0% found this document useful (0 votes)

26 views31 pages

Ultrasound Assessment of The Intracranial Arteries

Uploaded by

Nitro Maldini

We take content rights seriously. If you suspect this is your content, claim it here.

Available Formats

Download as PDF, TXT or read online on Scribd

0% found this document useful (0 votes)

26 views31 pages

Ultrasound Assessment of The Intracranial Arteries

Uploaded by

Nitro Maldini

We take content rights seriously. If you suspect this is your content, claim it here.

Available Formats

Download as PDF, TXT or read online on Scribd

You are on page 1/ 31

ULTRASOUND ASSESSMENT OF THE

INTRACRANIAL ARTERIES 10
Darius G. Nabavi, MD, Martin A. Ritter, MD, and E. Bernd Ringelstein, MD

Introduction The detection of high intensity transient signals

(HITS) or microembolic signals (MES) by means
In 1965, Miyazaki and Kato1 first reported the of TCD constitutes another developmental land-
use of continuous-wave Doppler ultrasound for mark by allowing the noninvasive estimation of
the assessment of extracranial cerebral vessels. microemboli reaching the intracranial arteries.10
Despite its rapid development in other medical The therapeutic use of ultrasound-assisted
fields, this technique was not applied to the intra- thrombolysis (sonothrombolysis)11 offers an
cranial vessels until 1982. At that time, Aaslid alternative to endovascular arterial recanalization
and colleagues2 developed a transcranial Doppler during an evolving stroke.
(TCD) device with a pulsed-wave sound emission This chapter provides an overview of the main
of 2 MHz that could successfully penetrate the technical and clinical aspects of intracranial
skull and accurately measure blood flow velocities ultrasonography and briefly introduces the latest
in the basal arteries and the circle of Willis. With technical and clinical developments.
the introduction of TCD, it became possible to
record intracranial blood flow velocity directly, and
TCD became an important noninvasive method Examination Techniques
for assessing cerebral hemodynamics and for
evaluating intracranial cerebrovascular disease. General prerequisites
The continuous development and refinement of Two prerequisites should be fulfilled before
ultrasonography during the past two decades led to performing a TCD examination: (1) the status
a broad spectrum of clinical TCD applications. The of the extracranial arteries has to be known, and
introduction of transcranial color-coded duplex (2) the patient needs to rest comfortably to avoid
sonography (TCCS) into clinical use was an impor- major fluctuations in blood carbon dioxide levels
tant technical refinement. TCCS combines B-mode and movement artifacts. In addition, two main
imaging with frequency-based color flow imaging anatomic considerations must be dealt with by the
and Doppler sonography.3 By means of TCCS, direct examiner: (1) the ultrasonic “windows” through
online visualization of the basal cerebral arteries which the ultrasound beam can penetrate the skull
and their flow directions became possible, allowing are often limited or difficult to identify, and (2)
for angle-corrected measurements of blood flow the arteries at the base of the skull vary greatly
velocities at defined depths. Subsequently, power- with respect to size, course, development, and
based4 and three-dimensional TCCS5 were added, site of access.12–15 The transmission of ultrasound
and ultrasound contrast agents were introduced,6 signals through the cranium has been extensively
further enhancing the diagnostic capability of studied.16,17 It depends on the skull structure, with
this innovative technique.7 Transcranial B-mode each of the three layers influencing ultrasound
sonography also offers insights into alterations transmission in different ways. Grolimund17 has
in the brain parenchyma seen in patients with performed a number of in vitro experiments
movement disorders. showing that a wide range of energy loss occurs
Ultrasound contrast agents have likewise pro- in different skull samples, and that the energy
vided the opportunity to detect right-to-left cardiac loss varies greatly between individuals and with
shunts8 and to perform perfusion studies of the skull location. In no case was the power measured
brain parenchyma based on indicator dilution behind the skull greater than 35% of the transmit-
principles.9 ted power. It was further shown that the skull

203

Descargado para MARIA GONZALEZ ([email protected]) en Private Technical University of Loja de ClinicalKey.es por Elsevier en enero 08,
2025. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2025. Elsevier Inc. Todos los derechos reservados.
204 SECTION 2 Cerebral Vessels

can provide the effect of an acoustic lens, and transtemporal, transorbital, suboccipital (i.e., trans-
that refraction or distortion of the beam depends foraminal), and submandibular approaches.18,19
more on the variation of bone thickness than on An extensive nomenclature has been developed
the angle of insonation. for describing the segments of the intracranial
cerebral arteries and this terminology is used in
Transcranial Doppler and transcranial this chapter. If you are unfamiliar with cerebral
color-coded duplex sonography devices artery nomenclature, please refer to Fig. 10.2.
Transcranial ultrasound applications require a large
signal-to-noise ratio. This is one of the reasons why Transtemporal approach
the available transcranial instruments have a lower The probe is placed on the temporal aspect of the
bandwidth, and therefore a larger and less-defined head, above the zygomatic arch and immediately
sample volume than most other pulsed Doppler anterior and slightly superior to the tragus of the
devices. Commercial TCD systems mostly use a ear conch (Fig. 10.3, position 1). This is usually the
2-MHz, pulsed, range-gated Doppler device with most promising examination site. A more posterior
good directional resolution. TCCS is performed window immediately cephalad and slightly dorsal
with 1.8- to 3.6-MHz phased-array sector trans- to the first one (see Fig. 10.3, position 2) may be
ducers. Further instrumental requirements are more appropriate in a minority of cases, especially
(1) transmitting powers ranging between 10 and for insonation of the P2 segment of the posterior
100 mW/cm2, (2) adjustable Doppler gate depth, cerebral arteries (PCAs). In some patients, a more
(3) pulse repetition frequency up to 20 kHz, (4) frontally located temporal window may be present
focusing of the ultrasonic beam at a distance of 40 (see Fig. 10.3, position 3). Starting from these
to 60 mm from the probe, and (5) online display transtemporal windows, the ultrasound probe can
of the time-averaged velocity and peak systolic be angulated anteriorly or posteriorly relative to
velocity (PSV) derived from the Doppler waveform the corresponding probe positions on the opposite
contour generated following spectral analysis of the side of the head. The anterior orientation of the
ultrasonic signals. Several commercially available ultrasound beam allows insonation of the M1
TCD devices are equipped with special headbands and M2 segments of the middle cerebral arteries
or helmets to enable continuous monitoring. (MCAs), the C1 segment of the carotid siphon
(CS), the A1 segment of the anterior cerebral artery
Ultrasonic windows (ACA), and often the anterior communicating
Four main ultrasound approaches (Fig. 10.1) artery (Fig. 10.4A). Posterior angulation of the
are used to examine the intracranial arteries: the ultrasound beam allows examination of the P1
and P2 segments of the PCA, the top of the basilar
artery (BA), and the posterior communicating
arteries (see Fig. 10.4B).

Transorbital approach
Components of the anterior cerebral circulation
may be evaluated by placing the transducer against
the closed eyelid.13 To avoid damage to the lenses
of the eyes, the power of the ultrasound transmis-
sion has to be reduced. The ophthalmic artery can
usually be insonated at depths of 45 to 50 mm,
whereas the C3 segment (anterior knee of the CS)
is normally met at insonation depths of 60 to
65 mm (Fig. 10.5A). At slightly greater insonation
depths of 70 to 75 mm, the C2 segment shows
flow away from the probe, and the C4 segment
shows flow toward the probe. These blood flow
FIG. 10.1 Relationship of ultrasonic probes to the available
directions apply only when the beam is nearly
ultrasound windows within the skull and to the basal sagittal (slight medial obliquity) and enters the
cerebral arteries. skull through the supraorbital or infraorbital

ACoA
OA OA
A2 A2
C3 C3
C2 C2
CS A1 A1 CS
C1 C1
ACA
M2 M1 M2
M1

MCA PCoA MCA

ICA ICA

P2 P1 P1 P2

PCA PCA
BA

VA VA
FIG. 10.2 Nomenclature of the basal cerebral arteries of the circle of Willis. ACA, Anterior cerebral
artery (segments A1, A2); ACoA, anterior communicating artery; BA, basilar artery; CS, carotid
siphon (segments C1 to C3); ICA, internal carotid artery; MCA, middle cerebral artery (segments
M1, M2); OA, ophthalmic artery; PCA, posterior cerebral artery (segments P1, P2); PCoA, posterior
communicating artery; VA, vertebral artery.

Suboccipital (transforaminal) approach

The suboccipital (transforaminal) approach is
essential for screening the distal part of the ver-
tebral artery (VA), the so-called V4-segment and
2 the basilar artery (BA). The probe is placed exactly
3 1 between the posterior margin of the foramen
magnum and the palpable spinous process of the
first cervical vertebra, with the beam aimed at the
bridge of the nose (Fig. 10.6A).2 The insonation
depth is set at 65 mm, and the right and left VAs
are tracked individually from this (deepest) point
FIG. 10.3 Available temporal ultrasonic windows and
probe placement. The probe should first be placed in back toward the foramen magnum, using progres-
the preauricular region to identify the middle cerebral sively smaller insonation depths (from 65 down to
artery. Very subtle movements of the probe should be 35 mm). As the depth decreases, the sound beam
performed in each position. If position 1 is not success- is angled increasingly sharply toward the side of
ful, position 2 should be tried next, before position 3
the head. The extradural part of the VA, on the
is chosen. 1, Preauricular position; 2, posterior window;
3, anterior window. posterior arch of the atlas (V3 segment), can also
be screened. Flow is toward the transducer in this
segment. The BA can be tracked cephalad from
the point at which the VAs join. The superior end
fissures. Typical insonation depths and velocities of the BA is reached at a depth of approximately
are shown in Fig. 10.5B. Measurements made 95 to 125 mm. Blood flow in the intradural VAs
through the transorbital approach are less well and the BA is normally directed away from the
established and validated than those made through probe. Typical insonation depths and blood flow
the transtemporal and suboccipital approaches. velocities are shown in Fig. 10.6B.

Z Z'

µ X T P' X'
Z' ω
X X' P Y

A B
FIG. 10.4 Position of the probe in the temporal region to insonate the anterior and posterior
parts of the circle of Willis. (A) Line X–X′ indicates a frontal plane that runs through the regular
placement of the probe on either side and, simultaneously, perpendicular to the sagittal midline
of the skull. Z′ indicates the site of the intracranial internal carotid artery bifurcation. The X′–Z′
distance is 63 ± 5 mm. The angle µ is the angle with which the probe is aimed more anteriorly
toward the middle cerebral artery and anterior cerebral artery segments. This angle was found
to be 6 ± 1.1 degrees. (B) The angle ω indicates the angle with which the beam is directed more
posteriorly to insonate the top (T) of the basilar artery (BA) and the P1 segments (P′ ) on both
sides. This angle was found to be 4.6 ± 1.2 degrees. The BA bifurcation could be insonated at
depths of 78 ± 5 mm, corresponding to the distance X–T or X′–T, respectively. Y indicates the
fictional point at which the pathway of the beam then transits the contralateral skull (i.e.,
approximately 2 to 3 cm behind the external acoustic meatus). The P2 segments (P) can also be
insonated if the beam is directed even more posteriorly and slightly caudally (line X′–P). W lies
approximately 5 cm behind the contralateral external acoustic meatus.

43 ± 13.8 cm/s
70 mm 21 ± 4.8 cm/s
45 mm
C1
OA
C2
P C3
C4
60 mm

47 ± 12.7 cm/s
70 mm

A B
FIG. 10.5 Insonation of the ophthalmic artery (OA) and carotid siphon (CS) by the transorbital
approach. (A) Probe (P) location and relationship to the OA and CS. (B) Representative insonation
depths and normal flow values within various segments of the CS (C1 to C4) and OA.

Submandibular approach artery (ICA). This particular imaging window

The submandibular approach complements the facilitates the detection of ICA dissection and
examination permitting the Doppler interrogation chronic ICA occlusion with abundant collateraliza-
of the retromandibular and more distal extradural tion through the external carotid artery. With the
parts (C5 to C6 segments) of the internal carotid transducer positioned as shown in Fig. 10.7A, the

41 ± 9.3 cm/s
60 mm 40 ± 9.9 cm/s
65 mm
P2 P1 P1 P2

B 39 ± 10.6 cm/s
33 ± 8.8 cm/s 95 mm
65 mm
V4

V V
V3

B
FIG. 10.6 (A) Transcranial Doppler examination of the vertebral system by the suboccipital approach.
(B) Representative insonation and normal flow values within the distal vertebral arteries (V) and
the basilar trunk (B). The P1 and P2 velocities are measured transtemporally. P, Probe.

