Applications and Advantages of Power Motion-Mode

Doppler in Acute Posterior Circulation Cerebral Ischemia

Georgios Tsivgoulis, MD, RVT; Vijay K. Sharma, MD, RVT; Steven L. Hoover, MD;
Annabelle Y. Lao, MD; Agnieszka A. Ardelt, MD, PhD;
Marc D. Malkoff, MD; Andrei V. Alexandrov, MD, RVT
Background and PurposeEvaluation of posterior circulation with single-gate transcranial Doppler (TCD) is technically
challenging and yields lower accuracy parameters in comparison to anterior circulation vessels. Transcranial power
motion-mode Doppler (PMD-TCD), in addition to spectral information, simultaneously displays in real-time flow signal
intensity and direction over 6 cm of intracranial space. We aimed to evaluate the diagnostic accuracy of PMD-TCD
against angiography in detection of acute posterior circulation stenoocclusive disease.
MethodsConsecutive patients presenting to the emergency room with symptoms of acute (24 hours) cerebral ischemia
underwent emergent neurovascular evaluation with PMD-TCD and angiography (computed tomographic angiography,
magnetic resonance angiography, or digital subtraction angiography). Previously published diagnostic criteria were
prospectively applied for PMD-TCD interpretation independent of angiographic findings.
ResultsA total of 213 patients (119 men; mean age 6516 years; ischemic stroke 71%, transient ischemic attack 29%)
underwent emergent neurovascular assessment. Compared with angiography, PMD-TCD showed 17 true-positive, 8
false-negative, 6 false-positive, and 182 true-negative studies in posterior circulation vessels (sensitivity 73% [55% to
91%], specificity 96% [93% to 99%], positive predictive value 68% [50% to 86%], negative predictive value 95% [92%
to 98%], accuracy 93% [90% to 96%]). In 14 patients (82% of true-positive cases), PMD display showed diagnostic flow
signatures complementary to the information provided by the spectral display: reverberating or alternating flow, distal
basilar artery flow reversal, high-resistance flow, emboli tracks and, bruit flow signatures.
ConclusionsPMD-TCD yields a satisfactory agreement with urgent brain angiography in the evaluation of patients with
acute posterior circulation cerebral ischemia. PMD display can depict flow signatures that are complimentary to and can
increase confidence in standard single-gate TCD spectral findings. (Stroke. 2008;39:1197-1204.)
Key Words: angiography ischemia power motion-mode Doppler stroke transcranial Doppler

osterior circulation ischemia is an important cause of

acute neurological disease and accounts for up to 20% of
ischemic stroke events.1 Delayed, incorrect, or missed diagnosis of vertebrobasilar ischemia is frequent and may result in
serious morbidity or mortality.1 The benefit of intraarterial
thrombolytic therapy in patients with basilar2 4 (BA) or
vertebral4 (VA) artery occlusions has been established as
potentially lifesaving if given within 12 to 24 hours after
symptom onset. Therefore, emergent noninvasive neurovascular assessment of posterior circulation is critical not only
for rapid confirmation of vertebrobasilar stenoocclusive disease, but also for identification of patients at higher risk of
poor outcome as candidates for interventional treatment.
Bedside transcranial Doppler (TCD) is a fast, noninvasive,
widely available diagnostic tool that can detect, localize, and

grade the severity of intracranial arterial obstruction in the

setting of acute ischemic stroke.5,6 However, the ultrasonographic assessment of the vertebrobasilar system is complex
due to difficult access (insufficient ultrasound penetration to
the distal parts of BA or in cases of adipose necks), anatomic
variability, and tortuosity of this vascular region.7 In addition,
evaluation of posterior circulation vessels with single-gate
TCD is technically challenging because it relies on onedepth-at-a-time waveform display without any image guidance and thus yields lower accuracy parameters in comparison to anterior circulation vessels.8 10
Transcranial power motion-mode Doppler (PMD-TCD)
was recently invented by Mark Moehring and Merrill Spencer.11 In its present configuration, PMD-TCD uses 33 overlapping Doppler samples to simultaneously display flow

