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symmetric stenosis without sinus dilatation however, the
model can only be transferred with caution to real ICA
stenoses which are frequently axis-asymmetric, of variable length, and of different distal resistance depending on
the presence of collaterals. Considering waveform appearance together with flow velocities will therefore help to
recognize a hemodynamically relevant stenosis.
Unfortunately, the terminology of the pre- and poststenotic flow signals is not well standardized. In this book, we
use the terms pre- and poststenotic flow pattern for detectable proximal or distal flow signal alterations.
The prestenotic flow pattern comprises a mostly normal
systolic flow velocity and always a normal rise in systolic
flow. However, the distal flow obstruction leads to raised
peripheral resistance, reduced prestenotic diastolic flow,
and subsequently raised pulsatility. In cases with unclear
cause of the distal flow obstruction (occlusion or stenosis)
but highly pulsatile flow signals, the term high-resistance
flow with increased pulsatility might be more appropriate.
A poststenotic flow pattern requires a relevant proximal
obstruction, which then leads to the phenomenon of a
delayed systolic rise. For exact assessment of a poststenotic flow pattern, clearly the insonation has to be performed outside of the stenosis. The compromised blood
flow results in a compensatory dilatation of the resistance
vessels to avoid downstream hypoperfusion. This results
in a rising total arterial cross-sectional area with subsequent reduction of the peripheral resistance causing a
raised diastolic flow component and reduced pulsatility.
For these flow patterns, terms such as “blunted flow,”“low
resistance flow,” or, in case of distinct alterations, “venouslike flow” have been used. A delayed systolic flow rise and
reduced velocity may coexist. However, one or the other
may also be the dominating feature of the Doppler spectrum alteration. The term poststenotic flow pattern can be
generally used in proximal stenosis and occlusion as the
remaining distal flow is never postocclusive but always a
result of an upstream functional stenosis, i. e., in a collateral. The only relevant differential diagnoses of a poststenotic flow pattern are low-resistance flow patterns in
AVMs (which, however, are usually associated with raised
and not reduced flow velocities) and general low-resistance flow patterns in all brain-supplying arteries, for
example, in those caused by severe aortic valve stenosis.
To reach the greatest diagnostic certainty during everyday clinical practice, we recommend that signals should be
obtained from all three vessel segments (i. e., prestenotic,
intrastenotic, and poststenotic) when possible. The above
criteria are of special help when performing serial measurements over long periods to detect diseaseprogression.
For instance, if initially absent indirect hemodynamic criteria develop over time, an increase of the stenosis to a
range of at least 80 % is likely. Follow-up assessment of an
extracranial low-grade progressive stenosis < 50 % is more
difficult. We recommend considering a lumen reduction of
at least 10 % as sign of progression. In stenoses > 50 % until
indirect hemodynamic signs are present, an increase of
Stenoses and Occlusions 85
Fig. A5.21 Left: Schematic drawing of severe extracranial ICA
stenosis. Right: Extracranial duplex, longitudinal view. Doppler spectrum analysis proximal, within and distal to a hemodynamically
relevant high-grade 90 % ICA stenosis. CCA flow velocity: 38/
12 cm/s. ICA flow velocity within the stenosis was 360/105 cm/s
and distal from the stenosis was 36/10 cm/s. Note the reduced
pulsatility in the prestenotic CCA and the distinctly delayed systolic
flow rise in the poststenotic ICA.
peak systolic velocity > 50 cm/s should be considered as
progress, only if good insonation conditions are present
and angle correction can performed without difficulties.
Ultrasound Criteria of Occlusions
Direct Morphologic Assessment
Extracranial B-mode duplex ultrasound may reveal complete filling of the vessel lumen with thrombotic material
of varying echogenicity. In chronic occlusion, precise vessel identification and differentiation of the vessel lumen
might be difficult, a fresh thrombotic occlusion usually
presents with hypoechogenic thrombotic material. Bmode insonation alone however is not sufficient for diagnosis of occlusion. It should always be combined with
color-mode and Doppler spectrum analysis.
Direct Hemodynamic Assessment
Occlusions result in a complete absence of color-flow signal, even after adjustment for very low flow signals (lowest pulse repetition frequency and increased color-gain
settings). Doppler spectrum analysis reveals a small stump
signal near the zero line but no flow signals. In cases with a
proximal vessel stump, a distinctly reduced, alternating
flow pattern with a short systolic peak and a small retrograde flow component (“to-and-fro signal”)canbefound.
Diagnostic certainty may be increased by using intravenously applied ultrasound contrast agents. On transcranial
insonation, a missing flow signal does not necessarily imply occlusion. For example, P1-PCA segment might be
absent due to P1 hypo- or aplasia in case of a fetal-type
PCA. Also, the A1-ACA segment might be missing in dis-
5 Vascular Pathology86
tinct hypo- or aplasia. In these circumstances, indirect
hemodynamic criteria might help to distinguish the normal variant from a pathologic finding.
