(Stroke. 1999;30:87-92.)
© 1999 American Heart Association, Inc.
Original Contributions |
Assessment of 
50% and <50% Intracranial Stenoses by Transcranial Color-Coded Duplex Sonography
From the Department of Neurology, University Hospital of Zürich (R.W.B.), and Departments of Neurology (H.P.M.) and Neuroradiology (G.S.), University Hospital of Bern (Switzerland).
Correspondence to Ralf W. Baumgartner, MD, Department of Neurology, University Hospital, Frauenklinikstr 26, CH-8091 Zürich, Switzerland. E-mail Strusbmg{at}neurol.unizh.ch
 |
Abstract |
|---|
 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Background and Purpose—A favorable risk-benefit ratio for warfarin compared with aspirin has been reported for the prevention of major vascular events in symptomatic
50% intracranial stenoses.
Transcranial color-coded duplex sonography (TCCS) criteria
providing an accurate detection of 50% and <50% stenoses
of the anterior, middle, and posterior cerebral arteries and basilar
and vertebral arteries were evaluated retrospectively with angiography
used as the standard of reference.
Methods—Prospectively collected TCCS, extracranial color-coded
duplex sonography, and intra-arterial digital subtraction
angiography data of 310 patients were reviewed. The patients had
angiography for confirmation of symptomatic extracranial
70% carotid stenoses, symptomatic
stenoses (peak systolic velocity higher than the
corresponding mean value +2 SDs of 104 normal subjects), and occlusions
of the middle cerebral or basilar artery previously assessed by
ultrasound. The sonographer was not aware of angiographic findings.
Results—TCCS would have detected all 31 of 50% intracranial
stenoses with 1 false-positive and 35 of 38 <50%
stenoses with 3 false-positives. One of 69 stenoses
(1%) and 280 of 2741 normal arteries (10%) were missed because of
inadequate insonation windows. The corresponding peak systolic
velocity cutoffs for 50%/<50% stenoses were 155/120
cm/s (anterior cerebral artery), 220/155 cm/s (middle cerebral
artery), 145/100 cm/s (posterior cerebral artery), 140/100 cm/s
(basilar artery), and 120/90 cm/s (vertebral artery).
Conclusions—TCCS may reliably assess 50% and <50% basal
cerebral artery narrowing and prove useful for noninvasive management
of patients with symptomatic intracranial stenoses.
Key Words: anticoagulants • aspirin • stenosis • ultrasonography, transcranial
|
Introduction |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Atherosclerotic narrowing of the intracranial cerebral arteries is assumed to cause approximately 10% of ischemic strokes.1 2 Secondary stroke prevention in patients with transient ischemic attack or ischemic stroke caused by a stenosed intracranial artery has been empirical. The recently published Warfarin-Aspirin Symptomatic Intracranial Disease study, however, suggests that oral anticoagulation is more effective than aspirin for preventing major vascular events in patients with
50% symptomatic intracranial
stenoses.3 This study used catheter angiography
for the assessment of cerebral artery narrowing. Because of the risk,
inconvenience, and cost4 5 associated with angiography,
the primary use of a noninvasive diagnostic method such as
transcranial color-coded duplex sonography (TCCS) would be
preferable. Conventional transcranial Doppler sonography is of established value for detecting stenoses of the intracranial arteries.6 7 8 9 10 11 12 13 14 TCCS criteria for detection and quantification of intracranial stenoses have not yet been established.
The purpose of the present study was to evaluate TCCS criteria
providing the best possible diagnostic accuracy for
detecting 50 and <50% intracranial stenoses with cerebral
angiography used as the standard of reference.
|
Subjects and Methods |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Patient Recruitment and Inclusion and Exclusion Criteria
Between November 1992 and December 1996, 310 consecutive patients (102 women, 208 men; mean±SD age, 56±16 years) with cerebral or ocular ischemic events were first examined by TCCS and extracranial color-coded duplex sonography (ECCS) and thereafter by cerebral intra-arterial digital subtraction angiography. Cerebral angiography was done for confirmation of symptomatic
70% carotid stenoses,
symptomatic stenoses, and occlusions of the middle
cerebral (MCA) or basilar (BA) arteries. Angiograms were done in
symptomatic 70% carotid stenoses for
confirmation of ultrasonic diagnosis before carotid
endarterectomy,15 in MCA or BA
occlusions with strokes of 
6 hours' duration to evaluate whether
subjects were candidates for local arterial
fibrinolysis,16 and with strokes of >6
hours' duration for diagnostic purposes. TCCS, ECCS,
cerebral angiographic, and the corresponding clinical, CT, or MRI
findings were collected prospectively in a database.
