. Seventy
percent of patients with dissection of the internal carotid
artery (ICA) have no or only mild neurologic decits, while
25% present with severe neurologic symptoms. Spontaneous
5.7 Diagnosis ofBrain Death
resolution is common when the false lumen becomes thrombosed and subsequent shrinkage of the thrombus causes the
An elevated intracranial pressure associated with trauma,
hemorrhage, or edema is reected in signs of increased
peripheral resistance in proximal arterial segments. In the
Doppler waveform from the internal carotid artery (ICA),
increasing intracranial pressure is indicated by a corresponding decrease in the diastolic ow component or even to-andfro ow with a systolic forward and diastolic backward
component (. Figs.5.43 and 5.95 (Atlas)). However, the cor-
compression of the true lumen to recede.
ere are three underlying causes of carotid dissection
with dierent symptoms, treatments, and prognoses:
5 Spontaneous dissection
5 Traumatic dissection (blunt trauma or iatrogenic aer
puncture) (. Fig.5.75 (Atlas))
5 Aortic dissection (Stanford type A) with subaortic exten-
sion (. Fig.5.73 (Atlas))
relation between intracranial pressure and the pulsatility
index varies as it is aected by individual factors and autoregulatory processes as well as the underlying disease. erefore, no reproducible absolute values of intracranial pressure
can be derived from the Doppler waveform or the pulsatility
index.
Nevertheless, interpretation of the Doppler waveform
will yield information on relevant elevations of intracranial
pressure. When intracranial pressure exceeds diastolic blood
pressure, the diastolic ow component disappears or
becomes retrograde (to-and-fro ow) (see . Fig. 5.95
(Atlas)), suggesting cessation of cerebral blood ow (Hassler
etal. 1991). Transcranial Doppler sonography has been an
accepted diagnostic modality for shortening the waiting
time for diagnosing cerebral circulatory arrest in Germany
since the early 1990s. If, for technical reasons, the typical
changes in the Doppler waveform cannot be demonstrated
in the basal cerebral arteries, cerebral circulatory arrest can
be diagnosed by using duplex sonography to demonstrate
these changes in the ow prole (. Fig.5.43) of the extracranial ICA or in the vertebral arteries. In this situation, care
must be taken to clearly identify the arteries supplying the
brain and to dierentiate them from other segments such as
the ECA.
Common carotid artery (CCA) dissection resulting from
aortic dissection begins in the proximal portion, from where
it can progress into the carotid bifurcation. In patients with
suspected CCA dissection, the artery is examined in the
transverse plane, starting as far anteriorly as possible using a
convex or curved array transducer. Spontaneous dissection
of the CCA is very rare but may occur in patients with Marfan’s syndrome (Harrer etal. 2006).
Traumatic and spontaneous
carotid dissection typically
aects the ICA including the portion near the skull base,
which is why the ultrasound examination must focus on
these segments.
Cerebral infarction due to dissection is primarily seen in
adolescents, and dissection accounts for approx. 20% of
strokes in younger patients. It is typically due to trauma and
rarely occurs spontaneously, commonly aecting arterial
segments prone to injury from bony structures such as the
skull base (carotid arteries) or the transverse foramina (vertebral arteries). Following an acute phase with a relatively
high risk of embolization and occlusion, dissection has a
good prognosis due to spontaneous recanalization over time.
e location and supercial course of the carotid arteries
allow good B-mode evaluation of the sonomorphologic
abcde
5.8 · Rare (Nonatherosclerotic) Vascular Diseases oftheCarotid Territory
347
5
. Fig. 5.44 a Diagrams of the sonomorphologic ndings in dierent
forms of dissection. The rst drawing shows intimal dissection with
entry and re-entry. The second drawing illustrates the situation in
internal dissection with narrowing of the true lumen due to thrombosis
of the false lumen. The third drawing presents the situation in external
dissection, which is characterized by intramural hemorrhage between
the media and adventitia with spindle-shaped or saccular dilatation
but with little or no compression of the true lumen; this may lead to
the formation of a pseudoaneurysm. b Ultrasound ndings in older
posttraumatic dissection of the internal carotid artery (ICA) with a relatively hyperechoic dissection membrane (D) in transverse and longitudinal orientation. The dissection begins in the carotid bulb and extends
4cm cranially (ECA=external carotic artery, CCA=common carotid
artery). To-and-fro ow in the false lumen is common, especially when
there is distal thrombosis in external dissection (see a)
features of carotid dissection with a high-resolution trans-
ducer (. Fig.5.44):
5 An intraluminal intimal ap separating the true and
false lumen; the ap can oen be seen apping back and
forth with pulsation (see . Figs.5.73 and 5.75 (both
Atlas)).