Indirect Hemodynamic Assessment
Inocclusion,thesamecriteriaasforhemodynamic,highgrade stenoses can be applied for the analysis of flow
profiles proximal and distal to the occlusion (see “Ultrasound Criteria of Stenoses,” p. 81). A flow signal post occlusion can of course only be observed if anastomosing
collateral vessels distal to the occlusion compensate for
the occluded vessel (for further details, see “Collateral
Pathways,” p. 101).
Extracranial Pathology
Extracranial Anterior Circulation
ICA—Stenosis
Since the development of imaging methods that permit
visualization of intravascular pathology in vivo, the evaluation of ICA pathology and grading of ICA stenosis has
been a matter of extensive analysis and debate. In contrast
with most other brain-supplying arteries, the ICA has a
bulbous physiologic dilatation at its origin—the carotid
sinus. Within this region, the blood flow is oftennonlinear,
leading to increased shear stress to the vessel walls, subsequent micro injury, and reparation processes which finally result in atherosclerotic vessel wall changes. Precise
analysis of vessel lumen reduction within this region is a
challenge for all currently available imaging methods.
Fig. A5.22 Schematic drawing of a stenosed ICA, similar to the
images derived from DSA. Illustration of three angiographic methods to determine the grade of ICA stenosis. Note, that the ECST
method uses an “eye ball” estimate of the nonvisible outer wall of
the ICA at the carotid sinus (dashed grey line). Comparative analysis
of the three methods yielded a linear relationship, allowing an
estimated conversion to be performed.
Grading of ICA Stenosis by Digital Subtraction Angiography
Evaluation of stenoses and occlusions in the past has been
dominated by the first available method: conventional
angiography. Based on angiographic data, a number of
important clinical trials have been performed, the results
of which form the basis for current treatment decisions in
carotid stenosis. The European Carotid Surgery Trial (ECST
1991) and the North American Symptomatic Carotid Endarterectomy Trial (NASCET 1991) compared medical treatment and carotid endarterectomy (CEA) in patients with
different grades of symptomatic ICA stenosis. They found
that patients with stenoses between 70 % and 95 % significantly benefit from the surgical intervention. However,
both studies used different approaches to determine the
grade of stenosis. The North American trial used the diameter of the nonaffected distal ICA and the narrowest stenosis diameter for calculation of stenosis (distal grade of
stenosis). The ECST used the stenosis diameter and the
estimated diameter of the nonvisualized outer walls of
the stenosed ICA (local grade of stenosis). A third method,
defining the grade of stenosis between the stenosis diameter and the proximal nonaffected CCA (CC method) has
not yet been used in a large clinical trial (de Bray and Glatt
1995) (Fig. A5.22). Current treatment decisions of whether
or not to perform CEA relies on the NASCET and ECST data.
Although numerically identical, a 70 % NASCET ICA stenosis is not equal to a 70 % ESCT ICA stenosis. Rothwell and
coworkers compared NASCET and ECST grades of stenosis
and found a linear correlation which allows an estimated
conversion between approaches with the formula: NASCET (%) = (ECST—40 %)/0.6. The same relationship can be
applied to the CC criteria: NASCET (%) = (CC—40 %)/0.6
(Rothwell et al. 1994).
Following this conversion, a 70 % ECST ICA stenosis
equals a 50 % NASCET stenosis. Despite this correlation
and the positive findings in the above two clinical studies,
both approaches have considerable methodologic problems (Alexandrov et al. 1993). The NASCET approach is
unable to account for low-grade stenosis as a 40 % ECST
stenosis equals 0 % NASCET, and for example, a 30 % ECST
stenosis transfers into a –16 % NASCET stenosis. The ECST
approach on the other hand relies on an “eyeball” estimation of the presumed carotid sinus diameter, which has the
potential for considerable error (Fig. A5.23). To reduce this
error some authors use the carotid stenosis index which is
mostly based on a publication by Williams and Nicolaides,
who found a fixed carotid sinus to proximal CCA ratio of 1.2
in96%of61angiogramsofpresumablynormalcarotid
bifurcations (Williams and Nicolaides 1987). Indeed, this
ratio improved the comparability between both angiographic methods but did not improve their diagnostic
accuracy. In fact other studies found an ICA/CCA ratio
ranging from 0.7 to 1.4 (Rothwell et al. 1994). A more
recent CTA approach has questioned a fixed ICA/CCA ratio
(Bartlettetal.2007).
Considering these shortcomings, it is surprising that
DSA has so far remained the diagnostic gold standard
Extracranial Pathology 87
Fig. A5.23 DSA, selective CCA injection, lateral view. A–C Potential
error in ICA stenosis estimation using the ECST method. Different
estimates of the presumed carotid sinus will result from A to C in a
higher calculated grade of stenosis. Diameter of stenosis: 3.3 mm.
