Extracranial and Intracranial Sonographic Findings in ...€¦ · The optimal clinical management of VB strokes remains a matter of debate: antiplatelets and statins are recom-mended

Extracranial and IntracranialSonographic Findings in VertebralArtery Diseases

Edoardo Vicenzini, MD, PhD, Maria Chiara Ricciardi, MD,Gaia Sirimarco, MD, Vittorio Di Piero, MD, PhD, Gian Luigi Lenzi, MD

Objective. The aim of this review is to illustrate the sonographic features that can be detected in ver-tebral artery (VA) diseases. Methods. We conducted a review of sonographic findings in VA diseases.Results. Various VA diseases are described, and sonographic techniques and features are discussed.Conclusions. Posterior circulation vascular imaging can be performed by means of various neu-roimaging techniques. Intra-arterial angiography remains the reference standard. The use of this tech-nique has become even more widespread since it has become possible to perform endovascularprocedures; it is, however, an invasive procedure that is associated with a not irrelevant level of risk.Computed tomographic angiography and magnetic resonance angiography with and without contrastagents have been proposed as less invasive alternatives, although these techniques can only beperformed in the radiology unit and may not be readily available in daily clinical management.Sonography, which combines an extracranial and intracranial evaluation, is highly suited to the assess-ment of the vertebrobasilar system on account of its widespread availability and its unique capacity tostudy real-time hemodynamics. Furthermore, new sonographic applications and sonographic contrastagents have improved the sensitivity and specificity of this technique with regard to diagnostic accu-racy for the posterior circulation. Key words: posterior circulation diseases; sonography; transcranialDoppler sonography; vertebral arteries.

Received June 8, 2010, from the Department ofNeurologic Sciences, Stroke Unit, SapienzaUniversity of Rome, Rome, Italy. Manuscript accept-ed for publication July 10, 2010.

Address correspondence to Edoardo Vicenzini,MD, PhD, Department of Neurologic Sciences,Sapienza University of Rome, Viale dell’Università30, 00185 Rome, Italy.

E-mail: [email protected]

AbbreviationsCE-MRA, contrast-enhanced magnetic resonanceangiography; CTA, computed tomographic angiography;IAA, intra-arterial angiography; PICA, posteroinferiorcerebellar artery; SA, subclavian artery; TCCD, transcra-nial color-coded duplex; TCD, transcranial Doppler; VA,vertebral artery; VB, vertebrobasilar

osterior circulation strokes account for one-fifth ofall ischemic strokes,1,2 with 20% of such strokesbeing caused by an artery-to-artery embolism aris-ing from vertebral artery (VA) stenosis.3–5 The prog-

nosis of vertebrobasilar (VB) strokes is far from benign, therisk of subsequent strokes and mortality rates being high-er than those associated with carotid diseases.6,7

The optimal clinical management of VB strokes remainsa matter of debate: antiplatelets and statins are recom-mended by the American Heart Association preventionguidelines8,9 for secondary acute stroke prevention; war-farin reduces the risk of ischemic stroke and vasculardeath in patients with basilar artery stenosis but does notprevent strokes in the basilar artery territory or providebenefits for VA stenosis or posterior circulation disease ingeneral.10 Identification of the underlying vascular dis-ease in posterior circulation strokes and the possibility ofconsequent surgical treatment have thus been consid-ered other alternatives for secondary stroke prevention in

© 2010 by the American Institute of Ultrasound in Medicine • J Ultrasound Med 2010; 29:1811–1823 • 0278-4297/10/$3.50

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such patients. Experienced vascular surgeonscan even directly reconstruct VA stenosis.Endovascular procedures such as angioplastyand stenting, sometimes in conjunction withintra-arterial thrombolysis, have proved feasible,yielding promising results, although with highercomplication risks than in the carotid territo-ry.11–14 The existence of specific surgical strategiesfor VA disease has conferred greater importanceon accurate vascular imaging of the posterior cir-culation. Until very recently, detection of a poste-rior circulation stenosis did not indeed alterclinical management of this condition, therebeing no specific treatment available other thanmedial therapy: antiplatelets or anticoagulation.

Cerebrovascular Imaging

The 4 methods available to date for VB vascularimaging are extracranial and intracranial sonog-raphy, computed tomographic angiography(CTA), magnetic resonance angiography with(CE-MRA) and without contrast agents, and con-ventional catheter intra-arterial angiography(IAA). Each of these techniques has its advan-tages and disadvantages.

