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ICA
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
ECA
CCA
VA
BrA
Fig. A5.85 Middle: Ce-MRA with a high-grade stenosis of the brachiocephalic trunk (BCT) type III according to Brunhölzl and von
Reutern (1989). Left and right: Doppler spectra analyses from
the right ICA, ECA, CCA, V2-VA, and brachial artery (BrA). Note
the hemodynamic consequences of the severe BCT stenosis leading to steal phenomena of grade 1 (ICA), grade 2 (CCA and ECA),
and grade 3 (V2-VA). Note the monophasic BrA fl ow pattern in ac-
cordance with a grade 3 subclavian steal phenomenon instead of a
n o r m a l t r i p h a s i c fl ow pattern.
139Arterial Pathology
Fig. A5.86 DSA, left ICA injection, posteroanterior view revealing
a high-grade M1-MCA stenosis of hemodynamic relevance (short
arrow). The hemodynamic signifi cance is underlined by the faster
fi lling of the ACA compared with the MCA (large arrow) and the
leptomeningeal anastomoses coming from the ACA (arrowheads).
by autopsy in more than 60% of patients and a stenosis
of >30% in more than 40% of patients after fatal stroke.
In these, the stenosis was considered to be causal in
5.8% of cases (Mazighi et al 2008). In the United States
intracranial stenoses of atherosclerotic origin account
for ~10% of stroke or TIA and the risk of recurrence is
~15% per year despite treatment (Chimowitz et al 2005).
The distribution of stenosis varies according to the diagnostic method used and the population studied. Using
CTA and considering a stenosis as a luminal reduction
of at least 30%, in a group of 786 symptomatic patients
the intracranial VA was the most aff ected vessel with
a prevalence of 30%, followed by the PCA (prevalence
26%), MCA (prevalence 16%), BA (prevalence 11%), ICA
(prevalence 10%), and ACA (prevalence 6%) (Homburg
et al 2011). A similar study in 652 symptomatic white
patients analyzed by CTA showed a diff erent distribu-
tion pattern with dominance of the anterior circulation
aff ecting mostly the MCA in 37% of patients, followed
by the PCA in 25%, ICA in 23%, VA in 9%, BA in 4%, and
ACA in 3% when analyzing stenoses ≥30% (Ovesen et al
2013). In the aforementioned autopsy study the most
frequently aff ected vessel with a stenosis of at least 30%
was the MCA in about 28% of patients, followed by the
ICA in 25%, the BA in 24%, the VA in 12%, and the PCA in
11%. The ACA was not considered (Mazighi et al 2008).
Reports about the distribution of intracranial stenosis in symptomatic patients, detected by TCCS and
graduated according to the Baumgartner criteria alone
or in addition to other imaging modalities, are rare. In
a Danish population-based study on 195 TIA patients
using TCCS the MCA was the main site of stenosis ≥50%
according to the Baumgartner criteria (33.3%), followed
by the ICA (25.9%), V4-VA (14.8%), PCA and BA (each,
11.1%), and ACA (3.7%). As ICA stenoses were originally
not considered by the Baumgartner group, a cut-off of
peak systolic fl ow velocity of 120 cm/s was used (von
Weitzel-Mudersbach et al 2012). A similar TCCS study
was done on 292 Italian patients with TIA or stroke,
but with addition of a second imaging modality (MRA,
CTA, or DSA). To confi rm a nonembolic stenosis, ultra-
sound assessment was repeated 6 months after the
event. Again, the MCA was the preferential site (48.4%)
for a stenosis ≥50%, followed by the PCA (29.5%), BA
(11.6%), V4-VA (6.5%), and ACA (4.3%). Here, the ICA
was not considered (Viaro et al 2012). In a highly selective French study of 102 mostly Caucasian stroke
patients with relapsing ischemia despite best medical
treatment and intracranial stenoses of ≥50% confi rmed
by at least two modalities, one of them TCCS, the main
artery involved was the MCA in 26.5%, followed by the
BA and ICA in 25.5% each, and the VA in 22.5%. In this
study, however, the PCA and ACA were not considered
(Mazighi et al 2006).
DSA is the gold standard for the evaluation of intracranial vessel pathologies. It allows excellent visualization of the intracranial arteries, the direct assessment
of a stenosis, and also the evaluation of hemodynamic
criteria, e.g., the delayed contrast infl ow in the poststen-
otic vessel segment and/or the activation of leptomeningeal collaterals (Fig. A5.86). The grading system for
stenoses developed for the WASID study included 24
stenoses (9 ICA, 7 MCA, 5 BA, and 3 VA). Using a magnifying glass (× 10) and calipers, the intrastenotic diameter was compared with the proximal normal diameter.
The distal or contralateral vessel segment was studied
if the proximal vessel segment was diseased or in case
of poststenotic vessel dilation. Stenoses were graded
in three categories: 30–49%, 50–69%, and 70–99%. Despite methodical shortcomings and the small number
of stenoses included, the interobserver agreement of
three observers ranged between 75% and 88% (Samuels
140 5 Vascular Pathology
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
Fig. A5.87 CTA with M1-MCA stenosis but limited direct judgment
options (short arrow). The hemodynamic relevance is revealed
by indirect signs—the visible cortical vessel dilatation indicating
c o l l a t e r a l s ( a r r o w h e a d s ) a n d t h e r e d u c e d s i g n a l i n t h e p o s t s t e n o t i c
M1-MCA segment (large arrow).
et al 2000). The main limitation of DSA is its invasiveness while “low-risk” methods like MRA and CTA and
“no-risk” techniques like TCD and TCCS are widely available. A large European survey including 25 countries
and 886 hospitals showed that the most frequently
used method to detect ICAS in stroke patients was CTA
in 69.9%, followed by MRA in 56.2% and TCCS in 39.7%.