Diameter of the carotid sinus, assessed by duplex ultrasound:
9.2 mm. Resulting degree of stenosis: 64 %, best corresponding to
the estimate in C.
with which all other methods have to compete. It also
questions the relevance of extended metaanalyses which
try to analyze sensitivity and specificity values for the less
invasive methods (duplex ultrasound, MRA, CTA) in comparisontoaninferiorstandard(Pateletal.2002,Wardlaw
et al. 2006). Like all other nonangiographic methods, the
findings on duplex ultrasound have to be imported into
the inexact angiographic scales. In our opinion, however,
thefuturestandardwillbeamoreaccurateevaluationof
the real, cross-sectional vessel narrowing using CTA and/or
duplex ultrasound, the latter technique also able to consider hemodynamic flow parameters (Staikov et al. 2000).
Continuous-wave Doppler sonography in contrast can no
longer be recommended because of its low diagnostic
accuracy. For instance, in a comparative Doppler and angiographic study that aimed to identify patients with ICA
stenoses > 60 % (NASCET criteria), the Doppler technique
yielded 41 % false-positive results (Qureshi et al. 2001). For
further details, see Case 1 (p.128).
Grading of ICA Stenosis by Duplex Ultrasound
Despite the ability of duplex ultrasound to directly measure the cross-sectional area and its lumen reduction,
clinical practice today requires grading of ICA stenosis
according to the angiographically defined scales. Duplex
ultrasound best determines the local grade of stenosis, i. e.,
to grade according to ECST criteria (Fig. A5.24). To achieve
this goal, all morphologic as well as direct and indirect
hemodynamic criteriashould be considered (Fig.A5.25). A
direct assessment of an ICA stenosis at its origin is mostly
unproblematic. However, a direct assessment may be hinderedorevenbeimpossibleinupto7%ofcasesbecauseof
severe plaque calcification and subsequent acoustic shad-
Fig. A5.24 Corresponding extracranial duplex. A B-mode image,
longitudinal plane: Large mid-echogenic structure in the carotid
sinusaswellasattheECAorigin.B Color-mode, cross-sectional
plane: Following the ECST criteria, the diameter of the vessel
(9.2 mm) and the residual lumen (3.3 mm) are assessed, resulting
in a 64 % stenosis. C Color-mode, longitudinal plane: Clear delineation of the remaining perfused lumen and confirmation of the
plaque extension. D Doppler spectrum analysis. Flow velocity: 185/
102 cm/s indicating local stenosis, grade 60–70 %.
Fig. A5.25 Assessment of pre- and poststenotic blood flow. Left:
Doppler profiles in an unaffected vessel. Right: Example of flow
profiles in a case with 90 % ICA stenosis. Prestenotic flow pattern in
the CCA with reduced flow velocity and increased pulsatility. Intrastenotic elevated flowvelocity and spectral broadening. Poststenotic
flow pattern in the distal ICA with reduced flow velocity and delayed
systolic flow rise.
owing (Polak et al. 1989) (Fig. A5.26)oralsointhecaseofa
deeply located and angulated vessel course. Prestenotic
flow alterations within the distal CCA are easy to find.
Extracranial measurements distal of the stenosis are often
hindered if the bifurcation is near the mandible or if the
stenosis extends over a long ICA segment. In these cases,
thedistalextracranialICAcanbeassessedintheaxial
plane, which allows evaluation of a probable poststenotic
flow pattern or alternatively the intracranial ICA, preferably at its C6 segment. The ipsilateral MCA may also be
5 Vascular Pathology88
analyzed. However, in MCA assessment it has to be considered that collateral filling might have already occurred
via ACoA, PCoA, and/or OA, and the observed MCA profile
does not really reveal the poststenotic flow pattern of the
ICA.
A synopsis of the currently recommended duplex ultrasound criteria for graduation of a proximal ICA stenosis
considering direct and indirect flow parameters, in part
based on the proposed criteria of de Bray and Glatt (1995)
is given in Ta ble A5.2. In many centers in Europe the
combination of velocity and hemodynamic parameters
are well-accepted, and a graduation in 10 % categories is
increasingly used, which has been shown to be a reliable
approach if applied by experienced sonographers (Dippel
et al 1997). The 95 % grade represents the specific findings
in near occlusion.In North America, however, a graduation
ofICAstenosisissolelybasedonvelocityparameters
whichhavebeenadaptedtotheroughNASCETgrading
system. According to a recently published consensus report the following criteria were proposed (Grant et al.
2003):
• < 50 % stenoses (peak systolic velocity: < 125cm/s, ICA/
CCA ratio: < 2.0).
• 50–69 % stenoses (peak systolic velocity: 125–230cm/s,
ICA/CCA ratio: 2.0–4.0).
• Stenoses ≥ 70 % (peak systolic velocity: > 230 cm/s, ICA/
CCA ratio: > 4.0).
• Near occlusion with variable velocities and ICA/CCA ratio and occlusion.
