Ultrasound of the extracranial vertebral artery

© The British Institute of Radiology

T M Buckenham, FRACRFRCRMBChB, , , , and I A Wright, PhD,

Department of Radiology, Christchurch Hospital, Private Bag 4710, Christchurch, New

Zealand
DOI: http://dx.doi.org/10.1259/bjr/70447093
Received: June 06, 2003
Accepted: August 29, 2003
Published Online: March 05, 2014

Abstract
Ultrasound of the extracranial vertebral artery (VA) is a valuable technique. This review
outlines VA anatomy and the technical aspects of ultrasound scanning of the VA, then
proceeds to demonstrate and discuss the use of ultrasound of the VA in identifying vertebral–
subclavian and coronary–subclavian steal syndromes, aortic valve disease, stenosis or
occlusion of the VA itself, dissection and aneurysm of the VA, and vertebrobasilar
insufficiency.
Ultrasound of the extracranial vertebral artery (VA) is a valuable technique, providing direct
or indirect evidence of abnormal VA circulation, including lesions that lie proximal or distal
to the VA itself. This review discusses the role of ultrasound in assessing the extracranial VA,
and defines its role in the investigation of VA disease.

Vertebral artery anatomy

The VA is divided into four segments [1]. Segments 1–3 represent the extracranial VA. The
first vertebral (V1) segment, or pre-transverse segment, extends from the origin of the
subclavian artery (SCA) to its entry into the foramen of the transverse process of C6.
Visualization by ultrasound of the V1 segment is variable, but in most patients it can be
adequately insonated [2]. The V1 segment arises from the craniodorsal but rarely from the
caudoventral half of the SCA; is tortuous and often describes a significant loop prior to
entering the transverse foramen of C6 [3]. The significance of the V1 segment of the vertebral
artery is as the most prone to atherosclerotic change, particularly at its origin [1].
The V2 segment extends from the transverse process of C6 to where the VA exits the axis.
The V3 segment extends from the point of exit from the axis to its entry into the spinal canal
[1]. The V4 segment is intracranial and terminates as the basilar artery. The V2 segment can
only be insonated in the intervertebral component, as the acoustic shadowing which occurs
during the passage through the bony canal precludes adequate visualization. The V3 segment
can be insonated until it enters the spinal canal.

Anatomical variation
Anomalous origins
The most common anomalous origin is a VA arising directly from the aortic arch on the left
side, occurring in up to 5% of cases [3, 4]. The VA enters the bony canal at C5 rather than C6
in this variation. Other variations described include an aortic origin distal to the left SCA, or
rarely it may arise from the left common carotid artery (CCA) or left external carotid artery.
Origin of the right VA from the arch or right CCA is very rare.

Applied anatomy
The VA communicates with multiple intracranial and extracranial arteries which can provide
collateral circulation if stenosis or occlusion occur [2, 5]. These can be divided into the
following [4]:
a) Pre-Willisian. The most common example seen is communication between the deep
cervical artery, which is a branch of the costocervical trunk, and the VA itself, allowing
antegrade filling of the VA in ostial stenosis or occlusion. Other examples include occipital
branch of the external carotid artery filling the ipsilateral VA via its atlantic branch and the
rete mirabile across the subdural space.
b) Willisian. The posterior communicating arteries allow vascular connection between the
right and left sided circle of Willis posteriorly.
c) Post-Willisian. Supratentorial cortical anastomoses between the cortical branches of the
posterior cerebral arteries at the surface of the brain allow collateral cross-over circulation.