ICA

C5
32 ± 8.7 cm/s 30 ± 9.0 cm/s
50 mm 60 mm

34 ± 8.7 cm/s
40 mm

A B
FIG. 10.7 (A) Transcranial Doppler examination of the petrous portion of the internal carotid
artery (ICA) by the submandibular approach. The ICA can be traced from depths of 25 to 80 mm,
corresponding to the C5 segment of the ICA. (B) Representative insonation depths and normal
blood flow velocities of the distal intracranial ICA.

beam is directed slightly medially and posteriorly. Diagnostic approach

The ICA can regularly be tracked to a depth of 80
to 85 mm, at which point it bends medioanteriorly Basic transcranial Doppler examination
to form the CS. Typical insonation depths and It is practical to start the examination at the
blood flow velocities are shown in Fig. 10.7B. transtemporal window, identify the MCA on
either side at an insonation depth of 50 to
55 mm, and then track the ipsilateral arterial
PRACTICAL TIPS network, step by step, in various directions.
Proof of traceability of the MCA is necessary for
• The transmitted ultrasound power
its unequivocal identification. This is also true for
penetrating the skull is at most 35%.
other arteries at the base of the brain. Traceability
• TCD systems mostly use a 2-MHz, pulsed,
refers to the fact that the MCA (and usually other
range-gated Doppler device with good
arteries) can be tracked in incremental steps from
directional resolution, whereas TCCS uses
shallow insonation depths (35 mm) to deeper
1.8- to 3.6-MHz phased-array sector
sites (55 mm) without showing changes in the
transducers.
character of the blood flow profile and direction.
• The transtemporal window permits:
When tracking the MCA medially (65 to 70 mm),
• Anterior orientation of the ultrasound
an abrupt change in flow direction (away from,
beam and interrogation of the M1 and
rather than toward the probe) indicates insonation
M2 segments of the MCAs, the C1
of the A1 segment of the ACA. Blood flow signals
segment of the CS, the A1 segment of
toward the probe at this depth usually emanate
the ACA, and often the anterior
from the CS at its junction with the MCA. Typical
communicating artery.
depths and blood flow velocities are shown in
• Posterior angulation of the beam allows
Fig. 10.8.
examination of the P1 and P2 segments
By angling the beam more posteriorly from
of the PCA, the top of the BA, and the
the transtemporal approach, the P1 segment of
posterior communicating arteries.
the PCA can be picked up most readily at an
• The transorbital approach requires the
insonation depth of 65 to 70 mm. The PCA can
application of less power and is used to
then be tracked to the top of the BA (75 mm)
insonate the ophthalmic artery and the C2
and from there to the contralateral PCA (80 to
and C4 segments of the ICA.
85 mm) (see Fig. 10.4B). The two criteria of trace-
• The suboccipital (foraminal) approach is
ability (i.e., the display of bilateral blood flow at
used to evaluate the vertebral and basilar
the junction with the BA and the change of flow
arteries.
direction within the contralateral PCA) are very

55 ± 12.8 cm/s

P 51 ± 13 cm/s 58 ± 15.6 cm/s

60/65 mm 50/55 mm

A1
M1
50 ± 11 cm/s
C1 39 ± 8.7 cm/s
65 mm

A B
FIG. 10.8 Typical transtemporal distances and velocities for the anterior cerebral artery and the
middle cerebral artery. (A) The beam axis is in line with the C1, M1, and A1 segments of the cerebral
vessels. (B) Representative insonation depths and blood flow velocities are illustrated. P, Probe.

important features for identifying the PCAs without

compression tests.
After the completion of the examination from
both temporal windows, additional information
may be obtained through the orbital, suboc-
cipital, or submandibular windows. The arterial
segments that are accessible from these windows
and insonation depths, as well as the techniques
for identifying these vessels, have previously been
described. A protocol for TCD examination is
described in Table 10.1.

Transcranial color-coded duplex

sonography examination
TCCS is a well-established diagnostic method, A
allowing direct noninvasive imaging of intra-
cranial vascular structures.3,19 This visual approach Ipsilateral
provides for more rapid and reliable vessel
identification, permitting exact localization of
MCA
the Doppler sample volume, and shortening the
examination time.19,20 This technique has evolved PCA
rapidly and now includes not only vascular (i.e.,
arterial and venous) imaging but also imaging of
ACA
the brain parenchyma. Usually the transtemporal
and suboccipital approaches are used during TCCS
ACA
examinations. No systematic data exist for the
submandibular approach. The transorbital TCCS
PCA
investigation now offers a means of monitoring
intracranial pressures by measurement of the width MCA Contralateral
of the sheath of the optical nerve (i.e., in intensive B
care units [intracranial pressure]), or in cases of
suspected benign intracranial hypertension.20 FIG. 10.9 Illustration of a typical transtemporal transcranial
color-coded Duplex sonography examination. (A) For initial
For transtemporal insonation, the probe is spatial orientation, the examination is started with a
positioned axially along the orbitomeatal line large-scale, B-mode cranial view, which is usually achieved
and the hypoechoic, butterfly-shaped midbrain at a depth of 14 to 17 cm. Visualization of the hyperechoic
is visualized as an anatomic landmark at a depth contralateral skull (arrowheads) proves the presence of
of 6 to 8 cm. From this perspective, the circle adequate transcranial ultrasound penetration. If the
hypoechoic, butterfly-shaped midbrain (arrows) and the
of Willis can then easily be depicted (Fig. 10.9). hyperechoic sphenoid bone (asterisks) can be visualized,
Other landmarks that can be seen as the beam is then the correct insonation plane has been achieved. (B)
tilted more cranially are the third ventricle in the For the color-mode examination, the insonation depth
midline, the pineal gland and the choroidal plexus is reduced to 8 to 10 cm; the precommunicating (P1) and
(both hyperechoic), and the cella media. For the postcommunicating (P2) segments of the posterior cerebral
artery (PCA) can be visualized as they follow the edge of
suboccipital approach, the hypoechoic foramen the midbrain. More anteriorly, the sphenoidal (M1) and
magnum and the hyperechoic clivus serve as the the insular (M2) parts of the middle cerebral artery (MCA),
anatomic landmarks, with both VAs located at and the precommunicating (A1) part of the anterior
their lateral edges (Fig. 10.10). The origin of the cerebral artery (ACA) can be depicted. In rare cases and
BA can also be visually identified in most cases at with excellent bone insonation conditions (as illustrated),
the entire circle of Willis can be displayed. The distal part
a depth of 75 to 95 mm. Generally, the reference of the internal carotid artery is also assessable with the
depths of the target vessels are similar to the values probe tilted downward.
given previously for the TCD examination. TCCS
also allows for the examination of cerebral venous
sinuses and large basal cerebral veins, although

TABLE 10.1 Transcranial Doppler Protocol: Identification Criteria and Normal

Flow Velocities.
Insonation Depth
Normal Flow Main Features for
Position of Range Reference Velocity (Mean Identification of Vessel
Probe Arterial Segment (mm) Depth (mm) ±SD) (cm/s) Segment
Transtemporal MCA 30–60 50 55 ± 12 M1: Insonation depth
M1 45–60 50 55 ± 12 50 mm; traceability
forward and
backward; flow
toward probe;
slightly anterior
angulation of beam
ACA 60–75 70 50 ± 11 Insonation depth; flow
away from probe;
traceability with
slight anterior
angulation of beam;
for clear-cut
differentiation from
carotid siphon
C1 (C2) (carotid 60–70 65 39 ± 9 Insonation depth;
siphon relatively low flow
transtemporal velocity compared
approach) with M1 segment;
slightly anterior and
caudal angulation
of beam; flow
toward probe
P1 (posterior cerebral 60 (55)–75 70 39 ± 10 Insonation depth; flow
artery) toward probe
(ipsilateral P1);
traceability to top
of basilar and
contralateral P1;
slightly posterior
and caudal
angulation of beam;
relatively low flow
velocity compared
with M1 segment
P1 and P1’ (top of 70–80 75 40 ± 10 Insonation depth;
basilar) bidirectional flow;
traceability
backward and
forward; angulation
of beam
P2 (PCA) 60–65 65 40 ± 10 Flow away from probe;
placement of probe;
posterior angulation
of probe;
modulation by
opening and
closing eyes

TABLE 10.1 Transcranial Doppler Protocol: Identification Criteria and Normal

Flow Velocities.—cont’d
Insonation Depth
Normal Flow Main Features for
Position of Range Reference Velocity (Mean Identification of Vessel
Probe Arterial Segment (mm) Depth (mm) ±SD) (cm/s) Segment
Suboccipital Extradural distal 40–55 50 34 ± 8 Suboccipital placement
vertebral artery of probe; insonation
depth; strongly
lateral angulation
of beam; flow
toward probe
Intradural distal 60–95 (100) 70 38 ± 10 Insonation depth
vertebral artery Beam aimed at bridge
of nose or slightly
laterally; traceability
forward and
backward
Basilar trunk 70 (65)–115 95 (100, if 41 ± 10 Insonation depth; flow
(120) possible) away from probe;
often slight increase
of flow velocity
compared with
vertebral artery;
traceability of
vertebrobasilar axis
Ophthalmic C2 (carotid siphon, 65–80 70 41 ± 11 Sagittal or slightly
transorbital oblique angulation
approach) of beam; flow away
from beam; flow
away from probe;
insonation depth
C3 (carotid siphon, 65 (60) 65 (Bidirectional, Bidirectional signal;
transorbital not measured) sagittal angulation
approach) of beam; insonation
depth
C4 and distal part of 65–80 (85) 70 47 ± 14 Sagittal or slightly
C5 (carotid oblique and caudal
siphon, angulation of beam;
transorbital flow toward probe;
approach) insonation depth
Ophthalmic artery 35–55 45 21 ± 5 Insonation depth; flow
toward probe
Contralateral A1 75–80 Not defined Measurements Strongly oblique
(ACA; transorbital in a few cases angulation of beam
approach, only through optic canal;
ancillary flow toward probe;
approach if lack compression test
of temporal necessary for
window) differentiation from
carotid siphon and
MCA
Submandibular C6 and 35–80 (85) 60 30 ±9 Flow away from probe;
retromandibular medial angulation
segment of ICA of beam; insonation
extradural ICA; depth
submandibular)

ACA, Anterior cerebral artery; ICA, internal cerebral artery; MCA, middle cerebral artery; PCA, posterior cerebral artery; SD, standard deviation.

TABLE 10.2 Normal Values of Mean

Blood Velocity for Arteriesa
(Transtemporal Approach).
Mean Blood Velocity (cm/s)
Age (Years) MCA (M1) ACA (A1) PCA (P1)
10–29 70 ± 16.4 61 ± 14.7 55 ± 9.0
30–49 57 ± 11.2 48 ± 7.1 42 ± 8.9
50–59 51 ± 9.7 46 ± 9.4 9 ± 9.9
60–70 41 ± 7.0 38 ± 5.6 36 ± 7.9
Insonated 50–55 60–65 60–65
depth (mm)
a
Measurements for the middle (MCA), anterior (ACA), and posterior
A (PCA) cerebral arteries according to age.

Vessel identification
The primary TCD parameters for identifying the
cerebral arteries are the following:
1. Insonation depth
VA VA
2. Direction of blood flow at insonation depth
3. Flow velocity (mean flow velocity and systolic
or diastolic peak flow velocity)
4. Probe position (e.g., temporal, orbital, suboc-
cipital, submandibular)
5. Direction of the ultrasonic beam (e.g., posterior,
anterior, caudad, cephalad)
BA 6. Traceability of vessels
B Compression of the extracranial carotid arteries, as
FIG. 10.10 Illustration of a typical suboccipital (or trans- a means for intracranial vessel identification, has
foraminal) transcranial color-coded duplex sonography gradually been excluded from the clinical routine
TCCS examination. (A) For initial spatial orientation, because of the low, but definite, risk for cerebral
the examination is started with a large-scale, B-mode embolism.22,23 This is especially the case since the
cranial view, which is usually achieved at a depth of 11 to
advent of TCCS used in conjunction with ultra-
13 cm. Visualization of the hypoechoic foramen magnum
(asterisks) and the hyperechoic clivus (arrow) proves the sound contrast agents because the identification
adequacy of transcranial ultrasound penetration. (B) of the major cerebral arteries and their collateral
For the color-mode examination, the insonation depth pathways is possible, for the most part, without
is usually reduced to 8 to 11 cm, visualizing segments (V4) compression maneuvers. Carotid compression
of both vertebral arteries (VAs) as they follow the edges
should be avoided in patients with extracranial
of the foramen magnum. The Y-shaped conjunction of
the VAs with the basilar artery (BA) is usually located atheromatous disease.
close to the clivus. Note, however, that the origin of the
BA is highly variable and all three arteries are not always Blood flow velocity measurements
visible within the same insonation plane. The mean blood flow velocities of various arterial
segments, and their age dependency, are shown in
Tables 10.2 and 10.3. Normal blood flow velocity
values in adults show little variation among differ-
this has not become part of the clinical routine. ent investigators.14,19,24,25 The highest velocities are
Transcranial B-mode ultrasound can be used to almost always found in the MCA or the ACA. The
follow intracranial hemorrhages and to assess the PCAs and BAs have lower Doppler frequency shifts
brain parenchyma in movement disorders. The than the MCA in normal patients. This pattern
method is especially helpful in differentiating has not been observed in cerebral blood flow
Parkinson syndromes.21 studies where volume blood flow is measured in

TABLE 10.3 Normal Values of Mean Normals (Ages 20–75) N = 40

Blood Velocity for Arteriesa (Suboccipital 200
Approach). Vasomotor reactivity: 87.8%
Mean Blood Velocity (cm/s)
152.5
Age (Years) PCA (P1) BA VA

Velocity (%)
10–29 54 ± 8.0 46 ± 11 45 ± 9.8
30–49 40 ± 8.5 38 ± 8.6 34 ± 8.2 100
50–59 39 ± 10.1 32 ± 7.0 37 ± 10.0
64.7
60–70 35 ± 11.1 32 ± 6.7 35 ± 7.0
Insonated 60–65 85–90 60–65 r1 = 0.9157
depth (mm) r2 = 0.9490
0
a
Measurements for the posterior cerebral (PCA), basilar (BA), and
0 1 2 3 4 5 6 7 8
vertebral (VA) arteries according to age.
Volume CO2 (%)