Notable velocity cut-off values of the American consensus
group referring to NASCET criteria are similar to those
published by the European authors who uniformly refer
to ECST criteria. A possible explanation might be the only
rough American grading system which increases sensitivity by using lower cut-off flow velocities. Recently, a better
adapted “sonographic NASCET index” has been proposed
Fig. A5.26 Extracranial duplex, color-mode image, longitudinal
view. A, B Examples of a distinct acoustic shadowing phenomenon
caused by calcified ICA plaques impeding assessment of ICA flow
(arrows).
Tab l e A5. 2 Ultrasound grading of ICA stenosis at its origin according to the ECST and NASCET criteria. Flow velocities are given in cm/s.
ECST (%) < 50 60 70 80 90 95 Occlusion
NASCET(%) 50678392Occlusion
Diameter Direct assessment
Tur bu len ce – (+) + + + ∕ø
V
ICA syst
V
ICA diast
V
ICA post
ICA/CCA velocity ratio < 1.5 > 1.5 > 2 > 4 > 4 ∕ø
Poststenotic ICA
Prestenotic CCA –––(+) + + +
OA collateral –––Variable Variable Pathol Pathol
IC collaterals –––(+) + + +
dist
< 120 120 200 300 > 400 ∕ø
<40 40 80 130 >130 ∕ø
>60 >60 >60 >60 <60 ∕ø
–––(+) + +
which also takes the distal ICA flow information into account and which subsequently yielded better correlation
with angiographic findings than considering conventional
peak systolic flow velocity alone (Hathout et al. 2005).
Diameter = residual diameter assessed in cross-sectional plane; turbulence = aliasing in color-mode and/or systolic broadening in Doppler
spectrum analysis; V
poststenotic ICA peak systolic flow velocity;
reduced flow velocity, delayed systolic flow rise and/or reduced pulsatility; prestenotic CCA = prestenotic flow pattern = reduced flow velocity
and increased pulsatility; OA collateral = variable: OA flow may be normal, absent or retrograde, pathol: OA flow is mostly pathological, i. e.,
absent or retrograde; IC collaterals = intracranial collateral activation via: retrograde ipsilateral A1-ACA, raised flow velocities in P1-PCA and
PCoA, raised flow velocities in P2-PCA and P3-PCA branches in variable combinations
These data are valid in singular stenoses and for the ICA origin only
= peak systolic flow velocity within thestenosis; V
ICA syst
ICA
/
= peak systolic velocity ICA/CCA ratio; poststenotic ICA
CCA
= end-diastolicflow velocity within the stenosis;V
ICA diast
= poststenotic flow pattern =
dist
ICA post
=
Fig. A5.27 Extracranial duplex, color-mode image, longitudinal
plane. Image of a 80 % ICA stenosis with color-aliasing at the maximum point of the stenosis. Direction of the flow jet and vessel
course is not equivalent, complicating the exact placement of the
angle correction. Dotted line:Preferred placement following the flow
jet within the stenosis. Dashed line: Inappropriate angle correction
placement following the vessel course.
However, all the above grading criteria should be applied with caution. The given cut-off values for blood flow
velocities might not be applicable in patients with generally altered cerebral perfusion, e.g., in severe hyperemiaor
in young subjects who generally show higher blood flow
velocities of the brain-supplying arteries. As blood flow is
generally altered in the above circumstances, differentiation should usually be possible. A second problem
may be the exact flow velocity assessment particularly if
the vessel is elongated. Within a stenosis, the direction of
the flow jet may be different from the direction of the
vessel course. In these circumstances the angle correction
must follow the blood flow jet to avoid erroneous measurements (Fig. A5.27).
Furthermore, high-grade ICA stenosis or occlusion may
lead to a raised contralateral ICA flow velocity with subsequent overgrading of flow, especially if a contralateral
stenosis is present (Henderson et al. 2000). Subsequently,
reopening of a high-grade ICA stenosis often results in a
decrease in blood flow velocity of the untreated stenotic
side. Following stent treatment a significant drop of peak
systolic velocity with a mean of 60.3 cm/s has been reported on the contralateral side. Also, 71 % of patients with
significant contralateral stenosis according to duplex criteria prior to intervention did not have significant stenosis
by angiography (Sachar etal. 2004). In a furtherstudy, after
CEA a contralateral decrease of blood flow velocity was
observed in 52 % of cases leading to an average drop of
duplex defined stenosis defined in grading steps of 20 % of
stenosis by at leastone category (Busuttil etal. 1996). It can
be assumed that such effects will only occur if the untreated ICA serves as a collateral vessel supplying blood
via the ACoA before intervention. Interestingly, none of the
above studies analyzed the presence or absence of intra-
Extracranial Pathology 89
cranial collaterals, which probably explains why this phenomenon did not occur in all of their patients.