Received July 17, 2007; final revision received September 5, 2007; accepted September 13, 2007.
From the Comprehensive Stroke Center (G.T., A.A.A., A.V.A.), University of Alabama at Birmingham Hospital, Birmingham, Ala; the Neurosonology
and Stroke Research Program (G.T., V.K.S., S.L.H., A.Y.L., M.D.M., A.V.A.), Barrow Neurological Institute, Phoenix, Az; the Department of Neurology
(G.T.), University of Athens School of Medicine, Athens, Greece; the Division of Neurology, Department of Medicine (V.K.S.), National University
Hospital, Singapore; and the University of Santo Tomas (A.Y.L.), Manila, Philippines.
Correspondence to Andrei V. Alexandrov, MD, Comprehensive Stroke Center, University of Alabama at Birmingham Hospital RWUH M226, 619 19th
St S, Birmingham, AL USA 35294. E-mail avalexandrov@att.net
2008 American Heart Association, Inc.
Stroke is available at http://stroke.ahajournals.org

DOI: 10.1161/STROKEAHA.107.499392

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Figure 1. Normal low-resistance PMD flow signatures in posterior circulation vessels: (A) PCom (depicted as a blue band at a depth of
53 to 72 mm during transtemporal insonation; the middle cerebral artery is depicted as a more superficial red band); (B) VA (suboccipital insonation); (C) BA (transforaminal insonation; (D) top-of-the-basilar (ipsilateral PIPCA depicted as a red band at a depth of 56 to
73 mm and contralateral PIPCA depicted as a blue band at a depth of 74 to 86 mm during transtemporal insonation); (E) posterior inferior cerebellar artery (PICA, depicted as a red band at a depth of 58 to 67 mm during suboccipital insonation; note that the ipsilateral
VA and BA are simultaneously visualized in the PMD display). Note that PMD was configured to display Doppler signal power (brightness) with color coding red (depicting flow toward the probe) and blue (depicting flow away from the probe) for directionality of flow in
real-time motion-mode format.11 The vessels in the schematic drawing of the circle of Willis are colored red and blue according to the
direction of flow during PMD-TCD insonation (red: flow toward the probe; blue: flow away from the probe). PI indicates Gosling-King
pulsatility index. Normal PI values are in the range of 0.6 to 1.1 for normotensive individuals.18

signal intensities and direction over 6 cm of intracranial

space. PMD-TCD provides a color-coded display of all flow
signals detectable at a given position and direction of the
transducer in real time. The brighter PMD colors reflect
stronger intensities, and this road map can serve as a guide
for more complete spectral analysis. Our group and other
investigators have described potential applications and advantages of PMD- over single-gate TCD in detecting acoustic
windows12 and microembolic flow signatures,13 in diagnosing
acute middle cerebral artery occlusions,14 and for evaluating
cervical internal carotid artery stenosis.15 In the present study,
we aimed to evaluate the diagnostic accuracy of PMD-TCD
against angiography for the detection of acute posterior
circulation stenoocclusive arterial disease.

Subjects and Methods

Transcranial Power Motion-Mode Doppler
Our stroke treatment team routinely uses portable 2-MHz PMD-TCD
(Spencer Technologies, Inc) as a noninvasive screening test in the
emergency department for the evaluation of patients with acute (24
hours) stroke. Bedside TCD is carried out simultaneously with
clinical assessment and blood draws by experienced sonographers
using a standardized fast-track (15 minutes) insonation protocol to
identify suspected arterial obstruction.16 All TCD studies are performed and interpreted by stroke neurologists (V.K.S., G.T., A.Y.L.,
M.D.M., A.V.A.) with specialized training and credentials in cerebrovascular ultrasound (certified by the American Society of Neuroimaging and/or the American Registry for Diagnostic Medical
Sonographers).
Ultrasound results were interpreted at bedside by the members of
our neurosonology team who were blinded to angiography results