About 30% of hospitals off ered all three modalities,
and 19% were without access to these methods in
which DSA was usually implemented (Balucani
et al 2009).
CTA mainly follows the DSA criteria and classifi es
stenoses by luminal assessment into three categories:
30–49%, 50–69%, and 70–99%. Most frequently the maximum intensity projection (MIP) technique is being used
(Homburg et al 2011). CTA is minimally invasive, fast,
and therefore less aff ected by motion artifacts. Because
of its worldwide availability CTA is currently the primary diagnostic tool even in developing countries. At least
in the proximal vessel segments CTA is as reliable as DSA
in the determination of cerebral artery stenosis. In vessel segments beyond the fi rst 1 cm, however, it seems to
be less reliable (Villablanca et al 2007). CTA also allows
a better delineation than MRA but can be limited in the
visualization of the petrous and cavernous part of the ICA
because of overlying bone artifacts. This does not apply to
dual-source CTA, as the diff erent voltages applied by this
technique permit bone-subtracted images of superior image quality, especially at the skull base level (Buerke et
al 2009). Hemodynamic information is limited, but activated leptomeningeal collaterals considered as the extent
of contrast visualized distal to the occlusion can be examined and this has been shown to be a good prognostic
pattern in acute stroke (Miteff et al 2009) (Fig. A5.87).
The main stenosis grading principle in MRI and MRA
is again the comparison of the intrastenotic lumen
with the obvious unaff ected prestenotic or poststen-
otic segment. In TOF-MRA, the WASID method can in
part be applied by measuring intrastenotic diameters
Fig. A5.88 3D TOF-MRA, axial MIP: Signal void in the proximal M1MCA indicating high-grade stenosis (short arrow). The indirect hemodynamic signs are the decreased poststenotic M1-MCA signal
intensity (large arrow), the increased ipsilateral PCA signal intensity
and its extension to the periphery indicating leptomeningeal collateral fl ow (arrowheads).
and the diameter of the assumed normal vessel size,
defi ning stenoses less or more than 50%. A partial sig-
nal loss (fl ow gap) with distal fl ow signal resembles a
high-grade stenosis (≥70%). An occlusion is defi ned if no
distal fl ow signal is seen (Aizawa et al 2012). However,
a near-occlusion or generalized low fl ow (e.g., severely
impaired cross-fl ow in extracranial ICA occlusion) might
simulate MCA vessel occlusion (Ishimaru et al 2007).
Important information can be obtained from TOF-MRA
as it provides fl ow-related information and accentuat-
ed hemodynamic features. A stenosis will usually be
overestimated, but this phenomenon can be used as a
high-sensitivity screening method for stenosis which
then needs to be confi rmed by a second method. TOF-
MRA also provides important insights into the hemodynamic impact of a stenosis: The signal intensity of the
poststenotic vessel segment can be compared with the
signal intensity proximal to the stenosis. The signal intensity ratio of a poststenotic reduced intensity and a
prestenotic high intensity was shown to be moderately
correlated with the grade of stenosis (Leng et al 2013)
and was also correlated with the risk of recurrent stroke
(Liebeskind et al 2014). A similar approach can be used
to evaluate the leptomeningeal collateral activation in
intra- or extracranial steno- occlusive disorders. A prominent PCA sign, resulting from collateral fl ow in MCA
occlusion, characterized by a pronounced PCA brightness and the length of its visualization (termed prominent PCA laterality) was fi rst published by Uemura et al
(2004) and later proven to predict a good clinical outcome (Ichijo et al 2013) (Fig. A5.88). Further collateral
signs on MRI are hyperintense leptomeningeal vessels
on fl uid-attenuated inversion recovery (FLAIR) sequenc-
es. Their presence was associated with less parenchymal
loss in MCA occlusion (K.Y. Lee et al 2009).
In considering an individual patient one has to take
into account that all of the methods discussed above
measure fl ow-related parameters that are similar but
not identical. It may therefore sometimes be diffi cult
141Arterial Pathology
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
RL
Fig. A5.89 Schematic of stenosis locations. Arrows indicate locations where effi cient collateral pathways may prevent the devel-
opment of raised fl ow velocities and subsequent underestimation
or overlooking may occur (VA, P1-PCA, A1-ACA). Circles indicate
locations where a stenosis will always result in raised fl ow veloci-
ties, provided that no near-occlusion is present (all ICA segments,
M1- and M2-MCA, A2-ACA, P2- and P3-PCA).
or even impossible to bring them and the ultrasound
fi ndings into complete agreement. Knowledge of the
principles and the main advantages and disadvantages of DSA, CTA, and MRI/A in general and with regard
to a specifi c vessel segment is therefore mandatory for
a neurosonologist. For further details see Chapter 6
and Case 5.
Using ultrasound for the assessment of intracranial
stenoses detecting a focal increased fl ow velocity is the
most evident parameter. Also, the downstream and upstream segments have to be evaluated to be sure that the
maximum of a stenosis has been detected and to look
for waveform abnormalities that indicate hemodynamic
relevance of the stenosis. In certain intracranial vessel
segments there may be no marked fl ow velocity rise
despite the presence of a stenosis. This peculiarity may
occur if suffi cient collaterals take over the blood sup-
ply function. For example this may occur in the P1-PCA
segment (possible fl ow compensation via the ipsilateral
ICA and the PCoA) or in the A1-ACA segment (possible
fl ow 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, p rov id ed th at i t i s n ot hypop la st ic. I n o ther ve ssel
segments, such as the ICA, M1- and M2-MCA, A2-ACA,
and P2- and P3-PCA a single, short vessel narrowing
below the level of a near-occlusion will always result in
raised fl ow velocities as no direct collateral pathway ex-
ists (Fig. A5.89). Several second-line criteria can be used
which may further help in the evaluation of fi ndings.
