Review Article

Ultrasound in
Address correspondence to
Dr Georgios Tsivgoulis,
Second Department of
Neurology, University of

Neurology Athens School of Medicine,

Iras 39, Gerakas Attikis,
Athens, Greece 15344,
tsivgoulisgiorg@yahoo.gr.
Georgios Tsivgoulis, MD, PhD, MSc, RVT;
Relationship Disclosure:
Andrei V. Alexandrov, MD, RVT Dr Tsivgoulis serves on the
editorial boards of Stroke and
the Journal of Neuroimaging
and has received research/
ABSTRACT grant support from the European
Purpose of Review: Low cost, avoidance of irradiation, and high temporal resolution Regional Development Fund.
Dr Alexandrov serves on the
are inherent advantages of ultrasound imaging that translate into multiple clinical uses in editorial board of the Journal
many domains of neurology. This article presents clinical uses of ultrasound examination of Neuroimaging.
in cerebrovascular, neurodegenerative, and peripheral nervous system diseases. Unlabeled Use of
Recent Findings: Modern treatment and prevention of ischemic stroke rely on prompt Products/Investigational
Use Disclosure:
diagnosis. Ultrasonography has found a place as a noninvasive screening test and Drs Tsivgoulis and
bedside technique that provides estimates of the degree of stenosis as well as Alexandrov report
hemodynamic and structural information about intracranial and extracranial vessels no disclosures.
in real time. Other standard applications of neurosonology include detection of * 2016 American Academy
of Neurology.
vasospasm in patients with subarachnoid hemorrhage, selection of appropriate
candidates for blood transfusion among patients with sickle cell anemia (primary
stroke prevention), right-to-left shunt testing, emboli detection, vasomotor reactivity
assessment, and noninvasive confirmation of cerebral circulatory arrest. Improvement
in image quality permits novel uses of ultrasonography in neurodegenerative and
peripheral nervous system disorders, providing clinically important information that
is complementary to the clinical examination and electrophysiology. Transcranial
parenchymal sonography may assist in the differential diagnosis of movement dis-
orders, while peripheral nerve ultrasound using high-frequency probes may provide
structural information regarding the underlying etiology of entrapment neuropathies.
Summary: The indications for neurosonology are rapidly expanding, increasing its
applicability outside the field of cerebrovascular diseases. Ultrasound testing is a
noninvasive easily repeatable bedside investigation providing clinically relevant
information on a wide spectrum of neurologic disorders.

Continuum (Minneap Minn) 2016;22(5):1655–1677.

INTRODUCTION Vascular ultrasound was the first

Excellent safety, very high temporal
and high spatial resolution, real-time
evaluation, low cost, and the ability to
perform examinations at the bedside
are some of the key advantages of
medical ultrasound. These advantages
explain why diagnostic ultrasound has
revolutionized many medical special-
ties, including neurology. Several med-
ical schools in the United States already
include ultrasound in their curriculum
for all medical students, using it to teach
anatomy and instructing them in how
to scan with portable equipment.
modality adopted in clinical neurology
for the evaluation of extracranial
(1970s) and intracranial (1980s) vascu-
lature before the widespread availability
of multimodal CT and MRI. Brightness-
mode display (B-mode) consists of a
two-dimensional grayscale image de-
rived from scanning a plane through
the body by an array of transducers.
B-mode has been in clinical use for many
years for the evaluation of the vessel
wall and plaques in the extracranial
arteries (Figure 13-1). Doppler mode
makes use of the Doppler effect in

Continuum (Minneap Minn) 2016;22(5):1655–1677 www.ContinuumJournal.com 1655

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

 Ultrasound

sonology to describe a variety of non-

FIGURE 13-1
internal carotid artery (ICA) and external carotid artery
(ECA). Note an arterial branch originating from the ECA (red
asterisk). The presence of arterial branch is essential for the
ultrasound differentiation between cervical ECA (several
arterial branches) and cervical ICA (no arterial branch).
KEY POINT
h The extracranial internal
carotid, common
carotid, external carotid,
and vertebral arteries
can be assessed by
cervical duplex
(simultaneous
presentation of
brightness-mode image
and Doppler waveform)
ultrasonography, while
the middle cerebral,
anterior cerebral,
posterior cerebral,
ophthalmic, intracranial
vertebral, and basilar
arteries can be
investigated by
transcranial Doppler or
transcranial color-coded
duplex sonography.
1656 www.ContinuumJournal.com
Cervical duplex ultrasound (brightness
mode, horizontal plane). The common
carotid artery (CCA) is bifurcating into the
measuring blood flow. Information
about blood direction and velocity is
projected on the B-mode image,
encoded in colors. Spectral Doppler
depicts a waveform containing infor-
mation about velocity, resistance, and
flow direction. Imaging improvement in
B-mode has permitted the evaluation
of the adult brain parenchyma and
opened new horizons in the imaging
of neurodegenerative disorders. Novel
high-frequency probes have permitted
high-quality imaging of peripheral
nerves, providing morphologic infor-
mation that is complementary to the
neurophysiologic findings. However,
it should be noted that despite recent
technologic advances, neurosonology
continues to remain highly operator
dependent and requires extensive train-
ing to acquire both the required theo-
retical knowledge and the necessary
scanning skills. This article presents a
brief and practical overview of the
main current applications of ultra-
sound in neurology.
CEREBROVASCULAR DISEASES
A major cause of disability and death,
ischemic stroke ensues after occlusion
of extracranial or intracranial arteries.
This article uses the term neuro-
invasive imaging and nonimaging
ultrasound techniques that have
established clinical value in evaluating
patients with stroke or those at risk for
stroke. The extracranial internal carotid,
common carotid, external carotid, and
vertebral arteries can be assessed by
cervical duplex (simultaneous presen-
tation of B-mode image and Doppler
waveform) ultrasonography, while the
middle cerebral, anterior cerebral, pos-
terior cerebral, ophthalmic, intracranial
vertebral, and basilar arteries can be
investigated by transcranial Doppler
(TCD) or transcranial color-coded du-
plex sonography. Other specialized
tests that can be used to ascertain the
pathogenic mechanism of stroke or risk
of stroke recurrence include emboli
detection with or without contrast
injection, vasomotor reactivity testing,
and real-time spectral Doppler moni-
toring during treatment or specific
maneuvers (eg, head turn, blood pres-
sure manipulation).
Ultrasound Assessment of
Extracranial Arteries
Cervical duplex ultrasonography is a
noninvasive neuroimaging modality
for the evaluation of both vessel wall
features and blood flow parameters in
cervical arteries. Cervical duplex ultra-
sonography provides real-time infor-
mation about the presence of an
atherosclerotic plaque, including its
length, composition, protrusion and
surface, range of resulting vascular
stenosis or occlusion, presence of a
dissection, and other significant imag-
ing findings in patients with acute
ischemic stroke (Table 13-1). Cervical
duplex ultrasonography can directly
visualize atherosclerotic plaque com-
position that can be classified based on
its echogenicity. Uniformly hyperechoic
carotid plaques are mainly composed
of fibrotic tissue needed for plaque
October 2016

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

 KEY POINTS
h Cervical duplex
TABLE 13-1 Applications of Cervical Duplex Ultrasonography in
Patients With Acute Ischemic Stroke ultrasonography can
directly visualize
b Information about plaque composition and surface (eg, lipid, hemorrhage, atherosclerotic plaque
fibrous content, ulceration, superimposed thrombus) composition that can be
classified based on its
b Diagnosis of the degree of carotid artery stenosis (normal, 0Y49%,
echogenicity. Cervical
50Y69%, 70Y99%, near occlusion, occlusion)
duplex ultrasonography
b Diagnosis of the degree of vertebral artery stenosis (G50%, 950%, occlusion) also allows rapid
b Detection of intraluminal thrombus in cervical vessels detection of internal
carotid artery thrombosis
b Diagnosis of subclavian steal syndrome and differentiation
b Diagnosis/suspicion of uncommon causes of stroke (eg, cervical artery between chronic internal
dissection, fibromuscular dysplasia, aortic arch dissection) carotid artery occlusion
with or without preexisting
b Complementary information in the diagnosis of temporal arteritis
atheromatous stenosis.
b Indirect information for distal intracranial vessel occlusion
h Peak systolic velocity,
b Indirect information for heart rate and heart valves end-diastolic velocity,
and the systolic internal
b Diagnosis of other conditions not related to acute stroke (eg, carotid
body tumor) carotid artery/common
carotid artery velocity
ratio are essential
ultrasound parameters
stability. In contrast, heterogeneous be conducted with grayscale (B-mode), for North American
(and predominantly hypoechoic) power-mode, or color Doppler and Symptomatic Carotid
plaques consisting of matrix deposi- spectral Doppler ultrasound, and Endarterectomy Trial
tion, cholesterol accumulation, ne- reported using NASCET ranges of ICA grading ranges of
extracranial internal
crosis, calcification, and intraplaque stenosis (normal, 0% to 49%, 50% to
carotid artery disease.
hemorrhage are considered unstable, 69%, 70% to 99%, near occlusion,
being the source of artery-to-artery occlusion). A characteristic example of h Peak systolic velocity and
embolic strokes.1 severe (70% to 99%) ICA stenosis is end-diastolic velocity
must be assessed in the
Peak systolic velocity, end-diastolic presented in Case 13-1.
prestenotic, stenotic, and
velocity, and the systolic internal ca- Cervical duplex ultrasonography al-
poststenotic segments of
rotid artery (ICA)/common carotid ar- lows rapid detection of ICA thrombosis the vessel, and ultrasound
tery (CCA) velocity ratio are essential and differentiation from chronic ICA interpretation must refer
ultrasound parameters for grading the occlusion with or without preexisting to the North American
percentage of stenosis in extracranial atheromatous stenosis. These acute Symptomatic Carotid
carotid artery steno-occlusive disease. findings may prompt consideration of Endarterectomy Trial
Peak systolic velocity and end-diastolic carotid endarterectomy (Case 13-2). strata of internal carotid
velocity must be assessed in the Ultrasound diagnosis and classifica- artery stenosis.
prestenotic, stenotic, and poststenotic tion of vertebral artery stenosis is more
segments of the vessel. The Society of demanding. Vertebral artery asymme-
Radiologists in Ultrasound Consensus try is common, and a hypoplastic
Conference reached multidisciplinary vertebral artery may terminate in the
agreement on criteria to predict clini- posterior inferior cerebellar artery. An-
cally relevant strata of ICA stenosis atomic variants and abnormalities (eg,
corresponding to the North American stenosis, occlusion) of the contralateral
Symptomatic Carotid Endarterectomy vertebral artery influence vertebral
Trial (NASCET) criteria (Table 13-2).2 artery flow. Severe stenosis in the
All carotid artery examinations should carotid arteries may also affect blood