using previously published diagnostic criteria.9,16 22 An insonation

depth of 40 to 79 mm and of 80 to 105 mm was used for the
identification of VA and BA stenoocclusive disease, respectively,
during transforaminal or suboccipital insonation (Figures 1 to 5). An
insonation depth of 58 to 70 mm with posterior angulation of the
probe during transtemporal insonation was used for identification of
posterior cerebral artery (PCA) stenoocclusive disease.
Posterior circulation occlusions were diagnosed using the Thrombolysis in Brain Ischemia (TIBI) flow-grading system. Occlusion
was defined as the absence of flow (TIBI 0) or the presence of
minimal (TIBI I), blunted (TIBI II), or dampened (TIBI III) flow
signals throughout the VA, BA (Figure 3, Case 2), and PCA at the
respective insonation depths.16,22 Normal vertebral artery (if available) was used as s comparison vessel in cases of suspected basilar
artery occlusion. TIBI grade was compared with the contralateral
vertebral in patients with suspected VA occlusions.22 The presence
of reverberating (oscillating) flow signals in the VA (Figure 2, case
3) and BA (Figure 3, Case 3) both in the PMD and spectral display
was coded as TIBI I.
Maximum mean flow velocities (MFV) were obtained from the
BA, VA, and PCA with a 4-second spectral Doppler data acquisition
sweep. A stenosis of 50% was identified when MFV exceeded 80
cm/s20 and when the stenotic-to-normal MFV ratio was 2.18,19 For
the calculation of the stenotic-to-normal MFV ratio, the following
algorithm was used. If a focal stenotic velocity was found in the
distal VA (50 to 79 mm), BA (90 to 105 mm), or distal PCA (65 to
70 mm), a more proximal prestenotic segment was chosen as normal
(40 to 49 mm for VA, 80 to 89 mm for BA [if unaffected in the
presence of a more distal BA lesion], 58 to 64 mm for PCA). If a
proximal VA (40 to 49 mm) or proximal PCA (58 to 64 mm) stenotic
flow velocity was found, a contralateral depth-corresponding segment was used to calculate the ratio. In case of proximal BA (80 to
89 mm) stenosis, the highest MFV velocity documented in the right
or left VA was used for the calculation of the stenotic-to-normal
MFV. In case of bilateral proximal PCA stenosis (Figure 4, Case 2),

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Figure 2. Diagnostic PMD flow signatures in patients with VA stenoocclusive disease. Case 1: Stenotic PMD flow signatures in a
patient with angiographically proven VA stenosis (A). Note that the stenotic (C) to normal (B) MFV ratio is 2.7 (162/60). Also note the
presence of bruits on the PMD display depicted as flow gaps during systol (yellow circles) that correspond to a bidirectional appearance of systolic bruits (blue circles) on the spectrogram. Case 2: PMD high-resistance flow signatures in a patient with right extracranial VA occlusion (A) and reconstitution (B) of the distal intracranial segment on CTA. Note the difference in PMD flow signatures
between the right (high-resistance flow on PMD display with delayed systolic flow acceleration on spectrogram; (C) and left VA (lowresistance flow on PMD display with sharp systolic flow acceleration on spectrogram). Case 3: Stenotic (A) and occlusive (B) PMD flow
signatures in a patient with right VA stenosis (C; injection of contrast into the right extracranial VA) and left VA occlusion (C, inset; injection of contrast into the left extracranial VA) on DSA. PMD showed reverberating flow (red to blue) signals that correspond to oscillating
flow on spectrogram of the left VA (B). The BA has a blunted flow with delayed systolic acceleration (D; compare with normal BA systolic flow acceleration in Figure 1C) and a lower resistance PI of 0.55 (compare with Figure 1C; PI0.7) that indicates potential compensatory vasodilatation. Embolic track signatures (white circles) on PMD and high-intensity transient signals on spectrogram were
observed during insonation of the VA and PICA (E). PI indicates Gosling-King pulsatility index; PICA, posterior inferior cerebellar artery.

the highest MFV documented in the BA was used for the calculation
of the ratio.
The presence of the following collateral patterns was identified
during the emergent PMD-TCD evaluation:

anterior inferior cerebellar artery, and 90 mm for superior

cerebellar artery in the absence of PCom flow or suspicion of
the reversed BA flow signature) in case of terminal vertebral
artery or BA occlusions.9,18