First, turbulence— although this is also a frequent physiologic fi nding caused by the tortuosity of many intracra-
nial vessel segments such as the carotid siphon. Second,
the restriction of a velocity rise to a circumscribed vessel
segment; and third, diff erences between homologous
Fig. A5.90 Left: 3D TOF-MRA, coronal MIP, revealing generalized
dilated intracranial arteries except the left A1-ACA. Right: TCCS,
color-mode with corresponding Doppler spectra revealing low fl ow
velocities in all vessels. Top: Axial midbrain transtemporal plane:
Left M1-MCA (32/11 cm/s). Middle: Axial midbrain plane: Left P1PCA (30/12 cm/s). Bottom: Transforaminal approach: Right V4-VA
(24/10). Low velocities were even seen in the BA (21/6, not shown)
which can best be explained by its elongated course. Using the
Baumgartner criteria a low-grade stenosis can easily be overlooked.
segments of both sides which extend more than 30 cm/s
may indicate presence of a stenosis. The latter can only
be applied with confi dence to equally developed vessel
segments, which restricts it to the M1-MCA and P2/P3PCA. Even in these segments the vessel’s course has to
be considered and an obvious diff erence may then need
angle correction which should be done if a straight vessel segment of at least 1 cm is visible and the sample
volume is centered in the mid part of the visible vessel.
When a stenosis is located in a curved segment (impeding the use of angle correction), the position of the ultrasound probe should be optimized to obtain the smallest
possible insonation angle. Flow velocities may, however,
be normal or reduced despite a grave stenosis. This may
be the case in a tandem stenosis, long-segmented stenosis, or near-occlusion. Especially in the MCA, a stenosis
may also be overlooked if the vessel runs a downward
convex course, because of the unfavorable insonation
angle and the resulting false low fl ow velocities. An-
other condition potentially obscuring correct diagnosis
is dilatative arteriopathy, a condition with generalized
intracranial vessel dilatation commonly seen in patients
with long-standing arterial hypertension. Here generalized low fl ow velocities can usually be seen. In general,
the vertebrobasilar arteries are more frequently aff ected
but the anterior circulation may also be involved (Lou
and Caplan 2010) (Fig. A5.90). The unremarkable fl ow
velocity that may be seen in near- occlusion (Fig. A5.91)
can be challenging. The most crucial additional parameter helping to identify the condition in each case is the
evaluation of indirect signs, i.e., the pre- and poststenotic waveforms. In accordance with the Spencer’s curve
(see Fig. A5.34) a decrease of blood volume fl ow and
drop of perfusion pressure starts at 70–80% stenosis. In
this situation, the intrastenotic fl ow velo city is elevated;
142 5 Vascular Pathology
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
the poststenotic vessel segment reveals a poststenotic
fl ow pattern and the unaff ected basal arteries and their
branches may present higher fl ow and fl ow velocities
via leptomeningeal collaterals. Because of the comparable fl ow in the P2-and P3-segments, the PCA is the
favorite target for analyzing fl ow asymmetries in MCA
steno-occlusive lesions (Gómez-Choco and Valdueza
2013a, 2013b). A velocity comparison between the P1PCA and A1-ACA segments yields more uncertain results as anatomic variations including hypoplasia have
to be considered. However, this approach has also been
described and used (Kim et al 2009). Again, following
the Spencer’s curve, intrastenotic fl ow velocities may be
normal or reduced if the vessel is nearly occluded. Here a
leptomeningeal collateral fl ow has to be present, which
avoids a misinterpretation of the intrastenotic fi ndings.
In contrast to the extracranial vessel pathology,
there are no international accepted ultrasound criteria for the grading of intracranial stenoses. Using TCCS,
Baumgartner and co workers (1999) were the fi rst to
extensively correlate TCCS data of basal cerebral arteries with DSA. They analyzed 69 stenoses (10 ACA,
29 MCA, 15 PCA, 7 BA and 8 VA—no ICA stenoses) with
a mean delay after stroke of 31 days (range 2–126) and
a mean delay after DSA of 2 days (range 0–6). An intracranial stenosis was diagnosed when a focal increase of
fl ow velocity of 2 SD higher than the mean value for
the corresponding cerebral artery of 104 normal subjects previously studied was seen (Baumgartner et al
1994a). They reported cut-off values for <50% and ≥50%
intracranial stenoses. Angle correction was performed
if a straight vessel segment was visible over at least
2 cm of length.
Applying these criteria the reported sensitivity and
specifi city values for stenoses ≥50% were both 100%
for all insonated vessel segments. In the category <50%
specifi city for ACA stenosis detection was 99%, sensitiv-
ity for MCA stenosis detection 94%; all remaining sensitivity and specifi city values were 100%. In contrast to the
extracranial ICA with its confl icting bulb, intracranial
fl ow velocity changes are observed even with a diameter reduction of less than 50%, following Hagen–Poiseuille’s law, which states that there is an inverse relation
between fl ow velocity and the squared diameter of the
remaining vessel lumen (see Fig. A1.1). Also, the smaller intracranial vessel diameter facilitates earlier recognition of a focal velocity increase. Intracranially, also, a
30–50% stenosis will result in a detectable fl ow veloci-
ty increase. In Baumgartner’s <50% ultrasound stenosis
group, the mean angiographic grade ranged from 30% to
35%. Even those patients with an angiographic stenosis
of 20% were detected by ultrasound, which indicates a
high sensitivity of ultrasound for the detection of lowgrade intracranial stenoses.