FIG. 10.11 Vasomotor reactivity in 40 normal individuals

cubic centimeters per second. Two explanations (ages 20 to 75 tears). Blood flow velocity changes are
have been offered for this discrepancy between shown during CO2-induced hypercapnia (upper curve)
velocity and volume flow: (1) the measurement and hypocapnia (lower curve). The average change was
sites may be different26 or (2) more likely, different 87.8% (52.5% and 35.3% hypercapnia and hypocapnia,
respectively). (From Ringelstein EB, Sievers C, Ecker S, et al.
velocities occur as a compensatory mechanism to Noninvasive assessment of CO2-induced cerebral vasomotor
keep volume flow constant in arteries of different response in normal individuals and patients with internal
sizes.19 Thus velocities are slower in large vessels carotid artery occlusions. Stroke. 1988;19:964. Copyright
and faster in small ones. Normal angle-corrected © American Heart Association.)
blood flow velocity values using TCCS have
likewise been established and are only slightly
higher than those obtained with TCD.27,28 The TCD MCA with changing CO2 concentrations show a
documentation of decreasing flow velocities with biasymptotic, S-shaped curve (Fig. 10.11).
increasing age25,27 correlates well with age-related A “preserved” vasomotor reserve implies that a
changes in cerebral blood flow26 and underlines drop in perfusion pressure can be counterbalanced
the validity and accuracy of TCD and TCCS for by vasodilatation of cortical arterioles to maintain
estimating cerebral blood flow. sufficient cortical blood supply. The vasomotor
reserve may become exhausted if the resistance
Functional reserve testing vessels in brain areas with low perfusion pressure
TCD is an ideal functional test for detecting distal to a high-grade stenosis are already maxi-
rapid changes in cerebral perfusion because mally dilated.29–32 In this state, the resistance vessels
the technique provides excellent resolution of are refractory to any further vasodilatory stimuli,
blood flow velocity changes occurring over time. and hypercapnia cannot increase blood flow. This
Functional tests are predominantly aimed at condition may be critical because ischemic brain
the evaluation of the reserve mechanism of the injury can occur if the perfusion pressure is further
cerebral vasculature, using various stimuli such reduced for any reason. Measurements of the
as hypocapnia or hypercapnia, shift in the pH vasomotor reserve capacity are useful in evaluating
by acetazolamide, increased or reduced systemic the hemodynamic impact of extracranial occlusive
arterial pressure, and hypoxia. The CO2 (carbon carotid disease or of a high-grade proximal middle
dioxide) dilatory effect is mainly restricted to the cerebral artery stenosis.
peripheral arterial vascular bed, particularly the The pulsatility index, as defined by Gosling
small cortical vessels.26 With changing CO2 con- (see Chapter 3), reflects the resistance in the
centrations, the relationship between flow velocity peripheral vascular bed and has been suggested
and volume flow within a large cerebral artery as a sensitive index of diastolic runoff, that is, with
is linear,29 provided that the CO2 level does not increased peripheral vasodilatation, diastolic runoff
directly affect the diameter of the large proximal is expected to increase and the pulsatility index to
arterial segment.30 Velocities measured from the decrease.33 However, in a large series of patients

with carotid artery occlusion, the pulsatility index

appeared to be much poorer for predicting the Definition of stenosis with
intracranial hemodynamic situation than the transcranial Doppler
vasomotor reserve capacity.34 The following are typical TCD features of circum-
scribed stenosis of a large basal cerebral artery (Fig.
10.12): (1) increased flow velocity; (2) disturbed
Diagnostic Parameters for Specific flow (spectral broadening and enhanced systolic
Clinical Applications and low-frequency components); and (3) covibra-
tion phenomena (vibration of vessel wall and
Intracranial stenosis and occlusion surrounding soft tissue).19,34 It is unclear whether
The detection of CS stenosis using TCD was first the PSV (>120 to 160 cm/s) or the mean systolic
reported in 1986 by Spencer and Whisler,13 who velocity (>80 to 120 cm/s) should be used as a
used similar criteria to those used for carotid threshold value.38 When detecting intracranial
bifurcation disease. Since then, a number of stenoses with a diameter of 50% or more with a
authors have reported similar findings for the mean velocity value of 100 cm/s, a sensitivity of
CS and have extended TCD applications to other 100%, a specificity of 97.9%, as well as positive
brain arteries.35–38 and negative predictive values of 88.8% and 94.9%

3 1

2
1

3
FIG. 10.12 Middle cerebral artery stenosis and associated transcranial Doppler changes: (1) normal
proximal flow; (2) increased systolic and diastolic peak velocity and spectral broadening (turbulent
flow) at the center of the stenosis; (3) distal turbulent flow.

TABLE 10.4 Thrombolysis in Brain Ischemia Criteria for Transcranial Doppler Monitoring
of the Middle Cerebral Artery Recanalization During and After Thrombolytic Therapy.40
TIBI Score Status of the MCA Flow TCD Criteria
0 Occlusion • No flow signal
1 Near occlusion or minimal • Early systolic low-flow signal
residual flow • No diastolic flow signal
2 Strongly reduced • Reduced systolic and diastolic velocity
• Flattened early systolic increment
• Pulsatility index <1.2
3 Moderately reduced • Normal systolic increment
• Pulsatility index >1.2
• Relative reduction of blood flow velocity of >30% as
compared with the contralateral side
4 Stenotic signal • Mean blood flow velocity >80 cm/s or relative increase of
velocity >30% as compared with the contralateral side
• Detection of turbulent flow
5 Normal signal • Side-to-side difference of blood flow velocity <30%
• Comparable values of pulsatility index

MCA, Middle cerebral artery; TCD, transcranial Doppler; TIBI, Thrombolysis in Brain Ischemia.

were reported.37 For the vertebrobasilar system, the MCA status during and after thrombolysis. The
a threshold of more than 2 kHz peak-systolic TIBI scale, ranging from 0 (MCA occlusion) to 5
Doppler shift showed a sensitivity of 80% and a (normal MCA), is given in Table 10.4. The TIBI
specificity of 97% in detecting stenoses of 50% or criteria were found to be accurate in the prediction
more.36 Most authors agree that, in comparison of the clinical outcome in acute stroke patients
with the contralateral vessel segment, a relative undergoing thrombolytic therapy.41
increase in PSV of more than 30% is suspicious
for hemodynamically significant stenosis and a Pitfalls and diagnostic accuracy
relative increase of more than 50% indicates a Noninvasive demonstration of intracranial arterial
definite intracranial artery stenosis. stenosis and occlusion is a valuable clinical tool,
but various errors can occur: (1) lack of Doppler
Definition of occlusion with flow signal due to an inadequate temporal window;
transcranial Doppler (2) misinterpretation of hyperdynamic collateral
Basal cerebral artery occlusion can be detected channels33 or arteriovenous malformation (AVM)
by three observations: (1) the absence of arterial feeders19,42 as stenosis; (3) displacement of arteries
signals at an expected depth; (2) the presence because of a space-occupying lesion; (4) misin-
of signals in vessels that communicate with the terpretation of physiologic variables in the circle
occluded artery; and (3) altered flow in com- of Willis;19 (5) misdiagnosis of vasospasm as
municating vessels, indicating collateralization. stenosis;43 and (6) misinterpretation of reactive
For example, occlusion of the MCA is diagnosed hyperemia following spontaneous recanalization
from the lack of an MCA signal in the presence of as stenosis.44 In most of these situations, however,
Doppler signals from other vessels (i.e., the PCA, the velocity increases are generally seen throughout
the ACA, or the distal CS). This combination of the course of the involved arteries thereby distin-
findings also confirms that the temporal window guishing these conditions from the typically
is satisfactory. TCD has shown a sensitivity of 83% localized areas of increased velocity seen with a
and a specificity of 94.4%, with an overall accuracy stenosis.
of 91.6%, in the detection of intracranial vessel Diagnostic accuracy of TCD in the VA–BA system
occlusion.39 Using coronary angiography-based remains a particular problem. Difficulties with
Thrombolysis in Myocardial Infarction (TIMI) VA–BA diagnosis result from the following: (1)
criteria as a model, Demchuk and colleagues40 the range of normal blood flow and the size of
have proposed Thrombolysis in Brain Ischemia the vessels are highly variable; (2) the location
(TIBI) criteria for the TCD-based classification of and course of the arteries are unpredictable; (3)

often the junction of the VAs cannot reliably be

identified; (4) absence of VA Doppler flow signals
on one side may not represent disease (e.g., so-
called posterior inferior cerebellar artery [PICA]-
ending anomaly in severe VA hypoplasia); and
(5) occlusion of one VA or a “top of the basilar”
occlusion does not necessarily lead to relevant
flow abnormalities.45

Detection of intracranial stenosis and

occlusion with transcranial color-coded
duplex sonography
For TCCS, usually the angle-corrected PSV is
used as the main parameter for the definition of
intracranial stenosis. In 1999, Baumgartner and A
co-workers46 published the results of the largest
TCCS validation study yet on the detection of
intracranial stenosis. Table 10.5 gives the cutoff
values of PSV for the different intracranial arteries.
These values show excellent accuracy for the iden-
tification of stenoses of 50% or greater diameter
reduction. Cutoff values ranged from 220 cm/s
for the MCA to 120 cm/s for the VA. The TCCS
accuracy in the detection of stenoses between
30% and 50% (diameter reduction) showed a
high negative predictive value (100%) but only a
moderate positive predictive value, ranging from
73% to 100%. The latter results can be explained
by the weak hemodynamic effects of low-grade
stenosis. Others have used much lower PSV cutoff B
values of 120 cm/s or more, or a side-to-side dif-
FIG. 10.13 An axial insonation plane through the tem-
ference of more than 30 cm/s, for the definition poral bone window. (A) Prestenotic flow signal of the
of TCCS-based intracranial stenosis.47 Fig. 10.13 middle cerebral artery. (B) Doppler waveform at the
shows an example of a high-grade MCA stenosis stenosis (300 cm/s).
in a young man.
TCCS diagnosis of an intracranial artery occlu-
sion is based on the absence of Doppler flow

TABLE 10.5 Threshold Values of Angle-Corrected Peak Systolic Velocity for the Detection
of Intracranial Stenoses of ≥50% With Transcranial Color-Coded Duplex Sonography.46
PSV Cutoff Sensitivity Specificity Positive Predictive Negative Predictive
Vessel (cm/s) (%) (%) Value (%) Value (%)
MCA ≥220 100 100 100 100
ACA ≥155 100 100 100 100
PCA ≥145 100 100 100 91
BA ≥140 100 100 100 100
VA ≥120 100 100 100 100

ACA, Anterior cerebral artery; BA, basilar artery; MCA, middle cerebral artery; PCA, posterior cerebral artery; PSV, peak systolic velocity; VA,
vertebral artery.

MCA
PCA

MCA Right

PCA
ACA

ACA
PCA
A
A

MCA I

PCA
ACA

ACA
PCA

B B
FIG. 10.14 Middle cerebral artery (MCA) occlusion and FIG. 10.15 (A) Preserved blood flow in the posterior
recanalization detected with transcranial color-coded cerebral artery (PCA) ipsilateral to a middle cerebral
duplex sonography (TCCS). (A) Typical finding of a artery (MCA) occlusion and following the administration
proximal MCA occlusion, with echocontrast-enhanced TCCS of contrast material. Note the typical “blooming” effect
(Levovist) in an acute stroke patient. Note the excellent that occurs if the gain settings are not adjusted with
visualization of both posterior cerebral arteries (PCAs) only short flashes of red visible in the ipsilateral (right)
around the midbrain and both anterior cerebral artery MCA. Low amplitude Doppler spectral velocities were
(ACAs). No flow is present within the presumed course acquired from the right temporal bone window. The M1
of the MCA using both the color mode (arrows) and the segment is functionally occluded by Doppler waveform
Doppler spectral mode (not shown). (Compare this image evaluation (Thrombolysis in Brain Ischemia [TIBI]). (B) By
with Fig. 10.9B.) (B) Several days later, spontaneous MCA contrast, Doppler blood flow signals in the left MCA as
recanalization has occurred, with the entire MCA (arrows) imaged from the left temporal bone window are normal.
depicted with contrast-enhanced TCCS.

signals using both the color Doppler images and in an older adult woman with acute stroke, whereas
the Doppler spectral waveforms (Fig. 10.14). In Fig. 10.16 shows evidence of severe vertebrobasilar
some cases, the occluded arterial segment appears occlusive disease.
slightly hyperechoic on B-mode imaging. In con- The value of TCCS for the monitoring of
trast to the TCD technique, the use of the correct thrombolysis in acute stroke patients has been
insonation site and the presence of an adequate convincingly shown by a multicenter trial.47 A
insonation window can be easily confirmed with recent meta-analysis of 25 studies demonstrated
TCCS. Diagnostic confidence of TCCS for intra- the early vessel status to be highly predictive of
cranial vessel occlusion is up to 100%48,49 and the clinical outcome in patients suffering from
can be further supported by the use of ultrasound acute stroke.52 The main parameters and criteria
contrast agents.50,51 Fig. 10.15 illustrates a case of for the use of TCCS in acute stroke trials have
acute MCA occlusion and insufficient bone window been well defined.53

Assessment of the effects of

extracranial occlusive disease
An important clinical application of TCD is the
evaluation of the hemodynamic effects of extracra-
nial vascular disease on the intracranial circulation.