1. Collateralization through the posterior communicating (PCom)

artery (normal, increased velocity or stenotic-like lowresistance flow directed either away from or toward the probe
in case of BA or internal carotid artery/middle cerebral artery
occlusion, respectively [Figure 4, Case 1] found at depths of
58 to 70 mm with posterior angulation of the transducer over
the temporal window).9,16 In case of proximal BA occlusion
with distal flow reversal through PCom collateralization, the
MFV in the PCom was expected to be equal or greater than the
highest MFV velocity documented in the BA, whereas in cases
with middle cerebral artery/internal carotid artery occlusion,
the MFV in the PCom was expected be equal or greater than
the highest MFV velocity documented in the middle cerebral
artery.
2. Reversed flow in basilar artery (low-resistance flow moving
toward the probe at depths of 80 to 105 mm in the absence of
antegrade basilar flow signals during suboccipital insonation
with or without confirmation of anterior circulation flow with
carotid tapping [Figure 4, Case 3]).17 Of note, carotid tapping
was performed only if extracranial ultrasound examination
previously confirmed the absence of significant stenosis or
hypoechoic plaques in carotid arteries.
3. Compensatory flow increase in the contralateral VA or cerebellar collaterals (arterial flow directed toward the probe with
higher MFV than in VA at depths of 55 to 70 mm for the
posterior inferior cerebellar artery, 75 to 85 mm for the

The presence of the subclavian steal phenomenon was diagnosed if

an alternating flow with reversal of direction toward the probe at the
beginning of the cardiac cycle was displayed both in PMD and
spectral displays.21 In cases in which flow reversal was incomplete
(ie, camelback waveform), the ischemia hyperemia test was
performed either to provoke the steal or to augment flow reversal.
The cuff was inflated to oversystolic blood pressure values and flow
reduction to the arm was maintained for at least 0.5 to 1 minute with
patients opening and closing their fists. The cuff was then quickly
released and any augmentation of flow was monitored (Figure 5,
Case 1). In all patients with no temporal windows, a noncontrastenhanced TCD examination of the orbital (transorbital insonation)
and vertebrobasilar (transforaminal insonation) vessels was routinely
performed. These limited studies were also included in the present
analysis.

Angiography
Computed tomography angiography (CTA) was obtained routinely
as part of our standard neuroimaging assessment of patients with
acute cerebral ischemia and was used as the gold standard for
comparison with TCD in determining the presence of stenoocclusive
intracranial lesions. The elapsed time between symptom onset and
CTA was less than 48 hours for all study subjects and less than 24
hours in 90% of cases. Patients with contraindications to CTA (renal
failure or creatinine levels 1.5 mg/dL, contrast allergy) were

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Figure 3. Diagnostic PMD flow signatures in patients with BA stenoocclusive disease. Case 1: PMD signatures in a patient with BA dissection depicted on brain MRI (A; axial T1 sequence showing intimal flap in the BA lumen, double lumen sign) and MRA (B; dynamic
contrast-enhanced sequence showing smooth tapering of the mid-BA portion, a characteristic feature of dissection resulting from poor
contrast enhancement in the false lumen).28 Insonation of the mid-BA portion with PMD-TCD (90 mm) shows antegrade flow on PMD
display (depicted as a continuous blue band) with elevated MFV (120 cm/sec) on spectral display corresponding to the true lumen as
well as high-resistance retrograde flow on PMD display (depicted as intermittent narrow red bands) with systolic spikes (white circles)
and absent diastolic flow in the spectral display corresponding to the false lumen. Case 2: High-resistance PMD flow signatures in a
patient with angiographically proven mid-BA occlusion (A). PMD showed a high-resistance flow (B) with PI of 1.7 in the BA segment
proximal to occlusion (depth, 78 mm). PMD showed an occlusive flow signature with minimal spectral signals (TIBI grade I) during
insonation of the mid-BA at 91 mm (C). Case 3: Reverberating PMD flow signatures with oscillating flow on spectral display (B) in a
patient with a proximal BA occlusion on CTA (A). PMD and spectrogram showed high-resistance flows (PI1.3) in the left VA (C). PI
indicates Goslin-King pulsatility index.

evaluated with magnetic resonance angiography (MRA). In these

cases, MRA was considered the gold standard for comparison with
TCD. Digital subtraction angiography (DSA) was performed in
selected cases when clinically indicated (intraarterial thrombolysis,
mechanical thrombectomy, discrepant results between CTA/MRA
and ultrasound, poor-quality nondiagnostic MRA or CTA).
High-resolution brain CTA was performed with a multidetector
helical scanner and CT scans were obtained at a 1.3-mm slice
thickness with a 1-mm interval during a bolus injection of 70 mL of
contrast material. Multiplanar reformats were created in the axial,
coronal, and sagittal plane. In patients who underwent both DSA and
noninvasive angiography, DSA was used for final analysis. If both
MRA and CTA were performed in a patient, we used the test done
closest in time to TCD. The degree of stenosis was defined as the
narrowest vessel diameter divided by a normal diameter of the vessel
by the Warfarin-Aspirin Stroke in Intracranial Disease (WASID)
trial criteria.23 The choice of a normal diameter was made according
to a standard algorithm for selection of a nonaffected denominator
(choice 1: prestenotic segment, choice 2: poststenotic segment,
choice 3: feeding vessel).23 Significant intracranial artery stenosis
was considered when the narrowest diameter of the residual lumen
was less than 50%. Intracranial artery occlusion was diagnosed when
no reconstitution of distal flow was detected. An attending-level staff
neuroradiologist and stroke neurologist evaluated neurodiagnostic
imaging studies independently of TCD results. The neuroradiological interpretation in the medical records was considered the official
reading for the purposes of the study. This study was approved by the
Institutional Review Board of our institution.