Another potential pitfall to be considered is the occurrence of tandem stenoses, i. e., the simultaneous presence
of an extra- and intracranial ICA stenosis. In such cases
flow velocity and therefore also the stenosis grade may be
underestimated. A tandem stenosis should be considered
if indirect signs of a hemodynamically relevant distal flow
obstruction are present, which cannot solely be explained
by the findings of the extracranial ICA stenosis. Finally, it
has to be mentioned that the presented stenosis categories
are based on the presence of an isolated,short, andcircumscribed ICA stenosis. In long-segmented ICA stenoses, such
as are seen in dissection, lower flow velocities might be
observed due to the increased flow resistance. For further
details, see Cases1 (p.128) and 11 (p.183).For details of ICA
near occlusion, see Cases 15 (p. 215) and 18 (p. 238).
ICA—Occlusion
A proximal ICA occlusion below the origin of the ophthalmic artery (OA) (infraophthalmic occlusion) is characterized bya missing color-mode signal and a missing Doppler
flow signal. In case of a preserved stump, a small alternating “to-and-fro” Doppler signal might be found
(Fig. A5.28). Flow pattern in the depending distal vessel
segments, i. e., the carotid siphon,MCA andACA depend on
the presence and qualityof collateral pathways (for further
details, see “Collateral Pathways,” p.101). In case of a
supraophthalmic ICA occlusion (distal to the OA origin)
the ICA only provides blood supply mainly to the OA. In
this constellation the ICA canbe considered as an extended
OA. Consequently, the lumen of the ICA often diminishes
to a level below the ECA diameter and the flow profile
resembles that of the OA with low flow velocities and a
higher pulsatility but preserved diastolic flow (Fig. A5.29).
For further details, see Cases 11–13 (pp . 183–209), 20
(p. 251), 24 (p.287), and 28 (p. 319).
CCA—Stenosis and Occlusion
In contrast to the ICA, an exact grading system of CCA
stenoses does not exist. However, the relation of diameter
and area assessments as well as the diameter/flow velocity
relation and the criteria for local findings, pre- and poststenotic alterations do also apply as in ICA stenoses (see
“ICA—Stenosis,” p.86). Stenoses in the mid- and distal CCA
are easily accessible on duplex ultrasound (Fig. A5.30).
Proximal low- and medium-grade CCA stenoses are probably often missed as the CCA origin is not directly accessible and a poststenotic flow pattern can only be observed
in high-grade stenoses > 70–80 %. In CCA occlusion, two
patterns may be observed:
• The CCA, ICA, and ECA may all be occluded resulting in
totally absent flow signals.
• The CCA shows a proximal occlusion whereas the ICA
and ECA remain patent.
5 Vascular Pathology90
Fig. A5.28 Proximal ICA occlusion. Left: DSA, selective left CCA fill-
ing, lateral view. Missing contrast filling of the ICA (arrow). Right:
Extracranial duplex. Top: Color-mode image, longitudinal view. Absent color filling within the proximal ICA. Bottom: Doppler spectrum
analysis. Alternating “to-and-fro” stump signal.
Fig. A5.30 Extracranial duplex. A B-mode image, longitudinal
plane: Large mid-echogenic structure in the CCA. B Color-mode,
cross-sectional plane: Diameter of the vessel (8.8 mm), residual lumen (4.4 mm) with a resulting stenosis of 50 %. C Color-mode,
longitudinal plane: Delineation of the remaining perfused lumen
and confirmation of the plaque extension. D Doppler spectrum
analysis revealing a spectral broadening and increased velocity in
moderate CCA stenosis (flow velocity: 168/53 cm/s).
Fig. A5.29 Distal, supraophthalmic ICA occlusion. Left: DSA, selective right CCA filling, lateralview. A Earlyarterialphase:ProximalICA
contrast filling but apparent contrast stop after 4 cm. B Late arterial
phase demonstrates preserved contrast filling of the total ICA (arrows). Note: The ICA lumen is smaller than the ECA lumen. Right:
Extracranial duplex. Top: Color-mode image, longitudinal plane.
Preserved color filling within the proximal ICA. Bottom: Doppler
spectrum analysis: Small orthograde flow with reduced flow velocities and increased pulsatility resembling OA flow pattern (flow
velocity: 40/12 cm/s).
ECA—Stenosis and Occlusion
ECA stenoses and occlusions are usually of little clinical
relevance. Only in cases of ICA occlusion and required
collateral pathways via ECA and retrograde OA will a hemodynamically relevant ECA stenosis have a direct effect
on cerebral perfusion and also be a possible source of
cerebral emboli. Also, patients being considered for extra-intracranial bypass, e. g. in extracranial ICA occlusion
require ECA evaluation and search for stenoses. Again, for
ultrasound evaluation the same diagnostic criteria as in
ICA stenosis can be applied. Main stem ECA stenoses can be
graded according to the peak systolic velocity into moderate (140 ± 49 cm/s) and high-grade stenoses (230 ±
95 cm/s) (Paivansalo et al. 1996). High flow velocities
may also be found in nonpathologic ECA and in stenoocclusive ICA disorders. For practical purposes we suggest
that spectral broadening and turbulences are therefore
regarded as major criteria of a stenosis (Fig. A5.31). ECA
occlusions are usually well compensated for by the available collaterals and might be easily be overlooked if distal
segmentsareaffectedandthemainstemisspared.