The presenting ischemic ocular or cerebral deficits were
classified as amaurosis fugax (monocular blindness lasting 24 hours),
retinal infarct (monocular blindness lasting >24 hours), transient
ischemic attack (focal neurological deficit lasting 24
hours), or stroke (focal neurological deficit lasting >24 hours). Two
hundred one patients had ischemic strokes, 78 had transient
ischemic attacks, 21 had amaurosis fugax, and 10 had retinal
infarcts. The median interval between ultrasonic studies and the onset
of stroke was 31 days (range, 2 to 126 days), and that between
ultrasonic studies and cerebral angiography was 2 days (range, 0 to 6
days).
Patients were excluded from the study if the indication for cerebral angiography was search for a tumor, aneurysm, vasospasm, arteriovenous fistula, sinovenous thrombosis, or a diagnostic workup of intracranial hemorrhage and vascular malformation.
ECCS Studies
The extracranial cerebral arteries were examined with an Acuson
128 XP/10 equipped with a 5.0/7.0-MHz linear scan.
Ultrasonographic evaluation of arterial stenoses
and occlusions was performed according to previously published
criteria.17 18
TCCS Studies
The intracranial cerebral arteries were studied with an
Acuson 128 XP/10 equipped with a 2.0/2.5-MHz 90° sector scan with the
same Doppler energy output and method of examination as described
previously.19 In brief, the MCA, anterior (ACA),
precommunicating (P1), and postcommunicating (P2) posterior (PCA)
cerebral arteries were insonated through the temporal window with the
patient in a supine position, whereas the BA and intracranial vertebral
(VA) arteries were investigated through the foramen magnum with the
patient in a sitting position. Each large cerebral artery was
investigated by spectral Doppler sonography with the color-coded
Doppler signal used as a "road map" for the presence of
stenoses, occlusions, and cross-flow through the circle of
Willis (see below). Flow direction (antegrade or reversed) and peak
systolic (PSV) and end-diastolic (PDV) velocities
were noted for every insonated artery. In case of suspicion of an
intracranial stenosis (see below), the presence of
low-frequency, high-intensity Doppler signals was also evaluated.
Angle correction was performed when the Doppler sample volume was
located within a straight vessel segment 20 mm in
length.20
The sonographer was aware of extracranial ultrasonographic findings but was blinded to the results of cerebral angiography.
An intracranial stenosis (Figures 1
and 2)
was diagnosed during prospective data collection when spectral
Doppler sonography showed both a focal increase of PSV and/or PDV
that was higher than the mean value +2 SDs for the corresponding
cerebral artery of 104 normal subjects reported
previously21 and low-frequency, high-intensity Doppler
signals. ACA velocity is often increased in the presence of cross-flow
through the anterior communicating artery22 and in
high-grade stenosis or occlusion11 23 of the
ipsilateral MCA. A high-grade stenosis of the MCA was diagnosed
with the use of the velocity cutoffs established by Röther et
al.13 P1 PCA velocity is enhanced in case of collateral
flow through the posterior communicating artery to the carotid
artery.8 22 24 Consequently, no ACA and P1 PCA
stenoses were diagnosed when TCCS findings suggested the
presence of cross-flow through the anterior communicating artery and
posterior communicating artery, respectively, and no ACA
stenosis was diagnosed when TCCS findings suggested the
presence of high-grade stenosis or occlusion of the ipsilateral
MCA.