5 In internal dissection (intimal tear) with thrombosis of
the false lumen
, the thrombotic material will appear as
a hypoechoic eccentric structure narrowing the true
lumen over a variable length. e thrombosed false
lumen typically has a somewhat higher echogenicity
than the adjacent patent lumen (see . Fig.5.74 (Atlas)).
5 In external dissection, intramural hemorrhage with
thrombosis will result in aneurysmal dilatation with low
echogenicity of content and a visibly elevated adventitia.
5 In patients with an intimal tear, the intima will be
visualized as a apping structure of higher echogenicity
Distal
stenosis
ICA
CCA
. Fig. 5.45 Diagrams of dierent ow proles in dissection of the
internal carotid artery (ICA). The waveform changes depend on the location and extent of dissection, presence of thrombosis, and sites of entry
and re-entry (From Widder 1995). a Long ICA dissection with varying
ow velocities due to caliber irregularities of the patent segment. bShort
dissection with circumscribed ow acceleration at the site of luminal
narrowing, which may be dicult to dierentiate from atherosclerotic
stenosis or bromuscular dysplasia. c Dissection-induced occlusion of
the ICA with thump pattern (to-and-fro sign) in the patent segment and
externalization of the common carotid artery (CCA). dIf the true and
false dissection lumina are patent, ow proles vary widely with the sites
of entry and re-entry. The waveform from the true lumen depends on
the degree of ow obstruction caused by the dissection. Fluttering of
the intimal ap leads to a multiphasic waveform. eDistal formation of a
pseudoaneurysm (typically beneath base of skull) cannot be detected by
ultrasound because proximal ow is normal
Proximal
stenosis
Occlusion Aneurysm
Intimal
flap
within the arterial lumen. In older dissection, the intimal
ap may assume the appearance of a circumscribed wall
deposit in an otherwise normal-appearing artery. Short
dissection can be iatrogenic– the result of inadvertent
injury to the opposite arterial wall with the needle
during catheterization and may cause short stenosis due
to a structure protruding into the lumen and dicult to
distinguish from plaque-like deposits.
Spectral Doppler ndings obtained in a patent false lumen are
highly variable, depending on the individual constellation and
the site of sampling relative to the entry and re-entry points.
ere may be to-and-fro ow or even retrograde ow. e
ow signal from the true carotid artery lumen may be obscured
by the more intense signal from the moving intimal ap.
rombosis of the false lumen is usually identied by a
slightly higher echo level compared with the patent lumen.
e Doppler waveform varies widely with the extent and
type of dissection (see
. Fig.5.73 (Atlas)). In patients with
dissection- induced occlusion distal to the ICA origin, a
knocking waveform (thump pattern) is obtained, and there
is externalization of the CCA.Dissection with luminal narrowing is characterized by a waveform with a higher Doppler shi frequency and an increased angle-corrected ow
velocity in the residual lumen over a long stretch of the
ICA. With only minimal luminal narrowing, the spectral
Doppler tracing from the ICA and CCA appears fairly
normal (. Fig.5.45).
348
Chapter 5 · Extracranial Cerebral Arteries
Carotid dissection can be caused by blunt trauma to the
neck or hyperextension of the cervical spine. Additionally, it
may be iatrogenic, the result of puncture of a cervical vein, or
secondary, the result of an aortic dissection extending into
the CCA (type I according to De Bakey) (. Fig.5.73 (Atlas)).
Rarely, CCA dissection extends into the ICA with patency of
long stretches of the true and false lumen. In this form there
may be forward ow in both lumina or, depending on the site
of re-entry, to-and-fro ow or retrograde ow in the false
lumen (see . Fig.5.74 (Atlas)).
5
A study evaluating the usefulness of dierent duplex cri-
teria
in 23 patients with ICA dissection conrmed by MRI/
MR angiography or conventional angiography revealed a
detection rate of only 47.8% when morphologic criteria alone
were used (intramural hematoma, double lumen). Additional
use of hemodynamic criteria (hemodynamic evidence of distal stenosis or occlusion) increased the detection rate to
73.9%. Sonographic follow-up aer 3–6weeks established a
correct diagnosis in 91.3% of cases (hemodynamic signs of
distal stenosis or occlusion with signs of resolution). Using
both morphologic and hemodynamic criteria, duplex
ultrasound is highly sensitive in detecting dissection; however, in some cases a sonographic follow-up examination is
necessary for a denitive diagnosis (Arning 2005).