Carotid stenosis or occlusion

Significant changes occur in the intracranial
circulation because of the reduced perfusion
pressure caused by extracranial flow-limiting
disease. With ICA obstruction of 80% or more,
the ipsilateral MCA velocity and the pulsatility
index generally decrease as a result of vasodilata-
FIG. 10.16 Severe vertebrobasilar disease. The probe is tion in the distal arterial circulation ipsilateral
in a suboccipital position and directed in an axial plane, to the obstruction.29,34 Increased velocities and
slightly angulated upward (transnuchal approach; see Fig. turbulence are encountered and usually indicate
10.10 for normal findings). The Doppler waveform shows
reversed direction of blood flow and decreased pulsatility
collateralization. The identification of collateral
in the basilar artery. flow in patients with extracranial carotid disease
is possible with TCD12,14,54 and TCCS.55 Four main
collateral pathways can be distinguished: (1) via
the anterior communicating artery (ACoA), (2)
via the posterior communicating artery (PCoA),
PRACTICAL TIPS (3) via the ophthalmic artery, and (4) via ipsilat-
eral leptomeningeal arteries. Because the small
• Intracranial blood flow patterns indicate
communicating arteries are not always visible
that blood flow velocities:
with TCCS,55 indirect hemodynamic signs of the
• Are slower in larger arterial segments
involved arteries are of considerable importance
than is smaller ones
for identifying and localizing collateralization.
• Decrease with age
Sonographic criteria for intracranial collateral-
• Increase in response to breath holding
ization are given in Table 10.6. In general, the
or titrated increases in CO2
more sonographic criteria that are present, the
• Traceability refers to the fact that the MCA
more confident is the TCCS diagnosis of col-
and other intracranial arteries can be
lateralization. Fig. 10.17 illustrates findings in a
tracked in incremental steps from shallow
patient with ICA occlusions and the ACA collateral
insonation depths (35 mm) to deeper sites
pathway.
(55 mm) without changes in the character
Evaluation of hemodynamic disturbances
of the blood flow profiles and blood flow
within the carotid artery–MCA pathway is of
directions.
particular interest in patients with subtotal
• With TCD, a relative increase in PSV of
ICA obstruction, both unilateral and bilateral.
more than 30% as compared with a
Although the predominant mechanism of stroke is
contralateral arterial segment is suspicious
thromboembolism, a small subgroup of patients
for hemodynamic significant stenosis and
experience transient ischemic attacks, permanent
a relative increase of more than 50%
stroke, or progressive ischemic eye disease because
indicates a definite intracranial artery
of critically reduced blood flow.56,57 This subgroup
stenosis.
of patients may benefit from recanalization surgery,
• Absolute angle corrected velocity cut-
including external carotid–internal carotid bypass.
points are favored in the detection of
The identification of these individuals is based on
stenosis by TCCS.
the detection of an exhausted cerebral vascular
• TCCS is superior to TCD for confirming
reserve, which can be assessed through TCD
the presence of intracranial artery
measurement of the CO2 responsiveness of the
occlusion.
cerebral arteries.29

TABLE 10.6 Sonographic Criteria for Transcranial Doppler and Transcranial Color-Coded
Duplex Sonography for the Detection of Intracranial Collateralization in Case of Severe
Extracranial Artery Disease.55
Collateral Pathway TCD/TCCS Criteria
ACoA • Retrograde and increased flow in ACAipsilateral
• Orthograde and increased flow in ACAcontralateral
• Strong turbulences in the region of the ACoA (mostly with TCCS)
PCoA • Direct visualization of the PCoA (TCCS)
• Increased velocity in P1 segment of the PCAipsilateral
• Velocity ratio of P1/P2 segment of the PCAipsilateral >1.5
• Velocity ratio of P1ipsilateral/P1contralateral >1.5
• Increased velocity within the BA (and sometimes VAs)
Ophthalmic artery • Retrograde flow in ipsilateral ophthalmic artery
• Additional findings in extracranial ultrasonography (e.g., reduced pulsatility index
within ipsilateral external carotid artery)
Leptomeningeals • Increased velocity in the entire ipsilateral PCA (P1ipsilateral = P2ipsilateral)
• Increased velocity in ACAcontralateral without retrograde flow within ACAipsilateral

ACA, Anterior cerebral artery; ACoA, anterior communicating artery; BA, basilar artery; PCA, posterior cerebral artery; PCoA, posterior
communicating artery; TCCS, transcranial color-coded duplex sonography; TCD, transcranial Doppler; VA, vertebral artery.

Vertebrobasilar system
PRACTICAL TIPS
The subclavian steal mechanism is the classic
paradigm for studying hemodynamic disturbances • Lesions causing more than 80% ICA
in the human vertebrobasilar system. In case of stenosis may decrease pulsatility and
severe obstruction of the proximal subclavian velocities of the ipsilateral middle cerebral
artery on either side, blood to the affected arm artery.
will flow retrograde through the ipsilateral VA and • In the case of severe ICA stenosis and
be “stolen” from the contralateral vertebral and occlusion, TCCS can show:
sometimes BA. Rapid flow changes caused by any • Collateral pathways such as the ACA
type of VA blood flow restriction can be measured • Signs of possible low cerebral perfusion
directly within the BA. Under resting conditions, • Proximal subclavian artery stenosis can
blood flow within the BA is almost never critically cause:
impaired, even if the subclavian steal is continuous. • To-and-fro or reversed blood flow in the
However, if the contralateral feeding VA is also ipsilateral vertebral artery
diseased (or hypoplastic), BA blood flow may • Rarely affects basilar artery blood flow
become reduced, may demonstrate a to-and-fro
flow pattern within each cardiac cycle, or may
even be reversed. During hyperemia testing of the Monitoring of cerebral vasospasm
stealing arm, blood flow velocity and direction of Monitoring of vasospasm using TCD is a well-
blood flow within the basilar trunk may become recognized tool in the clinical management of
more or less affected (Fig. 10.18). BA blood flow patients suffering from subarachnoid hemor-
is very resistant to any critical changes resulting rhage.14,43 There is a close correlation between
from the subclavian steal mechanism. Actually, the increased flow velocities within the spastic basal
subclavian steal, as such, is a benign condition, arteries (MCA, PCA, ACA) and the severity of the
and even in patients with vertebrobasilar stroke subarachnoid hemorrhage.58,59 This correlation is
or transient ischemic attack, most symptoms are valid with respect to the size and extent of the
caused by cerebral microangiopathy rather than subarachnoid clot, the clinical state of the patient,
large artery flow disturbances.12 Subclavian artery and angiographic documentation of the severity of
disease, however, is a strong indicator of coexist- spasm (if the Doppler shift is greater than 3 kHz
ing coronary artery disease and future cardiac or PSV above 120 cm/s). The side with the more
death. severe blood flow changes on TCD examination

A B

MCA
PCom
ACA P1

C D

E F
FIG. 10.17 Doppler studies from a young man with thrombotic occlusion of his right internal
carotid artery (ICA) are shown first. (A) Doppler waveforms are not detected in the occluded
right ICA. (B) Intracranially, this carotid occlusion is well collateralized: color Doppler signals and
Doppler waveforms in the middle cerebral artery (MCA) appear normal. (C) Blood flow signals
in the anterior cerebral artery (ACA) are retrograde (red, should be blue), the posterior com-
municating artery (PCom) is also visible (color filled and reversed), and the P1 segment is hyper-
perfused (aliasing effect). The blood flow profiles and velocities of the ipsilateral right MCA (B)
and the contralateral left MCA (D) show no significant difference, confirming the establishment
of good collateral flow. In a second case, a middle-aged man presents with occlusion of the right
ICA. His MCA is also occluded distally. (E) Blood flow profiles show increased pulsatility in the
MCA and (F) a similar pattern with retrograde perfusion of the ACA that is also suggestive of a
distal MCA occlusion.

Latent steal Manifest steal

Top of basilar artery

or
B B
or

Junction of vertebral artery

F S F S

FIG. 10.18 Schematic representation of flow conditions in various vertebrobasilar vessel segments
in patients with the subclavian steal mechanism (see Chapter 9). With latent steal, flow in the
feeding (contralateral) vertebral artery (F) is increased during brachial hyperemia and is normal
in the basilar artery trunk (B). By contrast, the blood column shows an alternating flow direction
in the stealing vertebral artery (S). During manifest steal, blood flow in the stealing vertebral
artery (S) is continuously reversed. This either has no effect on basilar artery blood flow or causes
alternating or reverse flow within the basilar artery trunk. During transcranial Doppler examination,
each of the three vessel segments can be clearly differentiated by means of their characteristic
changes in blood flow pattern during brachial hyperemia.

TABLE 10.7 Clinical Relevance of Increased Middle Cerebral Artery Flow Velocities After
Subarachnoid Hemorrhage.
Time-Averaged Peak
Middle Cerebral Artery Flow Velocity Velocity (Mean; cm/s) Clinical Consequences
Normal or nonspecifically increased ≤80 Should be observed further
Subcritically accelerated >80–120 Moderate vasospasm; preventive therapy
indicated
Critically accelerated >120–140 Severe vasospasm; consequent treatment
necessary
Highly critical flow acceleration >140 Severe vasospasm; delayed ischemic
deficit highly probable

Modified from Harders A. Neurosurgical Applications of Transcranial Doppler Sonography. New York: Springer-Verlag; 1986.

corresponds to the predominant location of the Recent data indicate that TCCS is likewise useful
blood clot and the presumed site of the aneurysm. for vasospasm detection, using the criteria previ-
A steep increase in blood flow velocity (>20 cm/s/ ously defined with TCD.60–62 In some patients,
day) within the first few days after the bleed is TCCS may directly visualize the aneurysm,62–64
associated with a poor prognosis. Usually, an depending on localization, size, and the experi-
MCA velocity exceeding 200 cm/s in patients with ence of the examiner. The minimum-size aneurysm
vasospasm is associated with a critical reduction in that can be detected is reported to be greater
cerebral blood flow (Table 10.7). The time course than 6 to 8 mm.59 Due to the availability of
of the development of vasospasm is also of clinical other noninvasive angiographic techniques (e.g.,
interest. In general, vasospasm occurs from 4 to 14 computed tomography and magnetic resonance
days following subarachnoid hemorrhage, but a angiography), however, TCCS has not become
TCD-detectable increase in velocity often precedes a routine diagnostic modality in the search for
the onset of symptoms by hours to days. aneurysms.65

blood flow that result from extracorporeal bypass

PRACTICAL TIPS
(a pumping technique that severely alters blood
• Increases in Doppler velocities parallel the flow physiology).66 Brain damage and perioperative
severity of a recent subarachnoid stroke may occur during extracorporeal bypass.
hemorrhage. TCD measurements have thrown considerable
• The side of the more severe blood flow doubt on the theory that such injury is caused by
velocity elevation tends to identify the site critical hypoperfusion. On the contrary, accidental
of hemorrhage. cerebral hyperperfusion may play a more decisive
• Elevations in TCD detected velocities can role, as well as air microemboli and loss of cerebral
precede the onset of symptoms. autoregulation. In addition, the frequency of
• Transcranial color-coded duplex cerebral microemboli detected with TCD during
sonography is not a reliable diagnostic test open heart surgery correlates with the degree of
for the detection of aneurysms that have neuropsychologic deficit.71,72
caused an active subarachnoid
hemorrhage.
PRACTICAL TIPS
• The M1 segment of the middle cerebral
Intraoperative monitoring artery is typically used for prolonged
Another ostensibly important application of TCD is intervals of TCD monitoring.
intraoperative monitoring. The unique advantages • TCD is typically used in open heart surgery
of TCD, in comparison with other cerebral blood with cardiopulmonary bypass and carotid
flow measurement techniques, are its complete endarterectomy.
noninvasiveness and its potential for detecting • TCD has shown that intraoperative air
rapid alterations in blood flow on a real-time microemboli are linked to postoperative
basis. TCD monitoring delivers direct, immedi- neuropsychologic deficits following open
ate information regarding cerebral perfusion, heart surgery with cardiopulmonary
thus anticipating potential hazards or permitting bypass.
rapid modification of therapy. TCD monitoring has • TCD changes in M1 segment velocities can
been used during carotid endarterectomy, open indicate the need for shunting during
heart surgery with cardiopulmonary bypass, and carotid endarterectomy.
intensive care therapy.12,66 In most studies, the M1
segment of the MCA is insonated at a depth of
50 to 55 mm. TCD monitoring can be performed Intensive care unit monitoring
either with repeated examinations at extremely TCD is a useful technique for monitoring critically
short intervals or continuously, using a headband ill patients in the intensive care unit.73 Eligible
to hold the transducer in place. patients are predominantly those with raised
Most experience with TCD monitoring has been intracranial pressure (e.g., after head injury) and
accumulated during carotid endarterectomy.67–69 It those with severe cerebrovascular occlusive disease,
has been shown that MCA flow is affected far less including cervical artery dissections.74,75 Monitoring
during intraoperative clamping of the carotid artery may also be informative, and possibly beneficial,
than expected, raising the possibility that shunts for the patient’s outcome in high-pressure and
are inserted too often. An MCA velocity of more low-pressure hydrocephalus and in low-flow states
than 10 cm/s during clamping has been associated associated with extracranial occlusive disease, heart
with adequate collateral circulation.69 It has further failure, or valvular disease, as well as impending
been shown that the amount of microembolization brain death. TCD monitoring may provide further
detected with TCD during the dissection and information about the pathophysiology of various
wound closure is predictive of postoperative abnormal conditions that affect intensive care
stroke.69 This online acoustic feedback from TCD patients and ultimately may be helpful for therapy.
signals has indicated that cerebral microembolism The use of TCD modified the diagnostic and thera-
is linked to surgical technique.70 peutic management in 36% of critically ill patients
TCD monitoring during open heart surgery has in one study.76 Although Aaslid and Lindegaard77
revealed a number of disturbances in cerebral have proposed certain TCD parameters that are

likely to reflect the cerebral perfusion pressure, hands TCD constitutes an accepted and reliable
and thus intracranial pressure, these parameters noninvasive diagnostic test to confirm brain death
have not yet been validated. Only a few TCCS by demonstrating the stoppage of the cerebral
studies have been conducted concerning critical circulation.82
care applications.78
PRACTICAL TIPS
PRACTICAL TIPS
• TCD has good accuracy in confirming
• TCD can be used to monitor patients with brain death.
raised intracranial pressure (e.g., after • Typical blood flow patterns include:
head injury) and those with severe • Reciprocating
cerebrovascular occlusive disease, including • Low amplitude systolic peaks
cervical artery dissections. • Absent flow signals
• Additional candidates are patients with
high-pressure and low-pressure
hydrocephalus and those with low-flow Arteriovenous malformations
states associated with extracranial and fistulas
occlusive disease, heart failure, or valvular Although an AVM is a developmental abnormality,
disease, as well as impending brain death. the arteries and veins involved in supplying blood
to the AVM are anatomically normal and are the
same arteries that supply the region of the brain
Brain death where the AVM is located. These arteries, which
The accurate diagnosis of brain death has become exclusively or partially feed AVMs, can unequivo-
more important in view of the ethical issues that cally be identified with TCD by means of their
surround the transplantation field. Determination significant blood flow abnormalities: (1) increased
of brain death was for a long time based on three blood flow velocity, (2) reduced pulsatility, and (3)
parameters: (1) clinical criteria, (2) electroencepha- reduced responsiveness to CO2.83 In a consecutive
lographic criteria, and (3) angiographic demon- series, more than 80% of large- to medium-sized
stration of absent intracranial circulation.79 The AVMs were detected, but more than 60% of smaller
arrest of intracranial flow results in a characteristic AVMs were missed with TCD.84 TCCS also allows
reflux phenomenon in the basal cerebral arteries the direct visualization of the AVM.60,63 For TCCS,
during late systole. This to-and-fro movement is a similar diagnostic sensitivity of 80% in the
easily noted in the TCD flow velocity waveform80 identification of AVMs was reported.85 In addition
(Fig. 10.19). In several large clinical studies, TCD to AVMs, other types of intracranial arteriovenous
findings correlated well with ancillary diagnostic shunts can be detected with TCD and TCCS, such
tests to confirm brain death, with few false-positive as carotid siphon–cavernous sinus fistulas or dural
and false-negative findings.81 Therefore in proper fistulas.60,86

60 25
Depth Depth

08 10
Mean Mean

Middle cerebral artery Common carotid artery

FIG. 10.19 Brain death. Transcranial Doppler changes are noted in the left middle cerebral and
extracranial common carotid arteries. The characteristic reflux phenomenon seen during late
systole is demonstrated.

