Intracranial stenosis/occlusion
Chapter
10 Claudio Baracchini and Kurt Niederkorn
Introduction
A systematic assessment of intracranial vessels by
ultrasound in stroke/stroke-at-risk patients is useful
in diagnosing intracranial stenosis/occlusion, under-
standing the hemodynamic effects and possibly the
nature of the stenosis and identifying patients at a
higher risk of stroke recurrence. Indeed, ultrasound
can provide real-time flow information (grade of ste-
nosis, collaterals), study hemodynamic changes with
time (progression/regression/stability of stenosis) or in
response to various stimuli (vasomotor reactivity) and
it can also detect transient emboli. All this information
might have immediate therapeutic implications: anti-
coagulants for a partially recanalized embolus, calcium
channel blockers for vasospasm, antiplatelet agents for
dissection, immunosuppressants for vasculitis, inten-
sive risk factor management and dual antiplatelet
treatment for intracranial atherosclerosis. In patients
with recurrent symptoms despite best medical therapy,
ultrasound can detect a progression of the stenosis, an
increased embolic count downstream; it can also assess
intracranial arterial hemodynamics postoperatively
(angioplasty alone or combined with stenting) and
verify treatment efficacy.
Focused questions
While scanning patients with possible intracranial
artery disease, there are few key questions to focus on:
• Is there an intracranial stenosis/occlusion?
• What are the hemodynamic effects?
• What is the nature of the stenosis/occlusion?
Once the diagnosis has been made, the questions dur-
ing follow-up are as follows:
154 Manual of Neurosonology, ed. László Csiba and Claudio Baracchini. Published by Cambridge University Press. © Cambridge
University Press 2016.
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• Is there a progression/regression/stability of the
intracranial occlusive disease?
• In patients who have undergone cerebral artery
stenting, was the endovascular treatment effective?
Anatomical diagnosis
Stenosis
Intracranial artery stenosis is a frequent finding in
stroke patients; in particular, intracranial athero-
sclerotic disease (ICAD) represents a major cause of
ischemic stroke in the world [1]. Its incidence varies
by ethnicity, being highest among Asians, black people
and Hispanics, but it is still underestimated in white
people [2,3,4,5]. ICAD is considered a malignant
cause of stroke due to a very high stroke recurrence
rate: highest rate for 70–99% stenosis and during the
first 2–3 weeks after the initial event [6].
Due to the heterogeneity in vascular anatomy
and physiology, ICAD in different vessels may rep-
resent diseases with fundamentally distinct courses.
Furthermore, intracranial stenosis is a dynamic dis-
ease, consequently static neuroimaging studies (com-
puted tomography [CT], magnetic resonance imaging)
characterize this process only partially; instead, ultra-
sound monitoring in parallel with clinical evaluation
offers invaluable information on the pathophysiology
of stroke allowing for tailored treatment.
The main goal of transcranial ultrasound in patients
with ischemic stroke is to detect hemodynamically sig-
nificant stenosis (≥50%) of intracranial vessels. Several
diagnostic criteria have been developed to identify
hemodynamically significant stenosis in various intrac-
ranial arteries, for both transcranial Doppler (TCD)
 Chapter 10: Intracranial stenosis/occlusion

Table 10.1  TCD criteria for intracranial stenosis

Artery Stenosis ≥ 50% Stenosis ≥70% Diffuse disease or near occlusion

(MFV, SPR) (MFV, SPR) (MFV, SPR)
MCA ≥ 100 cm/s, ≥2 ≥ 120cm/s, ≥3 <30cm/s, <1
ACA ≥ 80 cm/s, ≥2 n.a., ≥3 <30cm/s, <1
PCA ≥ 80 cm/s, ≥2 n.a., ≥3 <30cm/s, <1
BA ≥ 90 cm/s, ≥2 ≥ 110 cm/s ≥3 <20cm/s, <1
VA ≥ 90 cm/s, ≥2 ≥ 110 cm/s ≥3 <20cm/s, <1
ACA: anterior cerebral artery; BA: basilar artery; MCA: middle cerebral artery; MFV: mean flow velocity; n.a., not available; PCA: posterior
cerebral artery; SPR: stenotic/prestenotic MFV ratio; VA: vertebral artery.