Hemodynamically relevant high-grade stenosis
(>70–80%) was not separately analyzed in this study. As
the grade of an intracranial stenosis is directly related to
the risk of stroke recurrence, it is desirable to use reliable ultrasound parameters for this purpose. In addition
to the cut-off values of the Baumgartner classifi cation,
we therefore recommend diff erentiating hemodynam-
A
B
Fig. A5.91 (A) 3D TOF-MRA, coronal view suggestive of M1-MCA
occlusion (arrows) as only a proximal M1-segment is visible (arrowhead). (B) Ce-MRA of the same patient revealing an open M1-MCA
segment. Note the marked reduced vessel lumen (arrows). (C,D)
TCCS , tr anst empor al app roac h, a xial m idbrain plane with co rresponding Doppler spectra demonstrating aff ected M1-MCA with a
normal color signal but a turbulent fl ow and reduced fl ow velocity
(54/19 cm/s) at a depth of 49 mm. (E,F) TCCS, same transtemporal approach showing an M2-MCA branch with a marked poststenotic fl ow pattern and reduced velocities (16/9 cm/s) at a depth of
39 mm, indicating M1-MCA near-occlusion.
C
D
E
F
ically relevant stenoses >70–80% by the presence of a
poststenotic fl ow pattern in the downstream vessel seg-
ments. An additional crucial parameter is the detection
of increased velocities in the unaff ected basal arteries
and their branches, indicating leptomeningeal collateral
fl ow. Raised fl ow velocities are therefore not mandato-
ry for the diagnosis of a high-grade stenosis and even
normal or low intrastenotic velocities may be observed.
Currently, intracranial stenoses can therefore be graded roughly into three categories: mild stenosis (<50%),
moderate stenosis (50–70%) and high-grade, hemodynamically relevant stenosis (>70–80%).
The Baumgartner reference values and our suggestions are presented in Fig. A5.92. A DSA- or CTA-based
evaluation of the proposed third category of intracranial stenoses is currently not available. It would also be
desirable to expand the study of Baumgartner and coworkers for other reasons. First, it included a relatively
small number of 69 stenoses which is, however, already
higher than the 24 stenoses (9 ICA, 7 MCA, 5 BA, and
3 VA) which were used to defi ne the intracranial ste-
nosis grades with catheter angiography for the WASID
study (Samuels et al 2000). Second, Baumgartner did
not include intracranial ICA stenoses, probably because
of the tortuous course of the carotid siphon and the unfavorable insonation angle of the terminal intracranial
carotid artery (TICA). Third, the time delay between ultrasound and catheter angiography lasted up to 6 days
which might have allowed changes of vascular pathology, subsequently limiting the study’s informative value. Despite all this, the Baumgartner criteria should
currently always be used when classifying intra cranial
stenoses with TCCS.
143Arterial Pathology
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
Stenosis
M1
MCA
A1
ACA
P1–P3
PCA
BA
V4
VA
Fig. A5.92 Ultrasound grading of intracranial stenoses, provided that no other intracranial stenosis ≥50% is present. The provided fl ow
velocity values represent the peak systolic velocity in cm/s. The entries preceded by an asterisk denote a possible additional hemodynamic fi nding. In high-grade stenosis, the opportunity to analyze pre- and/or poststenotic signals strongly depends on the localization
(proximal or distal) of the stenosis and may not always be available. Note that in severe hemodynamically relevant stenoses the intrastenotic fl ow velocities may be normal or even reduced. All data are validated only for the proximal vessel segments with the largest
diameter. For more peripheral segment stenoses of the A2-ACA, M2-MCA, and M3-MCA the velocity ranges should in fact be lower,
but currently only the same cut-off s as for the main segments can be used for approximation. No ICA values are presented as it was not
studied by Baumgartner. Alternatively, the velocity criteria for the A1-ACA stenoses can be used for a fi rst orientation. For the diff erent
ICA segments (C1/2-ICA, siphon and C6-ICA) cut-off values may be calculated using the reported mean velocities + 3 standard deviations
(see Table A2 .3). In dilated vessels (and therefore normal low velocities) the proposed velocity criteria are not applicable but the indirect
criteria remain valid. In hypoplasia of the A1-ACA and P1-PCA none of the mentioned criteria are applicable. FV = fl ow velocity; FP = fl ow
pattern. (The data in the <50% and ≥50% columns are from Baumgartner et al 1999.)
<50%
Mild
≥120
≥100
≥100
≥90
≥50%
Moderate
≥220≥155
≥155
≥145
≥140
≥120
≥70%
High
FV ≥220 or variable FV
Distal M1/M2 poststenotic FP
* Raised FV ipsilat. A1 and/or PCA
FV ≥155 or variable FV
A2 poststenotic FP
* Raised FV ipsilat. M1 and/or contralat. A1
FV ≥145 or variable FV
Distal PCA poststenotic FP
* Raised FV ipsilat. M1 and/or A1
FV ≥140 or variable FV
Distal BA/PCA poststenotic FP
* Proximal BA prestenotic FP
FV ≥120 or variable FV
Distal VA/BA poststenotic FP
* Ipsilat. proximal VA prestenotic FP
So far, TCD is the main ultrasound approach for
intracranial stenoses in many countries and cut-off
velocities have been presented by several groups for a
limited distinct number of vessel segments (de Bray et
al 1988, Felberg et al 2002, Ley-Pozo and Ringelstein
1990, Mattle et al 1988, Navarro et al 2007, Röther et
al 1994, Tsivgoulis et al 2007). With regard to proximal
vessel identifi cation, TCD seems comparable to TCCS
although it does not allow angle-corrected fl ow velocity
measurements (Krejza et al 2007a, Schöning et al 1993).
However, TCCS is the only reliable method to diff erenti-
ate between a proximal M1-MCA trunk and a terminal
ICA stenosis, identify MCA branch stenosis (Klötzsch
et al 2000), identify the carotid siphon, or assess the C6ICA segment. Finally, even an expert in TCD would not
be able to iden tify the P3-PCA, A2-ACA, M3-MCA, and
branches of the PCA; this is only possible with TCCS.