Dissection causing high-grade stenosis of the patent
artery (ECA) can be involved in Takayasu’s arteritis (with
occlusion being quite common) but not the internal carotid
artery (ICA). Involvement of the latter suggests Horton’s disease.
Horton’s disease of the extracranial cerebral arteries has
a prevalence of 0.75% in individuals older than 50, and continues to become more prevalent with age. is form of giant
cell arteritis also aects medium-sized and large arteries, predominantly the arteries of the abdomen and extremities as
well as the supra-aortic arteries.
e etiology is unknown but an immunologic basis is
likely. Takayasu’s arteritis predominantly occurs in younger
women, while Horton’s giant cell arteritis is more common
aer age 60. General symptoms include weakness, headache,
fever, and weight loss. ese symptoms as well as unspecic
signs of inammation are present before vascular stenosis or
occlusion occurs, and an ultrasound examination of the preferred sites of these conditions– the subclavian artery and
the CCA – should be performed whenever either of these
two diseases is suspected. If the suspicion is conrmed by
sonography, cortisone therapy is initiated to prevent vascular
complications. In patients with suspected Horton’s arteritis,
the ultrasound examination should include not only the subclavian and axillary arteries but also the temporal artery
(which may be tender and rm on palpation).
lumen can be diagnosed with 96% sensitivity using ultrasound with determination of hemodynamic parameters
(Benninger etal. 2006).
5.8.2.1 Ultrasound Findings
inTakayasu’s Arteritis
e B-mode ultrasound appearance of Takayasu’s arteritis is
characterized by circumferential, homogeneous, and
5.8.2 Vasculitis
hypoechoic thickening of a long arterial wall segment, which
primarily aects the media but may also extend to the intima
Primary and secondary forms of vascular inammation are
distinguished. Secondary vasculitis is associated with autoimmune diseases (collagen disease, systemic rheumatic disease), infections, and malignancies. ese typically aect
smaller vessels, and therefore rarely involve the large arteries
supplying the brain.
ree categories are distinguished according to the size of
the vessels aected: small-cell vasculitis (Wegener’s granulomatosis, Churg-Strauss syndrome, hypersensitivity vasculitis), which is not amenable to diagnosis by ultrasound;
vasculitis of medium-sized vessels (Kawasaki’s disease, polyarteritis nodosa – oen with dilatative changes), which is
amenable to diagnosis by ultrasound; and vasculitis of large
vessels (giant cell arteritis with two subtypes: Takayasu’s arteritis and Horton’s disease/temporal arteritis).
Takayasu’s arteritis, occasionally called pulseless disease,
can aect the large arteries supplying the brain. It is a primary vasculitis and typically occurs before age 40. It is a giant
cell arteritis, predominantly of the aorta and its major
branches, with the common carotid artery (CCA) and the
subclavian artery as the extracranial cerebral arteries most
frequently aected. e mesenteric, renal, and iliac arteries
may also be aected. As with all other forms of vasculitis,
inammatory thickening of the arterial wall (media) causes
various degrees of luminal narrowing. e external carotid
(the so-called macaroni sign). In color duplex ultrasound, a
hypoechoic halo is seen around the patent lumen. With progression, the thickening wall can cause stenosis, and even
secondary thrombotic occlusion may occur. When repair of
an occluded subclavian or common carotid artery is contemplated, it is pivotal to carefully dierentiate thromboembolic
from atherosclerotic occlusion and to establish whether
occlusion is attributable to inammatory wall thickening.
e latter requires initial immunosuppressive treatment
before any attempt at repair can be made.
Concentric wall thickening distinguishes vasculitis from
dissection with thrombosis of the false lumen, which instead
causes eccentric narrowing of the true lumen (see
. Fig.5.76
(Atlas)). e appearance is also distinct from that of athero-
sclerotic lesions
, which primarily involve the intima, exhibit
focal variation, are more hyperechoic, and have irregular surfaces. While atherosclerosis can cause concentric luminal
narrowing in patients with lipid metabolism disorders or
diabetes mellitus, atherosclerotic lesions are primarily seen
in the carotid bulb and the ICA.Conversely, Takayasu’s arteritis aects the CCA and very rarely extends beyond the
carotid bifurcation. Arteritis may also cause dilatation of the
proximal aortic branches.