Statistical Analysis
Continuous variables are presented as mean (SD) or as median
(range). Noncontinuous variables are presented as percentages. The
accuracy parameters (sensitivity, specificity, positive predictive

value, negative predictive value, and overall accuracy) with their

corresponding 95% CI of the screening test (TCD) against angiography were calculated after computation of true positive, falsepositive, true-negative, and false-negative values. Patients with
absent temporal windows were included in the computation of
accuracy parameters with only results in the posterior circulation
assessment being considered for the analysis. The Statistical Package
for Social Science (SPSS Inc, version 11.5 for Windows) was used
for statistical analyses.

Results
A total of 213 patients (119 men, mean age 6516 years)
presenting with symptoms of acute (24 hours) cerebral
ischemia underwent emergent neurovascular assessment with
PMD-TCD within 24 hours from symptom onset and angiography (CTA, MRA, or DSA) within 48 hours from ictus
(Table 1). Thirty-eight (18%) patients received intravenous
(n29) or intraarterial thrombolysis (n9) (median National
Institutes of Health Stroke Scale score 10; range, 4 to 26
points). No delay in treatment resulted from ultrasound
testing. One hundred thirteen (53%) patients were found
ineligible for thrombolysis and 62 patients (29%) were
diagnosed with transient ischemic attacks.
Bedside PMD-TCD revealed intracranial artery stenosis or
occlusion in the posterior circulation in 24 cases: VA (n11),
BA (n8), and PCA (n5). Temporal acoustic windows
were absent in 20 cases (9%). Angiography findings were
positive for the posterior circulation stenoocclusive disease in
12% (n26) of the study population and revealed unremark-

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Figure 4. Diagnostic PMD flow signatures in patients with collateralization through the PCom artery or stenoocclusive disease in the
PCA. Case 1: PMD flow signatures in a patient with angiographically proven moyamoya-type disease affecting the anterior circulation
vessels and collateralization through the right PCom artery (AC). Transtemporal insonation showed a stenotic-like, low-resistance flow
directed toward the probe (accompanied by a soft wind-blowing sound) in the right PCom (E). The BA has a compensatory flow
velocity increase (G; stenotic-to-normal ratios 2 throughout the vertebrobasilar system). Insonation of the anterior circulation vessels
showed blunted flow with delayed systolic flow acceleration and low PI in the right middle cerebral artery (D) and the terminal internal
carotid artery (F). Case 2: Stenotic PMD flow signatures (BC) in a patient with bilateral P1-PCA stenoses on CTA (A). The highest MFV
documented in the distal BA (47 cm/sec, depth 94 mm; image not shown) was used for the calculation of stenotic-to-normal ratio in
the right (103/472.2) and left (138/472.9) PCA. Case 3: Reversed mid and distal BA flow signatures on PMD (C) in a patient with a
proximal BA occlusion on CTA (A). Both PMD and spectrogram showed a response to the left carotid tapping (white arrows, E) indicating that the reversed BA flow is supplied from the anterior circulation vessels. Transtemporal insonation showed the stenotic-like, lowresistance flow directed away from the probe in the left PCom (D) also seen on axial CTA sequences (B; white square).