Table 10.2  TCCS criteria for intracranial stenosis

Artery Mild stenosis Moderate stenosis Severe stenosis

Stenosis ≤50% Stenosis ≥50% Stenosis >80%
(PSV) (PSV)
MCA ≥155 cm/s ≥220 cm/s + Indirect signs
ACA ≥120 cm/s ≥155 cm/s + Indirect signs
PCA ≥100 cm/s ≥145 cm/s + Indirect signs
BA ≥100 cm/s ≥140 cm/s + Indirect signs
VA ≥90 cm/s ≥120 cm/s + Indirect signs
Modified from reference [11].
ACA: anterior cerebral artery; BA: basilar artery; MCA: middle cerebral artery; PCA: posterior cerebral artery; PSV: peak systolic velocity;
VA: vertebral artery. Indirect signs: proximal and/or distal flow alterations (i.e., diastolic velocity drop and high resistance in the feeding
vessel or in the proximal segment of the stenotic vessel, a delayed systolic flow rise and velocity drop downstream, flow diversion and
signs of collateralization).

[7,8,9,10] (Table  10.1) and transcranial color-coded
Doppler sonography (TCCS) [11] (Table 10.2).
However, none of these criteria are absolute, conse-
quently it is important to validate these velocity values
in each neurosonological laboratory against angio-
graphic findings.
For a more systematic approach, we recommend
following these direct criteria:  the first criterion for
intracranial stenosis, applicable only to TCCS, is rep-
resented by a color aliasing phenomenon, which may
indicate the presence of raised flow velocities, such as
those caused by a stenosis, and will help guide spectral
Doppler interrogation [12] (Figure 10.1); note that a
turbulent flow is also a frequent physiological finding
caused by a tortuous vessel course.
The second criterion is a progressive focal increase
of blood flow velocities in ≥50% stenosis (Figure 10.2)
or paradoxical velocity decrease with very severe ste-
nosis, near-occlusion or diffuse intracranial disease. As
a rule for a vessel with straight walls, a 50% diameter
reduction doubles the velocity, and a 70% stenosis may
triple the velocity at the end of the stenosis compared
with a prestenotic segment or with the contralateral
nonaffected side [13].
It is noteworthy that the velocity values measured
by TCCS are higher than those by TCD if there is angle
correction. Angle correction should be performed
when the Doppler sample volume is located within
a straight vessel segment ≥20  mm in length [14]. In
contrast with the extracranial internal carotid artery,
intracranial arteries do not have a bulbous widening
at their origin; this means that flow velocity changes
are already observed with a diameter reduction <50%,
hence even a 30–50% stenosis will result in a detect-
able flow velocity increase. On the contrary, in certain
vessels segments of the intracranial circulation (e.g.,
P1-PCA, A1-ACA) there might be no significant flow
velocity increase, despite the presence of a stenosis,
due to efficient collateralization (via ipsilateral internal
carotid artery and posterior communicating artery –
PCoA, and via contralateral A1 and anterior commu-
155
nicating artery – ACoA, respectively).

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 Chapter 10: Intracranial stenosis/occlusion

Figure 10.1  Color aliasing

phenomenon indicates the presence of
a stenosis. (A) M1 segment of the MCA;
(B) P1 segment of the PCA.

Figure 10.2  A focal increase of

blood flow velocities indicating a
hemodynamic significant stenosis. (A) M1
segment of the MCA; (B) P1 segment of
the PCA.

A third diagnostic criterion for intracranial ste-
nosis is a significant (≥30%) side-to-side difference of
velocity; however, this criterion can only be applied to
symmetrical vessel segments after accurate angle cor-
rection. In the case of severe stenosis, two additional
frequent findings are co-vibrations (i.e., high-intensity
156 signals at the zero line) and musical murmurs, which
have a visual correlate called mirror-image parallel
strings (Figure 10.3).
Musical murmurs, in very high-grade stenosis,
are harmonic phenomena resulting from harmonic
frequencies generated from regular vibrations of the
vessel walls caused by the increased flow velocities
and sound like a musical tone (sea gull cry, goose cry,

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 Figure 10.3  Signs of a severe stenosis
of the M1 segment of the MCA.
(A) Co-vibrations; (B) mirror-image
parallel strings.