Intra-arterial angiography remains the refer-ence standard for the identification of VAstenosis; it is, however, an invasive techniquethat is accompanied by a risk of proceduraliatrogenic stroke in up to 2% of cases15 anddoes not offer the possibility of obtaining struc-tural images of the brain simultaneously withthe vascular images. Moreover, there may bespecific technical procedural difficulties suchas selectively finding and injecting the contrastagent into the origin of the vessel, with reducedsensitivity if the injection is performed in thesubclavian artery (SA).

Magnetic resonance angiography with andwithout contrast agents, also with new arterialspin labeling techniques to detect vascularintegrity, and CTA have been proposed as power-ful alternatives, with higher sensitivity and speci-ficity for CE-MRA, lower for CTA, with respect tosonography, even when compared with IAA.16–18

Computed tomographic angiography can beperformed extremely rapidly, although despitebeing less invasive than IAA, it is associated witha potentially toxic load from contrast agents and

ionizing radiation. Although CE-MRA partiallyavoids the toxicity- and radiation-related prob-lems, this technique may be less widely availableand is more time-consuming than CTA. All ofthese conventional radiologic techniques, whichare becoming more and more diffuse even innonspecialized centers, are expensive andrequire patients to be delivered to a radiologyunit. However, their main limitation is that imag-ing is based on the flow within the vessels, whichmeans that definition may be scarce in cases inwhich flow is turbulent or severely reduced, alsomaking interpretations of radiologic imaginghighly operator dependant.

Sonography has been extensively used in theevaluation of the VB system, owing to its lowcosts, widespread availability, noninvasiveness,and the possibility of being performed at thebedside.19–21 Its main disadvantages, which arecommon to all sonographic examinations, arethat it is operator dependent and that its sensi-tivity is reported to be lower than that of eitherCTA or MRA. However, it should be borne inmind that sonography offers opportunities thatcannot be explored by means of other imagingtechniques, ie, its unique capability to investi-gate real-time hemodynamics, which is impossi-ble with conventional neuroimaging, for bothintracranial and extracranial segments in thesame session. Moreover, new advances forexamining the whole intracranial segment “at aglance” have been made even with only tran-scranial Doppler (TCD), with new software thattransforms the signals from different depths intoa tracing similar to the cardiac M-mode withcolor intensity indicating the direction andvelocity of the flow: the “power motionmode.”22,23 The use of sonographic contrastagents for transcranial color-coded duplex(TCCD) imaging have further enhanced intracra-nial VA tract imaging,24–28 thereby increasing itsdiagnostic sensitivity.

The aim of this review is to describe the sono-graphic features that can be detected in VA diseases.

Anatomy of the VA

The VA is divided into 4 segments.29V0 is the origin.The V1 tract extends from the SA, anterior to the C7transverse process, to the entry point of the C6

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foramen transversarium. The V2 tract lies withinthe C6–C1 intertransverse foramina. The V3 seg-ment, at the Tillaux point, extends in a loop fromthe arch of the atlas to the foramen magnum. TheV4 intracranial segment extends intradurally, givesrise to the posteroinferior cerebellar artery (PICA),and extends from the foramen magnum to thecontralateral VA to form the basilar artery. Theartery is most vulnerable anteriorly at C7, laterallyfrom C3 to C7, and posteriorly at C1 and C2.30

Sonographic Technique

The extracranial V1–V3 segments can beapproached anteriorly on the neck (V1–V2) andfrom the lateral posterior suboccipital region(V3), with longitudinal and transversal projec-tions. The left V0 origin is more difficult to visual-ize than the right V0 because it arises fromdeeper in the chest. Lower-frequency lineartransducers, with a higher penetration capacity,yield better results, whereas velocity measure-ments with continuous Doppler imaging havebecome less used in clinical practice because ofits limitation of being a “blind” technique.31–33