Ultrasonography allows early diagnosis of the disease
(Taniguchi et al. 1997) and is the method of choice for
5.8 · Rare (Nonatherosclerotic) Vascular Diseases oftheCarotid Territory
349
5
a
c
. Fig. 5.46 a Longitudinal and transverse images of circumferential wall thickening in Takayasu’s arteritis. The longitudinal view (left) nicely
illustrates that hypoechoic inammatory wall thickening predominantly involves the media. In this patient the innermost layer, or intima, is additionally thickened by atherosclerosis. b Inammatory wall lesions in Takayasu’s arteritis predominantly involve arterial segments close to the aorta,
in particular the subclavian artery and the common carotid artery (CCA), while the internal carotid artery (ICA) is not involved. The image shows
the transition from the thickened wall of the CCA to the carotid bifurcation, which is free of arteritis (arrow). In the left part of the image, the
thickness of the artery wall is normal (Courtesy of K.Amendt). c Patient with arterial wall thickening due to arteritis of the posterior branch of the
temporal artery (A.TEMP). The aected branch has a thin residual lumen, while the anterior branch appears normal without relevant wall thickening. The right image shows the situation during compression (KOMP): the thickened wall of the aected branch prevents compression, indicated
by a lumen diameter of 1.8mm while pressure is being applied with the transducer (versus 2.0mm without compression). The unaected anterior
branch is fully compressible (no ow signals, no wall thickening)
b
follow- up (Park etal. 2001; Fukudome etal. 1998), especially
for documenting the regression of inammatory wall thickening in patients on immunosuppressive treatment. e
Doppler waveform will show a continuously but only moderately increased ow velocity, depending on the degree of concentric narrowing. Ultrasound has a markedly higher
accuracy than angiography, in particular in early disease.
Severe inammatory wall thickening can cause vascular
occlusion (
. Fig.5.46). Medical therapy with the administra-
tion of anti-inammatory and immunosuppressive agents is
the treatment of choice. Bypass surgery is discouraged, even
in occlusion, as the patency rate is poor.
In Takayasu’s arteritis (and other inammatory vas-
cular conditions such as Horton’s disease), contrast-
enhanced ultrasound (CEUS)
allows good dierentiation
of the thickened media (hypoechoic, thickened intimamedia complex) from the hyperechoic, patent lumen and
from the adventitia and also allows evaluation of vasa vasorum proliferation. is information is useful for estimat-
ing inammatory activity and monitoring the response to
immunosuppressive treatment. A study of Takayasu’s arteritis using CEUS demonstrated microbubble accumulation
in the concentrically thickened carotid wall as a sign of
neovascularization in acute disease and a strong decrease
in enhancement during immunosuppressive treatment
(Schinkel etal. 2014).
5.8.2.2 Ultrasound Findings
inHorton’s Disease
Although historically referred to as temporal arteritis, Horton’s giant cell arteritis can also involve the extracranial cerebral arteries (like Takayasu’s arteritis) as well as the subclavian
and axillary arteries. Involvement of the ophthalmic artery is
dreaded as it can lead to blindness. Horton’s disease is an
immunovasculitis of individuals beyond age 50. ickening
of the temporal artery, if involved, points to the diagnosis.
Histologic workup of a segment of the diseased temporal
artery was long considered the diagnostic gold standard. In
350
Chapter 5 · Extracranial Cerebral Arteries
the sonographic examination, the main branch of the supercial temporal artery is identied in transverse orientation at
the level of the jaw and traced upward until it divides into
frontal and parietal branches, which are also examined.
ickening of the temporal artery may be segmental rather
than continuous, which is why the entire temporal artery
must be imaged and evaluated in longitudinal and transverse
planes in the B-mode (. Fig. 2.103d). Care must be taken to
use a low PRF and sensitive receive gain. Temporal arteritis,
like any form of vasculitis, causes circumferential wall thick-
5
ening (halo or macaroni sign) with a wall thickness of 0.5–
1.5 mm (Schmidt etal. 1997, 1993; Stammler et al. 2000).
Blood ow velocity is decreased, and wall pulsation is absent
or lower in the diseased temporal artery than on the contralateral side. ese parameters have a high positive predictive
value (Schmidt and Gromnica-Ihle 2002; Schmidt 2006), but
normal ndings in the temporal artery do not rule out Horton’s disease as the temporal artery is involved in only approx.
60% of patients. e axillary artery is involved in approx.