|
|
An intracranial occlusion was diagnosed when the Doppler signal of the corresponding cerebral artery was lacking and other ipsilateral basal cerebral arteries were identified.23 25 For diagnosis of occlusions of the intracranial VA or BA, the criteria established by von Büdingen and Staudacher26 also had to be fulfilled. Cross-flow through the circle of Willis was assessed as reported recently.27
Angiographic Studies
Selective intra-arterial digital subtraction
angiography (Philips Diagnost ARC A) was performed by a femoral artery
approach in both ICAs in all patients, in both VAs in 261 patients, and
in 1 VA in 49 patients. The injected volume of contrast medium was 5 to
8 mL Ultravist 300 (Iopromidum, Schering AG). Standard anteroposterior
and lateral views (512x512 matrix; since December 1993, 1024x1024
matrix) of the extracranial and intracranial circulation were obtained
routinely. The angiograms were reviewed retrospectively and
independently at separate reading sessions by 2 of the authors (H.P.M.,
G.S.), who were not aware of ultrasound findings. Extracranial carotid
stenosis was measured by the North American
Symptomatic Carotid Endarterectomy
Trial technique.15 For the assessment of intracranial
stenosis, the vessel being evaluated was measured at its
point of maximal narrowing and compared with the angiographically
normal section of the vessel adjacent to the stenosis
to determine the degree of stenosis (normal lumen
diameter-residual lumen/normal lumen diameter). Finally, each
intracranial artery was graded separately as follows: no
stenosis, stenosis <50%, stenosis 50%,
occlusion.
Statistical Analysis
Differences of cerebral artery velocities in patients without,
with <50%, and with 50% intracranial stenoses
at angiography were compared by nonparametric ANOVA
(Mann-Whitney U test). The same statistical test was used to
compare intrastenotic MCA velocities and the degree of
intracranial stenosis at angiography in patients with and
without additional 70% to 100% obstructions of the ipsilateral
extracranial carotid arteries. The nonparametric Spearman
rank correlation coefficient was used to assess consistency
of interpretation of cerebral angiograms between both
observers.28 Two-sided probability value of <0.05
was considered significant.
|
Results |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Angiography showed intracranially 69 stenoses (31
50%,
38 <50%) in 51 patients (16%) and 20 occlusions in 18 patients
(6%). Thirty-nine patients had 1, 8 patients had 2, 2 patients had 3,
and another 2 patients had 4 stenoses. Ten stenoses
were located in the ACA, 29 in the MCA, 15 in the PCA, 7 in the BA, and
8 in the VA. Sixteen patients had 1 occlusion, and 2 patients had 2
occlusions. One occlusion was located in the ACA, 8 were located in the
MCA, 2 in the distal P2 PCA, 3 in the BA, and 6 in the VA. TCCS identified 2461 of 2741 intracranial arteries (90%) examined by cerebral angiography. In detail, TCCS identified 515 of 620 ACAs (83%), 563 of 620 MCAs (91%), 557 of 620 PCAs (90%), 291 of 310 BAs (94%), and 535 of 571 VAs (94%).
According to the criteria shown in Tables 1 and 2, TCCS would have detected 66 of
69 stenoses (96%) with 4 false-positives; 1 narrowed ACA was
missed because of an inadequate temporal bone window. In addition, 18
of 20 occlusions (90%) were identified by ultrasound.
|
|
PSVs in arteries with 50%, with <50%, and without stenoses
are reported in Table 3. PDVs are not
reported because they were not found to be as sensitive and accurate as
the PSV values for the assessment of stenoses.
|
Ultrasonic Detection of 50% Stenoses
When we use the PSV cutoff values given in Table 1
as
diagnostic criteria, TCCS would have detected all 31
stenoses with 1 false-positive PCA stenosis. The
false-positive PCA stenosis was insonated 4 days before
angiography and showed a PSV of 154 cm/s; no angle correction was done.
Reexamination 1 day after angiography showed a PSV of 128
cm/s.
Ultrasonic Detection of <50% Stenoses
Using the PSV cutoff values reported in Table 2 as
diagnostic criteria provided 2 false-negative MCA and 3
false-positive ACA stenoses; no angle corrections were done.
Both false-negative stenoses were located in MCAs with downward
convex courses at angiography. In 1 false-positive ACA
stenosis, the contralateral ACA was hypoplastic at angiography,
and PSV was 48 cm/s. The other 2 false-positive ACA stenoses
had symmetrical ACA diameters at angiography, and the contralateral ACA
showed PSVs of 78 to 85 cm/s.
Intrastenotic PSVs in the MCAs of 7 Patients With and 22
Patients Without Additional 70% to 100% Obstructions of the
Ipsilateral Extracranial Carotid Arteries
Intrastentotic PSVs were slower in MCAs with (mean±SD, 174±24
cm/s; range, 157 to 215 cm/s) compared with MCAs without (mean±SD,
237±73 cm/s; range, 172 to 400 cm/s) additional 70% to 100% carotid
obstructions (P<0.05). The degree of narrowing showed a
nonsignificant trend to be lower in MCAs with (mean±SD, 39±4%;
range, 36% to 41%) compared with MCAs without (mean±SD, 55±16%;
range, 30% to 80%) additional 70% to 100% carotid obstruction.