Continuum (Minneap Minn) 2016;22(5):1655–1677 www.ContinuumJournal.com 1657

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

 Ultrasound

TABLE 13-2 Peak Systolic Velocities, End-Diastolic Velocities, and Doppler Spectra With
Varying Degrees of Extracranial Internal Carotid Artery Stenosisa

Peak Systolic
ICA Stenosis Peak Systolic End-Diastolic Velocity ICA/
Range Velocity (cm/s) Velocity (cm/s) CCA Ratio Plaque
Normal G125 G40 G2 None
0Y49% G125 G40 G2 G50% diameter reduction
50Y69% 125Y230 40Y100 2Y4 Q50% diameter reduction
70Y99% 9230 9100 94 Q50% diameter reduction
Near occlusion High/low or Variable Variable Significant, detectable
undetectable lumen
Occlusion Undetectable NA NA Significant, no detectable
lumen
CCA = common carotid artery; ICA = internal carotid artery; NA = not applicable.
a
Modified with permission from Grant EG, et al, Radiology.2 B 2003 Radiological Society of North America. pubs.rsna.org/doi/full/10.1148/
radiol.2292030516.

KEY POINT flow in the vertebral artery due to
h Ultrasonography recruitment of collaterals. Vertebral
may assist in the artery stenoses are most commonly
diagnosis of carotid or located in the origin from the subcla-
vertebral artery vian artery (V0 segment) followed by
dissection. Cervical
the atlas loop/intracranial segments,
duplex ultrasonography
while intertransverse segments are less
may detect reversed
systolic blood flow commonly affected. Criteria for verte-
at the origin of the bral artery stenoses are not based on a
vessel and absent or peak systolic velocity cutoff but on
minimal diastolic focal and significant peak systolic ve-
blood flow that locity increase, since tortuosity of the
concurs with proximal vertebral artery segment, ICA
high-resistance lesions, and vertebral artery asymmetry
bidirectional may result in relatively high velocities.
Doppler signal. The velocity increase should be found
over a relatively short segment of the
vertebral artery with normal or de-
creased prestenotic and poststenotic
velocities.7 Elongated and multiple ste-
noses in the vertebral artery may not
produce focal velocity elevations, which
could be a source of false-negative cer-
vical duplex ultrasonography studies.
Ultrasonography may assist in the
diagnosis of carotid artery dissection.
Cervical duplex ultrasonography may
detect reversed systolic blood flow at
the origin of the ICA and absent or
minimal diastolic blood flow that con-
curs with high-resistance bidirectional
Doppler signal. In B-mode imaging, a
tapered lumen with a characteristic
string sign appearance may be shown,
as well as a floating intimal flap. The
true lumen can be compressed by the
false lumen thrombus, and subse-
quently a low-velocity Doppler wave-
form can be recorded. The flow
direction in a patent false lumen may
fluctuate from forward to reverse or
may be bidirectional. If a dissection is
found ascending from the proximal
CCA, it indicates aortic dissection. In
patients with a distal cervical ICA
dissection (that has not descended to
the proximal ICA), a retromandibular
high-velocity signal may be the only
sign of dissection.8
Ultrasound detection of vertebral
artery dissection in the V2 through V4
segments (Figure 13-4) is challenging
since no well-defined and predictable
imaging findings have been identified.
Absent blood flow, low bidirectional
flow, or low poststenotic velocities can
be detected at the level of the atlas
loop, a frequent site of dissection. A

1658 www.ContinuumJournal.com October 2016

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

 Case 13-1
A 58-year-old man with a history of hypertension, hypercholesterolemia, and smoking presented with
recurrent episodes of transient hemiparesis lasting between 20 and 40 minutes over the previous 2 days.
His blood pressure was 178/94 mm Hg, and his ABCD2 score (age, blood pressure, clinical features,
duration, presence of diabetes mellitus) was 4. He reported that he developed symptoms after standing
up or walking for a period longer than 30 minutes. Emergent neurosonology evaluation disclosed the
presence of hypoechoic material in the distal right internal carotid bulb coupled by the absence of flow
in color-mode display on cervical duplex ultrasound (Figure 13-2). Transcranial duplex sonography showed
the presence of collateral flow via ipsilateral ophthalmic artery flow reversal (Figure 13-2), while the
flow in the ipsilateral proximal middle cerebral artery was severely blunted (mean flow velocity of
60 cm/s, pulsatility index of 0.42; normal values being less than 100 cm/s and 0.6 to 1.1, respectively).
The diagnosis of acute internal carotid artery occlusion causing orthostatic hypoperfusion syndrome was
made.3 Digital subtraction angiography confirmed the presence of an acute right internal carotid artery
occlusion. Brain MRI with diffusion-weighted imaging excluded the presence of an acute infarction.
The patient was put in the head-down position and treated with IV isotonic fluids and the combination of
oral aspirin (100 mg) and clopidogrel (75 mg) while his systolic blood pressure was maintained at the
levels of 160 mm Hg to 180 mm Hg for the first 5 days of acute cerebral ischemia. The patient did not
develop any recurrent symptoms during his hospitalization.

FIGURE 13-2 Imaging of the patient in Case 13-1. Acute internal carotid artery occlusion originally
diagnosed by cervical duplex ultrasound (A) and subsequently confirmed by digital
substraction angiography (C). Note the presence of hypoechoic material in the
distal internal carotid artery bulb coupled by absence of flow in color-mode display. Transcranial
color-coded duplex sonography displays the presence of collateral flow via ipsilateral ophthalmic
artery flow reversal (B, detection of retrograde low-resistance flow in ipsilateral ophthalmic artery).

Comment. This case highlights the importance of neurosonology in identifying patients with acute cerebral
ischemia due to hypoperfusion caused by steno-occlusive intracranial or extracranial arterial disease. Acute
blood pressure lowering in this subgroup of patients may be harmful and cause further neurologic
deterioration. Putting the patient in the head-down position and maintaining a moderately elevated blood
pressure level appears to be the preferable therapeutic approach in patients with orthostatic transient ischemic
attacks or strokes caused by cerebral hypoperfusion distal to an extracranial or intracranial large vessel occlusion.4

Continuum (Minneap Minn) 2016;22(5):1655–1677 www.ContinuumJournal.com 1659

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

 Ultrasound

Case 13-2
A 64-year-old man with a history of hypertension, diabetes mellitus, coronary artery disease, and
smoking presented with a mild right hemiparesis 12 hours following symptom onset. His National Institute
of Health Stroke Scale (NIHSS) score was 3. Emergent neurovascular ultrasound disclosed the presence of
a heterogeneous plaque with an overlying thrombus in his left internal carotid artery (Figure 13-3)
causing severe stenosis (70% to 99% North American Symptomatic Carotid Endarterectomy Trial
range). Transcranial Doppler monitoring of the ipsilateral proximal middle cerebral artery recorded the

FIGURE 13-3 Imaging of the patient in Case 13-2. Cervical duplex ultrasound (A, B) depicts a
heterogeneous plaque (A, green arrowheads) with an overlying thrombus
(A, white arrowheads) causing a hemodynamically (70% or greater) significant
carotid artery stenosis. Note the presence of aliasing on color-mode display (A) and the
elevated peak systolic velocity (236 cm/s) and end-diastolic velocity (112 cm/s) on spectral
display (B). CT angiography (C, D) confirms ultrasound findings and depicts the presence of an
overlying thrombus protruding in the vessel lumen (C, red circle; D, white arrowhead). The
patient underwent emergent carotid endarterectomy, removing both atherosclerotic plaque
and overlying thrombus (E).