PRACTICAL TIPS PRACTICAL TIPS—cont’d

• Blood flow patterns in the feeding artery • Criteria of thrombosis include:
of an AVM include: • Increased blood flow velocities
• Increased blood flow velocity • Direct visualization of the affected veins
• Decreased pulsatility and associated decreases in blood flow
• Reduced responsiveness to CO2 velocities
• Although sites of intraparenchymal
hemorrhage present as hyperechoic
Cerebral venous thrombosis and areas, this sign is not sensitive enough
intracerebral hemorrhage to be reliably used clinically.
Studies on healthy volunteers indicate that cerebral
sinuses and veins can be visualized in 50% to
90% of cases, depending on the vessel segment
examined.87 Preliminary data suggest that cerebral Microembolic signals/high intensity
venous thrombosis can be diagnosed using TCCS.88 transient signals
Ultrasonographic criteria are (1) abnormal eleva- The first reports on gaseous microemboli detected
tion of blood flow velocities within intracranial with ultrasound were published by Spencer and
sinuses and veins, and (2) direct visualization of colleagues93 in 1969 and were associated with
cerebral sinuses with decreased or absent flow. In a decompression sickness and open heart surgery.
recent study in patients suffering from thrombosis Since then, numerous experimental and clinical
of cerebral sinuses and veins, monitoring of venous studies have been published concerning micro-
hemodynamics was a significant predictor of the embolic signals (MES), including two consensus
long-term outcome.89 Direct visualization of the statements.10,94 The latter provide internationally
intracranial sinuses, however, requires significant accepted definitions of MES and cover major issues
expertise and, generally, the use of ultrasound involving TCD instrumentation and software
contrast agents. systems. The consensus opinions state that a
TCCS studies have shown that a sharply microembolic TCD signal must (1) be short in
demarcated, hyperechogenic area within the duration (<300 ms), (2) be at least 3 dB above the
brain tissue in stroke patients is indicative of background signal, (3) be mainly unidirectional
intracerebral hemorrhage.60,90 Although sensitiv- within the Doppler spectrum, and (4) produce
ity and specificity values were as high as 94% a characteristic sound (e.g., chirp, snap, moan).
and 95% in 133 consecutive stroke patients with Typical MES detected with TCD are illustrated in
sufficient temporal bone windows,91 TCCS still Fig. 10.20. It has been shown that the emboli
cannot replace computed tomographic or magnetic underlying MES are usually too small to elicit
resonance brain imaging in this cohort of patients. clinical symptoms. Nevertheless, there is now
Hemorrhagic transformation following thrombo- overwhelming evidence that MES possess clinical
lytic therapy of acute stroke has been detected and prognostic relevance in patients with various
with a sensitivity of 90% in one series.92 Thus sources of cardiac, arterial, or extracorporeal brain
ultrasound can serve as a complementary bedside embolism.95–99 Several studies have shown that the
technique to noninvasively monitor acute stroke amount of detected microemboli is a marker of
patients and their treatment effects but cannot stroke risk on an individual basis, thus serving as
replace radiologic brain imaging techniques as a a valuable surrogate parameter in clinical trials.99
prerequisite for thrombolytic therapy. In part, they also permit the monitoring of treat-
ment efficacy.100 MES detection represents a useful
tool for improving the stratification of individuals
PRACTICAL TIPS prone to cerebral embolic events and for evaluating
new primary and secondary prevention strategies
• In experienced hands, the venous sinuses
(Table 10.8). However, the procedure is time
and veins of the brain can be evaluated
consuming and needs the continuous presence
with TCCS facilitated by ultrasound
of a human observer. This limits the routine use
contrast agents.
of this technique.

cm/s indicator-dilution principles (see Chapter 35).102

This makes it possible to monitor the tissue
100 perfusion of the brain in patients suffering from
cerebrovascular disease during TCD examinations
performed at the bedside. Transtemporal brain
50
perfusion mapping can be achieved by combining
harmonic imaging techniques with an injection
of ultrasound contrast agent.9 In the first clinical
series reported on acute stroke patients, a positive
0
correlation was found between TCCS-derived brain
A perfusion maps and incident brain infarction.103,104
Ultrasound perfusion measurements have been
cm/s made with bolus tracking, a technique that
uses indicator-dilution principles to track signal
100
intensity after the injection of a bolus of contrast
agent creating time-intensity curves that can then
be processed mathematically.105 An alternative
60 approach, using refill kinetics during a constant
infusion of an ultrasound contrast agent has also
proven to be useful for brain perfusion measure-
ments.106 Automated brain perfusion measurements
0 have been evaluated in the clinical setting107 (Fig.
B 1 [s] 10.21). Limitations include the low spatial resolu-
FIG. 10.20 Illustrative examples of typical microembolic tion of TCCS systems used for ultrasound-based
signals (MES), detected with transcranial Doppler (TCD), brain perfusion measurements and the restricted
in a patient with artificial heart valves. These appear brain volume that can be investigated through
randomly within the systolic (A) or the diastolic (B) phase
of the Doppler spectrum (arrows). The origin of the MES
the temporal bone (one plane, limited access
and the maximum intensity elevation are always located to ipsilateral cortical tissue, limited signal from
within the Doppler spectrum; however, with strong contralateral side due to energy loss) that are
MES intensity gradients (mostly seen with systolic MES), impossible to circumvent. Therefore ultrasound
the upper edges and, rarely, also the lower edges, of the perfusion imaging is used only in the preclinical
signal may run off the Doppler spectrum. Note that the
intensity of the background TCD signal has to be decreased
stage and in experimental settings.
for MES monitoring (as seen) to allow for effective MES
identification.
PRACTICAL TIPS
• The administration of ultrasound contrast
PRACTICAL TIPS
agents can be used to evaluate cerebral
• MES/HITS associated with microemboli perfusion by use of either:
have the following characteristics: • Time-intensity curve analysis
• Short in duration (<300 ms) • Ultrasound tissue replenishment
• At least 3 dB above the background
signal
• Mainly unidirectional within the Doppler Sonothrombolysis
spectrum In 1942, Lynn and co-workers108 showed for the
• Produce a characteristic sound (e.g., first time that focused, in vivo ultrasound could
chirp, snap, moan) induce selective tissue damage without affecting the
surrounding areas. It is now well known that tissue
insonation may lead to various physiochemical
Ultrasound perfusion imaging tissue reactions, such as heating and denaturation,
Ultrasound contrast agents have opened the microstreaming effects, release of free radicals, and
possibility of ultrasound-mediated measure- alterations of blood cells and coagulation.11 The
ment of tissue perfusion, based on fundamental ability of ultrasound to augment the dissolution

TABLE 10.8 Amount and Clinical Relevance of Intracranially Circulating Microemboli

Detected by Transcranial Doppler.93–101
Prevalence of
Microembolic Prognostic
Clinical Collective Signals (Range; %) Impact Remarks
Normal probands 0 —
Acute ischemic stroke 9–71 (+) Higher MES load early after stroke;
Positive correlation to cause of stroke;
Subgroup of studies showed correlation
with short-term risk for recurrent stroke.
Carotid artery stenosis 2–29 + MES-positive patients showed higher rate of
Asymptomatic 18–100 cerebral ischemia;
Symptomatic More MES with higher degree of stenosis.
Intracranial artery stenosis 0 + MES-positive patients showed slightly higher
Asymptomatic 22–75 rate of cerebral ischemia;
Symptomatic More MES with short latency to recent
symptoms.
Acute dissection of 36–75 (+) In one study positive correlation of MES
brain-supplying prevalence to risk for recurrent cerebral
arteries ischemia
Aortic source of embolism 13–48 — Minor correlation to plaque thickness
Prosthetic heart valves 69–100 — High prevalence of cavitation-induced
gaseous microemboli without clinical or
prognostic impact;
No correlation to intensity of antihemostatic
treatment.
Left ventricular assist 28–100 (+) In part correlation of MES prevalence to risk
devices for recurrent cerebral ischemia;
No correlation to intensity of antihemostatic
treatment.
AF 15–40 (+) Higher MES prevalence in valvular than in
nonvalvular AF;
Higher MES prevalence in symptomatic AF
and in patients with recent cerebral
ischemia.
Interventions on brain- 38–100 — Mostly very high MES numbers without
supplying arteries clinical or prognostic impact
Open heart surgery 82–100 (+) Weak correlation of intraoperative MES load
to postoperative neuropsychologic
deficits

AF, Atrial fibrillation; MES, microembolic signal.

Prognostic impact: —, denotes no evidence; (+), minor/inconsistent evidence; +, clear evidence that has been confirmed and reproduced in
several studies.

of thrombus was first reported in 1989 by Kodo.109 been demonstrated.110 It is now believed that not
This capability has been confirmed by numerous macrostructural (e.g., clot disruption) but rather
experimental studies using in vitro and animal microstructural alterations (e.g., dysconfiguration
models.110,111 It has been shown that the insonation of fibrin molecules) are mainly responsible for
of thrombus alone112 or in combination with the sonothrombolytic effect, via a microcavitation
fibrinolytic agents113 significantly accelerates the process. In addition to several clinical studies in
thrombolytic process. This effect has been termed patients suffering from acute coronary syndromes,
ultrasound-assisted thrombolysis or sonothrombolysis. the first reports on successful sonothrombolysis
Using a variety of ultrasound frequencies (20 kHz in acute stroke patients have been published.114,115
to 3 MHz) and intensities (3 to 8 mW/cm2), a clear Sonothrombolysis is a very exciting, novel tool
dose-effect relationship of this phenomenon has that may increase the efficacy of the purely

PPI
2.5 h
B

TTP

A 4h C 180 h

FIG. 10.21 This figure shows corresponding axial planes of the computed tomographic (CT) scan
and the ultrasound perfusion imaging of a 70-year-old patient with middle cerebral artery infarction
(National Institutes of Health Stroke Scale [NIHSS]: 12). (A) Ultrasound perfusion studies were
done following a 2.5-mL SonoVue bolus injection as contrast agent. Ultrasound perfusion studies
are presented as pixelwise peak intensity (PPI) and time to peak intensity (TTP) maps. PPI is coded
as 0% to 100%, TTP as 0 to 20 seconds (color coded as levels of blue). CT scans were obtained
2.5 hours (B) and 180 hours (C) after symptom onset. The corresponding field of view of the
ultrasound perfusion studies is projected as a white frame over the CT scans.

pharmacologic approach of thrombolysis in

acute stroke and may be of use in regions without Detection of right-to-left shunts
access to endovascular interventions. Acceleration Overall, right-to-left shunts due to a patent foramen
of intracranial vessel recanalization could reduce ovale (PFO) are relatively common with a preva-
final cerebral infarct size and therefore improve lence near to 25% in the general population.119 A
the long-term outcome115,116 of stroke patients. The PFO is a risk factor for cryptogenic strokes in young
effect of sonothrombolysis can be enhanced by adults of ≤55 years of age.119 Transthoracic and
microbubble-induced cavitation.117,118 However, transesophageal echocardiography have been used
safety issues concerning the risk for intracerebral in the noninvasive evaluation of possible right-
hemorrhage are still under investigation. to-left shunts.120,121 TCD can also reveal evidence
of right-to-left shunts by detecting the presence
PRACTICAL TIPS of MES following the injection of microbubbles,
typically created by agitation of air with saline
• Sonothrombolysis uses sound waves of
in a syringe.122 Agitated saline does not normally
different frequencies to accelerate the
cross the pulmonary circulation into the arterial
effects of thrombolytic agents for
system (Fig. 10.22). The advantage of TCD is the
dissolving blood clots.
ability to perform the test at rest and during a
• Efficacy has been shown in multiple trials.
provocative test such as a Valsalva maneuver.122 A
• The effects of ultrasound can be enhanced
meta-analysis suggests that TCD might be more
by the administration of microbubbles
sensitive than echocardiography.123 At the very least,
(ultrasound contrast agents).
TCD offers a diagnostic option in the work-up
• Use may increase the risk of intracranial
of young adults suspected of having cryptogenic
hemorrhage.
stroke.

A B

C D
FIG. 10.22 This composite figure shows the effect of an injection of agitated saline in a patient
with a patent foramen ovale. (A) Baseline transcranial Doppler signals before the injection. (B)
Early arrival of the gas bubbles causes a series of prominent high intensity transient (microembolic)
signals on the tracing. (C) This progresses to a “curtain” or “shower” of color at 14 seconds. (D)
Some residual embolic signals persist late after the injection.

Recent trials comparing the value of patent

PRACTICAL TIPS—cont’d
foramen closure with medical treatment for stroke
prevention suggest a benefit for PFO closure.124 • Agitated saline does not normally cross
This may increase the role of the bubble test in into the systemic arterial circulation.
the diagnostic work-up of cryptogenic stroke. • A repeat injection can be easily
performed during a provocative test
such as the Valsalva maneuver.