Ultrasound assessment of the vertebral artery

t is possible to insonate the V1 and V2 sections of the VA with relative ease in most patients.
On Duplex ultrasound, it is estimated that the VA origin is visible in approximately 65–85%
of cases, with the right being more easily visualized than the left [3, 6]. The V2 segment is
visible in approximately 95% of patients [7], although failure to identify VA flow does not
conclusively indicate VA occlusion, as hypoplasia can mimic occlusion. The V3 section as it
exits the transverse process of C1, whilst not apparently routinely imaged by many centres,
may be visualized on ultrasound [6]. The V4 section lies intracranially although it may be
interrogated by transcranial Doppler ultrasound.
Normal Doppler parameters
Normal peak systolic velocity (PSV) for the V2 segment is approximately 20–60 cm
s−1 [6, 8, 9]. This range is poorly defined in the literature, but a PSV of <10 cm s−1 is probably
abnormal [2], and a focal PSV of >100 cm s−1 probably indicative of a significant stenosis [9].
At the origin of the VA the mean velocities are slightly higher (mean velocity of 64 cm
s−1 with a range of 30–100 cm s−1 [10]). Note that, due to asymmetry in VA diameter (present
in 73% of normal individuals [2]), there can be considerable difference in PSV between an
individual's (normal) VA. A normal VA diameter on ultrasound is regarded as approximately
4 mm, with a tendency for the left VA to be larger than the right [2].
A normal VA Doppler waveform is shown in Figure 1. There should be cephalad flow
throughout the cardiac cycle and a low-resistance flow pattern should be evident, i.e. a low
peak systolic: end diastolic velocity ratio.
Scanning technique
For optimal insonation of the VA the patient should be supine with head straight and the neck
extended; it may be necessary to rotate the head to assess postural changes in VA flow. In
order to better visualize the VA between the acoustic shadows from the transverse processes,
a 5 MHz or 7.5 MHz linear probe should be used. The sonographer should firstly image the
mid CCA in longitudinal section on B-mode from a lateral approach. Once the probe has been
positioned over the long axis of the CCA, it is slid posteriorly (without any rotation); acoustic
shadows from the transverse processes of the vertebrae will appear and one segment (or more)
of the V2 section should be seen between the shadows. Once the orientation of the relevant
segment of the VA has been established, the vessel should be imaged with colour Doppler
(with a suitably low pulse repetition frequency/high colour gain) and the direction of flow
established. Next the pulsed wave Doppler should be used to display the waveform in the VA
to identify any abnormalities in the flow pattern, and to measure the peak systolic velocity.
Often it is only the V2 segment that is assessed during a carotid ultrasound examination,
which provides a cursory check on flow direction and waveform shape. However, it may be
desirable to image the V1 section, particularly the origin as this is the most common site of
disease, especially if indicated by a distal tardus VA waveform. This is visualized by either
tracing the V2 segment proximally, or by imaging the supraclavicular SCA in transverse
section, where the VA origin and a short segment of the VA are usually evident. If desired,
lumen diameter and/or volume flow may be measured.

Duplex ultrasound of the vertebral artery as an indicator of proximal disease

Vertebral–subclavian steal syndrome
Haemodynamically significant abnormalities of the SCA proximal to the VA origin may
cause characteristic changes in the ipsilateral VA. A reduction in diameter of the proximal
SCA which produces a pressure gradient between the cerebral circulation (donor) and the left
SCA (recipient) will alter VA flow. The clinical manifestations of this are known as the
vertebral–subclavian steal syndrome (VSSS) [11]. It was initially thought to be responsible
for brainstem ischaemia and stroke, although subsequent studies have suggested that, whilst it
is a marker for atherosclerosis in general, VSSS itself does not necessarily lead to
cerebrovascular events and is probably a harmless haemodynamic phenomenon [5, 12, 13].
Complete reversal of VA flow caused by severe proximal SCA disease has been well
documented, but there appear to be several intermediate VA waveforms in which substantial
antegrade flow is maintained in the presence of mild to moderate SCA stenosis:
i) “Pre-bunny” waveform (Figure 2): A proximal SCA (diameter) stenosis of the order of 45%
or less may manifest itself in the VA as a pre-bunny waveform, which is associated with the
preservation of antegrade flow and the presence of a sharp mid-systolic deceleration, with a
sharp first systolic peak and a more rounded, lower second systolic peak. It is thought to be
due to the Venturi effect, creating a negative pressure at the ostium of the vertebral artery
transiently during the duration of the systolic jet [14].
ii) “Bunny” waveform (Figure 3): An SCA stenosis in the range of 55% may produce a
deeper cleft between the two systolic peaks, whereby the nadir of the cleft is at approximately
the same level and end diastole [14].

iii) To-and-fro/bidirectional waveform (Figure 4): Significant (∼ 80% or greater) stenosis of