Continued on page 1661

1660 www.ContinuumJournal.com October 2016

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

 Continued from page 1660
presence of high-intensity transient signals indicative of microembolism in real time. CT angiography
confirmed the ultrasound findings and depicted the presence of a large atherosclerotic plaque with an
overlying thrombus protruding in the left internal carotid artery lumen (Figure 13-3). Brain MRI with
diffusion-weighted imaging showed numerous small foci of restricted diffusion in the territory of
the left middle cerebral artery. Artery-to-artery embolism distal to a symptomatic carotid artery
stenosis was considered as the underlying mechanism of acute cerebral ischemia. The patient underwent
emergent carotid endarterectomy at 29 hours following symptom onset (Figure 13-3). He was discharged
on the fifth day of hospitalization with an NIHSS score of 1.
Comment. This case highlights the importance of neurosonology in identifying patients with
symptomatic carotid artery stenosis causing distal microembolization. These patients carry an
excessively high risk (nearly tenfold) of recurrent stroke5 and should undergo carotid endarterectomy
during the first 14 days after transient ischemic attack or nondisabling stroke.6 Neurosonology is a
noninvasive and inexpensive neuroimaging modality that can be rapidly applied at the bedside of
patients with acute cerebral ischemia; it may provide real-time diagnostic and prognostic information
to help make patient management decisions.

dissection causing stenosis at the V1 or cerebral arteriogram) should be

segment may be detected by ultra-
sound; absent blood flow may be
found in the intertransverse segments,
and a localized broadening of a vessel
diameter at V1 may be seen with se-
vere stenosis or occlusion. Direct visu-
alization of intramural hematoma by
ultrasound is rare; it can be easily missed
if no significant stenosis is evident or
if it is located outside an accessible
intratransverse arterial segment.9 When
a clinical suspicion of vertebral artery
dissection exists, further imaging work-
up (MRI with fat-saturation sequences
performed even if ultrasound results
are inconclusive.
Takayasu arteritis presents with
smooth homogenous concentric thick-
ening of the arterial wall on B-mode
imaging in proximal cervical vessels
(common carotid artery, innominate
artery, and subclavian artery), which
can be easily identified by cervical
duplex ultrasonography by the typi-
cal macaroni sign (Figure 13-5). In
contrast to atherosclerotic disease,
patients with Takayasu arteritis have an
affected CCA with sparing of the ICA

FIGURE 13-4 Extracranial vertebral artery (VA) segments on cervical duplex ultrasound. VA
origin (V0) from the subclavian artery is displayed on the right panel, the
pretransverse VA segment (V1) located proximally to the C6 transverse process
is displayed in the middle panel, and the transverse VA segment (V2) is displayed in the
left panel.
RVA = right vertebral artery.

Continuum (Minneap Minn) 2016;22(5):1655–1677 www.ContinuumJournal.com 1661

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

 Ultrasound

FIGURE 13-5 Cervical duplex ultrasound showing typical macaroni sign in the right common carotid artery (CCA)
of a 32-year old woman with Takayasu arteritis (A, B-mode). The macaroni sign represents smooth,
homogeneous, and moderately echogenic circumferential thickening of the arterial wall (red
arrowheads) that occurs in Takayasu arteritis. Note the elevation of velocities (peak-systolic velocity: 257 cm/s,
end-diastolic velocity: 76 cm/s) due to constriction of CCA lumen in color-mode display (B).

KEY POINT
h Intracranial cerebral
vasculature can be
assessed by transcranial
Doppler or transcranial
color-coded duplex
sonography to provide
real-time flow findings
that are complementary
to information provided
by CT angiography or
multimodal MRI.
and external carotid artery. More-
over, contrast-enhanced cervical du-
plex ultrasonography can reliably
identify vulnerable plaques at the
vessel wall lumen, by providing direct
visualization of intraplaque neovas-
cularization and improving delinea-
tion of plaque ulcers. 10 Takayasu
arteritis may also present with subcla-
vian steal syndrome caused by subcla-
vian artery stenosis.
Giant cell arteritis can present
with stroke symptoms, typically of the
vertebrobasilar territory. In these cases,
the vertebral artery may rarely show
hypoechoic wall thickening on cervical
duplex ultrasonography. An examina-
tion of the superficial temporal artery
with high-frequency 12-MHz to 15-MHz
B - m o de transducers can detect
hypoechoic circumferential thickening
(the halo sign) (Figure 13-6).11 The
halo sign is moderately sensitive (68%)
but highly specific (91%) when present
at the superficial temporal artery and
can also be used to guide biopsy as
well as monitor treatment.12
Ultrasound Assessment of
Intracranial Arteries
Intracranial cerebral vasculature can be
assessed by TCD or transcranial color-
coded duplex sonography to provide
real-time flow findings (Figure 13-7)
that are complementary to information
provided by CT angiography (CTA) or
multimodal MRI. TCD is a diagnostic
method increasingly used for the
diagnosis of cerebrovascular diseases
(Table 13-3). TCD identifies intracra-
nial stenoses, distal emboli, and col-
lateral flow and helps determine
hemodynamic significance of extra-
cranial or intracranial steno-occlusive
lesions, monitor recanalization during
thrombolytic therapy in real time, deter-
mine the stroke pathogenic mechanism,
and select the next and most appro-
priate step in patient management.13
A fast-track insonation protocol
has been developed for rapid extra-
cranial and intracranial artery eval-
uation in the emergency setting of
acute ischemic stroke to diagnose large
artery intracranial steno-occlusive le-
sions, recanalization, and reocclusion.14
The choice of fast-track insonation
steps is determined by clinical localiza-
tion of the ischemic arterial territory.
Most studies can be accomplished
within minutes by experienced sonog-
raphers at the bedside in parallel with
the neurologic examination in the

1662 www.ContinuumJournal.com October 2016

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

FIGURE 13-6 Ultrasound findings in giant cell arteritis. Extracranial duplex ultrasound of the left superficial temporal artery
(STA) shows reduced color filling and vessel-wall thickening in the form of a dark halo (hypoechoic
circumferential thickening) in axial (A, red arrows) and longitudinal (B, blue arrow) planes. Note the normal
color filling in the right STA in axial (C) and longitudinal (D) planes. The ultrasound findings in the left STA wall (unilateral
halo sign) are indicative of giant cell arteritis. The diagnosis is confirmed by magnetic resonance angiography (MRA) (E)
depicting unilateral severe left STA stenosis/obstruction (red arrow) and temporal artery biopsy showed inflammatory
infiltrates (including giant cells) involving the entire vessel wall with marked intimal thickening. Note the normal appearance
of the right STA (E, blue arrow).

emergency department without evaluating patients with acute ischemic

delaying treatment. Overall, bedside
TCD examination in the emergency
department had a satisfactory agree-
ment to brain CTA in the evaluation of
patients with acute ischemic stroke.
TCD is a highly accurate and reliable
bedside diagnostic examination for
stroke with acute proximal arterial oc-
clusion or stenosis of an intracranial
artery (Figure 13-8). Its efficacy de-
pends on symptomatic artery localiza-
tion, onset-to-insonation time, and
acute ischemic stroke severity. TCD
can reveal artery occlusion in more

FIGURE 13-7 Depiction of proximal intracranial arteries of the circle of Willis in a healthy individual using
transcranial color-coded duplex sonography (A). The intensity mode, or power mode,
allows better visualization of the arterial flow (B).
ACA = anterior cerebral artery; MCA = middle cerebral artery; PCA = posterior cerebral artery.

Continuum (Minneap Minn) 2016;22(5):1655–1677 www.ContinuumJournal.com 1663

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

 Ultrasound

TABLE 13-3 Applications of Transcranial Doppler or Transcranial

Color-Coded Duplex Sonography in Patients With Acute
Ischemic Stroke

b Bedside confirmation of vascular origin of the presenting symptoms and

determination of underlying stroke mechanism
b Fast detection and localization of occlusion/stenosis
b Mapping of the collateral circulation
b Detection of cerebral embolism in real time and quantification of
right-to-left shunt
b Real-time monitoring of recanalization in patients treated with systemic
thrombolysis
b Selection of patients for intraarterial reperfusion procedures
b Monitoring of rescue intraarterial procedures (eg, detection of
reocclusion, air embolism, hyperperfusion syndrome)
b Detection of supratentorial intracerebral hemorrhage at the bedside
following acute reperfusion therapies (application of transcranial
color-coded duplex sonography)
b Potential augmentation of clot lysis and clinical recovery
(sonothrombolysis)

than 90% of patients with acute ische-
mic stroke treated with recombinant
tissue-type plasminogen activator
within 3 hours from symptom onset
when NIHSS score is 10 or more.14
Ultrasound may also assist in map-
ping of collateral cerebral circulation.
Efficient collateral circulation helps
maintain cerebral perfusion in the set-
ting of acute ischemic stroke and is

FIGURE 13-8 Transcranial Doppler findings in intracranial stenosis. A, Power-motion-mode transcranial Doppler
depicts the presence of a hemodynamically (70% or greater) significant right proximal middle
cerebral artery stenosis. Note the presence of elevated mean (141 cm/s) and peak (209 cm/s)
systolic flow velocities and the presence of systolic bruit on power-motion-mode (depicted as systolic flow gaps) and
spectral (circles) displays. B, Digital substraction angiography confirmed the diagnosis of severe (79%) proximal
middle cerebral artery stenosis (arrow).