50% of patients (Schmidt etal. 2008) and should be examined as well (see
. Figs. 2.46 and 2.49). Inammatory wall
thickening recedes under immunosuppressive treatment,
which correlates with a drop in laboratory inammatory
parameters.
High-resolution ultrasound of the temporal artery (if
resolution ultrasound images (the so-called string-of- beads
sign). Color duplex or power Doppler imaging will detect
ow in the residual lumen, allowing dierentiation of the
patent lumen from the dysplastic arterial wall. e sonomorphologic appearance allows dierentiation from atherosclerotic lesions, aided by the fact that bromuscular dysplasia
typically occurs in young women without atherosclerotic
lesions in other vascular territories.
e duplex ultrasound appearance is characterized by
multiple stenoses, which may alternate with dilated segments. Depending on the severity of steno-occlusive lesions,
direct and indirect signs of stenosis may be present. Carotid
bromuscular dysplasia is rarely diagnosed with duplex
ultrasound as the rst imaging test because the lesions causing the string-of-beads appearance usually spare the proximal 3–5 cm of the ICA. When bromuscular dysplasia is
suspected, the examiner must follow the ICA as far cranially
as possible using a curved array transducer and lowering
both the transmit frequency and the pulse repetition frequency toward the skull base. In general, ultrasound can only
detect advanced disease with hemodynamically relevant stenosis located not too far cranially. Ultrasound studies report
a prevalence of 0.05–0.14% (Labropoulos etal. 2007; Arning
2004) compared with 0.61% in a catheter angiography study
(Sandok 1983).
involved) has 97% specicity (Schmidt and Blockmans 2005),
and if the sonographic examination provides denitive evidence of vasculitis, treatment can be started without obtain-
5.8.4 Aneurysm
ing a biopsy (guidelines of the German Association of
Scientic Medical Societies, AWMF guidelines). A biopsy is
only required when ultrasound ndings are inconclusive or
normal but clinical signs suggest arteritis. A biopsy should be
obtained from a sonographically suspicious wall segment to
preclude false-negative results (as involvement is segmental).
Since demonstration of ow in small vessels crucially relies
on adequate instrument settings (gain, PRF), the diagnosis
can be corroborated by testing for compressibility. e temporal artery can be compressed against the skull, and incompressibility of the residual lumen conrms inammatory wall
thickening (Aschwanden etal. 2013).
Aneurysm of the ICA is rare and may occur secondary to
atherosclerotic or inammatory vascular disease (. Figs.5.70,
5.71, and 5.72 (Atlas)).
A true aneurysm is an aneurysm involving all three arterial wall layers and can be congenital, typically in patients
with connective tissue disease, or it can be acquired. Mycotic
or inammatory aneurysm is caused by a localized infection
of the arterial wall in the setting of inammatory conditions
of the head or neck region or in individuals in whom hematogenous spread has occurred, for example, in endocarditis.
True aneurysms of the carotid territory must be distinguished
from pseudoaneurysms, which typically develop aer surgery or trauma.
5.8.3 Fibromuscular Dysplasia
True aneurysms of the extracranial cerebral arteries are
very rare with reported rates of 0.4% (Painter etal. 1985) to
Fibromuscular dysplasia is a rare nonatheromatous and noninammatory vascular disease of unknown etiology that
typically involves the renal arteries (hypertension). It is a disease of medium-sized arteries and can therefore also aect
the extracranial carotid territory, causing TIAs or even stroke.
Approx. 30% of patients with bromuscular dysplasia have
intracranial aneurysm. In the vast majority of cases, stenoocclusive disease is due to hyperplasia of smooth muscle cells
and must be dierentiated from degenerative and inammatory vascular conditions.
Fibromuscular dysplasia is characterized by multiple stenoses alternating with normal or dilated arterial segments,
producing a beaded appearance on angiograms and high-
5.5% (Liapis etal. 1994). ey are accounted for by atherosclerosis in 32% of cases, thrombosis in 17%, and dissection
in 37% (Moreau etal. 1994). Before the era of antibiotic treatment, most true aneurysms were mycotic aneurysms developing secondary to tuberculosis and syphilis (Konstantinidis
etal. 1998). Only 5% of mycotic aneurysms were reported to
involve the extracranial carotid arteries (Brown etal. 1995).
Mycotic aneurysms have become very rare and are usually
caused by staphylococci or streptococci, or less commonly by
salmonella infections.