A recent multicenter TCD study of patients with hemodynamic relevant stenoses >70% correlated ultrasound with catheter angiography (Zhao et al 2011). The
best sensitivity and specifi city for a ≥70% MCA stenosis
(68% and 95%, respectively) was achieved for a mean
fl ow velocity >120 cm/s and a stenotic/prestenotic velocity ratio (SPR) ≥3. Using the above velocity threshold
or a SPR ≥3 or an asymmetry index >30% (velocity dif-
ference compared with the homologous contralateral
side) or with the presence of a downstream fl ow pat-
tern alteration (corresponding to a poststenotic fl ow
pattern) increased the sensitivity to 91%, but the specifi city decreased to 80%. In the intracranial VA and BA a
≥70% stenosis was best detected using a mean velocity
threshold of 110 cm/s or an SPR ≥3 or a poststenotic fl ow
pattern, yielding a sensitivity of 80% and a specifi city of
81%. A velocity threshold of 140 cm/s alone increased
the specifi city to 99% but reduced the sensitivity to 35%.
A critical point, comparable to other studies, is the small
patient number of 102. More relevant, however, is that
patients were included within 4 weeks after conventional angiography. As all patients suff ered from recent
cerebral ischemia a lot of vascular changes, especially
clot recanalization, must be expected.
A TCCS approach using a velocity index (termed “continuity equation method”) was recently proposed by
Logallo and coworkers. This approach, analyzing relative
velocity increases, was assumed to be less aff ected by the
individual magnitude of velocities and to better avoid the
possibility of overlooking stenoses in patients with conditions such as hypertension-related dilatative angiopathy.
Compared with the classical cut-off velocity method the
study revealed a slightly higher sensitivity (78% versus
144 5 Vascular Pathology
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
Absent flow signal
AB
67%) and identical specifi city (86%) compared with CTA
in detecting MCA stenosis ≥50% (Logallo et al 2012).
For TCCS analysis of intracranial pathology we recommend the following strategy: To obtain the best orientation of the patient individual anatomy, start with the
presumably unaff ected side. As in extracranial pathol ogy,
the highest fl ow velocities for each vessel are sought and
documented. The depth of insonation of the maximal
systolic fl ow velocity should be documented. To facili-
tate follow-up examinations the use of angle correction
should be noted (this applies equally to the documentation of stenoses). Sometimes it may be diffi cult to fi nd the
highest velocities because the high-velocity components
are too weak and therefore not displayed. Slight probe
adjustment searching for the loudest Doppler signal (examiner acoustically guided as in the “blind” TCD method)
rather than movement of the sample volume and/or an
increase of the Doppler gain may facilitate the detection
of the highest velocities. Whenever a pathologic fi nding is
present, the proximal and distal vessel segments must be
evaluated (see above discussion). Also, potential collateral pathways should be considered (for further details, see
“Intracranial Collateral Pathways” below).
0
Complete proximal occlusion
Minimal flow signal
1
Absent end-diastolic flow
Blunted flow signal
2
Delayed systolic flow acceleration with reduced mean
flow velocity and Pl <1.2
Dampened flow signal
3
Pulsatile signal with normal
acceleration and decrease of
mean flow velocity >30%
compared to normal si de
Stenotic flow signal
4
Focal in crease of flow
velocity
Normal flow signal
5
Without relevant difference
to the contralate ral side
(<30% difference)
No flow
1
Low flow velocities
2
Absent end-diastolic flow
Low flow velocities
3
With diastolic flow
Established perfusion
4
a) Flow velocities equal to
contralate ral side
b) High focal flow
velocities (i.e. stenosis)
c) High segmental
flow velocities
(hyperperfusion)
proximal MCA, PCA, and ACA and the short lengths of the
studied arterial segments. In distal arterial main stem occlusion, velocity asymmetries may be of help. This particularly applies to the M1-MCA and P2-PCA segments, as both
usually reveal comparable velocities on both sides. However, anatomic variability of the vessel courses has to be
considered, which may infl uence the insonation angle and
therefore the measured fl ow velocities.
Most evaluations concerning intracranial occlusions are
reported in patients with acute stroke. The DIAS I (Duplex
Sonography In Acute Stroke) study analyzed the ability of
duplex ultrasound to diagnose main stem arterial occlusions within the anterior circulation within a 6-hour time
window. Diagnostic certainty of the sonographers varied
from 50% to 60% of studied vessels in unenhanced TCCS but
reached 80–90% after intravenous contrast administration
(Gerriets et al 2002). These fi ndings suggest that the qual-
ity of the bone window, i.e., the insonation conditions, determines whether a suffi cient transcranial evaluation can
be achieved. For Doppler spectrum analysis in occlusion
and evaluation of reperfusion patterns after thrombolysis,
a grading system similar to the TIMI criteria (Thrombolysis
In Myocardial Ischemia), the TIBI grading system (Thrombolysis In Brain Ischemia), has been developed for use in
Occlusions
Occlusions are characterized by missing color and Doppler
fl ow signals at the site of the occlusion or reduced fl ow
signals in vessel segments proximal to the occlusion. The
reduced fl ow signals are usually caused by the remaining
blood fl ow into small perforating arteries or vessel branch-
es located proximal to the occlusion. They may also be
caused by residual fl ow around an embolic clot or in-situ
acute stroke (Demchuk et al 2001). TIBI diff erentiates the
following grades of fl ow pattern (Fig. A5.93A):
• Grade 0: Absent fl ow.
• Grade 1: Minimal fl ow.
• Grade 2: Blunted fl ow.
• Grade 3: Dampened fl ow.
• Grade 4: Stenotic fl ow.