1664 www.ContinuumJournal.com October 2016

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.


associated with reduced infarct volume
and better functional outcome. The
main collateral pathways are the ante-
rior and posterior communicating ar-
teries, reversed ophthalmic artery, and
reversed basilar artery. These channels
come into play only if a change occurs
in pressure gradients between two
anastomosing arterial systems. TCD
can provide real-time information on
the blood flow direction and velocity
of the collateral pathways. Activation
of a collateral flow pathway implies
the presence of a flow-limiting lesion
proximal to the origin of the collateral
channel.15
TCD and transcranial color-coded
duplex sonography may assess recan-
alization and potential reocclusion in
real time in patients with acute ische-
mic stroke treated with systemic or
intraarterial reperfusion therapies.
Spontaneous recanalization of a mid-
dle cerebral artery (MCA) occlusion
occurs at a rate of approximately 6%
per hour after symptom onset, and IV
tissue plasminogen activator doubles
the chance of complete recanalization
to almost 13% during the first hour
of treatment, with a median time of
35 minutes after the bolus infusion.16
TCD provides a noninvasive bedside
tool for real-time monitoring of arterial
recanalization. The thrombolysis in
brain ischemia (TIBI) flow-grading
system was developed to evaluate
residual flow noninvasively and in real
time in analogy to the thrombolysis in
myocardial infarction (TIMI) flow
grades.17 TIBI grade 5 corresponds
to normal blood flow, grade 4 to stenotic
blood flow (accelerated), grade 3 to
dampened blood flow (decreased ve-
locities compared to the contralateral
intracranial artery), grade 2 to blunted
blood flow (flattened waveform),
grade 1 to minimal blood flow (absent
diastolic flow), and grade 0 to no flow.
Continuum (Minneap Minn) 2016;22(5):1655–1677
Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
KEY POINTS
TIBI flow grades were found to corre- h Transcranial Doppler
late strongly with stroke severity, assesses recanalization
mortality, and clinical improvement. and potential reocclusion
Rapid arterial recanalization is associ- in real time in patients
ated with better short-term improve- with acute ischemic
ment. On the contrary, slow flow stroke treated with
improvement and dampened TIBI systemic or intraarterial
flow signals are less favorable prog- reperfusion therapies.
nostic signs that indicate the need for h A novel application of
further reperfusion therapies, such as neurosonology is the
mechanical thrombectomy. TIBI flow assessment of an
intracranial arterial steal
grading can be used in follow-up after
syndrome and evaluation
initial CTA assessment to determine if of vasomotor reactivity
the patient still has a persisting occlu- of intracranial arteries.
sion or reocclusion or had full recanali-
zation without clinical improvement to
avoid the need for repeat CTA in acute
ischemic stroke within the time frame
for mechanical thrombectomy.
A novel application of neurosonology
is the assessment of intracranial arterial
steal syndrome and evaluation of vaso-
motor reactivity of intracranial arteries.
Once a feeding vessel is blocked,
compensatory distal vasodilation de-
creases resistance to attract blood flow
through collateral channels. Counter-
intuitively, this hemodynamic phenom-
enon may, in turn, lead to further
perfusion decrease of ischemic brain
tissues (in which arteries cannot dilate
any further). This lack of further dilation
may not counteract the steal of blood
by normally perfused areas that main-
tain the capability for vasodilation with
additional stimuli. This hemodynamic
steal phenomenon can be detected on
TCD in patients with acute ischemic
stroke and has been termed reversed
Robin Hood syndrome in analogy with
‘‘rob the poor to feed the rich.’’18
A TCD vasomotor study is a simple
method to assess vasomotor reactivity
in acute ischemic stroke and can iden-
tify patients at high risk for stroke in
the setting of symptomatic or asymp-
tomatic extracranial internal carotid
artery stenosis or occlusion. During this
www.ContinuumJournal.com 1665
 Ultrasound
KEY POINTS
h The transcranial noninvasive test, TCD is used to mea-
Doppler bubble sure velocity response to voluntary
test is more sensitive breath-holding for 30 seconds, which
than transthoracic induces hypercapnia and serves as a
echocardiography (with natural vasodilatory stimulus.19
or without contrast Another indication for TCD is the
injection) in detection of noninvasive detection of cerebral em-
a right-to-left shunt bolization and presence of right-to-left
through a patent shunts, such as patent foramen ovale,
foramen ovale. as a conduit of paradoxical embolism.
h Transcranial Doppler Microembolic signals can be detected
stratifies the risk of during TCD monitoring in patients with
patients with sickle cell acute ischemic stroke or transient is-
anemia and those in chemic attacks as signals of high inten-
need of blood
sity and short duration within the
transfusions for primary
Doppler spectrum; they represent solid
stroke prevention. Those
who meet transcranial
or gaseous particles within the blood
Doppler criteria for blood flow. Although not causing immediate
transfusions should stay symptoms, these embolic signals are
on transfusions since clinically important, as they can identify
these children remain an embolic mechanism and point to the
at high risk of stroke source of embolism in patients with
if transfusions stroke or transient ischemic attack.
are discontinued. TCD is the gold standard of detection,
h One of the first quantification, and localization of cere-
applications of bral embolization in real time. Patients
transcranial Doppler in with symptomatic carotid artery steno-
clinical use has been sis and microembolic signals on TCD
the identification of were found to benefit from early ca-
cerebral vasospasm rotid endarterectomy.20
after subarachnoid
Paradoxical embolism is a possible
hemorrhage.
mechanism of acute ischemic stroke in
patients with right-to-left shunts. The
TCD bubble test is equivalent or even
superior to both transthoracic and
transesophageal echocardiography in
detection of right-to-left shunt through
a patent foramen ovale. 13 Power-
motion-mode Doppler may further
increase the yield. TCD criteria for
grading right-to-left shunts have been
proposed to distinguish incidental
from pathogenic right-to-left shunts in
patients with acute ischemic stroke.21
TCD is a validated diagnostic tool for
children with sickle cell anemia be-
tween the ages of 2 and 16 years who
have not sustained a stroke to identify
those at high risk for stroke who could
1666 www.ContinuumJournal.com
Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
benefit from prophylactic transfusion
(Table 13-4).13 Ischemic strokes in
children with sickle cell anemia primar-
ily result after stenosis of the MCA or
distal intracranial ICA, and some chil-
dren may develop moyamoya syn-
drome. The Stroke Prevention in
Sickle Cell Anemia (STOP) trial showed
that time-averaged maximum mean
velocity greater than 200 cm/s in the
terminal ICA or MCA is associated with
a 10% annual risk for stroke.13 Trans-
fusion to lower hemoglobin S concen-
trations to less than 30% of total
hemoglobin in these children decreases
time-averaged maximum mean for
several weeks, reduces blood coagu-
lation biomarkers,22 and, most impor-
tant, reduces the relative risk of stroke
by 92%. Children at risk continue to
benefit from transfusions and should
continue to receive treatment to sustain
the primary stroke prevention benefit,
as shown in the STOP 2 trial.23 It should
be noted that not all pediatric strokes
in sickle cell anemia are predicted by
TCD as other mechanisms come into
play, such as artery dissection, embo-
lism, small artery infarction, and
hypercoagulable states.
One of the first applications of TCD
in clinical use has been the identifica-
tion of cerebral vasospasm after sub-
arachnoid hemorrhage (SAH). Blood
extravasation has a toxic effect on
brain arteries and leads to lumen
narrowing that, when severe enough,
can lead to ischemic lesions. TCD can
estimate the severity of vasospasm by
detecting increased blood velocities
in areas of vasospasm (Table 13-4).13
Baseline TCD measurements are
obtained, and the patient is monitored
every day or every other day through-
out Day 7 (all grades) and Day 10 (Hunt-
Hess grades 2+) or until vasospasm
resolution. It is recommended that
extracranial internal carotid artery ve-
locities be recorded to adjust for
October 2016
TABLE 13-4 Established Clinical Indications and Expected Outcomes of Transcranial Doppler
Testing in Sickle Cell Anemia, Subarachnoid Hemorrhage, and Brain Deatha
Broad Indication Specific Indications
Sickle cell anemia Children
Subarachnoid Days 2Y5
hemorrhage
Days 5Y12
Day 12Yend of ICU stay
Suspected brain Increased intracranial
death pressure, mass effect,
herniation
a
Modified with permission from Alexandrov AV, et al; American Society of Neuroimaging Practice Guidelines Committee, J Neuroimaging.13
B 2010 American Society of Neuroimaging. onlinelibrary.wiley.com/doi/10.1111/j.1552-6569.2010.00523.x/full.
increased velocities due to hyperdynamic
states. By recording velocity in the MCA
and the ipsilateral extracranial ICA, a
Lindegaard ratio between mean flow
velocities (MCA/ICA) can be calculated;
a ratio greater than 6 indicates severe
spasm. Secondary findings, such as rapid
daily mean flow velocity rise (greater
than 20% or greater than 65 cm/s) and
early appearance of MCA mean flow
velocity of greater than 180 cm/s, are
associated with adverse outcomes in
patients with SAH. Early recognition
of severe vasospasm can lead to the
prompt treatment of vasospasm with
Continuum (Minneap Minn) 2016;22(5):1655–1677
Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
Expected Outcomes
Robust first-ever stroke risk reduction based on transcranial
Doppler (TCD) criteria for the need of blood transfusion
and continuing use of blood transfusions.
TCD can detect development of vasospasm days before it
can become clinically apparent. This information can be
used by intensivists to step up hemodynamic management
of these patients.
TCD can detect progression to the severe phase of spasm
when development of the delayed ischemic deficit due to
perfusion failure through the residual lumen is the greatest.
This information can help in planning interventions (eg,
angioplasty, nicardipine infusions).
TCD can document spasm resolution after treatment or
intervention, sustainability of vessel patency, and infrequent
cases of late or rebound vasospasm development at the end
of the second or into the third week after subarachnoid
hemorrhage. At all specific time intervals, TCD is able to detect
changes in resistance to flow that may indicate increase in
the intracranial pressure and necessitate ventriculostomy.
TCD can rule out cerebral circulatory arrest if positive
diastolic flow is detected at any intracranial pressure values.
TCD can confirm the clinical diagnosis of brain death by
demonstrating complete cerebral circulatory arrest in both
middle cerebral arteries and the basilar artery. TCD offers
serial noninvasive assessments and can minimize the
number of nuclear flow studies needed to confirm arrest
of cerebral circulation.
hypertension-euvolemia or invasively
with balloon angioplasty or intraar-
terial vasodilators. Distal vasospasm
can be indirectly diagnosed when focal
pulsatile flow (pulsatility index greater
than 1.2) is detected.24 Similar to a
Lindegaard ratio, a Soustiel ratio (mean
flow velocity of basilar artery/extracranial
vertebral artery assessed at the first
cervical level) greater than 3 indi-
cates severe basilar artery vasospasm
after SAH.25
Brain death is a clinical diagnosis
that can be supported by TCD find-
ings, given the ability of TCD to detect
www.ContinuumJournal.com 1667
 Ultrasound
KEY POINTS
h Brain death is a clinical
diagnosis that can be
supported by transcranial
Doppler, given the ability
of transcranial Doppler to
detect cerebral
circulatory arrest.
h The midbrain appears
hypoechoic in transcranial
sonography, surrounded
by the hyperechoic basal
cisterns, while the
substantia nigra appears
as a thin hyperechoic strip
with total surface not
exceeding 0.20 cm2 in
normal subjects.
h Increased substantia
nigra hyperechogenicity
can be detected with
transcranial parenchymal
sonography in
approximately 90% of
patients with idiopathic
Parkinson disease.
FIGURE 13-9
1668 www.ContinuumJournal.com
Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
cerebral circulatory arrest (Table 13-4).
Increased intracranial pressure causes
increased pulsatility, followed by re-
duction, elimination, and reversal of
diastolic flow. Finally, a reverberating
flow pattern emerges, and, at that point,
TCD can confirm complete cerebral
circulatory arrest (Figure 13-9), offering
a pathophysiologic explanation of clin-
ical progression to brain death. TCD has
received a Class A, Level II evidence rat-
ing for determining cerebral circulatory
arrest/brain death by the American Aca-
demy of Neurology.26 False negatives
exist, especially when time has elapsed
between brain death and TCD examina-
tion, but specificity remains high (higher
than 95%). A recent meta-analysis in-
cluding 22 eligible studies (1671 pa-
tients total) showed that TCD had a
pooled sensitivity and specificity of
90% and 98%, respectively, for the
diagnosis of brain death.27
MOVEMENT DISORDERS
Technologic advances in ultrasound
have led to improved brain parenchy-
mal imaging that has permitted novel
uses of transcranial sonography in neu-
rologic disorders. The echogenicity and
surface of specific brain structures are
Power-motion-mode transcranial Doppler showing reverberating flow in middle cerebral arteries both
in power-motion-mode (red bands corresponding to antegrade flow, blue bands corresponding to
retrograde flow) and spectral displays in a patient with cerebral circulatory arrest.
evaluated in three predetermined exam-
ination planes: mesencephalic, thalamic,
and lateral ventricular (Table 13-5).
The midbrain appears hypoechoic in
transcranial sonography and is readily
recognized by its characteristic but-
terfly pattern, surrounded by the hyper-
echoic basal cisterns. The substantia
nigra appears as a thin hyperechoic
strip with total surface not exceeding
0.20 cm2 in normal subjects. In 87% of
patients with Parkinson disease (PD),
the substantia nigra shows increased
echogenicity (Figure 13-10) as com-
pared to 12% in controls.28 Hyperecho-
genicity is more pronounced in the side
of the midbrain contralateral to the
side of predominance of extrapyramidal
symptoms. In a minority of patients
with PD, around 10%, normal echo-
genicity of the substantia nigra is pre-
served, a finding that could be because
of a different genetic background or
secondary parkinsonism.29 Increased
iron deposition and reduction of fer-
ritin levels have been described in
autopsy studies of the substantia nigra
of patients with PD; iron is thus be-
lieved to bind to alternative proteins
and result in neurotoxicity locally.30
October 2016
TABLE 13-5 Standardized Examination Planes and Cerebral Structures to Be Evaluated
in Patients Diagnosed With Movement Disorders