PRACTICAL TIPS
Transcranial sonography
• PFO may be the source of cryptogenic (parenchyma ultrasound)
strokes in young adults.
In 1995, it was reported that patients with Par-
• TCD can confirm the diagnosis by showing
kinson disease (PD) showed a marked hyper-
the presence of microembolic signals in
echogenicity within the brainstem on transcranial
the intracranial circulation following the
B-mode ultrasound.125 The hyperechogenic area
injection of agitated saline.
corresponds to the substantia nigra and the
• Detection of a PFO with an agitated saline
changes were seen only on ultrasound images but
solution is facilitated by the fact that:
not on magnetic resonance or computed

tomographic images. Since then, a considerable

PRACTICAL TIPS—cont’d
number of papers described changes of B-mode
ultrasound in varying types of movement disor- • Offer some insights into pathological
ders.21 Meanwhile, the technique has gained changes within the brain of patients
acceptance and can be used to identify patients with movement disorders
at risk of Parkinson syndromes, to establish the
risk for symptomatic disease, and to differentiate
idiopathic PD from other Parkinson syndromes.21 Summary
In addition to the echogenic appearance of the
substantia nigra of the brainstem, other areas of Through continuous refinements and techni-
the brain can be used to establish a differential cal innovations during the past three decades,
diagnosis. These include structures easily visualized transcranial ultrasound is no longer limited to the
through the transtemporal window: the width of sonographic measurement of blood flow velocities.
the third ventricle, the echogenicity of the lenticular Today, transcranial ultrasound offers multimodal,
nucleus, the echogenicity of the Raphe, and the high-resolution, and real-time imaging of the
width of the cella media. The major limitation of brain’s structure and vasculature. Using modern
the investigation is in fact the quality of the bone equipment and a variety of ultrasound modali-
window, such that in patients with good insonation ties, information can be acquired about anatomy,
conditions, the reliability and the accuracy of the hemodynamic status, and function of the central
method is quite high. nervous system and its supplying arteries and
veins (Table 10.9). Nevertheless, TCD and TCCS
PRACTICAL TIPS remain portable, easy-to-access, dynamic, highly
reliable, and reproducible techniques in clinical
• Direct imaging of the brain parenchyma
medicine that support various therapeutic deci-
can:
sions. Noninvasiveness further advocates the use
• Help identify the landmarks where the
of TCD as a monitoring tool, particularly during
major intracranial arteries lie
surgical or neurointerventional procedures. Overall,

TABLE 10.9 Main Indications for Vascular Transcranial Doppler and Transcranial Color-
Coded Duplex Sonography in Clinical and Experimental Settings.
1. Detection of intracranial stenoses and occlusions in the major basal arteries.
2. Evaluation of intracranial hemodynamic effects and collateral flow of extracranial occlusive disease (e.g.,
occlusions, subclavian steal).
3. Monitoring of intracranial vessel recanalization in acute stroke.
4. Monitoring of intracranial cerebral hemodynamics:
a. After subarachnoid hemorrhage (e.g., presence and severity of vasospasms)
b. In patients with increased intracranial pressure (e.g., on the intensive care unit)
c. During and after extracranial revascularization procedures (e.g., carotid endarterectomy, endovascular
carotid stent placement)
d. Before and during neuroradiologic interventions (e.g., balloon occlusion) for presence of collateral
pathways
e. During open heart surgery
f. In the evaluation of brain death
5. Detection and quantification of cerebral circulating microemboli.
6. Detection and quantification of right-to-left shunts.
7. Functional tests:
a. Stimulation of intracranial arterioles with carbon dioxide or other vasoactive drugs (e.g., assessing
vasomotor reserve capacity)
b. Language lateralization (e.g., before neurosurgery)
c. External stimulation of visual cortex
8. Still under investigation:
a. Brain perfusion imaging
b. Ultrasound-assisted thrombolysis

transcranial ultrasound with TCD and TCCS has 14. Aaslid R, Markwalder TM, Nornes H. Noninvasive
transcranial Doppler ultrasound recording of flow veloc-
improved our understanding of cerebrovascular
ity in the basal cerebral arteries. Journal of Neurosurgery.
disease. TCD and TCCS play important roles in the 1982;57:769.
diagnostic work-up of cerebrovascular disorders. In 15. Arnolds B, von Reutern GM. Transcranial Doppler
most countries, TCD and TCCS are in the hands sonography: examination technique and normal reference
of physicians and technicians with neurologic values. Ultrasound in Medicine and Biology. 1986;12:115.
16. White DN, Curry GR, Stevenson RJ. The acoustic charac-
training who deal appropriately and carefully with
teristics of the skull. Ultrasound in Medicine and Biology.
its capabilities and limitations. However, we must 1978;4:225.
be aware that all these methods require sufficient 17. Grolimund P. Transmission of ultrasound through the
knowledge, practical skills, and technical expertise. temporal bone. In: Aaslid R, ed. Transcranial Doppler
In other words, we have to ensure continuous Sonography. New York: Springer-Verlag; 10.
18. Aaslid R, ed. Transcranial Doppler Sonography. New York:
education and adequate training in the fascinating
Springer-Verlag; 39.
field of neurosonology. 19. Ringelstein EB, et al. Transcranial Doppler sonography.
Anatomical landmarks and normal velocity values.
Ultrasound in Medicine and Biology. 1990;16:745–761.
REFERENCES 20. Bäuerle J, Nedelmann M. Sonographic assessment of the
1. Miyazaki M, Kato K. Measurement of cerebral blood optic nerve sheath in idiopathic intracranial hypertension.
flow by ultrasonic Doppler technique. Japanese Circulation Journal of Neurology. 2011;258:2014.
Journal. 1965;29:375. 21. Berg D, Godau J, Walter U. Transcranial sonography in
2. Aaslid R, Markwalder TM, Norris H. Noninvasive movement disorders. The Lancet. Neurology. 2008;7:1044.
transcranial Doppler ultrasound recording of flow 22. Mast H, Ecker S, Marx P. Cerebral ischemia induced by
velocity in basal cerebral arteries. Journal of Neurosurgery. compression tests during transcranial Doppler sonogra-
1982;57:769. phy. The Clinical Investigator. 1993;71:46.
3. Bogdahn U, et al. Transcranial color-coded real-time 23. Khaffaf N, et al. Embolic stroke by compression maneuver
sonography in adults. Stroke; a Journal of Cerebral Circula- during transcranial Doppler sonography. Stroke; a Journal
tion. 1990;21:1680. of Cerebral Circulation. 1994;25:1056.
4. Bude RO, Rubin JM, Adler RS. Power versus conventional 24. Hennerici M, et al. Transcranial Doppler ultrasound for
color Doppler sonography: comparison in the depiction the assessment of intracranial arterial flow velocity—part
of normal intrarenal vasculature. Radiology. 1994;192: I. Examination technique and normal values. Surgical
777. Neurology. 1987;27:439.
5. Klötzsch C, et al. Contrast-enhanced three-dimensional 25. Grolimund P, Seiler RW. Age dependence of the flow
transcranial color-coded sonography of intra-cranial velocity in the basal arteries—a transcranial Doppler
stenoses. AJNR. 2002;23:208. ultrasound study. Ultrasound in Medicine and Biology.
6. Otis S, Rush M, Boyajian R. Contrast-enhanced transcranial 1988;14:191.
imaging. Results of an American phase-two study. Stroke; 26. Frackowiak RSJ, Lenzi GL, Jones T. Quantitative measure-
a Journal of Cerebral Circulation. 1995;26:203. ments of cerebral blood flow and oxygen metabolism in
7. Nabavi DG, et al. Diagnostic benefit of echocontrast man using 15-oxygen and positron emission tomography.
enhancement for the insufficient transtemporal bone Theory, procedure and normal values. Journal of Computer
window. Journal of Neuroimaging. 1999;9:102. Assisted Tomography. 1980;4:727.
8. Jauss M, Zanette E. Detection of right-to-left shunt with 27. Schöning M, Buchholz R, Walter J. Comparative study
ultrasound contrast agent and transcranial Doppler of transcranial color duplex sonography and transcranial
sonography. Cerebrovascular Diseases. 2000;10:490. Doppler sonography in adults. Journal of Neurosurgery.
9. Wiesmann M, Seidel G. Ultrasound perfusion imaging of 1993;78:776–784.
the human brain. Stroke; a Journal of Cerebral Circulation. 28. Baumgartner RW, et al. A validation study on the
2000;31:2421. intraobserver reproducibility of transcranial color-coded
10. Ringelstein EB, et al. Consensus on microembolus duplex sonography velocity measurements. Ultrasound in
detection by TCD. International Consensus Group on Medicine and Biology. 1994;20:233.
Microembolus Detection. Stroke; a Journal of Cerebral 29. Ringelstein EB, et al. Noninvasive assessment of CO2-
Circulation. 1998;29:725. induced cerebral vasomotor response in normal individu-
11. Francis CW, Behrens S. Ultrasonic thrombolysis. In: als and patients with internal carotid artery occlusions.
Hennerici M, Meairs S, eds. Cerebrovascular Ultrasound. Stroke; a Journal of Cerebral Circulation. 1988;19:963.
Theory, Practice and Future Developments. Cambridge, UK: 30. Huber P, Handa J. Effect of contrast material, hypercapnia,
Cambridge University Press. hyperventilation, hypertonic glucose and papaverine
12. Ringelstein EB. A practical guide to transcranial Doppler on the diameter of the cerebral arteries—angiographic
sonography. In: Weinberger J, ed. Noninvasive Imaging of determination in man. Investigative Radiology. 1987;2:17.
Cerebral Vascular Disease. New York: AR Liss; 75. 31. Markwalder TM, et al. Dependency of blood flow velocity
13. Spencer MP, Whisler D. Transorbital Doppler diagnosis of in the middle cerebral artery on end-tidal carbon dioxide
intracranial arterial stenosis. Stroke; a Journal of Cerebral partial pressure—a transcranial ultrasound Doppler study.
Circulation. 1986;17:916. Journal of Cerebral Blood Flow and Metabolism: Official

Journal of the International Society of Cerebral Blood Flow tool for future stroke trials. Stroke; a Journal of Cerebral
and Metabolism. 1984;4:368. Circulation. 2000;31:2342.
32. Ringelstein EB, Otis SM, Schneider PA. Noninvasive 48. Seidel G, Kaps M, Gerriets T. Potential and limitations
assessment of CO2-induced cerebral vasomotor reactiv- of transcranial color-coded sonography in stroke
ity. Comparison with rCBF findings during 133-xenon patients. Stroke; a Journal of Cerebral Circulation. 1995;26:
inhalation measurement. Journal of Cerebral Blood Flow 2061.
and Metabolism: Official Journal of the International Society 49. Kenton AR, et al. Comparison of transcranial color-coded
of Cerebral Blood Flow and Metabolism. 1989;1:161. sonography and magnetic resonance angiography in acute
33. Gosling RG, King DH. Arterial assessment by Doppler-shift stroke. Stroke; a Journal of Cerebral Circulation. 1997;
ultrasound. Proceedings of the Royal Society of Medicine. 28:1601.
1974;67:447. 50. Nabavi DG, et al. Potential and limitations of
34. Ley-Pozo J, Willmes K, Ringelstein EB. Relationship echocontrast-enhanced ultrasonography in acute stroke
between pulsatility indices of Doppler flow signals patients: a pilot study. Stroke; a Journal of Cerebral Circula-
and CO2-reactivity within the middle cerebral artery in tion. 1998;29:949.
extracranial occlusive disease. Ultrasound in Medicine and 51. Postert T, et al. Contrast-enhanced transcranial color-
Biology. 1990;16:763. coded real-time sonography: a reliable tool for the
35. Niederkorn R, Neumayer K. Transcranial Doppler diagnosis of middle cerebral artery trunk occlusion in
sonography: a new approach in the noninvasive diagnosis patients with insufficient temporal bone window. Stroke;
of intracranial brain artery disease. European Neurology. a Journal of Cerebral Circulation. 1998;29:1070.
1987;26:65. 52. Stolz E, et al. Can early neurosonology predict outcome
36. de Bray JM, et al. Detection of vertebrobasilar intra- in acute stroke?: a metaanalysis of prognostic clinical
cranial stenoses: transcranial Doppler sonography versus effect sizes related to the vascular status. Stroke; a Journal
angiography. Journal of Ultrasound in Medicine. 1997;16: of Cerebral Circulation. 2008;39:2355.
213. 53. Nedelmann M, et al. Consensus recommendations for
37. Felberg RA, et al. Screening for intracranial stenosis with transcranial color-coded duplex sonography for the
transcranial Doppler: the accuracy of mean flow velocity assessment of intracranial arteries in clinical trials on
thresholds. Journal of Neuroimaging. 2002;12:9. acute stroke. Stroke; a Journal of Cerebral Circulation. 2009;
38. Rorick MB, Nichols FT, Adams RJ. Transcranial Doppler 40:3238.
correlation with angiography in detection of intra- 54. Anzola GP, et al. Transcranial Doppler sonography and
cranial stenosis. Stroke; a Journal of Cerebral Circulation. magnetic resonance angiography in the assessment of
1931;25:1994. collateral hemispheric flow in patients with carotid
39. Demchuk AM, et al. Accuracy and criteria for localizing artery disease. Stroke; a Journal of Cerebral Circulation.
arterial occlusion with transcranial Doppler. Journal of 1995;26:214.
Neuroimaging. 2000;10:1. 55. Baumgartner RW, et al. Transcranial color-coded duplex
40. Demchuk AM, et al. Thrombolysis in brain ischemia sonography in the evaluation of collateral flow through
(TIBI) transcranial flow grades predict clinical severity, the circle of Willis. AJNR. American Journal of Neuroradiol-
early recovery, and mortality in patients treated with ogy. 1997;18:127.
intravenous tissue plasminogen activator. Stroke; a Journal 56. Caplan LR, Sergay S. Positional cerebral ischemia. Journal
of Cerebral Circulation. 2001;32:89. of Neurology, Neurosurgery, and Psychiatry. 1976;39:385.
41. Saqqur M, et al, CLOTBUST Investigators. Residual flow at 57. Ringelstein EB, et al. The pathogenesis of strokes from
the site of intracranial occlusion on transcranial Doppler internal carotid artery occlusion: diagnostic and therapeu-
predicts response to intravenous thrombolysis: a multi- tic implications. Stroke; a Journal of Cerebral Circulation.
center study. Cerebrovascular Diseases. 2009;27:5. 1983;14:867.
42. Schwartz A, Hennerici M. Noninvasive transcranial 58. Harders A, Gilsbach JM. Time course of blood velocity
Doppler ultrasound in intracranial angiomas. Neurology. changes related to vasospasm in the circle of Willis
1986;36:626. measured by transcranial Doppler ultrasound. Journal
43. Aaslid R, et al. Evaluation of cerebrovascular spasm with of Neurosurgery. 1987;66:718.
transcranial Doppler ultrasound. Journal of Neurosurgery. 59. Seiler RW, et al. Cerebral vasospasm evaluated by
1984;60:37. transcranial ultrasound correlated with clinical grade
44. Ringelstein EB, et al. Type and extent of hemispheric and CT-visualized subarachnoid hemorrhage. Journal of
brain infarctions and clinical outcome in early and Neurosurgery. 1986;64:594.
delayed middle cerebral artery recanalization. Neurology. 60. Baumgartner RW. Transcranial color duplex sonography
1992;42:289. in cerebrovascular disease: a systematic review. Cerebro-
45. Brandt T, et al. CT angiography and Doppler sonography vascular Diseases. 2003;16:4.
for emergency assessment in acute basilar artery ischemia. 61. Proust F, et al. Usefulness of transcranial color-coded
Stroke; a Journal of Cerebral Circulation. 1999;30:606. sonography in the diagnosis of cerebral vasospasm. Stroke;
46. Baumgartner RW, Mattle HP, Schroth G. Assessment of a Journal of Cerebral Circulation. 1999;30:1091.
≥50% and <50% intracranial stenoses by transcranial 62. Becker G, et al. Diagnosis and monitoring of subarach-
color-coded duplex sonography. Stroke; a Journal of noid hemorrhage by transcranial color-coded real-time
Cerebral Circulation. 1999;30:87. sonography. Neurosurgery. 1991;28:814.
47. Gerriets T, et al. DIAS I: duplex-sonographic assessment 63. Martin PJ, et al. Intracranial aneurysms and arteriovenous
of the cerebrovascular status in acute stroke. A useful malformations: transcranial colour-coded sonography