able posterior circulation vessels in the remaining cases

(n187 [88%]). DSA was performed in 16 cases, whereas a
total of 31 patients with contraindications to CTA were
evaluated with MRA. Compared with angiography, PMDTCD showed 17 true-positive, 8 false-negative, 6 falsepositive, and 182 true-negative studies (sensitivity 73% [55%
to 91%], specificity 96% [93% to 99%], positive predictive
value 68% [50% to 86%], negative predictive value 95%
[92% to 98%], accuracy 93% [90% to 96%]). The accuracy
parameters with their corresponding CIs for TCD in detecting
arterial stenosis or occlusion in VA, BA, and PCA are
presented in Table 2.
Absent temporal windows led to one false-negative PCA
study. Three of the remaining 7 false-negative studies occurred in the distal BA (n2) or in the distal P2-PCA
segment (n1). Also, incorrect insonation of a single existing
VA (VA was insonated from both sides during suboccipital
insonation) led to 2 other false-negative studies. Finally, in
cases of missed VA stenosis, the MFVs were within the
normal range (72 cm/s and 67 cm/s) despite an abnormal
stenotic-to-normal ratio (2.2 and 2.4, respectively). These
patients were 72 and 81 years old.
Two of 6 false-positive TCD cases were attributed to the
minimal flow signals due to suboptimal angle of insonation in
tortuous distal VA (n1) and distal BA (n1). Also, the
presence of a blunted flow signal (TIBI grade II) with low
MFV throughout a dolichoectatic BA led to another falsepositive study.

Misinterpretation of collateral flow signals in PCom (n1)

in a patient with extracranial internal carotid artery occlusion
led to the diagnosis of a false-positive PCA stenosis. In a
patient with dampened flow signals (TIBI grade III) in the
intracranial VA, CTA findings were attributed to hypoplasia
and not an acute occlusion. Finally, in one patient, the
stenotic VA velocities were not confirmed by CTA after
intravenous thrombolytic therapy. This patient had a 4-point
reduction in the National Institutes of Health Stroke Scale
score during thrombolysis with complete recanalization and
time delay of 105 minutes between TCD and CTA causing
this discrepancy.
In 16 cases (8%), PMD showed findings complementary to
brain CTA or MRA: (1) flow reversal in the distal BA with
the proximal BA occlusions; (2) flow reversal in the distal
VA with the proximal intracranial VA occlusions; (3) realtime embolization distal to a stenoocclusive disease (Figure 2,
Case 3); (4) blunted flow signals throughout intracranial VA
in patients with extracranial severe stenoocclusive disease
(both cases confirmed by subsequent neck CTA; Figure 2,
Case 2); and (5) alternating PMD flow signals indicative of
subclavian steal phenomenon (Figure 5, Case 1).
Furthermore, in 14 patients (82% of true-positive cases),
PMD flow signatures were also complementary to the findings of the spectral TCD display: (1) reverberating flow
signatures (Figure 2, Case 3, Figure 3, Case 3); (2) alternating
flow signature (Figure 5, Cases 1 and 2); (3) high-resistance

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Figure 5. PMD alternating flow signatures.

Case 1: Alternating flow signals in the left
VA at 46 mm (B) with complete flow reversal after hyperemiaischemia cuff test (C)
indicating subclavian steal phenomenon
in a patient with left subclavian artery
stenosis on MRA (A). Note that the
high-resistance flow toward the probe
(depicted as narrow intermittent red bands
on PMD display) corresponds to the flow
reversal in the VA during systole, which
now supplies the high-resistance system
of the arm. Low-resistance flow (depicted
as wide intermittent blue bands on PMD
display) in the VA is seen during late systolic diastole and has a normal direction
because lesser pressures are necessary to
perfuse the low-resistance brain vasculature. Case 2: Alternating flow signals in
the left VA in a patient with intracranial
VLA dissection on CTA (1) and MRA
(1, inset; fat-saturation axial T1 sequence
depicting the intramural hematoma).29
PMD-TCD showed alternating flow signatures with high-resistance flow reversal
during systole (narrow red bands on PMD
display) in the left VA (C) and normal lowresistance antegrade flow in the right VA
at a depth of 66 mm. No flow reversal
augmentation was found during the hyperemia cuff test (images not shown) and the
left subclavian artery stenosis was also
excluded by neck CTA (image not shown).

flow signature (Figure 3, Cases 2 and 3); (4) embolic tracks

flow signature (Figure 2, Case 3); and (5) disturbed flow
(bruit) signature (Figure 2, Case 1).
Explanations as to how these PMD findings provide
additional diagnostic value are given in the figure legends.