The intracranial V4 segments can be insonatedthrough the suboccipital transforaminal windowby TCD imaging with a 2-MHz pulsed wave probeand by TCCD imaging with a 2.0- to 3.5-MHz sec-tor array transducer, with regard to the ultra-sound apparatus. The left and right VAs are moreeasily identified with TCCD imaging. With anadequate subnuchal acoustic window, the originof the PICAs in the distal V4 tract can also beinsonated, resulting in flow directed in the oppo-site position with respect to the VAs.31–33 In a caseof an inadequate transforaminal window orwhen the neck conformation and forward bend-ing are particularly difficult, sonographic contrastagents can be used to improve detection of the V4segments, the PICAs, and the proximal tract ofthe basilar artery.24–27 Contrast agents thusmarkedly increase the sensitivity and diagnosticaccuracy, particularly in the detection of acutebasilar artery occlusion34 and in follow-up forbasilar stenting.28 However, under the best condi-tions, through the suboccipital window, sonogra-phy allows visualization of two-thirds of thebasilar artery, even with the aid of contrastagents.35–37 The basilar artery tip can be examined

by means of a transtemporal approach, and themedian/distal part of the vessel may sometimesthen be identified with some difficulty by TCCDimaging.

Pathologic Findings

Pathologic findings of the VA that can be detect-ed by sonography include (1) caliber variationsand hypoplasia, (2) course anomalies and cervi-cal compression, (3) proximal and distal occlu-sion, (4) proximal stenosis with and withoutcervical compensation, (5) V4 intracranial steno-sis, (6) dissection, and (7) subclavian steal.

The most frequent locations of VA atheroscle-rotic damage are at the sites of vessel bifurcation,namely at the V0/V1 origin and in the distal V4tracts, ie, the VB junction.38 Arterial dissectionmay be located more frequently in the V2 and V3segments (35% and 34%), the V1 segment (20%),and the V4 segment (11%).39

Asymmetries, Hypoplasia, and Abnormal PICATerminationCongenital variations in the posterior circulationare commonly observed in routine clinical diag-nosis but are of no clinical relevance in mostcases.40 Several diagnostic techniques havedetected caliber asymmetry, with most observa-tions revealing a larger left- than right-side VAdiameter.31,37,41–43 Asymmetry can easily beobserved using standard color duplex imaging,which highlights any differences in the vesselcaliber throughout the whole vessel course,measured in the intertransverse V2 segment.44

When these differences are minimal, no alter-ations in the Doppler spectra and the resistiveand pulsatility indices emerge (Figure 1).

The vessel caliber criteria used to diagnose VAhypoplasia remain, however, a matter of debate.In an early pathoanatomic study, hypoplasiawas defined as a lumen diameter of less than 2mm,45 this definition being supported by asonographic study that revealed a decrease inblood flow velocity in VAs with diameters of lessthan 2 mm.46 Nonetheless, other authors haveproposed a diagnosis of hypoplasia when thecaliber is less than 3 mm47 and when theDoppler spectrum shows a high resistive pat-tern.31 When the caliber is congenitally smaller

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than 3 mm, resistive indices increase as the bloodflow through the artery is reduced; this is consid-ered a hypoplastic vessel with reduced wall disten-sibility.31 The diameter of the contralateral normalvessel is usually larger. Furthermore, a hypoplasticVA is frequently associated with an abnormal ter-mination in the homolateral PICA; in these cases,post-PICA occlusion and an abnormal PICA ter-mination cannot easily be differentiated exclu-sively with cervical sonography and with noevident clinical symptoms (Figure 1B).48–50

When the diameter of the hypoplastic vessel isvery small (ie, <2.0 mm), a further increase in theresistive indices may be observed (Figure 1C). Insuch cases, an extracranial investigation alone isunlikely to reveal pre-PICA occlusion, althoughwith more reduced diagnostic velocities in thelatter case,49,50 TCD or TCCD being required toprovide further diagnostic information; a simi-larly high resistive pattern in the intracranial V4segment confirms the patency of the distal vesseland thus indicates vessel hypoplasia. In suchcases, the presence of a clinical history may beimportant to make a differential diagnosisbetween acute symptomatic distal occlusion ofan eventual dysplastic/ hypoplastic vessel andcongenital asymptomatic non–clinically relevanthypoplasia, a second test being confirmative.

Tortuous VA Course and CervicalIntertransverse Segment CompressionVertebral artery course anomalies due to con-genital variations related to their embryogenesisare frequent.51 Indeed, length anomalies, tortu-osity, and kinking of the V2 segment are com-monly observed in routine clinical practice,although without any related clinical symptoms(Figure 2, A–C). Cases in which a VA interverte-bral loop causes radicular compression andwidens the intertransverse foramen, consequent-ly requiring decompressive surgery, are rare.52

Cervical spine arthrosis may, like rheumatoidarthritis, cause vertebral atlantoaxial and subaxi-al subluxation with spinal cord compression, VAloop formation, and vascular compression.53

A tortuous course of the intertransverse V2 seg-ment of the VA may be observed in such cases,accompanied by an increase in the resistiveindices and changes in blood flow velocities(Figure 2, D and E).