An aneurysm of the extracranial cerebral arteries
becomes apparent as a pulsating neck mass. B-mode ultrasound depicts the focal dilatation of the artery (saccular or
5.8 · Rare (Nonatherosclerotic) Vascular Diseases oftheCarotid Territory
351
5
spindle-shaped), and color duplex imaging allows evaluation
of the patent lumen and demonstration of thrombotic
deposits.
e denition of aneurysm that applies to the extracranial carotid and vertebral arteries (abrupt doubling
of the lumen diameter) cannot readily be applied to the
wider carotid bulb. Here, normal diameter variation must
be dierentiated from true aneurysmal dilatation, which
is usually assumed when the external diameter reaches
14–15mm. Clinically, however, it is more relevant to identify thrombotic deposits in saccular, dilated arterial segments, which can give rise to embolism and cause cerebral
infarction.
A spontaneous stroke rate of up to 50% has been reported
for untreated carotid aneurysm (Valentine 2003), suggesting
that even smaller aneurysms should be operated on. Other
complications may result from local compression of adjacent
structures such as the internal jugular vein, the trachea, the
esophagus on the le side, and occasionally of a cerebral
nerve (Numenthaler 1986). Rupture of carotid aneurysm is
rare.
Color duplex ultrasound (or MR angiography) is the
method of choice, enabling precise evaluation of the diameter and extent of the aneurysm as well as dierentiation of
thrombotic deposits (which is not possible with angiography) (see . Fig.5.72 (Atlas)).
Suture aneurysm is a pseudoaneurysm that may be
noted as a pulsatile mass of the neck or may be detected
at sonographic follow-up after carotid endarterectomy.
Color duplex ultrasound differentiates flow within the
aneurysm from thrombotic material, and the characteristic “steam engine sound”, caused by a high-frequency systolic signal and retrograde flow throughout diastole, can
be heard in the aneurysm neck when Doppler interrogation is performed (see . Fig.5.71 (Atlas)). The indication
for surgical revision can be established without preoperative angiography.
volume on the ipsilateral side by multiplying the mean ow
velocity with the cross- sectional area of the CCA proximal
to the stula and then subtracting the CCA ow volume of
the contralateral side.
When a dural AV stula is suspected (typically presenting
with pulse-synchronous tinnitus), sonographic evaluation of
the occipital artery in the retroauricular area directly in front
of the mastoid can conrm the stula by demonstration of a
characteristic high-frequency signal. A stula with a large
blood ow volume is identied by a unilateral increase in
ow velocity in the ECA (and CCA). e increase in PSV is
apparent in a long ECA segment, distinguishing stula from
stenosis (short focal PSV increase).
5.8.6 Idiopathic Carotidynia
Idiopathic carotidynia was first mentioned in 1927 and
has been recognized as a distinct clinical entity by the
International Headache Society (IHS) since 1988. It is a
neck pain syndrome presenting with severe unilateral
pain of the upper neck region and responding well to
treatment with nonsteroidal anti-inflammatory drugs.
Ultrasound demonstrates echolucent, often eccentric
thickening of the vessel wall, usually causing only moderate luminal narrowing (
part of the thickening extends outward. While the findings resemble the appearance in dissection or vasculitis,
carotidynia differs from dissection (with thrombosed false
lumen) in that it involves the bifurcation with the distal
CCA and proximal ICA and presents with local pain,
while dissection tends to involve more cranial segments of
the ICA and causes headache. Magnetic resonance imaging (MRI) was reported to show no evidence of intramural hematoma but enhancement after administration of
contrast medium, suggesting an inflammatory wall lesion
. Fig. 5.47) because the main
5.8.5 Arteriovenous Fistula
An arteriovenous (AV) stula is usually a sequela of trauma
or iatrogenic manipulation (puncture, central venous catheter) and is conspicuous as a mosaic of colors due to perivascular tissue vibration. Spectral Doppler interrogation
will not always demonstrate the stula directly, which is
why the diagnosis relies on the demonstration of high ow
velocity in the feeding artery, especially during diastole,
and arterialized ow in the vein. e Doppler waveform
obtained within the stula depends on the ow volume but
resembles the pattern in a stenosis with high systolic and
diastolic ow velocities. AV stulas in the carotid system
primarily involve the common carotid artery (CCA) and
the internal jugular vein because they lie close together. e
stula ow volume can be estimated by calculating the ow
. Fig. 5.47 Idiopathic carotidynia with wall thickening at the origin
of the internal carotid artery (ICA). Thickening primarily involves the
outer wall layer (two-layered appearance of the arterial wall)
352
Chapter 5 · Extracranial Cerebral Arteries
(Burton etal. 2000; Arning 2004). As the thickened wall
does not constrict the lumen, no hemodynamic signs of
stenosis can be detected. Carotidynia is an example of a
well-established clinical entity that required the advent of
state-of-the-art imaging to identify underlying morphologic changes (high- resolution ultrasound and MRI). The
symptoms resolve spontaneously with follow-up imaging
after 4 weeks demonstrating a return to almost normal
wall thickness.