Examination Plane Structure Normal Findings Abnormal Findings

Mesencephalic plane
Thalamic plane
Lateral ventricular plane
Substantia nigra Echogenicity: weak
Size of echoic area:
G0.2 cm2
Red nucleus Echogenicity: medium
to significant
Midbrain raphe Echogenicity: medium
to significant
Thalamus Echogenicity: hypoechoic
to isoechoic
Lentiform nucleus Echogenicity: isoechoic
Caudate nucleus Echogenicity: isoechoic
Third ventricular Age G60 years: G7 mm
diameter
Age 960 years: G10 mm
Lateral ventricular Age G60 years: G19 mm
diameter
Age 960 years: G22 mm
Size of echoic area 90.2 cm2:
medium hyperechogenicity
Size of echoic area 90.25 cm2:
significant hyperechogenicity
Unknown
Reduced echogenicity
(hypoechoic to anechoic)
Increased echogenicity
(hyperechoic)
Increased echogenicity
(hyperechoic)
Increased echogenicity
(hyperechoic)
Age G60 years: 97 mm
Age 960 years: 910 mm
Age G60 years: 919 mm
Age 960 years: 922 mm

When extrapyramidal symptoms
become apparent in PD, 60% to 70%
of nigrostriatal neurons have been
lost. As a consequence, a preclinical
diagnosis of PD is critical for the
research and development of neu-
roprotective therapies. Large-scale
population screening is not feasible,
but in relatives of patients with PD,
who are at higher risk for developing
the disease, substantia nigra hyper-
echogenicity is present in 45%.31 An-
other subgroup at risk for PD is
patients with depression; in this group,
an increased incidence of substantia
nigra hyperechogenicity has been de-
scribed.32 In a cohort of 1847 asymp-
tomatic subjects over 50 years of age,
substantia nigra hyperechogenicity cor-
related with markedly increased risk KEY POINT
for PD development.33 h Substantia nigra
Neurosonology may provide nonin- hyperechogenicity may
serve as a preclinical
vasive information for the differential
marker of idiopathic
diagnosis of extrapyramidal disorders. parkinsonism.
Differentiating PD from other neuro-
degenerative disorders presenting
with parkinsonism, such as multiple
system atrophy, progressive supranu-
clear palsy, dementia with Lewy bod-
ies, and corticobasal degeneration,
can still be challenging despite re-
markable progress in brain imaging.34
Definite diagnosis of the aforemen-
tioned disorders necessitates autopsy,
and, in many instances, clinical diag-
nosis is proved erroneous by post-
mortem findings. Correct diagnosis is
crucial not only for treatment, but

Continuum (Minneap Minn) 2016;22(5):1655–1677 www.ContinuumJournal.com 1669

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

 Ultrasound

KEY POINTS
h Peripheral nerve
ultrasound may offer
structural information
regarding the underlying
etiology of entrapment
neuropathies.
Ultrasound findings are
complementary to
information offered by
neurophysiologic studies.
h Ultrasonography of a
peripheral nerve
examines five parameters:
(1) cross-sectional area
at certain sites of clinical
interest, (2) variability
of the cross-sectional
area along its course,
(3) echogenicity,
(4) vascularity, and
(5) mobility.