the pre-vertebral SCA produces a VA waveform with initial antegrade flow and subsequent
retrograde flow each cardiac cycle [15].
iv) Completely retrograde waveform (Figure 5): Occlusion or high grade pre-vertebral SCA
stenosis may produce complete VA flow reversal [16].
Such changes in the VA waveform at rest have been shown to be highly predictive of the
presence of atherosclerotic proximal subclavian disease, with a moderate correlation between
the type of VA waveform and the severity of disease [13, 14]. The presence of bidirectional or
completely retrograde VA flow has been shown to be 100% sensitive to high grade stenosis or
occlusion of the proximal SCA or brachiocephalic trunk [7, 13, 17], and that the more subtle
changes to VA waveform are highly sensitive to the presence of SCA disease. However, the
correlation between the altered but unidirectional VA waveform and the degree of SCA
stenosis is not high, and one author notes a bunny waveform in the presence of only a 25%
SCA stenosis [13].
It should be noted that mild to moderate SCA stenoses may only produce a pressure gradient
after exercise and that exercise [5, 13] may increase the stage of an already abnormal VA
waveform. Also, flow reversal in the VA is often associated with flow reversal in the
ipsilateral internal mammary artery [18]. It has been shown, using ultrasound, that following
satisfactory endoluminal recanalisation of a significantly diseased SCA, restoration of
antegrade VA flow is not immediate and can take between 20 s and several minutes, or even
days. This is thought to act as a protective mechanism against cerebral embolism [19].
There is very little information on the specificity/negative predictive value of VA waveform
alteration as a predictor of proximal disease, presumably due to the lack of angiographic
information on patients who appear to have normal VA waveforms.
Coronary–subclavian steal syndrome
Coronary–subclavian steal syndrome (CSSS) occurs when the left internal mammary artery
(LIMA) has been used as a bypass conduit for coronary revascularization and the presence of
a haemodynamically significant stenosis in the proximal SCA causes flow reversal in the
vertebral and ipsilateral LIMA, creating a steal away from the heart and/or the brain [20]. The
physiology is difficult to fully explain as the coronary artery in these cases is usually
stenosed, hence the need for the LIMA conduit; it is therefore difficult to perceive a pressure
gradient occurring between the stenosed SCA and the stenosed coronary circulation, allowing
a LIMA–subclavian steal. There are only two cases of CSSS in the literature which suggest
flow reversal in the LIMA without associated reversal in the ipsilateral left VA [21, 22]; all
others report ipsilateral vertebral flow abnormalities which usually manifest themselves as
complete VA flow reversal. In a recent case of CSSS at our institution, a bunny waveform
was evident in the left VA (Figure 3). It is estimated that the incidence of CSSS is less than
0.5% [23, 24], although its consequences are grave. Hence carotid and vertebral scanning
prior to coronary artery bypass grafting may be useful not only to better define the risks of
surgery due to significant carotid artery disease, but to also identify patients who may benefit
from prophylactic SCA stenosis/occlusion treatment.
Aortic valve disease
Other haemodynamically significant lesions such as aortic valve disease cause alteration in
the vertebral waveform and it may become bisferious (Figure 6), with the second systolic
peak greater than or equal to the first, both peaks being distinct from the dicrotic notch. This
appearance may also be seen in the carotid arteries [25] and if present bilaterally, is a non-
specific indicator of valvular disease, either incompetence or stenosis.
Atherosclerotic stenosis or occlusion of the vertebral artery
The extracranial VA develops atheromatous change with a similar frequency to the carotid
artery, although the clinical relevance is less clear. The origin of the VA is the most common
distribution, although strictures may occur throughout its length. Ostial stenoses may be
detected by a tardus waveform in the more distal VA (Figure 7), or by direct insonation of the
origin and detection of focal velocities in excess of 100 cm s−1 [9]. VA occlusions are less
easily diagnosed and it may be difficult to differentiate from hypoplasia or aplasia or
occlusion and an alternative cause such as a dissection. Detection of a VA in the bony canal
with no flow is suggestive of occlusion, particularly if calcified plaque can be identified. De
Bray et al [26], using direct visualization (measurement of diameter reduction and velocity
increase) or inference (tardus parvus Doppler waveform distal to the site of stenosis), found
ultrasound detection of >70% proximal VA stenosis to be 71% sensitive and 99% specific.
Nicolau et al [7] studied four tardus parvus VA waveforms and found two to be due to
significant proximal VA stenosis and two to hypoplasia of the VA.
Distal obstructions to the VA may manifest themselves as a high resistance (parvus, without
the tardus component) waveform (Figure 8). Nicolau et al [7] found the presence of such a
waveform to have a low positive predictive value as, out of 19 high resistance waveforms, one
was due to a proximal stenosis and a further seven due to VA hypoplasia.
In terms of the specificity and negative predictive value of the vertebral waveform in
identifying VA disease, Nicolau et al [7] report two normal VA waveforms with
angiographically proven high grade distal VA stenoses and one with a significant ostial
stenosis.
Dissection and aneurysms of the vertebral artery
Reports of the efficacy of Duplex ultrasound in identifying VA dissection are scant. The
prevalence of VA dissection (spontaneous or traumatic) is unknown, although it seems less
frequent than internal carotid artery dissection [27], appears to have a female preponderance
and mainly affects middle-aged (30–50 years) adults [28]. It appears that of the extracranial
VA segments, the V3 segment is the most frequently involved [27–29]. Several studies have
found that whilst Doppler ultrasound of the extracranial VA is high sensitive for flow
abnormalities (70–80% [27–29]), it is insufficiently specific for VA dissection. Bartels' study
[30], which contained a higher prevalence of VA dissection proximal to the V3 segment, cited
typical ultrasound findings of an irregular, stenosis dissecting membrane with biluminality,
localized increase in vessel diameter, pseudoaneurysm, intramural haematoma, and tapering
stenosis with distal occlusion. Other studies, which find a higher incidence of dissection in the
reportedly more difficult to visualize V3 segment [27], use more indirect Duplex criteria of
abnormally low PSVs, a high resistance waveform and absence of flow or reversal of flow to
identify a potentially abnormal VA which, if clinical symptoms concur, may warrant MRI to
confirm the diagnosis of dissection.
Aneurysms of the extracranial VA mainly arise from trauma and are extremely rare, possibly
due to their relatively protected course through the bony foramen [31]. Various studies find
the upper limit to the normal VA diameter of approximately 5–5.5 mm [32, 33], hence
anything larger should be regarded as significantly dilated. They appear to most commonly
occur in the distal V2 segment (at the level of C1/C2) [34], although a recent report detailed a
large, non-traumatic V3 segment VA aneurysm [35]. Dissecting aneurysms of the extracranial
VA appear more common [34]. A case of a VA pseudoaneurysm with associated
arteriovenous fistula of unknown aetiology has been reported [34].
Vertebrobasilar insufficiency secondary to hypoplasia or extrinsic compression
Apart from previously described pathologies, aplasia or hypoplasia of the VA may cause a
significant reduction in volume flow through the vertebrobasilar system, one of the suspected
causes of vertebrobasiliar insufficiency (VBI). The mean diameter of the extracranial VA is
approximately 3.5 mm [2, 3, 8], with a diameter of <3 mm suggestive of hypoplasia. Doppler
waveform analysis does not appear useful in identifying VA hypoplasia, with reports of
normal [5, 7], bidirectional, high- and low-resistance [7] waveforms in such vessels. In
response to Bendick and Glover's studies [36] which suggested that patients may be prone to
vertebrobasilar ischaemia if their net (right plus left) VA flow was less than 200 ml min−1,
Seidel et al [8] attempted to establish reference values for net VA flow using Duplex
ultrasound in adults without cerebrovascular disease or symptoms and representative in age of
patients with cardiovascular disease. Their conclusion was that a threshold of 100 ml
min−1 was more appropriate, although they acknowledged the technical difficulty of
measuring volume flow in the VA on ultrasound, which may explain the paucity of published
data from other centres.
An alternative explanation for VBI is extrinsic compression of the extracranial VA at all
levels, which can occur during cervical rotation [37]. Again, the role of Duplex ultrasound in
identifying extrinsic compression of the VA is not extensively reported, and it would appear
that, whilst there is evidence that a reduction or cessation of VA flow on cervical rotation in
patients with VBI is sometimes demonstrable on Duplex [37, 38], the potential technical
difficulties of insonation of the VA during head movement and achieving a significant degree
of cervical rotation in elderly patients, and the reports suggesting that cervical rotation may
induce flow cessation in patients without peripheral vascular disease [39], suggest that the
technique is neither sensitive nor specific in this application.
Conclusion
Duplex ultrasound of the VA is a useful non-invasive first line approach to imaging the VA. It
is a sensitive indicator of proximal disease in the subclavian and brachiocephalic arteries and
often ostial VA stenosis. It is less sensitive in the evaluation of dissection, as this is often
restricted to the V3 segment, although secondary manifestations indicative of dissection may
be useful. The relationship between VA disease and clinical neurological signs and symptoms
is much less defined than the carotid circulation and this has reduced the need to evaluate the
VA circulation in many patients. The advantage of VA ultrasound is that it is a quick, non-
invasive method of assessment which can indicate abnormality and clarify selection of
subsequent imaging modalities.