• Grade 5: Normal fl ow.
thrombus. Even if MRA, DSA, or CTA suggests a complete
cessation of fl ow, some minimal fl ow may still pass the ob-
stacle and be detectable with ultrasound. The fi nding of a
residual fl ow may make it diffi cult for the sonographer to
decide whether or not an occlusion is present, or indeed
at which site. The interpretation of fi ndings may be diffi -
cult because of the presence of perforator arteries in the
TIBI 0 and 1 refer to proximal occlusion, TIBI 2 and 3 to
distal occlusion, and TIBI 4 to induced recanalization.
Applying these criteria in acute stroke the TIBI classifi cation correlates with initial stroke severity, clinical
recovery, and mortality in patients treated with recombinant tissue plasminogen activator (rt-PA) (Demchuk et al
Fig. A5.93 (A) Ultrasound Thromboly-
sis In Brain Ischemia (TIBI) grading system according to Demchuk et al (2001).
(B) Consensus on Grading Intracranial
Flow obstruction (COGIF) score for assessment of baseline findings before thrombolysis and changes during the recanalization process according to Nedelmann
et al (2009).
145Arterial Pathology
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Fig. A5.94 Left: DSA, selective CCA injection, lateral view. C5/6ICA stenosis (arrow). Right: TCCS, transtemporal approach, axial
lower pontine plane. Color-mode and corresponding Doppler spectra visualize a stenosis with a turbulent fl ow and raised velocities
(199/50 cm/s).
2001). The grading system has also been used to predict
recanalization and to analyze recanalization patterns, for
example during thrombolysis, where it was shown that
the duration of recanalization correlates with the clinical
outcome (Alexandrov et al 2001, Tsivgoulis et al 2013).
For further details, see Case 10.
The TIBI score was developed for the TCD method, which
has some limitations in anatomic assessment of vessels.
Grades 0 and 1 appear clearly related to a proximal vessel
obstruction. An absent fl ow also means that the occlusion
has to be anterior to relevant perforator arteries. The dampened fl ow in grade 3 can be related to the asymmetry index
of Zanette and fi ts well with a main stem occlusion distal to
the perforator arteries or an occlusion of a relevant branch.
Grade 2, however, rather resembles a poststenotic fl ow pat-
tern, e.g., distal to a proximal high-grade stenosis. It could
also refer to a distal M1-MCA occlusion in the presence of
a prominent early temporal M1 branch. Here the temporal
branch tries to compensate for the M1 occlusion via leptomeningeal collaterals and the loss of resistance could then
explain the delayed systolic fl ow acceleration and the low
pulsatility. Despite these remarks, the TIBI criteria can also
be well assessed using TCCS. Alternatively, the COGIF classifi cation (Consensus on Grading Intracranial Flow obstruction), which allows better distinction between a proximal
occlusion (grades 1 and 2) and a distal occlusion (grade 3),
was introduced by groups using preferentially TCCS (Nedelmann et al 2009b) (Fig. A5.93B):
• Grade 1: No fl ow.
• Grade 2: Low fl ow without diastolic fl ow.
• Grade 3: Low fl ow with diastolic fl ow.
• Grade 4: Established fl ow with (a) normal fl ow ve-
locities, (b) focal high fl ow velocities (stenosis),
(c) segmental high fl ow velocities (hyperperfusion).
Intracranial Anterior Circulation
ICA Stenosis
The Baumgartner TCCS grading system does not include ICA stenoses, as mentioned above. One reason
A
C
Fig. A5.95 (A) CCT, pronounced calcifi cation of the right carotid
siphon (arrow). (B–D) TCCS, color-mode images. Note excellent
vessel visualization in the midbrain/thalamic plane (B) and the
lower pontine plane (C). In the upper pons/midbrain plane (D) the
PCA is also demonstrated in high quality but not the carotid siphon
(arrowhead) which can be best explained by its calcifi cation and
subsequent shadowing.
B
D
may be the tortuous anatomic course of the artery and
the unfavorable insonation angle. However, the proximal (C6-ICA) (see Video
15.11) and the distal (C1/2-
ICA) segments usually show a straight vessel course
and can be insonated in the axial or coronal insonation
plane respectively. Contrary to the usual assumption,
the main sites of intracranial ICA stenoses are found
to be variable. In the INTRASTENT multicentric registry of 388 patients with intracranial stenoses, 13.9% of
patients had a lesion at the C6 segment and 16.8% in
the carotid siphon while the MCA was aff ected in only
18.6% of cases (Kurre et al 2010). Therefore all available ICA segments, including C5-ICA and C6-ICA, have
to be studied in patients with ischemia of the anterior
circulation, in particular if no other reasonable explanation is found (Fig. A5.94). Insonation of the carotid
siphon may be limited in case of severe calcifi cations
(Fig. A5.95). A further problem aff ecting the detection
of siphon stenosis is that the mean vessel diameter at
the siphon is larger compared with the terminal ICA
diameter (5 ± 0.6 versus 3.6 ± 0.4 mm; Rai et al 2013).
This means that vessel diameter reduction of up to
50% may not lead to detectable fl ow alterations. ICA
stenoses >70–80% will result in activation of collaterals (ACoA or PCoA) and a poststenotic fl ow pattern in
the depending distal vessel segments may be seen (Fig.
A5.96). Depending on the grade and the location of the
stenosis (infraophthalmic or supraophthalmic) the extracranial ICA fl ow may show more or less pronounced
prestenotic fl ow alterations. The interpretation may be
diffi cult in intra- and extracranial ICA tandem stenoses.