as a diagnostic aid. Ultrasound in Medicine and Biology. 81. de Freitas GR, et al. Sensitivity of transcranial Doppler
1994;20:689. for confirming brain death: a prospective study of 270
64. Wardlaw JM, Cannon JC, Sellar RJ. Use of color power cases. Acta Neurologica Scandinavica. 2006;113:426.
transcranial Doppler sonography to monitor aneurysmal 82. Wijdicks EF. The diagnosis of brain death. The New England
coiling. AJNR. 1996;17:864. Journal of Medicine. 2001;344:1215.
65. Klötzsch C, Harrer JU. Cerebral aneurysms and 83. Diehl RR, et al. Blood flow velocity and vasomotor
arteriovenous malformations. Frontiers of Neurology and reactivity in patients with arteriovenous malformations:
Neuroscience. 2006;21:171. a transcranial Doppler study. Stroke; a Journal of Cerebral
66. von Reutern GM, et al. Transcranial Doppler ultrasonog- Circulation. 1994;25:1574.
raphy during cardiopulmonary bypass in patients with 84. Mast H, et al. Transcranial Doppler ultrasonography in
severe carotid stenosis or occlusion. Stroke; a Journal of cerebral arteriovenous malformations. Diagnostic sensitiv-
Cerebral Circulation. 1989;19:674. ity and association of flow velocity with spontaneous
67. Schneider PA, et al. Transcranial Doppler monitor- hemorrhage and focal neurological deficit. Stroke; a Journal
ing during carotid arterial surgery. Surgical Forum. of Cerebral Circulation. 1995;26:1024.
1987;38:333. 85. el Saden SM, et al. Transcranial color Doppler imaging
68. Padayachee TS, et al. Monitoring middle cerebral artery of brain arteriovenous malformations in adults. Journal
blood velocity during carotid endarterectomy. The British of Ultrasound in Medicine. 1997;16:327.
Journal of Surgery. 1986;73:98. 86. Sommer C, et al. Noninvasive assessment of intracranial
69. Ackerstaff RG, et al. Association of intraoperative fistulas and other small arteriovenous malformations.
transcranial Doppler monitoring variables with stroke Neurosurgery. 1992;30:522–528.
from carotid endarterectomy. Stroke; a Journal of Cerebral 87. Stolz E, et al. Transcranial color-coded duplex sonography
Circulation. 2000;31:1817. of intracranial veins and sinuses in adults. Reference
70. Jansen C, et al. Carotid endarterectomy with transcranial data from 130 volunteers. Stroke; a Journal of Cerebral
Doppler and electroencephalographic monitoring: a Circulation. 1999;30:1070.
prospective study in 130 operations. Stroke; a Journal of 88. Stolz E, Kaps M, Dorndorf W. Assessment of intracranial
Cerebral Circulation. 1993;24:665. venous hemodynamics in normal individuals and patients
71. Barbut D, et al. Determination of size of aortic emboli and with cerebral venous thrombosis. Stroke; a Journal of
embolic load during coronary artery bypass grafting. The Cerebral Circulation. 1999;30:70.
Annals of Thoracic Surgery. 1997;63:1262. 89. Stolz E, et al. Intracranial venous hemodynamics is a
72. Braekken SK, et al. Association between intraoperative factor related to a favorable outcome in cerebral venous
cerebral microembolic signals and postoperative neuro- thrombosis. Stroke; a Journal of Cerebral Circulation. 1645;
psychological deficit: comparison between patients with 33:2002.
cardiac valve replacement and patients with coronary 90. Seidel G, Kaps M, Dorndorf W. Transcranial color-coded
artery bypass grafting. Journal of Neurology, Neurosurgery, duplex sonography of intracerebral hematomas in adults.
and Psychiatry. 1998;65:573. Stroke; a Journal of Cerebral Circulation. 1519;24:1993.
73. Alvarez del Castillo M. Monitoring neurologic patients in 91. Maurer M, et al. Differentiation between intracerebral
intensive care. Current Opinion in Critical Care. 2001;7:49. hemorrhage and ischemic stroke by transcranial color-
74. Babikian VL, et al. Transcranial Doppler sonographic coded duplex-sonography. Stroke; a Journal of Cerebral
monitoring in the intensive care unit. Journal of Intensive Circulation. 1998;29:2563.
Care Medicine. 1991;6:36. 92. Seidel G, et al. Sonographic evaluation of hemorrhagic
75. Dittrich R, et al. Polyarterial clustered recurrence of transformation and arterial recanalization in acute
cervical artery dissection seems to be the rule. Neurology. hemispheric ischemic stroke. Stroke; a Journal of Cerebral
2007;69:180–186. Circulation. 2009;40:199.
76. Grupo de Trabajo de Neurointensivismo y Trauma de 93. Spencer MP, et al. The use of ultrasonics in the determina-
la Sociedad Espanola de Medicina Intensiva, Critica y tion of arterial aeroembolism during open-heart surgery.
Unidades Coronarias (SEMICYUC); Grupo de Trabajode The Annals of Thoracic Surgery. 1969;8:489.
Neurologia Critica de la Societat Catalana de Medicina 94. Consensus Committee of the Ninth International Cerebral
Intensiva i Critics (SOCMIC). Clinical use of transcranial Hemodynamic Symposium. Basic identification criteria
Doppler in critical neurological patients. Results of a of Doppler microembolic signals. Stroke; a Journal of
multicenter study. Medicina Clinica. 2003;120:241. Cerebral Circulation. 1995;26:1123.
77. Aaslid R, Lindegaard KF. Cerebral hemodynamics. In: 95. Droste DW, Ringelstein EB. Detection of high intensity
Aaslid R, ed. Transcranial Doppler Sonography. New York: transient signals (HITS): how and why? European Journal
Springer-Verlag; 60. of Ultrasound. 1998;7:23.
78. Shiogai T, et al. Morphological and hemodynamic evalu- 96. Nabavi DG, Sliwka U. Mikroembolusdetektion mittels
ations by means of transcranial power Doppler imaging transkranieller Dopplersonographie. Klin Neurophysiol.
in patients with severe head injury. Acta Neurochirurgica. 1999;30:275.
Supplementum. 1998;71:94. 97. Ritter MA, et al. Prevalence and prognostic impact of
79. Black PM. Brain death. Medical progress. The New England microembolic signals in arterial sources of embolism. A
Journal of Medicine. 1978;299:338. systematic review of the literature. Journal of Neurology.
80. Marinoni M, et al. The relevance of early TCD monitoring 2008;255:953.
in the intensive care units for the confirming of brain 98. King A, Markus HS. Doppler embolic signals in cerebro-
death diagnosis. Neurological Sciences. 2011;32:73. vascular disease and prediction of stroke risk: a systematic

review and meta-analysis. Stroke; a Journal of Cerebral 113. Lauer CG, et al. Effect of ultrasound on tissue-type
Circulation. 2009;40:3711. plasminogen activator-induced thrombolysis. Circulation.
99. Markus HS, et al. Dual antiplatelet therapy with 1992;86:1257.
clopidogrel and aspirin in symptomatic carotid stenosis 114. Alexandrov AV, et al. High rate of complete recanalization
evaluated using Doppler embolic signal detection. The and dramatic clinical recovery during tPA infusion when
Clopidogrel and Aspirin for Reduction of Emboli in continuously monitored with 2-MHz transcranial Doppler
Symptomatic Carotid Stenosis (CARESS) trial. Circulation. monitoring. Stroke; a Journal of Cerebral Circulation. 2000;
2005;111:2233–2240. 31:610.
100. Goertler M, et al. Rapid decline of cerebral microemboli 115. Eggers J, et al. Effect of ultrasound on thrombolysis of
of arterial origin after intravenous acetylsalicylic acid. middle cerebral artery occlusion. Annals of Neurology.
Stroke; a Journal of Cerebral Circulation. 1999;30:66–69. 2003;53:797.
101. Spencer MP, et al. Detection of middle cerebral artery 116. Eggers J, et al. Sonothrombolysis with transcranial
emboli during carotid endarterectomy using transcranial color-coded sonography and recombinant tissue-type
Doppler ultrasonography. Stroke; a Journal of Cerebral plasminogen activator in acute middle cerebral artery
Circulation. 1990;21:415. main stem occlusion: results from a randomized study.
102. Meier P, Zierler KL. On the theory of the indicator-dilution Stroke; a Journal of Cerebral Circulation. 2008;39:1470.
method for measurement of blood flow and volume. J 117. Alexandrov AV, et al. A pilot randomized clinical
Appl Physiol (1985). 1954;6:731. safety study of sonothrombolysis augmentation with
103. Federlein J, et al. Ultrasound evaluation of pathological ultrasound-activated perflutren-lipid microspheres for
brain perfusion in acute stroke using second harmonic acute ischemic stroke. Stroke; a Journal of Cerebral Circula-
imaging. Journal of Neurology, Neurosurgery, and Psychiatry. tion. 2008;39:1464.
2002;69:616. 118. Molina CA, et al. Microbubble administration acceler-
104. Meyer K, et al. Harmonic imaging in acute stroke: detec- ates clot lysis during continuous 2-MHz ultrasound
tion of a cerebral perfusion deficit with ultrasound and monitoring in stroke patients treated with intravenous
perfusion MRI. Journal of Neuroimaging. 2003;13:166. tissue plasminogen activator. Stroke; a Journal of Cerebral
105. Bolognese M, et al. Real-time ultrasound perfusion Circulation. 2006;37:425.
imaging in acute stroke: assessment of cerebral perfusion 119. Saver JL. Clinical practice. Cryptogenic stroke. The New
deficits related to arterial recanalization. Ultrasound in England Journal of Medicine. 2016;374:2065.
Medicine & Biology. 2013;39:745. 120. Fraker TD Jr, et al. Detection and exclusion of inter-
106. Kern R, et al. Real-time ultrasound brain perfusion atrial shunts by two-dimensional echocardiography
imaging with analysis of microbubble replenishment and peripheral venous injection. Circulation. 1979;59:
in acute MCA stroke. Journal of Cerebral Blood Flow & 379.
Metabolism. 2011;31:1716. 121. Bourdillon PD, Foale RA, Rickards AF. Identification of
107. Maciak A, et al. Automatic detection of perfusion deficits atrial septal defects by cross-sectional contrast echocar-
with Bolus Harmonic Imaging. Ultraschall in Der Medizin diography. British Heart Journal. 1980;44:401.
(Stuttgart, Germany: 1980). 2008;29:618. 122. Teague SM, Sharma MK. Detection of paradoxical cerebral
108. Lynn JG, et al. A new method for the generation and echo contrast embolization by transcranial Doppler
use of focused ultrasound in experimental biology. The ultrasound. Stroke; a Journal of Cerebral Circulation. 1991;
Journal of General Physiology. 1942;26:179. 22:740.
109. Kudo S. Thrombolysis with ultrasound effect. Tokyo Jikeikai 123. Katsanos AH, et al. Transcranial Doppler versus trans-
Med J. 1989;104:1005. thoracic echocardiography for the detection of patent
110. Ishibashi T, et al. Can transcranial ultrasonication increase foramen ovale in patients with cryptogenic cerebral
recanalization flow with tissue plasminogen activator? ischemia: a systematic review and diagnostic test accuracy
Stroke; a Journal of Cerebral Circulation. 2002;33:1399. meta-analysis. Annals of Neurology. 2016;79:625.
111. Eggers J, Ossadnik S, Seidel G. Enhanced clot dissolution 124. Sondergaard L, et al. Patent foramen ovale closure or
in vitro by 1.8-MHz pulsed ultrasound. Ultrasound in antiplatelet therapy for cryptogenic stroke. The New
Medicine and Biology. 2009;35:523. England Journal of Medicine. 2017;377:1033.
112. Rosenschein U, et al. Ultrasound imaging-guided non- 125. Becker G, et al. Degeneration of substantia nigra in chronic
invasive ultrasound—thrombolysis: preclinical results. Parkinson’s disease visualized by transcranial color-coded
Circulation. 2000;102:238. real-time sonography. Neurology. 1995;45:182.