In the latter cases, a retrograde ECA flow from the ipsilateral VA or ECA anastomoses toward the ICA may be
observed. For further details of CCA occlusion, see Cases
3 (p. 138) and 30 (p. 338).
Extracranial Posterior Circulation
VA—Stenosis
V0/V1—VA
TheoriginoftheVAisthesecondmostcommonlocationof
atherosclerotic stenosis. In contrast with the ICA origin,
however, the V0/V1 segment is less easy accessible to
duplex ultrasound due to its anatomic location behind
Extracranial Pathology 91
Fig. A5.31 Extracranial duplex, longitudinal plane. Left: Doppler
spectrum analysis with a turbulent flow signal and increasedvelocity
in moderate ECA stenosis (flow velocity: 190/20 cm/s). Right: Corresponding color-mode image. Aliasing phenomenon at the ECA
origin. Note the superior thyroid artery (arrow).
theclavicle(forfurtherdetails,seeChapter2,“Extracranial
Arteries,” p.18). Ultrasound-derived diameter measurement and analysis of cross-sectional area reduction are
in general are not obtainable. Similar to all other arterial
vessels, color aliasing and an altered Doppler flow profile
with raised flow velocities and spectral broadening can be
observed in stenoses starting at 50–60 % (Fig. A5.32). Indirect signs of a proximal high-grade stenosis >70–80 %
can be found in the VA segments, distal to the stenosis
(V1–V4) in the form of a poststenotic flow pattern. In V0VA stenosis, a prestenotic vessel segment cannot be assessed. If both VAs are equally well developed, a marked
flow rise may be absent despite the presence of a relevant
stenosis as the contralateral VA compensates for it. In VA
hypoplasia or when the contralateral VA terminates as the
posterior inferior cerebellar artery (PICA), however, the
specific criteria of stenosis are effective. For further details,
see Cases 12 (p.194) and 23 (p. 279).
V2—VA
Stenoses of the V2-VA segment are rare. Because of its deep
location and the small vessel size, it is not possible to
measure the diameter or cross-sectional area in most instances. For assessment of stenosis, identical criteria as for
the V0-VA segment are applied (Fig. A5.33). However,
evaluation of the prestenotic V1-VA segment should be
attempted and is feasible in most cases.
Fig. A5.32 Extracranial duplex, longitudinal plane: Left: Color-mode
image of the V0-VA and V1-VA segment. VA = vertebral artery; SA =
subclavian artery. Note the color-aliasing at the origin of the VA
(arrow). Right: Doppler spectrum analysis and color-mode image in
the V0-VA segment (top) and the V1-VA segment distal of the
stenosis (bottom). Velocity measurements in the stenosis: 186/
19 cm/s, and in the V1-VA: 64/25 cm/s. Note the difficulties in
performing angle correction. Obviously there is a turbulent flow
with increased flow velocity and a normal distal flow pattern which
characterizesa50–80 % stenosis.
Fig. A5.33 A Contrast-enhanced MRA,lateral projection: V2-VA stenosis (arrow). B, C Extracranial duplex, longitudinal plane. B Colormode image and Doppler analysis proximal to the stenosis (flow
velocity: 76/17 cm/s). C Color-mode image and Doppler analysis
withinthestenosis(flowvelocity:319/61cm/s).Thereisaincreased
prestenotic pulsatility and a high intrastenotic flow velocity indicating a hemodynamically relevant stenosis >80 %. A poststentotic flow
segment was not studied.
V3—VA
Similar criteria apply to V3-VA stenoses which occur more
frequently than those in the V2-VA segment. Exact angle
correction may be difficult because of its tortuous vessel
course.
5 Vascular Pathology92
VA—Occlusion
The analysis of VA occlusions requires specific knowledge
to avoid diagnostic errors. As in the diagnosis of ICA occlusion, an occluded vessel might be depicted by colormode sonography with an absent color signal (Fig. A5.34).
Within the V2-VA segment the usually preserved blood
flow of the concomitant vertebral vein might be of diagnostic aid (Fig. A5.35).
In contrast with the extracranial ICA which does not
show secondary filling from extracranial collaterals, the
VA has numerous extracranial anastomoses at all levels of
its extracranial course which can potentially serve as col-
Fig. A5.34 Extracranialduplex, longitudinal plane:V0/V1-occlusion.
A absent color filling and absent Doppler spectrum in the V0-VA
segment. B Normal color signal and Doppler spectrum of the SA.
laterals and prevent occlusion over its entire length. These
are anastomoses from the thyrocervical trunk and
branches of the ECA, especially from the occipital artery.