FIGURE 13-10 Transcranial sonography in a patient

with idiopathic Parkinson disease at axial
midbrain plane. Note the butterfly
appearance of midbrain (A, red arrow) and the presence
of mild ipsilateral substantia nigra hyperechogenicity
(B, green asterisk; planimetric measurement of substantia
nigra echoic area: 0.227 cm2 [normal reference value
G0.20 cm2, moderate substantia nigra hyperechogenicity
0.20 cm2 to 0.25 cm2, severe substantia nigra
hyperechogenicity 90.25 cm2]).

also for creating homogenous cohorts PNS that is complementary to electro-

for clinical trials. As a consequence, a
great need exists for novel noninva-
sive diagnostic methods. Transcranial
sonography, in conjunction with clin-
ical characteristics, has demonstrated
high sensitivity for the differential
diagnosis of movement disorders.35
Transcranial sonography findings in ex-
trapyramidal disorders are summarized
in Table 13-6.
PERIPHERAL NERVOUS SYSTEM
Ultrasonography of the peripheral
nervous system (PNS) is a noninvasive
diagnostic method that is increasingly
being used in clinical practice. It pro-
vides a morphologic evaluation of the
physiologic studies. Normal peripheral
nerves have a tubular form, with alter-
nating hypoechoic (nerve fibers) and
hyperechoic (perineurium) zones that
give the impression of a honeycomb
pattern (Figure 13-11). Five parame-
ters of a peripheral nerve are exam-
ined: (1) cross-sectional area (CSA) at
certain sites of clinical interest, (2) va-
riability of the CSA along its course,
(3) echogenicity, (4) vascularity, and
(5) mobility.
Entrapment Neuropathies
Peripheral nerve ultrasound may be
particularly useful in the diagnosis of en-
trapment neuropathies (Table 13-7).36,37

1670 www.ContinuumJournal.com October 2016

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

TABLE 13-6 Ultrasound Findings of Brain Parenchyma in Healthy Individuals and in Those With
Neurodegenerative Disease

Increase Increase of
Substantia Lentiform Caudate of Third Lateral
Nigra Nucleus Nucleus Ventricular Ventricular
Condition Hyperechogenicity Hyperechogenicity Hyperechogenicity Diameter Diameter
Healthy individuals Rare Rare Rare Very rare Rare
960 years old
Idiopathic Almost always Rare Often Never Very rare
Parkinson observed
disease
Multiple system Very rare Almost always Often Never Very rare
atrophy observed
Progressive Rare Almost always Almost always Almost Often
supranuclear palsy always
Corticobasal Almost always Almost always Almost always Never Rare
degeneration observed
Dementia with Almost always Rare Almost always Never Often
Lewy bodies observed

Carpal tunnel syndrome. Carpal
tunnel syndrome is the entrapment
neuropathy that has been most exten-
sively studied with ultrasound. The
most common ultrasound findings de-
tected in patients with symptomatic
carpal tunnel syndrome include:
& Enlarged CSA of the median nerve
proximal to the edge of the
flexor retinaculum
& Increased wrist to forearm
swelling ratio
& Hypoechogenicity and disturbed
fascicular echo structure
& Reduced slippage of the nerve
after finger flexion
& Increased vascularity
A diagnostic algorithm that takes
into consideration CSA of the median
nerve at the wrist and the forearm
presents similar sensitivity and speci-
ficity to electrophysiologic studies.36
However, in some cases of severe and
advanced carpal tunnel syndrome re-
sulting in nerve atrophy, CSA could be
within normal values.37 One of the KEY POINT
latest applications of neuromuscular h The most common
ultrasound is the preoperative detection ultrasound findings seen
in patients with
of persistent median artery or bifid
symptomatic carpal
median nerve that have been reported tunnel syndrome include
as causes of atypical carpal tunnel enlarged cross-sectional
syndrome.38 area of the median nerve
Radial neuropathy. The most com- proximal to the edge of
mon causes of compressive neuropa- the flexor retinaculum,
thy of the deep motor branch of the increased wrist to forearm
radial nerve are repetitive overuse of the swelling ratio,
forearm (repetitive pronation-supination hypoechogenicity and
disturbed fascicular echo
or flexion-extension). The most com-
structure, reduced
mon ultrasound findings are CSA en- slippage of the nerve after
largement of the posterior inferior finger flexion, and
nerve at the proximal portion of increased vascularity.
the compression site, hyperemia of
the nerve, and echo difference of the
dorsal extensor muscles caused by
denervation.37,39
Fibular neuropathy. Entrapment
neuropathy of the common fibular
nerve is usually located at the fibular
head region. Although reduction of mo-
tor conduction velocity and presence

Continuum (Minneap Minn) 2016;22(5):1655–1677 www.ContinuumJournal.com 1671

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

 Ultrasound

FIGURE 13-11 Median nerve ultrasound. A, Peripheral nerve ultrasound depicts a transverse view of a normal median nerve
(circled with dotted lines) at the wrist. The nerve appears with normal echotexture exhibiting a honeycomb pattern
and with a normal cross-sectional area (CSA) of 0.07 cm2. B, The same nerve is depicted in sagittal
view, exhibiting no signs of entrapment (dotted lines). C, Peripheral nerve ultrasound depicting a transverse view of the wrist of a
patient with carpal tunnel syndrome. The median nerve appears enlarged (circled with dotted lines) (CSA = 0.18 cm2, normal
value G0.11 cm2) and the echotexture has changed to hypoechoic with loss of the regular honeycomb pattern. D, Sagittal view
of the same nerve shows the structural entrapment and consecutive enlargement shortly before the constriction (dotted lines).

of conduction block are frequent elec-
trophysiologic findings, neuromus-
cular ultrasound may add useful
diagnostic data concerning the etiology
of entrapment: intraneural ganglia,
ganglion cyst, neurofibroma, or hema-
toma. Common pathologic ultrasound
findings include increased CSA of the
nerve at the fibular head or proximally
and increased fibular to popliteal fossa
swelling ratio.37,40
Cervical radiculopathy. Although
MRI remains the gold standard for
diagnosing cervical radiculopathy, so-
nography provides an alternative
method for evaluating cervical root
lesions. CSA of the clinically affected
cervical nerve roots are increased
compared to the unaffected sides and
correlate with symptom duration.41
Brachial Plexopathies
Ultrasound imaging of the brachial
plexus is routinely used to perform
nerve block, but diagnostic applica-
tions are growing fast. High specificity
and fair sensitivity of ultrasound in
brachial plexus pathology has been
reported, especially for the detection
of mass lesions.42 Ultrasound may