Figure 10.4  Indirect hemodynamic signs. (A) Prestenotic diastolic drop (with retained diastolic component) and increased peripheral
resistance in the ipsilateral ICA of a patient with (B) a severe MCA stenosis. (C) Poststenotic delayed systolic flow rise and velocity drop in a
patient with a severe MCA stenosis. 157

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 Chapter 10: Intracranial stenosis/occlusion
honks, cooing). Beware that murmurs are also found in
functional stenoses when blood flow is too high for the
size of the vessel (ACoA, PCoA).
In very severe stenosis (>80%), in addition to the
direct criteria described previously, there are indirect
hemodynamic criteria which include proximal or distal
flow alterations: a diastolic velocity drop and high resist-
ance in the feeding vessel or in the proximal segment of
the stenotic vessel, a delayed systolic flow rise and veloc-
ity drop (tardus et parvus) downstream, flow diversion
and signs of collateralization (Figures 10.4 and 10.5).
When the bone window is inadequate or absent,
ultrasound contrast agents should be used in order
not to miss hemodynamically significant stenoses
(Figure 10.6).
Analogously, if a high-grade intracranial vertebral
artery or basilar artery stenosis must be quickly ruled
out, contrast agents should be used generously for an
accurate diagnosis, being aware that prestenotic flow
in patients with distal basilar artery stenosis may be
normal.
Occlusion
Direct criteria for proximal occlusion include the com-
plete absence of color-flow signal (using lowest pulse
repetition frequency [PRF] and increased color-gain
settings) (Figure 10.7) or minimal flow signal in ves-
sel segments (branches or perforators) proximal to
the occlusion; criteria for distal occlusion are blunted
flow signal and dampened flow signal as discussed in
greater detail in Chapter  12, since most evaluations
concerning intracranial occlusions are made in acute
stroke patients.
It is noteworthy that a missing flow signal does not
necessarily imply occlusion – it could be hypoplasia/
aplasia. It is therefore helpful to use ultrasound contrast
agents and very important to check for indirect signs of
intracranial occlusion in the proximal and distal ves-
sel segments: a diastolic velocity drop and high resist-
ance in the feeding vessel or in the proximal segment of
the occluded vessel; a flow diversion; a post-occlusive
orthograde flow pattern if efficient collaterals distal to
the occlusion are activated; sometimes a flow inver-
sion is observed distally (Figure 10.8). For example, in
a proximal basilar artery occlusion, activation of the
PCoAs with retrograde flow in the posterior cerebral
arteries and in the distal segment of the basilar artery
is a frequent finding, along with a positive oscillation
158 phenomenon with carotid tapping. Beware that there
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are no indirect signs in patients with top of the basilar
artery occlusion, so that an apparent normal flow in
the vertebral arteries and in the proximal basilar artery
does not exclude distal basilar artery occlusion. A help-
ful trick in this case is to tap the vertebral arteries: if this
determines an oscillation of the flow in the posterior
cerebral arteries, then a complete basilar artery occlu-
sion can be excluded.
Transcranial ultrasound has a very high nega-
tive predictive value in excluding a 50–99% steno-
sis and occlusion, therefore it is a useful screening
test for exclusion of intracranial artery disease.
Although the administration of ultrasound con-
trast agent improves their diagnostic yield, TCD
and TCCS have only a moderate positive predictive
value, thus requiring confirmation by other imaging
modality such as angio-CT or conventional cerebral
angiography [7].
Functional diagnosis
Once the anatomical diagnosis of an intracranial ste-
nosis/occlusion is made, it is crucial to understand
the functional significance and the hemodynamic
effects of the stenosis/occlusion. Transcranial ultra-
sound can surely help by studying collaterals, testing
for vasomotor reactivity (VMR) and detecting emboli
(Figure 10.9).
In fact, TCD/TCCS can provide real-time informa-
tion on collateral flow and in case of vessel obstruction,
activation of collateral pathways is very important for
the clinical outcome of the patient [15]. A  complete
circle of Willis and the possibility to activate primary
collaterals (ACoA, PCoA) or secondary collaterals
(ophthalmic artery, leptomeningeal arteries) reduces
the risk of hemodynamic ischemic stroke; in patients
with intracranial artery obstruction, the most frequent
collaterals are the leptomeningeal arteries. Sometimes
we see a compensatory increase of blood flow veloc-
ity in the donor vessel due to recruitment of collaterals
by vasodilation in tissues with compromised perfusion
[16]. Other times (e.g., in MCA tight stenosis/occlu-
sion), flow diversion to the anterior or posterior cer-
ebral artery is observed; this is associated with earlier
and better neurological improvement, therefore flow
diversion has a protective effect on the ischemic brain
tissue [17].
TCD/TCCS provides also information on hemo-
dynamic changes in response to various vasodilatory
stimuli (apnea, acetazolamide):  if there is no velocity
 Figure 10.5  Indirect hemodynamic signs. (A) and (B) prestenotic diastolic drop and increased peripheral resistance in both vertebral
arteries. (C) A significant focal increase of blood flow velocities, and (D) angio-CT image indicating a severe basilar artery stenosis.