Ultrasonic Detection of Intracranial Occlusions
Ultrasound detected 18 of 20 angiographically confirmed
occlusions. Ultrasound misdiagnosed no stenosis as occlusion.
Conversely, 2 occlusions located in the distal P2 PCA were missed.
Interobserver Variability in the Interpretation of Cerebral
Angiograms
The Spearman rank correlation coefficient between both readers of
angiograms was statistically significant for differentiating between no
stenoses, stenoses <50%, stenoses
50%, and occlusions (r=0.93,
P<0.0001).
|
Discussion |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
With the use of the diagnostic criteria elaborated in this study, TCCS would have detected all
50% intracranial
stenoses with 1 false-positive and 92% of <50% intracranial
stenoses with 3 false-positives. In addition, 90% of
intracranial occlusions were identified by ultrasound. Adequate Doppler signals were obtained in 68 of 69 angiographically proven intracranial stenoses (99%). This finding is probably incidental because the detection rate for the different cerebral arteries was 83% to 94%, which is in accord with previous TCCS studies reporting rates of 80% to 98%.22 25 29 30 31 Recent studies using echo contrast agents provided conclusive TCCS examinations in 67% to 72% of patients with ischemic cerebrovascular disease and ultrasound-refractory temporal windows,32 33 suggesting that the evaluation of intracranial arteries may become possible in most patients with ischemic stroke.
The low number of false-negative intracranial stenoses found in
this study may be related to the angiographically proven absence of
branch occlusions in the territory of the narrowed arteries. Multiple
MCA branch occlusions are associated with decreased velocities in the
MCA main stem14 and in our experience may cause normal
intrastenotic velocities and false-negative TCCS findings in
case of MCA main stem narrowing. The principal reason for the absence
of intracranial branch occlusions was that most TCCS investigations
were performed in the chronic phase of cerebral infarction, when branch
occlusions were already recanalized.34 35 Another
explanation for the low number of false-negative stenoses is
that the color Doppler signal was used as a road map to visualize
both the vascular anatomy and focal areas with increased flow
velocities. Thus, the sonographer was able to investigate all vessel
segments by spectral Doppler sonography and to estimate whether the
placement of the angle indicator was adequate (Figure 1) or not
(Figure 2). When a stenosis was located in a curved
segment and prevented the use of angle correction, the position of the
ultrasound probe was changed to obtain the smallest insonation angle
possible. It is important to note that intrastenotic velocity
increase may persist for a few centimeters ("jet") and surpass the
anatomic extent of narrowing.36 The jet is likely to
increase the probability of detecting a stenosis and may lead
to a more favorable angle of insonation in curved vessels.
Nevertheless, TCCS missed 2 <50% stenoses located in MCAs
with downward convex courses at angiography. This suggests that the
absence of angle correction resulted in the failure to detect both MCA
stenoses and that stenoses located in curved
intracranial arteries may represent a diagnostic
pitfall of TCCS.
Interestingly, no intracranial stenosis would have been missed
in patients with additional 70% stenoses of the ipsilateral
extracranial carotid artery. As expected, intrastenotic MCA
velocities were lower in patients with compared with those without
additional 70% ipsilateral carotid stenoses
(P<0.05). This finding may also have resulted from the
trend of patients with additional 70% carotid stenoses to
have a lower average degree of MCA stenosis at angiography.
There were 1 false-positive 50% P2 PCA stenosis and 3
false-positive <50% ACA stenoses in this series. Inadequately
high insonation angles may result in the measurement of high flow
velocities and false-positive stenoses. No angle correction was
performed in ACA stenoses (Figure 2) and the
false-positive PCA stenosis because the angle corrector was
only used when color Doppler imaging suggested the presence of
straight vessel segments 20 mm in length.20 Thus,
inadequately high insonation angles were probably not the cause of the
false-positive stenoses. TCCS may misdiagnose intracranial
stenoses in conditions with increased cerebral blood flow, such
as cross-flow through the circle of Willis, leptomeningeal anastomoses
supplied by the ACA in the presence of high-grade stenosis or
occlusion of the MCA, and arteriovenous
malformation.8 11 23 37 38 No ACA stenosis was
diagnosed when ultrasonic findings indicated the presence of collateral
flow through the anterior communicating artery or high-grade
stenosis or occlusion of the ipsilateral MCA. Patients with
angiographic signs of arteriovenous malformations were excluded. Thus,
increased blood flow is a very unlikely explanation for the
false-positive stenoses. Asymmetrical ACAs are associated with
higher velocities in the larger vessel.39 This might be
the cause in 1 false-positive <50% ACA stenosis since the
contralateral ACA was hypoplastic and showed slow velocities.