Figure 1. Normal vertebral artery Doppler waveform.

Figure 2. A “pre-bunny” vertebral artery Doppler waveform. Duplex

ultrasound showed an ipsilateral subclavian artery origin stenosis of approximately 50%.

Figure 3. A “bunny” waveform from the left vertebral artery (VA) of a

patient with coronary–subclavian steal syndrome caused by a 90% stenosis within a left
subclavian artery stent. This usually manifests itself in complete reversal of VA flow,
although in this case there were concomitant ipsilateral common and internal carotid artery
origin stenoses of 50% and 90%, respectively, and the right VA was diffusely diseased on
arteriography.
 Figure 4. Bidirectional vertebral artery Doppler waveform.

Figure 5. Retrograde vertebral artery Doppler waveform.

Figure 6. Bisferious vertebral artery Doppler waveform in a patient with

severe aortic stenosis and mild aortic incompetence.

Figure 7. Tardus vertebral artery (VA) Doppler waveform, seen distal to a

tight VA origin stenosis (confirmed by MR angiography).

Figure 8. High resistance vertebral artery (VA) Doppler waveform seen in

the intertransverse segment. Distal occlusion of the VA was confirmed on angiography.
The authors would like to thank Dr Neil Pugh, Head of Vascular Ultrasound, University Hospital of Wales,
Cardiff, UK for kindly providing Figure 5.

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