Because the VAs can cause catastrophic iatro-genic complications during cervical spinesurgery and manipulation,30 all of these abnor-malities should be borne in mind by surgeonswhen they approach the cervical and cran-iospinal regions. Moreover, with the advent ofintravascular treatment for distal intracranial VA

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Figure 1. Cervical color Doppler images. A, Normal VA diameter in the V2 segment. B, Smaller VA diameter (2.0 mm). Note theincrease in the resistive indices. C, Hypoplastic VA (1.3 mm) with a marked increase in the resistive indices and interrupted diastolicflow that may be suggestive of V4 pre-PICA occlusion.


and basilar artery stenosis, the interventionalradiologist should also be aware of any vesselcourse anomalies that may impede, for example,the passage of an intravascular catheter andcause local traumatic dissections when repeatedunsuccessful selective VA catheterizations areattempted.

Proximal and Distal VA OcclusionHemodynamic changes can be indirectly detect-ed in the V2 segment in cases of both proximaland distal VA stenosis/occlusion.48–50

In cases of proximal occlusion, the flow may beabsent in the V2 segment, thus indicating exten-sion of the atherosclerotic process from the ori-gin to the whole cervical segment (Figure 3A).

However, if the V2 segment is patent, flow oftencan be detected through visible collateral cervi-cal branches arising from the external carotidartery and refilling the intertransverse segment.

In distal intracranial V4 occlusion, the V2 seg-ment may be patent. If evaluation of the VA islimited to the extracranial segment, the criteriaon which diagnosis of the distal V4 segmentocclusion is based are only indirect: they consistof the observation of a normal vessel caliber inthe intertransverse segment but with alteredresistive indices and interrupted diastolic flow(Figure 3B).49,50

However, the site of intracranial V4 occlusion,ie, before or after the origin of the PICA, is impor-tant to identify, as V4 occlusions distal to the ori-

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Figure 2. A–C, Cervical color Doppler images showing tortuosity of V1 (A) and V2 (B) and kinking of the intertransverse V2 segment(C). D and E, Cervical compression of V1 (D) with corresponding MRA (E, arrow).


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Figure 3. Top, Cervical color Doppler images of proximal VA occlusion. A, Absence of a signal and flow interruption in V2 (arrow).B, Absence of a signal in proximal V0–V1. Bottom, Cervical TCCD images of distal VA occlusion. C, Normal V2 diameter and visual-ization with dampened flow and diastolic interruption (arrow). D, Transcranial color-coded duplex image. The left (LT) V4 segment isnot visualized. BAS indicates basilar artery.


gin of the PICA may be overlooked with only cer-vical examination because no prominent changeof flow velocity and/or the flow signal is expectedin the intertransverse segment in this case. Someauthors have suggested that differences in the VAcaliber, velocity measurements, and aspect ofDoppler spectra may be used as criteria for dif-ferentiating intracranial VA occlusion fromhypoplasia and an abnormal termination,49

although agreement on the usefulness of suchmeasurements is not unanimous.50

Nonetheless, for the differential diagnosis, thealtered resistive indices in the V2 segmentobserved in cases of severe vertebral hypoplasiaor in an abnormal V4 segment that terminatesinto the PICA may be misinterpreted as V4 occlu-sion. Direct evaluation of the V4 segment bymeans of TCD and TCCD imaging yields impor-tant information on distal vessel patency andhemodynamics that may support and confirmthe diagnosis in these cases.26,27 Indeed, a hemo-dynamic sonographic evaluation is fundamentalbecause MRA and CTA may, in low-flow condi-tions, not visualize the vessel.

Proximal VA Stenosis With and WithoutCervical CompensationWhen the proximal V0–V1 segments presenthemodynamic stenosis but the intertransversesegment is patent, compensatory flow may arisefrom the cervical branches, refilling the V2 seg-ment.54 In such cases, the resistive and pulsatili-ty indices are reduced in V2, whereas minimalalterations are observed in V3 and V4 if compen-sation is sufficient (Figure 4, A–C). Evaluation ofthe complete vertebral axis is thus mandatorybecause proximal stenosis may escape diagnosisif only intracranial CTA or MRA, which would insuch cases show a normal distal V4 segment, isperformed.