In case of a hemodynamically relevant extracranial stenosis, fl ow velocity of the distal stenosis may be low
and its extent consequently underestimated. If the distal stenosis dominates, the proximal stenosis will be
underestimated. Turbulences at the proximal M1-MCA
may be confounded with upstream distal intracranial
ICA stenoses (Fig. A5.97). A carotid siphon stenosis may
also be detected by TCD. However, in a DSA-correlated study a high number of TCD-false-positive patients
146 5 Vascular Pathology
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A
CD
Fig. A5.96 (A) 3D TOF-MRA, coronal MIP. Signal void in the C1/
C2-ICA indicating high-grade stenosis (arrow). (B) TCCS, transtemporal approach, anterior coronal plane. Distal ICA stenosis
with turbulent fl ow and angle-corrected maximal velocities of
161/98 cm/s. (C) TCCS, transtemporal approach, axial midbrain
plane: Cross-fl ow activation via ACoA and retrograde ipsilateral
A1-ACA (arrow) confi rming a high-grade stenosis despite the only
moderately raised intrastenotic fl ow velocity. (D) TCCS, transtem-
poral approach, axial midbrain plane. Mild poststenotic ipsilateral M1-MCA fl ow pattern (69/39 cm/s, PI = 0.49: contralateral
118/58 cm/s, PI = 0.58) further supporting the diagnosis of a hemodynamically relevant stenosis.
B
were reported due to coexisting intracranial stenoses,
underlining the limitations of TCD for exact determination of the insonated anatomic site (You et al 2010). For
further details about intracranial ICA carotid-T stenosis
see Case 9 and Case 30, for siphon stenosis see Case 14,
and for C6-ICA stenosis see Case 31.
Fig. A5.97 TCC S, transte mpor al appro ach, anter ior corona l p lane.
Top: Normal fl ow velocity and turbulent fl ow are detected in
the C2/C3-ICA junction considered to be normal (103/22 cm/s).
Middle: Marked turb ulent fl ow in the C1/2-ICA with maximal veloc-
ities of 182/64 cm/s reveal a stenosis. Bottom: Turbulent proximal
M1-MCA with fl ow velocity within the normal range (138/41 cm/s).
Without knowledge of the distal ICA stenosis a mild proximal MCA
stenosis would probably be wrongly diagnosed.
ICA Occlusion
Long segmental intracranial ICA occlusions are usually
characterized by the absence of a color signal. However,
in infraophthalmic ICA occlusion, fi lling of the carotid
siphon may occur via a retrograde OA, the PCoA, or the
ACoA. In supraophthalmic ICA occlusion an antegrade
fl ow from the proximal C6-ICA segment to the carotid
siphon further draining antegrade into the OA may be
seen. In suspected intracranial ICA occlusion extracranial ICA analysis is of great value as a reduced fl ow
velocity and an increased pulsatility can be expected.
An infraophthalmic ICA occlusion may lead to an open
vessel (large blind sack) without cerebral or orbital perfusion and therefore a subsequent stump signal. A supraophthalmic ICA occlusion often results in a severely
reduced fl ow with a preserved diastolic fl ow compo-
nent, resembling OA fl ow. However, if the carotid blood
fl ow can canalize into a fetal-type PCA, the extracranial
ICA fl ow signal may appear at best only mildly reduced
(Fig. A5.98). Infraophthalmic ICA occlusion over time
will lead to a successive retrograde thrombosis of the
complete proximal ICA. In supraophthalmic ICA occlusion the proximal ICA remains open, functioning as a
prolonged OA. For further details about intracranial ICA
occlusion see Case 37.
Ophthalmic Artery Stenosis and Occlusion
OA stenos is has been repor ted by TCD in a patient with repeated episodes of amaurosis fugax which seemed to be
related to a vasospasm related to systemic autoimmune disease (Fig. A5.99). Following treatment with calcium chan-
nel blockers the attacks immediately ceased and repeated
Doppler examinations confi rmed resolution of the stenosis
(Ploner et al 1995). OA stenoses have been also reported in
giant cell arteritis (Pérez López et al 2009). TCCS-determined
OA occlusion was reported in patients with steno-occlusive
disorders of the ipsilateral ICA (Wilterdink et al 1994). In
this condition, however, a watershed phenomenon with a
zero OA fl ow seems more likely than real OA occlusion.
MCA Stenosis
Stenoses of the MCA usually aff ect its main M1 segment.
Here the stenoses can be allocated to the proximal, middle,
and distal M1 segment and graded according to fl ow veloc-
ity, turbulence, and asymmetry into mild (<50%), moderate (50–69%), and high-grade stenoses (≥70–80%) (see Fig.
A5.92). The latter requires the analysis of available pre- and
poststenotic vessel segments. If the stenosis is located within the proximal M1-MCA, signals should be obtained from
the distal M1-MCA as well as from the M2 segment which in
147Arterial Pathology
A
B
D
E
F
G
H
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All rights reserved. Usage subject to terms and conditions of license.
Extracranial ICA A1-ACA M1-MCA
A
B
C
C
D
E
F
Normal
Reduced
or normal
Reduced
OA-like
flow
Stump
signal or
no flow
Normal or
reduced
Normal
Raised or
normal
Raised or
normal
No flow
Retrograde
or reduced
Normal or
raised
Reduced
or normal
Reduced
flow in prox.
M1
No or
retrograde
flow in distal
M1
No or
retrograde
flow
Reduced
or normal
Reduced
or normal
P1/2-PCA
Normal
Raised or
normal
Raised or
normal
Raised or
normal
Raised or
normal
Raised or
normal
Fig. A5.98 Synopsis of hemodynamic eff ects
of ICA and MCA occlusions depending on the
localization of the occlusion. (A–E) Findings in
a normally developed circle of Willis. (F) Vari-
ant with a strong early temporal MCA branch.
(G–H) Findings in fetal-type PCA.
Normal or
G
H
reduced
Reduced
Raised or
normal
No flow
No or
retrograde
flow in distal
M1
No or
retrograde
flow
high-grade stenosis should show a poststenotic fl ow pat-
tern (Fig. A5.100 and Fig. A5.101). In high grades and near-
occlusions even a venous-like fl ow signal may be seen
together with normal or low intrastenotic fl ow velocities
(see Fig. A5.91). A hemodynamically relevant stenosis leads
to activation of a collateral fl ow in the ipsilateral ACA and PCA
segments via leptomeningeal anastomoses (Fig. A5.102). (For
collateral activation, see “Secondary Collaterals (Ophthalmic
Artery and Leptomeningeal Collaterals)” under “Intracranial Collateral Pathways in ICA Occlusive Processes” below.)