Intracranial vasospasm, vasculitis, and thromboembolism may change the
degree of luminal narrowing over time. Patients with cerebral vasospasm
and vasculitis were excluded. However,
recanalization is the most likely cause of the
false-positive PCA stenosis because the follow-up TCCS
examination performed 1 day after cerebral angiography indicated the
regression to a <50% stenosis.
Cerebral angiography was used as the standard of reference in the present study. Nevertheless, this technique may have some limitations. Biplanar assessment of intracranial stenoses is mostly not obtainable,12 and reliable measurement of intrastenotic diameter is often difficult because of the small vessel size. Conversely, velocities measured by ultrasound are inversely proportional to the diameter squared of the insonated vessel. TCCS may thus be more sensitive for detection of <50% intracranial stenoses by principles of mathematics over angiography that measures diameter only. However, there are no data available to prove this hypothesis. This or interindividual differences in arterial diameter13 may be the cause of the other 2 false-positive <50% ACA stenoses.
It is remarkable that no intracranial stenosis was misdiagnosed as occlusion. Conversely, ultrasound missed 2 occlusions located in the distal P2 PCA, probably because the adjacent superior cerebellar artery was misinterpreted as PCA. Because of the low number of cerebral artery occlusions observed in this study, the diagnostic accuracy for ultrasonic assessment was not calculated.
As expected, the prevalences for intracranial stenoses and occlusions were higher than those found in previous investigations.40 41 42 Difference in patient selection is the most likely cause since cerebral angiography was only performed when ultrasound suggested the presence of extracranial or intracranial occlusive vascular disease.
The Warfarin-Aspirin Symptomatic Intracranial Disease
study3 reported a favorable risk-benefit ratio for
warfarin compared with aspirin for the prevention of major vascular
events in patients with symptomatic 50% to 99%
intracranial stenoses. The present results indicate that
TCCS may provide a reliable and noninvasive assessment of such patients
and supply the information needed to initiate adequate medical
treatment. Intracranial stenoses may regress by
recanalization of thromboembolic
material.35 A recent study has shown good reproducibility
for TCCS velocity measurements.43 Thus, repetitive TCCS
examinations in patients with symptomatic 50%
stenoses may detect the regression to <50% (R.W. Baumgartner,
unpublished data, 1994) and prevent the inappropriate long-term
use of anticoagulation and its well-known adverse effects.
Because the diagnostic accuracy for TCCS diagnosis of
intracranial 50% stenoses is unlikely to be 100% in
clinical practice, some patients might erroneously receive warfarin
instead of aspirin and vice versa. Consequently, in case of TCCS
findings, which are close to the cutoff PSV values for 50%
stenoses, angiographic evaluation may be taken into
consideration.
The main limitation of TCCS was the difficulty in differentiating between patients with normal and <50% stenosed arteries. To our knowledge, there is no study suggesting that both groups of patients should have different treatments. Thus, we assume that this limitation is not relevant. Another drawback of TCCS is the temporal bony window, which prevents the reliable detection of stenoses located in branches of the basal cerebral arteries, such as the insular segment of the MCA or the pericallosal artery.
In conclusion, we have elaborated TCCS criteria for detecting 50%
and <50% intracranial stenoses. The criteria require
prospective testing in an angiography-correlated study because they may
prove useful for noninvasive assessment and long-term management of
patients with symptomatic intracranial
stenoses.
Received August 18, 1998; revision received October 1, 1998; accepted October 1, 1998.
|
References |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
1. Sacco R, Kargman D, Gu Q, Zamaillo M. Race-ethnicity and determinants of intracranial atherosclerotic cerebral infarction: the Northern Manhattan Stroke Study. Stroke. 1995;26:14–20.
2.
Wityk R, Lehman D, Klag M, Coresh J, Ahn H, Litt B.