In case of a proximal VA occlusion, they may lead to a
secondary VA filling, resulting in a “postocclusional” VA
flow, which might then be detected within the distal VA
segments (Figs A5.36, A5.37). Because of the bilateral VA
composition, the above collateral pathways are rarely of
importance as the contralateral VA will provide the blood
supply to the posterior circulation and also retrogradely to
the affected VA in most cases. However, in case of contralateral VA hypoplasia or when the contralateral VA terminates as the PICA, the extracranial anastomoses are indeed of relevance and the distal VA flow profile may then
be orthograde with a typical poststenotic flow pattern.
Although the term “poststenotic” seems slightly inaccurate in a vessel segment distal to an occlusion, we would
suggest its use nevertheless, as it clearly illustrates the
common problem of hemodynamic impairment in stenoses and occlusions. A distal extracranial VA occlusion may
cause a stump signal or a high pulsatile flow signal with
almost absent end-diastolic flow component (Fig. A5.38).
In a recently published study including 10 VA occlusions
proximal to the origin of the PICA, all subjects presented a
diastolic zero flow (Saito et al. 2004). Because of the high
variability of distal collateral filling, it has to be emphasized that the term “VA occlusion” alone is not sufficient
but has to be complemented by the exact location of the
occlusion and the information about possible secondary
VA filling by collaterals distal to the occlusion. For further
details, see Case 19 (p. 245).
Fig. A5.35 A DSA, selective SA filling, posteroanterior view: Proximal VA-occlusion (arrow). B–D Extracranial duplex, V2-VA segment. B B-mode image: Typical image constellation with the bilateral acoustic shadowing from the transverse processus and the
hypoechogenic transverse signal of the VA in between. Dashed
line: Estimated VA diameter. C Color-mode image demonstrates a
missing flow signal within the occluded VA but a preserved flow
signal in the vertebral vein. Long and short dashed lines: Estimated
and real diameter of the VA, respectively. D Doppler spectrum of the
vertebral vein.
Fig. A5.36 Left: DSA, selective thyrocer vical trunk filling, LAO view.
Proximal VA occlusion. Secondary, segmental collateral filling of the
V2- and V3-VA segments from numerous muscle anastomoses. 1–3
Extracranial duplex, longitudinal plane. 1 V2-VA with minimal flow;
2 Muscle branch anastomosis (flow velocity: 25/10 cm/s); 3 Postste-
notic flow pattern with reduced flow in the postocclusive V3-VA
(flow velocity: 16/5 cm/s).
Extracranial Pathology 93
Fig. A5.37 Left: DSA, selective right VA filling, posteroanterior view.
Occlusion of the left proximal VA and the right VA ending as the
posterior inferior cerebellar artery. Secondary segmental collateral
filling of the left VA via numerous segmental spinal anastomoses
from the right VA. 1–3 Extracranial duplex, longitudinal plane. 1
Proximal left V2-VA (flow velocity: 18/9cm/s); 2 Mid left V2-VA (flow
velocity: 22/10 cm/s); 3 Distal left V2-VA (flowvelocity: 27/10cm/s).
Note the improving flow in distal segments with increasing number
of collaterals.
Fig. A5.39 Schematic drawing of the two main variants of collateral
flow in case of a subclavian steal phenomenon. A Vertebrovertebral
overflow (regular type), B ICA-VA overflow (in cases with additional
contralateral VA pathology). Furthermore, a few rare collateral variants have been described with conventional angiography which are,
however, all difficult to assess with ultrasound.
Fig. A5.38 Left: DSA, selective VA-filling, lateral view: V3-VA occlusion (arrow). Note the only outflow pathway via a small muscle
supplying arterial branch. Right: Extracranial duplex of V2-VA with
normal diameter, longitudinal view: preserved color signalbut highly
pulsatile flow on Doppler spectrum analysis with small retrograde
flow component (flow velocity: 58/0cm/s) indicating that this vessel
does not participate in brain perfusion and strongly suggestive of VA
occlusion distal of the PICA origin.
Fig. A5.40 Subclavian steal syndrome in left proximal SA occlusion.
Left: DSA, selective right VA filling, posteroanterior view. Vertebrovertebral contrastoverflow. Right: Doppler spectrum analysis. SA-R:
Right SA with normal triphasic flow signal. V2-VA-R: Strong orthograde VA signal. V2-VA-L: Retrograde vertebral flow, which corresponds to a complete subclavian steal effect. SA-L: Monophasic
poststenotic distal SA signal.