1672 www.ContinuumJournal.com October 2016

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

TABLE 13-7 Overview of the Most Common Ultrasound Findings in
Entrapment Neuropathiesa
Entrapment Neuropathy
Carpal tunnel syndrome
Cubital tunnel syndrome
Radial nerve compression
Fibular nerve compression
Cervical radiculopathy
a
Modified with permission from Kerasnoudis A, Tsivgoulis G, J Neuroimaging.37 B 2015 American
Society of Neuroimaging. onlinelibrary.wiley.com/doi/10.1111/jon.12261/abstract.
reveal rupture, swelling, or loss of the
internal texture of the brachial plexus
in traumatic lesions and may assist in
the diagnosis of radiation plexitis,
tumor invasion (Pancoast tumor), neu-
rogenic tumors, and Parsonage-Turner
(also known as neuralgic amyotrophy
or brachial neuritis) and thoracic out-
let syndromes.43
Phrenic Neuropathies
Besides enhancing the accuracy of
needle positioning during EMG of
the diaphragm, ultrasound may reveal
atrophy (decrease of absolute thickness)
or decreased contractility (decrease in
thickening ratio at maximal inspiration)
of the diaphragm, providing additional
information to diaphragmatic EMG and
Continuum (Minneap Minn) 2016;22(5):1655–1677
Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
Ultrasound Findings
Cross-sectional area (CSA) 90.11 cm2
Wrist to forearm ratio 91.4
Reduced echogenicity
Increased vascularity
Reduced mobility
CSA 90.09 cm2
Elbow to upper arm ratio 91.4
Reduced echogenicity
Increased echogenicity of epineurium
Luxation/subluxation
CSA 90.06 cm2
Reduced echogenicity
CSA 90.12 cm2
Reduced echogenicity
Popliteal fossa to fibular head ratio 91.4
Side-to-side difference ratio 91.5
nerve conduction studies of the phrenic
nerve.44
Inflammatory Polyneuropathies
PNS ultrasound may also offer diag-
nostic information in patients with in-
flammatory polyneuropathies.37 The
main applications of neurosonology
in the diagnostic evaluation of inflam-
matory polyneuropathies are summa-
rized below.
Chronic inflammatory demyelinat-
ing polyradiculoneuropathy. Brachial
plexus hypertrophy and multifocal
peripheral nerve hypertrophy can be
seen on ultrasound images in patients
with chronic inflammatory demyelin-
ating polyradiculoneuropathy (CIDP),
probably due to recurrent episodes
www.ContinuumJournal.com 1673
 Ultrasound
of demyelination and remyelination
that lead to the classic onion-bulb his-
tologic appearance of the nerves. In-
creased intranerve CSA variability in
several peripheral nerves has also been
reported. The degree of correlation
between sonographic and electrophys-
iologic findings in CIDP still remains
unclear, and neither study correlates
sufficiently with functional disability.45
Nerve ultrasound scores have been de-
veloped to distinguish CIDP of sub-
acute or progressive onset from
Guillain-Barré syndrome (GBS). A sum
score of 2 points or more on the
Bochum ultrasound score has sensi-
tivity of 80% and specificity of 100%
for the distinction of subacute CIDP
from GBS. The score is more sensitive
than both classic electrophysiologic
and clinical parameters in diagnosing
the early onset of CIDP.46 In addition,
a distinction of CIDP from multifo-
cal motor neuropathy (MMN) or
multifocal acquired demyelinating
sensory and motor neuropathy
(MADSAM) can be made with the
Bochum ultrasound score.
Guillain-Barré syndrome. Both pe-
ripheral nerve and cervical root pa-
thology during the early stage of GBS
have been described with ultrasonog-
raphy, but nerve ultrasound findings
seem to show no significant correla-
tion to electrophysiologic findings or
functional disability in patients with
GBS.47 However, increased CSF protein
and reduced compound muscle action
potential amplitudes in motor conduc-
tion studies appear to predict both the
functional outcome and the develop-
ment of pathologic nerve ultrasound
changes in GBS.37
Other neuropathies. Nerve ultra-
sound abnormalities in MMN appear as
a multifocal pattern of nerve enlarge-
ment at sites with or without clinical or
electrophysiologic abnormalities. Nerve
ultrasound is a useful method for
1674 www.ContinuumJournal.com
Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
detecting focal nerve enlargement in
MMN and differentiating this condition
from amyotrophic lateral sclerosis.48
Peripheral nerve involvement is a
common complication of systemic
vasculitis and presents as a painful
sensorimotor polyneuropathy affect-
ing primarily the lower limbs or as a
mononeuritis multiplex. Diffuse thick-
ening of peripheral nerves, primarily
of the lower limbs, and reduction of
nerve diameter after corticosteroid
therapy have been described using
ultrasound.49 Abnormal ultrasound
findings have been reported in pa-
tients with paraproteinemia, and path-
ologic values of both of the nerve CSAs
in various peripheral nerves have been
found in patients with antiYmyelin-
associated glycoprotein antibodies
(MAG) polyneuropathy.50
CONCLUSION
TCD and cervical duplex ultrasonogra-
phy are two easily repeatable nonin-
vasive diagnostic tests that can be
performed at the bedside and may
provide hemodynamic information in
real time. Both tests broaden the
abilities of stroke physicians to rapidly
evaluate patients with stroke, deter-
mine the likely mechanism of stroke,
and decide on acute reperfusion and
secondary prevention therapies. Tran-
scranial parenchymal sonography has
recently been developed as a valuable
supplementary tool in the diagnosis
and differential diagnosis of move-
ment disorders by providing reliable
structural information on the substantia
nigra, basal ganglia, and ventricular
system. Peripheral nerve ultrasound is
a noninvasive and readily available
modality that may offer structural in-
formation regarding the underlying
etiology of entrapment neuropa-
thies that is complementary to the
findings offered by neurophysio-
logic studies.
October 2016
REFERENCES
1. Rundek T. Beyond percent stenosis: carotid
plaque surface irregularity and risk of stroke.
Int J Stroke 2007;2(3):169Y171. doi:10.1111/
j.1747-4949.2007.00135.x.
2. Grant EG, Benson CB, Moneta GL, et al.
Carotid artery stenosis: gray-scale and
Doppler US diagnosisVSociety of Radiologists
in Ultrasound Consensus Conference.
Radiology 2003;229(2):340Y346. doi:10.1148/
radiol.2292030516.
3. Saqqur M, Sharma VK, Tsivgoulis G, et al.
Real-time hemodynamic assessment of
downstream effects of intracranial stenoses
in patients with orthostatic hypoperfusion
syndrome. Cerebrovasc Dis 2010;30(4):
355Y361. doi:10.1159/000319567.
4. Pascual-Leone A, Anderson DC, Larson DA.
Volume therapy in orthostatic transient
ischemic attacks. Stroke 1989;20(9):1267Y1270.
doi:10.1161/01.STR.20.9.1267.
5. King A, Markus HS. Doppler embolic signals
in cerebrovascular disease and prediction of
stroke risk: a systematic review and meta-analysis.
Stroke 2009;40(12):3711Y3717. doi:10.1161/
STROKEAHA.109.563056.
6. Brott TG, Halperin JL, Abbara S, et al. 2011
ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/
SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the
management of patients with extracranial
carotid and vertebral artery disease. Stroke
2011;42(8):e464Ye540. doi:10.1161/
STR.0b013e3182112cc2.
7. Bartels E, Fuchs HH, Flügel KA. Duplex
ultrasonography of vertebral arteries:
examination, technique, normal values,
and clinical applications. Angiology
1992;43(3 pt 1):169Y180. doi:10.1177/
000331979204300301.
8. Sturzenegger M, Mattle HP, Rivoir A,
Baumgartner RW. Ultrasound
findings in carotid artery dissection:
analysis of 43 patients. Neurology
1995;45(4):691Y698. doi:10.1212/
WNL.45.4.691.
9. Nebelsieck J, Sengelhoff C, Nassenstein I,
et al. Sensitivity of neurovascular
ultrasound for the detection of
spontaneous cervical artery dissection. J Clin
Neurosci 2009;16(1):79Y82. doi:10.1016/
j.jocn.2008.04.005.
10. Schinkel AF, van den Oord SC, van der
Steen AF, et al. Utility of contrast-enhanced
ultrasound for the assessment of the
carotid artery wall in patients with Takayasu
or giant cell arteritis. Eur Heart J
Cardiovasc Imaging 2014;15(5):541Y546.
doi:10.1093/ehjci/jet243.
Continuum (Minneap Minn) 2016;22(5):1655–1677
Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
11. Tsivgoulis G, Heliopoulos I, Vadikolias K,
et al. Teaching NeuroImages: ultrasound
findings in giant-cell arteritis. Neurology
2010;75(16):e67Ye68. doi:10.1212/
WNL.0b013e3181f881e9.
12. Arida A, Kyprianou M, Kanakis M,
Sfikakis PP. The diagnostic value of
ultrasonography-derived edema of the
temporal artery wall in giant cell arteritis:
a second meta-analysis. BMC Musculoskelet
Disord 2010;11:44. doi:10.1186/
1471-2474-11-44.
13. Alexandrov AV, Sloan MA, Tegeler CH, et al;
American Society of Neuroimaging
Practice Guidelines Committee. Practice
standards for transcranial Doppler (TCD)
ultrasound. Part II. Clinical indications and
expected outcomes. J Neuroimaging