Figure 10.6  (A) Inadequate

transtemporal bone window;
(B) ultrasound contrast agent disclosing a
>50% MCA stenosis.

159

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 Chapter 10: Intracranial stenosis/occlusion

Figure 10.7  Intracranial artery occlusion. (A) Absent signal in the MCA and ACA, while it is present in the PCA. (B) Absent color Doppler
signal in ACA even after ultrasound contrast agent administration. (C) No color signal in the MCA, flow diversion in the ACA. (D) No color and
Doppler signal in the MCA.

increase during apnea, we speak of impaired VMR which
translates into a higher risk of hemodynamic stroke.
Sometimes we observe an intracranial steal, that is, a
paradoxical velocity decrease in the affected vessel and
a simultaneous velocity increase in normal vessels, in
response to vasodilatory stimuli. This represents the
“reversed” Robin Hood principle (i.e., rob the poor to
feed the rich). Thus, when a pressure gradient favors the
normally perfused brain parenchyma, a collateral vessel,
which normally acts with a compensatory mechanism
delivering sufficient supplies, can become deleterious
for the patient by further depriving brain regions at risk
of supply. If the steal is causing a clinical deterioration
we speak of reversed Robin Hood syndrome, which is
associated with a higher stroke recurrence rate [18].
160 Transcranial ultrasound is the only diagnostic
method that can detect clinically silent emboli; this
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requires continuous monitoring of the major intrac-
ranial arteries and according to the current consensus
the duration of the monitoring should be at least 1 hour
[19]. Microembolic signal (MES) detection identifies
patients who are at higher risk of atheroembolic stroke
[20], thus allowing to select those patients who could
benefit from a more aggressive treatment. MES are also
valid surrogate markers for verifying antithrombotic
or endovascular treatment efficacy.
Diagnosis of nature
Having detected and categorized the intracranial
arterial obstruction (stenosis or occlusion), defined
its severity and its hemodynamic effects, it is crucial
to understand its nature. The differential diagnosis
includes atherosclerotic disease, a partially recana-
lized embolus/thrombus, arterial dissection, vasculitis
 Chapter 10: Intracranial stenosis/occlusion

Figure 10.8  (A–C) Pre-posterior inferior cerebellar artery (PICA) occlusion of the intracranial segment – V4 – of the vertebral artery.
(A) Flow inversion in the V4 segment distally to a pre-PICA occlusion. (B) Missing V4 segment (red arrow) in magnetic resonance angiogram
(MRA). (C) Prestenotic very high resistance flow in the ipsilateral V2 segment (note that the diastolic component is missing). (D–F) Post-PICA
occlusion of the intracranial segment – V4 – of the vertebral artery. (D) No color signal in the V4 segment. (E) Missing V4 segment (red arrow) in
MRA. (F) Prestenotic high resistance flow in the ipsilateral V2 segment (note that the diastolic velocity component is reduced but present).