How To Perform and Interpret A DTC
No ratings yet
How To Perform and Interpret A DTC
7 pages
Ringelstein Et Al. - 1990 - Transcranial Doppler Sonography Anatomical Landma
No ratings yet
Ringelstein Et Al. - 1990 - Transcranial Doppler Sonography Anatomical Landma
17 pages
Doppler Transcraneal 1
No ratings yet
Doppler Transcraneal 1
14 pages
Transcranial Color-Coded Duplex Ultrasonography in
No ratings yet
Transcranial Color-Coded Duplex Ultrasonography in
6 pages
Practice Standards For Transcranial Dopp
No ratings yet
Practice Standards For Transcranial Dopp
8 pages
Transcranial Doppler Ultrasonography in Intensive Care: Original Article
No ratings yet
Transcranial Doppler Ultrasonography in Intensive Care: Original Article
7 pages
127 Williams
No ratings yet
127 Williams
9 pages
TCD Neurovascular
100% (1)
TCD Neurovascular
13 pages
Transcranial Dopler
No ratings yet
Transcranial Dopler
16 pages
Neuro-Ultrasonography 2020
No ratings yet
Neuro-Ultrasonography 2020
15 pages
Transcranial Doppler Ultrasonography in Anesthesia and Neurosurgery
No ratings yet
Transcranial Doppler Ultrasonography in Anesthesia and Neurosurgery
19 pages
Usg Cerebral Icm 2019
No ratings yet
Usg Cerebral Icm 2019
15 pages
Brain Ultrasonography: Methodology, Basic and Advanced Principles and Clinical Applications. A Narrative Review
No ratings yet
Brain Ultrasonography: Methodology, Basic and Advanced Principles and Clinical Applications. A Narrative Review
15 pages
Transcranial Doppler: An Introduction For Primary Care Physicians
No ratings yet
Transcranial Doppler: An Introduction For Primary Care Physicians
7 pages
0007RRCT PDF
No ratings yet
0007RRCT PDF
10 pages
TCD Presentation
No ratings yet
TCD Presentation
43 pages
Doppler Syme
No ratings yet
Doppler Syme
12 pages
Transcranial Doppler
No ratings yet
Transcranial Doppler
3 pages
Transcranial Doppler For Evaluation of Cerebral Autoregulation
No ratings yet
Transcranial Doppler For Evaluation of Cerebral Autoregulation
15 pages
Doppler Transcreaneal y Ecografía Del Nervio Óptico
No ratings yet
Doppler Transcreaneal y Ecografía Del Nervio Óptico
15 pages
Transcranial Doppler for Technologists
No ratings yet
Transcranial Doppler for Technologists
15 pages
Neurosonology in Acute Ischemic Stroke
No ratings yet
Neurosonology in Acute Ischemic Stroke
36 pages
1 s2.0 S0306452221001214 Main
No ratings yet
1 s2.0 S0306452221001214 Main
12 pages
Purkayastha 2012 Semin Neurology TCDReview
No ratings yet
Purkayastha 2012 Semin Neurology TCDReview
11 pages
TCCD For Fnvac
No ratings yet
TCCD For Fnvac
30 pages
Intracranial Pressure
No ratings yet
Intracranial Pressure
11 pages
Transcranial Doppler Ultrasound Examination For Adults and Children
No ratings yet
Transcranial Doppler Ultrasound Examination For Adults and Children
12 pages
Dev Med Child Neurol. 2024 Jun 28
No ratings yet
Dev Med Child Neurol. 2024 Jun 28
20 pages
Transcranial Doppler Guide
100% (2)
Transcranial Doppler Guide
58 pages
Indications and Utility in The Intensive Care Unit: Neuromonitoring
No ratings yet
Indications and Utility in The Intensive Care Unit: Neuromonitoring
11 pages
Transcranial Doppler (TCD)
100% (1)
Transcranial Doppler (TCD)
100 pages
Bja/aeh 205
No ratings yet
Bja/aeh 205
15 pages
Wendy C. Ziai, Christy L. Cornwell - Neurovascular Sonography-Springer (2022)
No ratings yet
Wendy C. Ziai, Christy L. Cornwell - Neurovascular Sonography-Springer (2022)
539 pages
20240821T105542 Rady 5034 Intracranial Cerebrovascular Examination
No ratings yet
20240821T105542 Rady 5034 Intracranial Cerebrovascular Examination
29 pages
10 Intracranial Stenosis Occlusion - 230706 - 135921 ( - 230921 - 105710
No ratings yet
10 Intracranial Stenosis Occlusion - 230706 - 135921 ( - 230921 - 105710
13 pages
J Permed 2012 03 002
No ratings yet
J Permed 2012 03 002
4 pages
Nedelmann Et Al Consensus Recommendations For Transcranial Color Coded Duplex Sonography For The Assessment of
No ratings yet
Nedelmann Et Al Consensus Recommendations For Transcranial Color Coded Duplex Sonography For The Assessment of
7 pages
Transcranial Doppler Hands-On Workshop: Lorraine Chisari, RDMS, RVT
No ratings yet
Transcranial Doppler Hands-On Workshop: Lorraine Chisari, RDMS, RVT
35 pages
s40140 021 00483 0 PDF
No ratings yet
s40140 021 00483 0 PDF
9 pages
TCD in ICU
No ratings yet
TCD in ICU
14 pages
Alejandro Cordoso Neuro UZV
No ratings yet
Alejandro Cordoso Neuro UZV
12 pages
Diagnostic Ultrasonography in Neurology.15
No ratings yet
Diagnostic Ultrasonography in Neurology.15
40 pages
Diagnostic Ultrasonography in Neurology.15
No ratings yet
Diagnostic Ultrasonography in Neurology.15
40 pages
Transcranial Doppler: - DR Himanshu Soni
No ratings yet
Transcranial Doppler: - DR Himanshu Soni
35 pages
3 NS Foreword
No ratings yet
3 NS Foreword
1 page
Remainder Ancillary Proc
No ratings yet
Remainder Ancillary Proc
21 pages
TCD Ultrasonography Principles
No ratings yet
TCD Ultrasonography Principles
51 pages
ACN - TCD Examination Techniques and Interpretation
No ratings yet
ACN - TCD Examination Techniques and Interpretation
8 pages
Transcranial Doppler
No ratings yet
Transcranial Doppler
20 pages
PIIS0025619612611501
No ratings yet
PIIS0025619612611501
11 pages
Doppler-Atlas Stroke Management
No ratings yet
Doppler-Atlas Stroke Management
7 pages
10 1002@jum 15317
No ratings yet
10 1002@jum 15317
12 pages
s13054 019 2700 6 PDF
No ratings yet
s13054 019 2700 6 PDF
4 pages
Focused Ultrasounds and Alzheimer's
No ratings yet
Focused Ultrasounds and Alzheimer's
10 pages
Intracranial Cerebrovascular TCDI
No ratings yet
Intracranial Cerebrovascular TCDI
11 pages
1 s2.0 S0033838924001106 Main
No ratings yet
1 s2.0 S0033838924001106 Main
16 pages
Transcranial Doppler
No ratings yet
Transcranial Doppler
37 pages
PH Food Service Laws & Safety
No ratings yet
PH Food Service Laws & Safety
3 pages
Legal Response in COVID-19 Case
100% (1)
Legal Response in COVID-19 Case
3 pages
Atrial Septal Defect
No ratings yet
Atrial Septal Defect
4 pages
Gilligan'S Theory of Moral Development
100% (4)
Gilligan'S Theory of Moral Development
2 pages
Policy On The Use of Lasers For Pediatric Dental
No ratings yet
Policy On The Use of Lasers For Pediatric Dental
4 pages
Reflective Writing
No ratings yet
Reflective Writing
2 pages
Kilitch Healthcare India Limited, N+Maharashtra, India 10.20.23 483
No ratings yet
Kilitch Healthcare India Limited, N+Maharashtra, India 10.20.23 483
19 pages
Anthropometric Result
No ratings yet
Anthropometric Result
2 pages
English Exam Paper Instructions
No ratings yet
English Exam Paper Instructions
7 pages
Speaking of Sadness Depression, Disconnection, and The Meanings of Illness (Updated and Expanded Edition) 2nd Edition Secure Ebook Download
No ratings yet
Speaking of Sadness Depression, Disconnection, and The Meanings of Illness (Updated and Expanded Edition) 2nd Edition Secure Ebook Download
15 pages
Amoul nCPAP Series Brochure-2
No ratings yet
Amoul nCPAP Series Brochure-2
3 pages
Para Pharmaceuticals
No ratings yet
Para Pharmaceuticals
19 pages
The Systemic Inflammation-Based Neutrophil-Lymphocyte Ratio: Experience in Patients With Cancer
No ratings yet
The Systemic Inflammation-Based Neutrophil-Lymphocyte Ratio: Experience in Patients With Cancer
13 pages
Problem Statement: Categories Time Required (Minutes)
No ratings yet
Problem Statement: Categories Time Required (Minutes)
4 pages
An Updated Comparison of Current Impression Techniques Regarding Time, Comfort, Anxiety, and Preference: A Randomized Crossover Trial
No ratings yet
An Updated Comparison of Current Impression Techniques Regarding Time, Comfort, Anxiety, and Preference: A Randomized Crossover Trial
8 pages
Test Acct
No ratings yet
Test Acct
20 pages
The Powertrain by Pavel: Plan Strong™ Strong Endurance™
No ratings yet
The Powertrain by Pavel: Plan Strong™ Strong Endurance™
3 pages
Safe Syringe Pump Management
No ratings yet
Safe Syringe Pump Management
3 pages
Marketing Communications A European Perspective 6th Edition Patrick de Pelsmacker Digital Download
No ratings yet
Marketing Communications A European Perspective 6th Edition Patrick de Pelsmacker Digital Download
82 pages
Ben-Porath Et Al., 2020 Dialectical Behavioral Therapy An Update and Review of The Existing Treatment Models Adapted For Adults With Eating Disorders
No ratings yet
Ben-Porath Et Al., 2020 Dialectical Behavioral Therapy An Update and Review of The Existing Treatment Models Adapted For Adults With Eating Disorders
21 pages
SANI-CLOTH® 70 XP00142 XP00159 E701000 E701010 E701020 E701030 Rev 4 3
No ratings yet
SANI-CLOTH® 70 XP00142 XP00159 E701000 E701010 E701020 E701030 Rev 4 3
14 pages
Pharmaceutical Industry Hazards and Safety
100% (1)
Pharmaceutical Industry Hazards and Safety
23 pages
TN Oxygen Suppliers Status
No ratings yet
TN Oxygen Suppliers Status
3 pages
ĐỀ SỐ 11 (HS) TNPT MAI PHUONG
No ratings yet
ĐỀ SỐ 11 (HS) TNPT MAI PHUONG
8 pages
MUSEC Briefing 39 What Is Direct Instruction
No ratings yet
MUSEC Briefing 39 What Is Direct Instruction
1 page
PEPSI Screening Case Study: Selena Espinosa EDU 220: Educational Psychology Ricardo Espinosa College of Southern Nevada
No ratings yet
PEPSI Screening Case Study: Selena Espinosa EDU 220: Educational Psychology Ricardo Espinosa College of Southern Nevada
13 pages
Cinco Jonila Joys For Hardbound
No ratings yet
Cinco Jonila Joys For Hardbound
153 pages
MCQ FOR BARASH - Connelly PDF
78% (9)
MCQ FOR BARASH - Connelly PDF
496 pages
CBCT
No ratings yet
CBCT
7 pages
Nuclear Medicine and Radiology
No ratings yet
Nuclear Medicine and Radiology
25 pages

Ultrasound Assessment of The Intracranial Arteries

Uploaded by

Ultrasound Assessment of The Intracranial Arteries

Uploaded by

ULTRASOUND ASSESSMENT OF THE

Introduction The detection of high intensity transient signals

MCA PCoA MCA

Suboccipital (transforaminal) approach

Submandibular approach artery (ICA). This particular imaging window

beam is directed slightly medially and posteriorly. Diagnostic approach

P 51 ± 13 cm/s 58 ± 15.6 cm/s

important features for identifying the PCAs without

Transcranial color-coded duplex

TABLE 10.1 Transcranial Doppler Protocol: Identification Criteria and Normal

TABLE 10.1 Transcranial Doppler Protocol: Identification Criteria and Normal

TABLE 10.2 Normal Values of Mean

TABLE 10.3 Normal Values of Mean Normals (Ages 20–75) N = 40

FIG. 10.11 Vasomotor reactivity in 40 normal individuals

with carotid artery occlusion, the pulsatility index

often the junction of the VAs cannot reliably be

Detection of intracranial stenosis and

Assessment of the effects of

Carotid stenosis or occlusion

Latent steal Manifest steal

Top of basilar artery

Junction of vertebral artery

blood flow that result from extracorporeal bypass

Middle cerebral artery Common carotid artery

PRACTICAL TIPS PRACTICAL TIPS—cont’d

cm/s indicator-dilution principles (see Chapter 35).102

TABLE 10.8 Amount and Clinical Relevance of Intracranially Circulating Microemboli

AF, Atrial fibrillation; MES, microembolic signal.

pharmacologic approach of thrombolysis in

Recent trials comparing the value of patent

tomographic images. Since then, a considerable

You might also like