2012;22(3):215Y224. doi:10.1111/
j.1552-6569.2010.00523.x.
14. Tsivgoulis G, Sharma VK, Lao AY, et al.
Validation of transcranial Doppler with
computed tomography angiography in
acute cerebral ischemia. Stroke
2007;38(4):1245Y1249. doi:10.1161/
01.STR.0000259712.64772.85.
15. Molina CA, Alexandrov AV, Demchuk AM,
et al. Improving the predictive
accuracy of recanalization on stroke
outcome in patients treated with tissue
plasminogen activator. Stroke
2004;35(1):151Y156. doi:10.1161/
01.STR.0000106485.04500.
16. Alexandrov AV, Burgin WS, Demchuk AM,
et al. Speed of intracranial clot lysis with
intravenous tissue plasminogen activator
therapy: sonographic classification and
short-term improvement. Circulation
2001;103(24):2897Y2902. doi:10.1161/
01.CIR.103.24.2897.
17. Tsivgoulis G, Ribo M, Rubiera M, et al.
Real-time validation of transcranial Doppler
criteria in assessing recanalization during
intra-arterial procedures for acute ischemic
stroke: an international, multicenter study.
Stroke 2013;44(2):394Y400. doi:10.1161/
STROKEAHA.112.675074.
18. Alexandrov AV, Nguyen HT, Rubiera M,
et al. Prevalence and risk factors associated
with reversed Robin Hood syndrome in
acute ischemic stroke. Stroke
2009;40(8):2738Y2742. doi:10.1161/
STROKEAHA.109.547950.
19. Silvestrini M, Vernieri F, Pasqualetti P, et al.
Impaired cerebral vasoreactivity and risk of
stroke in patients with asymptomatic carotid
artery stenosis. JAMA 2000;283(16):2122Y2127.
doi:10.1001/jama.283.16.2122.
www.ContinuumJournal.com 1675
 Ultrasound
20. Tsivgoulis G, Krogias C, Georgiadis GS, et al.
Safety of early endarterectomy in patients
with symptomatic carotid artery stenosis: an
international multicenter study. Eur J Neurol
2014;21(10):1251Y1257, e75Ye76.
doi:10.1111/ene.12461.
21. Lao AY, Sharma VK, Tsivgoulis G, et al.
Detection of right-to-left shunts: comparison
between the International Consensus and
Spencer Logarithmic Scale criteria.
J Neuroimaging 2008;18(4):402Y406.
doi:10.1111/j.1552-6569.2007.00218.x.
22. Tsivgoulis G, Kerasnoudis A, Krogias C, et al.
Clopidogrel load for emboli reduction in
patients with symptomatic carotid stenosis
undergoing urgent carotid endarterectomy.
Stroke 2012;43(7):1957Y1960. doi:10.1161/
STROKEAHA.112.657916.
23. Adams RJ, Brambilla D; Optimizing Primary
Stroke Prevention in Sickle Cell Anemia
(STOP 2) Trial Investigators. Discontinuing
prophylactic transfusions used to prevent
stroke in sickle cell disease. N Engl J Med
2005;353(26):2769Y2778. doi:10.1056/
NEJMoa050460.
24. Mizuno M, Nakajima S, Sampei T, et al. Serial
transcranial Doppler flow velocity and cerebral
blood flow measurements for evaluation of
cerebral vasospasm after subarachnoid
hemorrhage. Neurol Med Chir (Tokyo)
1994;34(3):164Y171. doi:10.2176/nmc.34.164.
25. Soustiel JF, Shik V, Shreiber R, et al. Basilar
vasospasm diagnosis: investigation of a
modified ‘‘Lindegaard Index’’ based on imaging
studies and blood velocity measurements of the
basilar artery. Stroke 2002;33(1):72Y77.
doi:10.1161/hs0102.100484.
26. Sloan MA, Alexandrov AV, Tegeler CH, et al.
Assessment: transcranial Doppler
ultrasonography: report of the Therapeutics
and Technology Assessment Subcommittee of
the American Academy of Neurology.
Neurology 2004;62(9):1468Y1481. doi:10.1212/
WNL.62.9.1468.
27. Chang JJ, Tsivgoulis G, Katsanos AH, et al.
Diagnostic accuracy of transcranial Doppler
for brain death confirmation: systematic
review and meta-analysis. AJNR Am J
Neuroradiol 2016;37(3):408Y414.
doi:10.3174/ajnr.A4548.
28. Vlaar AM, Bouwmans A, Mess WH, et al.
Transcranial duplex in the differential diagnosis
of parkinsonian syndromes: a systematic
review. J Neurol 2009;256(4):530Y538.
doi:10.1007/s00415-009-0143-8.
29. Walter U, Niehaus L, Probst T, et al. Brain
parenchyma sonography discriminates
Parkinson’s disease and atypical
1676 www.ContinuumJournal.com
Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
parkinsonian syndromes. Neurology
2003;60(1):74Y77. doi:10.1212/WNL.60.1.74.
30. Riederer P, Sofic E, Rausch WD, et al.
Transition metals, ferritin, glutathione, and
ascorbin acid in parkinsonian brains. J
Neurochem 1989;52(2):515Y520.
doi:10.1111/j.1471-4159.1989.tb09150.x.
31. Ruprecht-Dörfler P, Berg D, Tucha O, et al.
Echogenicity of the substantia nigra in
relatives of patients with sporadic Parkinson’s
disease. Neuroimage 2003;18(2):416Y422.
doi:10.1016/S1053-8119(02)00035-6.
32. Schuurman AG, van den Akker M, Ensinck KT,
et al. Increased risk of Parkinson’s disease
after depression: a retrospective cohort study.
Neurology 2002;58(10):1501Y1504.
doi:10.1212/WNL.58.10.1501.
33. Berg D, Seppi K, Behnke S, et al. Enlarged
substantia nigra hyperechogenicity and risk
for Parkinson disease: a 37-month 3-center
study of 1847 older persons. Arch Neurol
2011;68(7):932Y937. doi:10.1001/
archneurol.2011.141.
34. Respondek G, Roeber S, Kretzschmar H, et al.
Accuracy of the National Institute for
Neurological Disorders and Stroke/Society
for Progressive Supranuclear Palsy and
neuroprotection and natural history in
Parkinson plus syndromes criteria for the
diagnosis of progressive supranuclear palsy.
Mov Disord 2013;28(4):504Y509. doi:10.1002/
mds.25327.
35. Busse K, Heilmann R, Kleinschmidt S,
et al. Value of combined midbrain
sonography, olfactory and motor function
assessment in the differential diagnosis of
early Parkinson’s disease. J Neurol Neurosurg
Psychiatry 2012;83(4):441Y447. doi:10.1136/
jnnp-2011-301719.
36. Deniz FE, Oksüz E, Sarikaya B, et al.
Comparison of the diagnostic utility of
electromyography, ultrasonography,
computed tomography, magnetic resonance
imaging in idiopathic carpal tunnel
syndrome determined by clinical findings.
Neurosurgery 2012;70(3):610Y616.
doi:10.1227/NEU.0b013e318233868f.
37. Kerasnoudis A, Tsivgoulis G. Nerve
ultrasound in peripheral neuropathies: a
review. J Neuroimaging 2015;25(4):528Y538.
doi:10.1111/jon.12261.
38. Walker FO, Cartwright MS, Blocker JN, et al.
Prevalence of bifid median nerves and
persistent median arteries and their association
with carpal tunnel syndrome in a sample of
Latino poultry processors and other manual
workers. Muscle Nerve 2013;48(4):539Y544.
doi:10.1002/mus.23797.
October 2016
39. Djurdjevic T, Loizides A, Löscher W, et al.
High resolution ultrasound in posterior
interosseous nerve syndrome. Muscle Nerve
2014;49(1):35Y39. doi:10.1002/mus.23867.
40. Visser LH, Hens V, Soethout M, et al.
Diagnostic value of high-resolution
sonography in common fibular neuropathy
at the fibular head. Muscle Nerve
2013;48(2):171Y178. doi:10.1002/mus.23729.
41. Kim E, Yoon JS, Kang HJ. Ultrasonographic
cross-sectional area of spinal nerve roots in
cervical radiculopathy: a pilot study. Am J
Phys Med Rehabil 2015;94(2):159Y164.
doi:10.1097/PHM.0000000000000212.
42. Tagliafico A, Succio G, Serafini G, Martinoli C.
Diagnostic performance of ultrasound
in patients with suspected brachial plexus
lesions in adults: a multicenter retrospective
study with MRI, surgical findings and clinical
follow-up as reference standard. Skeletal
Radiol 2013;42(3):371Y376.
43. Lapegue F, Faruch-Bilfeld M, Demondion X,
et al. Ultrasonography of the brachial
plexus, normal appearance and practical
applications. Diagn Interv Imaging
2014;95(3):259Y275.
44. Boon AJ, Sekiguchi H, Harper CJ, et al.
Sensitivity and specificity of diagnostic
ultrasound in the diagnosis of phrenic
neuropathy. Neurology 2014;83(14):
1264Y1270.
45. Kerasnoudis A, Pitarokoili K, Behrendt V,
et al. Correlation of nerve ultrasound,
Continuum (Minneap Minn) 2016;22(5):1655–1677
Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
electrophysiological and clinical findings
in chronic inflammatory demyelinating
polyneuropathy. J Neuroimaging
2015;25(2):207Y216. doi:10.1111/
jon.12079.
46. Kerasnoudis A, Pitarokoili K, Behrendt V,
et al. Bochum ultrasound score versus
clinical and electrophysiological parameters
in distinguishing acute-onset chronic from
acute inflammatory demyelinating
polyneuropathy. Muscle Nerve 2015;
51(6):846Y852. doi:10.1002/mus.24484.
47. Grimm A, Décard BF, Axer H.
Ultrasonography of the peripheral nervous
system in the early stage of Guillain-Barré
syndrome. J Peripher Nerv Syst 2014;
19(3):234Y241. doi:10.1111/jns.12091.
48. Grimm A, Décard BF, Athanasopoulou I,
et al. Nerve ultrasound for differentiation
between amyotrophic lateral sclerosis and
multifocal motor neuropathy. J Neurol
2015;262(4):870Y880. doi:10.1007/
s00415-015-7648-0.
49. Grimm A, Décard BF, Bischof A, Axer H.
Ultrasound of the peripheral nerves in
systemic vasculitic neuropathies. J Neurol
Sci 2014;347(1Y2):44Y49. doi:10.1016/
j.jns.2014.09.017.
50. Lucchetta M, Padua L, Granata G, et al. Nerve
ultrasound findings in neuropathy associated
with anti-myelin-associated glycoprotein
antibodies. Eur J Neurol 2015;22(1):193Y1202.
doi:10.1111/ene.12554.
www.ContinuumJournal.com 1677