5
5.8.7 Vasospasm
Vasospasms can be induced by mechanical manipulation or
medications taken to treat vasculitis, or they can occur during episodes of migraine. ey can cause cerebral or ocular
ischemia, but the stenosis caused by spasm is usually of such
short duration that only a few reports describe it being visualized by ultrasound (Janzarik etal. 2007; Mosso etal. 2007).
It is assumed that most instances of vasospasms go undetected. Treatment is with calcium antagonists. Color duplex
imaging will show a narrow lumen with stenotic ow, returning to normal within hours. No morphologic wall changes
are apparent; recurrent vasospasms usually aect the same
arterial segment.
5.8.8 Compression by Tumor,
Carotid Body Tumor
. Fig. 5.48 a Longitudinal view of a carotid body tumor in the bifur-
Compression of a carotid segment by cervical tumors or
lymph node metastases is rare and more commonly aects
the internal jugular vein. Carotid body tumors are highly
vascularized masses located at the carotid bifurcation, where
they cause the typical saddle deformity (splaying of the internal and external carotid branches by the tumor mass) on
ultrasound. In the color duplex mode, multiple small tumor
vessels are demonstrated.
e tumor arises from the 3–4mm carotid body, a structure in the bifurcation that functions as a chemoreceptor and
regulates PO
, PCO2, and the pH value. Carotid body tumors
2
are primarily supplied with blood from external carotid
branches and rarely also from the thyrocervical trunk. ey
are assumed to develop from paraganglial tissue, probably a
residue of the neural crest. Hence, there may be multiple
tumors and rarely also parajugular or paravagal tumors as
well as tumors at the aortic arch.
Histologically, adenomatous and angiomatous subtypes
can be distinguished. e latter is very highly vascularized
with an impressive appearance on color duplex imaging.
Tumor growth in the area of the carotid bifurcation can
encase or compress the arteries (. Fig. 5.48). Color duplex
evaluation of the localization and vascularization of the
tumor contributes to the preoperative dierentiation, and the
information on tumor extension facilitates radical surgical
removal.
cation splaying the internal carotid artery (ICA) and external carotid
artery (ECA) in a 57-year-old patient. The tumor receives its blood
supply from ECA branches; tumor vascularization is relatively low.
The sample volume is placed in the ECA. b 64-year-old patient with a
palpable, pulsatile neck mass on the right side. The transverse color
duplex image shows a highly vascularized carotid body tumor measuring 4–5cm and encasing segments of the ICA and ECA.The Doppler
waveform from a tumor-feeding artery arising from the ECA shows a
very large diastolic ow component
Color duplex imaging is also the method of choice for
monitoring the outcome of tumor embolization in elderly or
multimorbid patients (. Fig.5.95 (Atlas)) in whom surgical
resection should be avoided. Serial ultrasound allows evaluation of tumor growth and tumor vascularization.
5.9 Diagnostic Role ofDuplex Ultrasound
inEvaluating theExtracranial
Cerebral Arteries
As a noninvasive diagnostic test, duplex ultrasound is the
method of choice for conrming or ruling out suspected
steno-occlusive lesions of the carotid system. In the stepwise
diagnostic workup, it follows aer the patient’s history has
been obtained and a physical examination performed. e
5.9 · Diagnostic Role ofDuplex Ultrasound inEvaluating theExtracranial Cerebral Arteries
353
5
. Table 5.16 Role of duplex ultrasound in carotid artery
surgery and stenting
Decision to be made Duplex criteria
Indication for surgery Degree of stenosis
Plaque morphology
Nonatherosclerotic vascular
narrowing/disease
Tandem stenosis
Timing of operation Early surgery, risk of occlusion/
reischemia
Type of surgery/
anesthesia
Technical success Degree of residual/recurrent stenosis
Outcome Recurrent stenosis, follow-up
CAS carotid artery stenting, CEA carotid endarterectomy,
ICAinternal carotid artery
Kinking: shortening of ICA
Site of plaque/plaque length: general
versus local anesthesia
Plaque morphology: surgery versus
stenting (CEA– CAS)
following surgery/stenting
Complications of surgery
formerly widely used CW Doppler technique is less expensive, easy to perform, and has an accuracy of over 90% in
detecting therapeutically relevant higher-grade carotid stenosis (Keller et al. 1988; Neuerburg-Heusler 1984). It is a
suitable screening modality for patients with a reasonable
suspicion of carotid stenosis if abnormal ndings are subsequently veried by duplex imaging. However, anatomic
anomalies and sudden changes in the angle of insonation due
to kinking or coiling of the carotid artery may give rise to
false-positive ndings, and low-grade stenosis escapes detection by CW Doppler.