Discussion
Our study showed that bedside PMD-TCD examination
yields satisfactory agreement with urgent brain angiography
in patients presenting with symptoms of acute posterior
circulation cerebral ischemia. Moreover, in a substantial
number of patients (82% of the true-positive cases), PMD
Table 1. Baseline Characteristics of the Study Population
(n213)
Variable
Mean age, years (SD)

Percent
65 (16)

Male sex

56

Hypertension

68

Diabetes mellitus

32

Ischemic heart disease

27

Hypercholesterolemia

49

Atrial fibrillation
Median National Institutes of Health Stroke Scale score
(range)*

19
12 (425)

Continuous variables are presented as mean (SD) or as median (range).

Noncontinuous variables are presented as percentages.
*Tissue plasminogen activator-treated patients.

display showed diagnostic flow signatures complementary to

the information provided by the spectral display: reverberating or alternating flow, distal BA flow reversal, highresistance flow, emboli-tracking, and disturbed flow
signatures.
The accuracy parameters of PMD-TCD in the present
study are higher than those of previous reports on the
diagnostic accuracy of single-gate TCD in the evaluation of
posterior circulation vessels.8 10,24 According to the recently
published results of the Stroke Outcomes and Neuroimaging
of Intracranial Atherosclerosis (SONIA) trial, the positive
predictive value of single-gate TCD for detection of stenosis
in the intracranial VA and BA were 45% and 36%, respectively (diagnostic cutoff for MFV was 80 cm/s) when
compared with DSA with negative predictive value of 84%
and 90%, respectively.24 We hypothesize that the higher yield
of PMD-TCD may be related to its ability to visualize flow on
the PMD display along tortuous and long arterial segments
(Figure 1) that may not be readily appreciated by sonographers during a single-gate TCD examination.12 In addition,
the ease of identification of turbulent flow on PMD display
(flow gaps during systole; Figure 2, Case 1) prompts sonographers to perform a more thorough spectral sample volume
interrogation because it topographically maps the location
and extent of turbulence. Finally, PMD permits easy identification of retrograde flow in the BA that may be caused
either by retroperfusion of the distal BA through the anterior
circulation in cases of proximal BA occlusion (Figure 4, Case
3) or by BA dissection (retrograde high-resistance flow in the
false lumen; Figure 3, Case 1).

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Table 2. Accuracy Parameters for Detecting Intracranial Stenoocclusive Lesions in the

Posterior Circulation Vessels by PMD-TCD
Sensitivity
(95% CI)

Specificity
(95% CI)

Positive Predictive
Value (95% CI)

Negative Predictive
Value (95% CI)

VA

66% (3993%)

98% (96100%)

72% (4598%)

98% (96100%)

BA

75% (50100%)

99% (98100%)

75% (50100%)

99% (98100%)

PCA

80% (45100%)

99% (98100%)

66% (28100%)

99% (98100%)

Vessel

In the present report, we implemented a stenotic-to-normal

MFV ratio 2 in addition to standard MFV thresholds in our
diagnostic criteria for the detection of intracranial stenosis,
because the addition of this ratio to the MFV cutoff improved
TCD accuracy in diagnosing anterior circulation stenoses.19,25
These ratios were not taken into account in the analysis of
WASID-SONIA findings.24 Because PMD simultaneously
shows vessel segments with turbulent and laminar flow over
a wide range of depths, it permits better interrogation of the
affected and nonaffected vessel segments. This, in turn,
facilitates a more reliable estimation of stenotic-to-normal
MFV ratios and possibly decreases erroneous vessel identification while resulting in a more thorough vessel interrogation
compared with a single-gate TCD examination.9
Detection of flow reversal in retroperfused BA on PMD
display may constitute another factor contributing to the
higher diagnostic accuracy of this neurovascular imaging
modality in the evaluation of posterior circulation stenoocclusive disease. According to our previous experience, BA
flow reversal can be missed with the single-gate TCD,
whereas its detection with PMD correlated with better outcomes after the proximal BA occlusion.17 Similar to our
present findings, 2 recent studies of posterior circulation
vessels with transcranial color-coded duplex ultrasound imaging, which allows simultaneous visualization of anatomic
structures in color-coded B-mode images and Doppler flow,
also reported satisfactory agreement with angiography in
cases of suspected BA occlusion.26,27
A plausible alternative explanation for the different accuracy parameters between our present report and previous
single-gate TCD studies may be related to the elapsed time
interval between the screening test and the gold standard.
Longer time delays between ultrasound and angiography may
provide ample time for thrombus propagation, dissolution, or
reocclusion to occur, accounting for the lower predictive
values in previous reports. Notably, in one study, 25% of
middle cerebral artery stenoses had completely disappeared 6
months after stroke, suggesting an embolic rather than atherothrombotic process.28
In our series, PMD display depicted diagnostic flow
signatures that were complementary to the information provided by the spectral display in the majority of the truepositive cases. The presence of reverberating or highresistance flow signatures on PMD can facilitate the rapid
diagnosis and localization of vertebrobasilar artery occlusion.
This observation is in keeping with the findings by Saqqur et
al who reported that absent or high-resistance PMD flow
signatures can reliably diagnose 87% of angiographic-proven
proximal middle cerebral artery occlusions.14 Furthermore,
subclavian steal phenomenon can be easily identified by

