British Journal of Radiology (2004) 77, 15-20
© 2004 British Institute of Radiology
doi: 10.1259/bjr/70447093
Ultrasound of the extracranial vertebral artery
T M Buckenham, FRACR, FRCR, MBChB
and
I A Wright, PhD
Department of Radiology, Christchurch Hospital, Private Bag 4710, Christchurch, New Zealand
Correspondence: Dr Isabel Wright
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Abstract
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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.
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Introduction
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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.
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Vertebral artery anatomy
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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.
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Anatomical variation
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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.
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Applied anatomy
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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.
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Ultrasound assessment of the vertebral artery
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It 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.
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Duplex ultrasound of the vertebral artery as an indicator of proximal disease
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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].
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Figure 2. A "pre-bunny" vertebral artery Doppler waveform. Duplex ultrasound showed an ipsilateral subclavian artery origin stenosis of approximately 50%.
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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].
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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.
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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.
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Figure 6. Bisferious vertebral artery Doppler waveform in a patient with severe aortic stenosis and mild aortic incompetence.
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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.
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Figure 7. Tardus vertebral artery (VA) Doppler waveform, seen distal to a tight VA origin stenosis (confirmed by MR angiography).
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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.
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Figure 8. High resistance vertebral artery (VA) Doppler waveform seen in the intertransverse segment. Distal occlusion of the VA was confirmed on angiography.
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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.
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Conclusion
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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.
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Acknowledgments
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The authors would like to thank Dr Neil Pugh, Head of Vascular Ultrasound, University Hospital of Wales, Cardiff, UK for kindly providing Figure 5.
Received for publication June 6, 2003.
Revision received July 28, 2003.
Accepted for publication August 29, 2003.
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Abstract
Introduction