and vasospasm. Differentiating between stenosis and
vasospasm can sometimes be difficult. In the case of
stenosis of atherosclerotic origin the aliasing phenom-
enon is usually visible in a circumscribed, short sec-
tion of the vessel, corresponding to the extension of the
stenotic segment, whereas in vasospasm several vessels
are frequently affected. Notably, increased flow veloci-
ties can also be registered in the case of obstructive
lesions in the contralateral hemisphere or in extrac-
ranial carotid disease due to a compensatory increase
of blood flow through collateral vessels. Diagnostic
errors can be avoided by considering the findings of all
arteries supplying the brain [21]. Intracranial steno-
sis can be a dynamic process and serial examinations
by TCD/TCCS will aid understanding of its nature; in
fact, cerebral artery stenosis may undergo progression
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(it is usually an atherosclerotic plaque), regression (it
could be an embolus, dissection, vasospasm, vasculi-
tis) or remain stable during follow-up.
Intracranial artery stenosis is assumed to represent
atherosclerotic plaque when no other obvious disor-
der, like vasculitis or dissection, is found on diagnostic
workup. However, we know relatively little about the
composition of these cerebral artery stenoses apparent
on noninvasive and invasive imaging studies. For this
reason, transcranial ultrasound should be repeated
after about 3 months to ascertain the atherosclerotic
nature of the stenosis.
With regard to the timing of diagnosis of intracra-
nial atherosclerosis, transcranial ultrasound detects
the advanced stages of the disease, as the vessel main- 161
tains the same lumen diameter up to 30–40% stenosis
 Chapter 10: Intracranial stenosis/occlusion

Figure 10.9  (A) and (B) A patient with impaired vasomotor reactivity, showing no significant velocity increase during apnea.
(C) Spontaneous microembolic signal (white arrow) detection during MCA insonation. (D) Flow inversion in the A1 segment (colored red like
the ipsilateral MCA) indicating the activation of a collateral pathway through the anterior communicating artery.

due to the remodeling of the arterial wall according to
Glagov et al., regardless of the progressing atheroscle-
rotic process [22]. When this compensatory mecha-
nism fails, a vessel stenosis develops.
The information obtained on the nature of the
intracranial stenosis will have immediate therapeutic
implications: anticoagulants for a partially recanalized
embolus of cardiac origin, calcium channel block-
ers for vasospasm, antiplatelet agents for dissection,
immunosuppressants for vasculitis, intensive risk fac-
tor management and dual antiplatelet treatment for
intracranial atherosclerosis.
Follow-up
Overall transcranial ultrasound provides accurate infor-
mation on cerebral hemodynamics and represents the
162
ideal modality for following disease progression and
therapeutic effects. In patients with recurrent symp-
toms despite best medical therapy, ultrasound can
detect a progression of the stenosis or a branch occlu-
sion, and check for a possible increase of the embolic
count downstream. The Stenting and Aggressive
Medical Management for Preventing Recurrent stroke
in Intracranial Stenosis (SAMMPRIS) study has shown
that early aggressive medical therapy is better than stent-
ing for prevention of recurrent stroke [23]. Nevertheless,
there are subgroups of patients who remain at high risk
of stroke despite aggressive medical therapy. In these
patients, angioplasty alone or in combination with new
stent types might still be an option [24], and transcranial
ultrasound can quickly assess vessel patency by record-
ing intracranial arterial hemodynamics changes post-
operatively. In particular, due to the metal composition
of the stent, TCCS can clearly display the stent, thereby

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 Chapter 10: Intracranial stenosis/occlusion

Figure 10.10  (A) Severe MCA stenosis. (B) One month after angioplasty and stenting, normalization of the blood flow velocities in the MCA.
(C) The metal stent is shown within the red circle. (D) Re-stenosis of the MCA detected 1 year later.

determining the location and shape of it. When the
treatment is effective, there is a significant and imme-
diate decrease of blood flow velocities; after about a
week, owing to the reshaping of the stent and vascular
remodeling, there is a further improvement in hemo-
dynamics with velocity values declining toward normal
[25]. A regular follow-up of these patients is advisable
in order to confirm the efficacy of stenting and to detect
residual stenosis or in-stent restenosis (Figure 10.10).
Conclusions
In stroke patients with propensity for intracranial ste-
nosis, transcranial ultrasound identifies those with high
risk of recurrent events (class I, level A). Serial moni-
toring of the stenosis by TCD/TCCS provides further
risk stratification (class I, level A). Digital subtraction
angiography (DSA) remains the “gold standard” for the
accurate measurement of lumen stenosis for intracra-
nial stenosis, especially for those with a plan for inter-
ventional therapy. However, TCD/TCCS can be used as
a minimally invasive screening test before DSA (class II,
level B). Use of contrast-enhanced agent improves the
diagnostic yield of TCD/TCCS (class II, level B).
Conflicts of interest
The authors have no conflicts of interest with regard to
the contents of this manuscript.
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