Most frequently, MCA stenoses have a proximal location but
they can also be found in the transition between M1- and
M2-MCA or in a detectable M2 branch itself (Fig. A5.103 and
Fig. A5.104; see also Video
15.12). A stenosis may even
be found in the M3-MCA segments, although this is rare
(Fig. A5.105). Cut-off velocity criteria for M2- and M3-MCA
stenoses do not exist. For a pragmatic approach, the criteria
for an M1-MCA stenosis can be applied. If a turbulent fl ow
is detected with a fl ow velocity higher than in the main
stem of MCA a stenosis seems very likely, but the angle of
insonation has to be considered. M1-MCA near-occlusions
have not been specifi cally reported on in the literature but
low fl ow velocities and marked poststenotic fl ow alterations
Raised
Raised
can be expected similar to extracranial ICA near-occlusions
(Tang et al 2006). For further details about MCA stenosis see
Case 5, Case 17, Case 24, Case 30, and Case 44, and for MCA
near-occlusion see Case 25 and Case 30.
MCA Occlusion
Depending on the location of the occlusion, the Doppler
spectrum may be completely absent or reduced. In the
M1 segment at least proximal, mid, and distal M1 occlusions should be diff erentiated.
In proximal M1-MCA occlusion no real fl ow signal is
seen (correlating to TIBI 0 and 1 and COGIF 1 and 2). Sometimes a hyperechoic B-mode signal can be observed which
might correspond to MCA main stem occlusion (Kadimi et
al 2000) (Fig. A5.106; see also Video
A5.13). A missing
M1-MCA and concomitantly preserved PCA signal may,
however, also be caused by an insuffi cient anterior acous-
tic bone window and this should not be overlooked. Good
insonation conditions and MCA visualization on the contralateral side argue in favor of a real occlusion. If the contralateral M1-MCA and A1-ACA are visible from the side
of the presumed occlusion, an M1-MCA occlusion can be
assured with certainty (Fig. A5.107). Visualization of the
148 5 Vascular Pathology
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All rights reserved. Usage subject to terms and conditions of license.
Fig. A5.99 Large image: DSA, selective ICA injection, lateral view:
OA stenosis at its origin (yellow circle). Small image: TCD, transorbital insonation at a depth of 48 mm at the proximal OA revealing a turbulent fl ow signal with a peak systolic velocity of 120 cm/s.
A
CD
Fig. A5.100 Center: 3D TOF-MRA, axial MIP: Short signal void in
the proximal M1-MCA indicating high-grade stenosis (arrowhead).
(A–D) TCCS, transtemporal approach, axial midbrain plane with corresponding Doppler spectra. (A) M1-MCA stenosis with a marked
turbulent fl ow and angle-corrected velocities of 385/234 cm/s.
(B,D) Ipsilateral anterior and posterior M2 branches showing a
poststenotic fl ow pattern assuring the hemodynamically relevance
of the M1 stenosis. (C) A contralateral M2 branch, on the contrary,
reveals a normal waveform.
A
B
B
Fig. A5.101 Left: 3D TOF-MRA, axial MIP: Signal void in the proximal M1-MCA indicating high-grade stenosis (arrow). Note the
increased signal intensity in the ipsilateral PCA (yellow circle) and
ACA (red circle). The PCA signal extends to the periphery indicating leptomeningeal collateral fl ow. Right: TCCS, transtemporal ap-
proach, axial midbrain plane with corresponding Doppler spectra.
Top: M1-MCA stenosis with a marked turbulent fl ow and a non-an-
gle-corrected velocity of 380/225 cm/s. Middle: Poststenotic M1-
MCA with increased acceleration time of 144 milliseconds. Bottom:
Decreased pulsatility of 0.64 in the same location—both secondary
signs of a hemodynamically compromised circulation.
deep middle cerebral vein alone, which usually follows
the M1-MCA in an opposite fl ow direction, also confi rms a
long- segmented M1-MCA occlusion (Fig. A5.108; see also
Case 39). If uncertainty remains echo contrast agents can be
administered.
In mid MCA occlusions, a small antegrade fl ow with
increased pulsatility remains present and may be detected depending on the amount of blood fl ow into the ante-
grade perfused lenticulostriate perforators (correspond-
C
Fig. A5.102 TCC S, tran stemporal appr oach , a xial planes wit h cor responding Doppler spectra of the same patient as in Fig. A5.101
showing leptomeningeal collateral fl ow. (A) Upper pons/mid-
brain plane: Ipsilateral A1-ACA with increased fl ow velocity
of 128/43 cm/s. (B) Cella media/thalamic plane: The A4-ACA
(pericallosal artery) can be detected as a marked collateral with a
fl ow velocity of 43/16 cm/s. (C) Thalamic plane: Increased fl ow ve-
locities in the distal P2-PCA segment (108/42 cm/s). (D) Midbrain/
thalamic plane: As expected, increased fl ow velocities are de-
tectable in PCA branches, here in the anterior temporal artery
(70/26 cm/s).
D
ing to TIBI 2 and 3 and COGIF 3). The amount of residual
fl ow also depends on the presence and size of an early
temporal branch which has its origin at the opposite of
the perforating arteries.
An early temporal M1-MCA branch also determines the
residual proximal MCA fl ow in distal M1-MCA occlusion.
Here, usually all lenticulostriate arteries show anterograde
perfusion. A distinctly reduced fl ow velocity can be expect-
ed with variable pulsatility (again corresponding to TIBI 2
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