By contrast, a “steal” phenomenon, ie, retro-grade flow during systole and orthograde flowduring diastole, may be observed in V4 in severeproximal V0–V1 steno-occlusive disease whencompensation via cervical vessels is insufficient.This finding has not yet been described in the lit-erature and refers to our experience in consecu-tive performing TCD or TCCD imaging to assessintracranial vessel patency in cases of VA proxi-mal diseases. It is reasonable to consider that,

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Figure 4. Top, Cervical TCCD images of V1 stenosis with cervical branch compensation to V2. A, Reduced velocities with altered resis-tive indices in V2. B, Cervical collateral compensatory branches supplying the V2 intertransverse segment. C, Normal flow velocitiesand resistive indices in V4. Bottom, Cervical TCCD images of V2 stenosis without cervical compensation and with a distal V4 stealphenomenon. D, Reduced velocities with altered resistive indices in V2. E, Absence of collateral branches in V2 with tortuosity due tocervical compression. F, Alternating flow in V4.


when the V4 segment distal to the occlusion ispatent, the steal phenomenon is directed towardthe PICA (Figure 4, D–F). This mechanism sup-ports blood flow to the cerebellum and clearlyindicates that the distal segment is patent andnot involved in the atherosclerotic process.Conventional neuroimaging may lead to falseinterpretations because the biphasic low flow inthe V4 segment may reduce visualization andconsequently be interpreted as occlusion.

V4 Intracranial StenosisStenosis of the V4 segment and the basilar arterycan be detected with either TCD or TCCD imag-ing. When using TCD imaging, the V4 segmentcorresponds to an insonation depth of 65 to 80mm,31–33 whereas the basilar artery can beinsonated at higher depths. The advent of thepower motion mode can help identify the wholeV4 segment at a glance even with TCD imaging,especially in cases of occlusive disease (Figure5A).22,23 Transcranial color-coded duplex imagingmay first help differentiate the left from the rightV4 segment and then to locate the site of thestenosis within the vessel by searching for analiasing effect or a color defect, which indicates ahigh or low velocity, respectively (Figure 5B).Depending on the extent of the stenosis, bothincreased and decreased flow velocities, accom-panied by Doppler spectrum broadening andaltered resistive indices, may be observed,55–60

with normal systolic and diastolic values rangingfrom less than 140/100 cm/s for the basilar arteryand less than 120/90 cm/s for the VA.60

Nonetheless, because a TCCD image of the ves-sel is derived from the inward flow, vascularimages must always be associated with a Dopplerhemodynamic evaluation because nonhemody-namic stenosis cannot be detected. In contrast,congenital tortuosity can easily be visualized, thusallowing it to be differentiated from a flow velocitymodification related to a course variation.

Vertebral Artery DissectionWith the progress of high-resolution sonography,it is possible to noninvasively diagnose a dissec-tion of the extracranial VA when it is located inthe proximal V1 segment, ie, at the entrance ofthe artery in the transverse foramen at C6 or atthe V0–V1 origin.19,29,61,62 Cervical sonographicfindings in the acute phase may vary from vesselocclusion to the observation of surface irregular-ities and intramural hematoma, especially in V1.Occasionally, 3 lumina with a mobile intimal flapmay be observed, although this requires high-resolution echographic systems and a skilledsonographer. A follow-up examination may con-firm the diagnosis when good recanalization isobserved because atherosclerotic lesions rarelydisappear.31

Dissections located in the V3 and V4 segmentscannot be visualized directly on the screen; the

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Figure 5. Intracranial V4 hemodynamic stenosis. A, Transcranial Doppler image showing increased flow velocities and the powermotion mode. B and C, Transcranial color-coded duplex images showing an aliasing effect in V4 (B) and an increase in flow velocitiesat the site of the stenosis (C). D, Magnetic resonance angiogram. The arrow marks the stenosis.


diagnosis in such cases is based on indirect signsin the course of the cervical intertransverseartery, such as a high-resistance flow pattern,indicating distally obstructed flow with a normalcaliber.31 Transcranial duplex imaging, with theuse of contrast agents if necessary, may confirmor support the diagnosis when the distal V4 seg-ment is occluded and cannot be visualized. Evenin this case, clinical symptoms are fundamentalfor correct interpretation of the findings.