SA—Proximal Stenosis and Occlusion
Direct signs of a hemodynamically relevant SA stenosis
> 50 % are, as in all other arteries raised flow velocities
and a turbulent flow, which is often difficult to directly
assess. In stenoses > 70–80 % and in proximal SA occlusion
indirect hemodynamic signs might be observed within the
dependent axillary, brachial, and radial arteries. These
vessels then show a poststenotic flow profile, i. e., a de-
layed systolic flow rise, reduced flow velocities as well as a
change of the typical triphasic flow profile to a bi- or
monophasic flow signal. A characteristic and pathognomonic sign of proximal high-grade SA stenosis or occlusion
is a flow alteration within the ipsilateral VA, which may
serve as a collateral for the blood supply of the arm—which
is then called subclavian steal phenomenon (Figs A5.39,
A5.40). Depending on the grade of SA stenosis a reduced
5 Vascular Pathology94
Fig. A5.41 Table of V2-VA Doppler flow spectrum findings in in-
creasing grade of subclavian steal phenomenon (grades 1 to 3). N =
normal
systolic flow (systolic deceleration), an alternating flow, or
even a retrograde flow within the ipsilateral VA may be
observed. According to the extent of the collateral flow the
subclavian steal phenomenon can be graded as: grade
1—incipient, grade 2—incomplete and grade 3—complete
(Fig. A5.41). For further detailed reading, see Cases 23
(p. 279) Case 28 (p. 319).
Intracranial Pathology
Stenoses
Intracranial stenoses of atherosclerotic origin account for
about 10 % of cerebral infarction. They are mainly diagnosed by detecting a focal increased velocity. In addition, a
numberofsecond-linecriteriahavebeenestablished
which may further help in theevaluation of findings.These
are turbulences which, however, are also a frequent physiologic finding caused by the tortuous vessel course of
many intracranial arterial segments, the restriction of a
velocity rise to a circumscribed vessel segment, and differences between the right and left sides, extending more
than 30 cm/s. The latter may only be applied to symmetrically developed vessel segments like, forexample, the M1segment of the MCA or the P2/P3-segments of the PCA,
ideally after accurate angle correction, which requires the
visualization of a straight vessel segment of at least
1.5–2 cm. This condition is seldom present in intracranial
arteries.
In contrast with the extracranial ICA pathology no internationally accepted criteria for grading of intracranial
stenoses are available. Using transcranial color-coded sonography (TCCS), Baumgartner and coworkers were the
first to extensively correlate TCCS data of basal cerebral
arteries with DSA. Their reported cut-of values for < 50 %
and ≥ 50 % intracranial stenoses are given in Ta b l e A5.3.
Applying these criteria the reported sensitivity and specificity values for stenoses ≥ 50 % were 100 % and 100 % for all
insonated vessel segments. In the category < 50% specificity for ACA stenosis detection was 99 %, the sensitivity for
MCA stenosis detection 94 %, all remaining sensitivity and
specificity values were 100 % (Baumgartner et al. 1999). In
contrast to the extracranial ICA, flow velocity changes are
already observed with a diameter reduction < 50 %. As
intracranial arteries do not show physiologic bulbous widening, flow velocities directly follow Hagen–Poiseuille’s
law, which states that there is an inverse relation between
flow velocity and the squared diameter of the remaining
vessel lumen (see Chapter 1, Fig. A1.1, p. 2). Accordingly,
even a 30–50%stenosiswillresultinadetectableflow
velocity increase. In addition to the cut-off values of Baumgartner and coworkers, we recommend differentiating
high-grade hemodynamically relevant stenoses that are
characterized by the presence of pre- and poststenotic
flow patterns in the up- and downstream vessel segments.
Additionally, increased velocities within the non-affected
basal arteries may indicated leptomeningeal collateralization. Intracranial stenoses can therefore be roughly graded
into three categories: mild stenosis (< 50 %), moderate
stenosis (50–80 %), and high-grade hemodynamicallyrelevant stenosis (> 80 %). A more detailed evaluation is currently not available because there are no comparative data
for the different diagnostic methods.
In certain vessel segments of the intracranial circulation,
there may be no marked flow rise despite the presence of a
stenosis. This peculiarity may occur if sufficient collaterals
take over the blood supply function as, for example, in the
P1-PCA segment (possible flow compensation via the ipsilateral ICA and the PCoA) or the A1-ACA segment (possible
flow compensation via the contralateral A1-ACA and the
ACoA). A similar problem may arise in extracranial VA
stenosis which can be compensated via the contralateral
VA,providedthatitisnothypoplastic.Inothervessel
segments, such as the ICA, M1- and M2-MCA, A2-ACA,
P2- and P3-PCA a vessel narrowing will always result in
raised flow velocities as no direct collateral pathway exists
(Fig. A5.42).
For the ultrasound analysis of intracranial pathology we
recommend proceeding as follows: To obtain the best
orientation of the individual anatomic constellations start
at the presumably nonaffected side. Like in extracranial
pathology, the highest flow velocities for each vessel are
searched for and then documented. Sometimes, the maximum flow velocity within a turbulence may be obtained
by onlyslightly adjusting the probe searching for the loudest Doppler signal (the examiner will be acoustically
guided like in the “blind” TCD method) rather than the
sample volume. Whenever a pathologic finding is present,
the proximal and distal vessel segments should be evaluated. Also, potential collateral pathways should be considered (for further details, see “Intracranial Collateral
Pathways,” p. 101).