Duplex ultrasonography is noninvasive and has a sensi-
tivity and specicity of over 90% in quantifying internal
carotid artery (ICA) stenosis, making it the diagnostic test
of choice
(. Table5.16). is is all the more so since angiography, the traditional gold standard, has its limitations as
well. Its accuracy, determined by comparing the image interpretations performed by two independent radiologists, is
88–93%, which is similar to the comparison of duplex ultrasound and angiography. is agreement is surprising since
duplex ultrasound is based on hemodynamic evaluation
while angiography is a morphologic method. Angiography is
limited by the fact that 3D plaques protruding into the vessel
lumen are reduced to the two lm dimensions, which impairs
the reliability of stenosis measurement– despite mandatory
assessment in two or three planes.
Duplex sonography is also the method of choice in all
patients with nonatherosclerotic vascular conditions (inammatory disease, dissection, aneurysm) because B-mode scanning depicts not only the luminal narrowing but wall changes
and perivascular structures as well.
e complications of angiography include a stroke rate of
1–3% (Waugh and Sacharias 1992), which is almost as high
as the rate of complications experienced centers achieve with
surgical management by carotid endarterectomy (CEA). For
this reason, the indication for CEA is increasingly based on
duplex ultrasound alone. In addition to the preoperative
localization and quantication of carotid stenosis, sonography is also preferred for follow-up aer CEA or carotid artery
stenting (CAS).
In patients with high-grade internal carotid artery (ICA)
stenosis (70% ECST stenosis/50% NASCET stenosis; see
. Fig.5.9b and . Table5.9), the stenosis degree alone estab-
lishes the indication for surgery and, if the sonographic
examination allows condent grading, no further stenosis
quantication or B-mode evaluation of plaque morphology
is necessary. Sonomorphologic evaluation of plaque vulnerability only has a role in stage II disease and moderate stenosis of 60–70% or in stage I disease with high-grade stenosis,
where a decision needs to be made between best medical
treatment and surgery.
Many studies have been performed to investigate sonographic properties of plaques (e.g., echogenicity, surface, and
contour) and to identify features that might allow prediction
of the risk of embolism, but no consistent picture has
emerged, and results are even contradictory. Furthermore,
published data are not easily comparable because investigators
use dierent study designs, descriptive criteria, and classication systems. Nevertheless, a few general conclusions
regarding plaque morphology and echogenicity appear to be
generally accepted. For one, the risk of stroke increases with
plaque thickness, which is why the same degree of stenosis is
associated with a greater risk of embolism when caused by an
eccentric plaque than when caused by a concentric plaque.
is is because an eccentric plaque protruding into the blood
stream is more susceptible to rupture of its cap. Such a plaque
is oen identied by characteristic longitudinal pulsation in
the direction of blood ow in real-time B-mode ultrasound.
An irregular surface seen on B-mode scans suggests atheromatous rather than brous plaque. Plaque with high lipid
content is assumed to be echolucent and has an up to four
times higher risk of embolism. In evaluating plaque echogenicity, however, the examiner must always bear in mind
the inherent technical limitations of ultrasound resulting
from the fact that a sonographic B-mode image is generated
from echoes reected o boundaries between tissues of different acoustic impedance. is means that low echogenicity
merely indicates that a tissue is homogeneous but allows no
conclusions to be drawn regarding other tissue properties
such as elasticity. Moreover, evaluation of echogenicity is
subjective and also depends on the equipment and settings
used. To overcome these limitations, a standardized measure
of plaque echogenicity, the gray-scale median (GSM), has
been proposed. While this standardized analysis shows good
interobserver correlation, agreement between sonomorphologic plaque classication and histopathologic examination
of eversion CEA specimens is poor. Again, no consistent