alternating PMD flow signatures (Figure 5, Case 1). Of note,

however, a differential diagnosis that needs to be kept in mind
is dissection of intracranial VA,29,30 because it can also
present with alternating flow signatures (Figure 5, Case 2).
Also, the PMD display has been shown to be more sensitive
for the detection of embolic flow signatures than the singlegate spectral display, because it allows simultaneous display
of flow over long arterial segments as well as more than one
vessel.13 In our series, we noted PMD embolic tracks in the
cerebellar arteries (depicted as red bands on PMD display
over different depths), whereas our sample volume interrogation was set in depths corresponding to VA or BA. Because
the cerebellar arteries are not routinely insonated during the
assessment of posterior circulation vessels with single-gate
TCD, the presence of embolization distal to an extracranial or
intracranial stenoocclusive arterial lesion may have not been
identified without PMD-TCD.
Our study has limitations, including the need for considerable sonographer expertise to complete and interpret testing
promptly and efficiently. Our study also identified clinical
situations when PMD-TCD could not be reliably interpreted,
including limited visualization of the distal BA, incorrect
insonation through both suboccipital windows of a single
existing VA, and absent temporal windows rendering unfeasible the insonation of PCA. Moreover, it needs to be
acknowledged that PMD cannot reliably differentiate a hypoplastic intracranial segment of VA with low-velocity, highresistance flow signals from that of an acutely occluded VA
with dampened residual flow signals. In addition, to avoid
interobserver variation, angiographic measurements of the
degree of stenosis by a second investigator would have been
methodologically advantageous should they had been performed. MFV values also decrease with increasing age and
the fact that we did not use age-dependent thresholds for
detection of intracranial stenoocclusive disease should be
acknowledged as another methodological shortcoming of the
present report. Finally, the present study was not designed to
compare the accuracy parameters of single-gate TCD with
PMD in the evaluation of posterior circulation ischemia and
therefore, direct conclusions regarding the potential superiority or inferiority of one imaging modality over another cannot
be inferred. In fact, PMD is complementary to spectral TCD,
which provides waveforms and velocities used for diagnosis
of arterial patency and lesions.
On the other hand, a methodological strength of the present
report is that both neurovascular assessments (PMD and
angiography) were performed in the emergency setting with a
relatively narrow time window. We also attempted to minimize selection bias by including consecutive patients presenting with symptoms of acute cerebral ischemia who under-

1204

Stroke

April 2008

went angiographic and PMD-TCD neurovascular assessment

irrespective of whether their clinical findings were indicative
of an anterior or posterior circulation ischemic event and of
whether their symptoms resolved or persisted during the first
24 hours of ictus.
In conclusion, emergent PMD-TCD yields a substantial
proportion of posterior circulation stenoocclusive arterial
lesions with satisfactory agreement with angiography in the
acute stroke setting. In addition, in selected cases, it offers
information complementary to noninvasive angiography or to
single-gate TCD. These findings provide preliminary evidence indicating that PMD-TCD is a promising and valuable
noninvasive imaging modality for the emergent bedside
assessment of posterior circulation that can be used as a rapid
vascular screening method to reliably exclude vertebrobasilar
artery occlusion and to select potential candidates for invasive angiography that may ultimately undergo subsequent
endovascular interventions if the ultrasound findings are
confirmed by DSA.

Acknowledgments
G.T. is recipient of a neurosonology fellowship grant from the
Neurology Department of Eginition Hospital, University of Athens
School of Medicine, Athens, Greece.

Disclosures
None.

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