Subclavian Steal EffectA subclavian steal effect can arise from anobstruction of the brachiocephalic trunk orwhen there is SA stenosis or occlusion in theproximal segment before the VA origin. If the cal-iber of the VA is normal, the blood supply to thearm is maintained through a steal effect fromthe contralateral side, via a vertebrovertebralcrossover from the intracranial V4 segments thatunite to form the basilar artery.63–65 In approxi-mately 25% of cases, a carotidobasilar supplywith retrograde flow in the basilar artery or asteal effect via the branches of the externalcarotid artery may be observed.66

Steal effects vary according to the severity andextent of the SA stenosis or occlusion, as report-ed by authors who have investigated this effecteven by means of the cuff upper arm compressiontest, which induces reactive arm hyperemia andconsequently the steal effect.21,46 Summarizing,steal effects are divided into 3 grades dependingon the severity of the hemodynamic effects67:

Initial Subclavian Steal EffectIf the SA stenosis is in the early stages and not yetsevere, the only signs may be a reduction in thesystolic blood flow velocity in the homolateral V2segment with a slight alteration in the resistiveindices. In such cases, blood steal and to-armflow are examined only during arm muscle exer-cise; hyperemia induced by the cuff compressiontest inverts the flow direction in the VA and isassociated with the appearance of to-arm flowon the release of compression (Figure 6A).

Incomplete Subclavian Steal EffectWhen the SA stenosis is moderate, to-arm bloodmay be carried partially through the stenotic SAand partially through a contralateral steal phe-

nomenon. In such cases, under basal conditions,the homolateral VA shows biphasic alternatingflow, which is in the to-arm direction during sys-tole and the to-brain direction during diastole.The cuff compression test increases the to-brainflow during compression and the to-arm flow onthe release of compression (Figure 6B).

Complete and Manifest Subclavian Steal EffectIn cases of high-grade proximal SA stenosis orocclusion, the blood supply to the arm is main-tained exclusively by the contralateral VA, inwhich blood flow velocity increases, and byinversion of the flow direction in the homolater-al VA. The hyperemia cuff compression test doesnot usually induce substantial hemodynamicchanges, except for a slight to-arm flow increaseon the release of compression (Figure 6C).

The subclavian steal effect should always betaken into account when an alteration in the V2segment resistive indices is observed. The possi-bility sonography offers of detecting functionalhemodynamic changes in response to hyper-emic arm compression tests may help identifyconditions that are still in their early stages andmay otherwise escape detection.

Final Considerations

Vascular imaging of posterior circulation may beperformed by means of several neuroimagingtechniques. Intra-arterial angiography is stillconsidered the reference standard, although thistechnique is invasive and carries procedure-related risks. Computed tomographic angiogra-phy and MRA with and without contrast agentsare not only highly sensitive for the posteriorcirculation but are also less invasive than IAA;they cannot, however, be used for vascularscreening purposes because CTA is potentiallytoxic on account of the contrast agents and radi-ation involved, whereas MRA is expensive andnot always available. Interpretation of imagesmay also be operator dependant. Sonography,which combines cervical imaging with TCD orTCCD imaging, contrast agents, and functionaltests, is noninvasive and widely available andsheds light on the pathophysiologic characteris-tics. However, its sensitivity is reported to belower than that of either CTA or CE-MRA

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Figure 6. Cervical color Doppler images of different grades of subclavian steal. A, Initial subclavian steal. Note the reduced systolicvelocity and altered resistive indices in V2. A1, Cuff compression induces the appearance of retrograde flow on the release of com-pression (arrow). B, Incomplete steal. In the basal condition, flow alternates in V2. B1, Cuff compression increases the retrograde flowon the release of compression (arrow). C, Complete steal. In the basal condition, flow is totally anterograde with increased flow veloc-ities on the normal side (left) and retrograde on the subclavian stenosis side (right). C1, Cuff compression increases the retrograde flowon the release of compression (arrow).


because it requires skilled neurosonologists, isoperator dependent, and provides a limited viewof the VAs. In specific cases, data collected frommore than one imaging technique may increasethe diagnostic accuracy of posterior circulationevaluation. In this regard, the advantage ofsonography is that it offers the possibility of cou-pling vascular imaging with real-time data onfunctional hemodynamics.

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