Race and sex differences in the distribution of cerebral
atherosclerosis. Stroke. 1996;27:1974–1980.
3.
Chimowitz MI, Kokkinos J, Strong J, Brown MB, Levine
SR, Silliman S, Pessin MS, Weichel E, Sila CA, Furlan AJ, Kargman DE,
Sacco RL, Wityk RJ, Ford G, Fayad PB. The Warfarin-Aspirin
Symptomatic Intracranial Disease Study.
Neurology.. 1995;45:1488–1493.
4.
Davies KN, Humphrey PR. Complications of cerebral
angiography in patients with symptomatic carotid territory
ischaemia screened by carotid ultrasound. J Neurol Neurosurg
Psychiatry. 1993;56:967–972.
5.
Hankey GJ, Warlow CP, Sellar RJ. Cerebral
angiographic risk in mild cerebrovascular disease. Stroke. 1990;21:209–222.
6.
American Academy of Neurology Therapeutics and
Technology Assessment Subcommittee. Assessment:
transcranial Doppler. Neurology. 1990;40:680–681.
7. De Bray J, Joseph P, Jeanvoine H, Maugin D, Dauzat M, Plassard F. Transcranial Doppler evaluation of middle cerebral artery stenosis. J Ultrasound Med. 1988;7:611–616.[Abstract]
8.
Grolimund P, Seiler RW, Aaslid R, Huber P, Zurbruegg
H. Evaluation of cerebrovascular disease by combined extracranial and
transcranial Doppler sonography: experience in 1039
patients. Stroke. 1987;18:1018–1024.
9. Ley-Pozo JA, Ringelstein EB, Willmes K. Noninvasive detection of occlusive disease of the carotid siphon and middle cerebral artery. Ann Neurol. 1990;28:640–647.[Medline] [Order article via Infotrieve]
10.
Lindegaard K, Bakke S, Aaslid R, Nornes H. Doppler
diagnosis of intracranial artery occlusive disorder. J
Neurol Neurosurg Psychiatry. 1986;49:510–518.
11.
Mattle HP, Grolimund P, Huber P, Sturzenegger M,
Zurbrügg H. Transcranial Doppler sonographic
findings in middle cerebral artery disease. Arch Neurol. 1988;45:289–295.
12. Rorick MB, Nichols FT, Adams RJ. Transcranial Doppler correlation with angiography in detection of intracranial stenosis. Stroke. 1994;25:1931–1934.[Abstract]
13. Röther J, Schwartz AS, Wentz KU, Rautenberg W, Hennerici M. Middle cerebral artery stenoses: assessment by magnetic resonance angiography and transcranial Doppler ultrasound. Cerebrovasc Dis. 1994;4:273–279.
14.
Zanette EM, Roberti C, Mancini G, Pozzilli C, Bragoni
M, Toni D. Spontaneous middle cerebral artery reperfusion in
ischemic stroke: a follow-up study with
transcranial Doppler. Stroke. 1995;26:430–433.
15. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade stenosis. N Engl J Med. 1991;325:445–453.[Abstract]
16.
Gönner F, Remonda L, Mattle HP, Sturzenegger M,
Ozdoba C, Lövblad KO, Baumgartner RW, Bassetti C, Schroth G.
Local arterial thrombolysis in acute
ischemic stroke. Stroke. 1998;29:1894–1900.
17.
Sitzer M, Fürst G, Fischer H, Siebler M, Fehlings
T, Kleinschmidt A, Kahn T, Steinmetz H. Between method correlation in
quantifying internal carotid stenosis. Stroke. 1993;24:1513–1518.
18. Von Büdingen HJ, Von Reutern GM. Ultraschalldiagnostik der hirnversorgenden Arterien. Stuttgart, Germany: Thieme; 1993.
19.
Baumgartner RW, Schmid C, Baumgartner I. Comparative
study of power-based versus mean frequency-based
transcranial color-coded duplex sonography in normal
adults. Stroke. 1996;27:101–104.
20. Giller CA. Is angle correction correct? J Neuroimaging. 1994;4:51–52.[Medline] [Order article via Infotrieve]
21. Baumgartner RW, Mattle HP, Kothbauer K, Schroth G. Transcranial color-coded duplex sonography in cerebral aneurysms. Stroke. 1994;25:2429–2434.[Abstract]
22. Baumgartner RW, Baumgartner I, Mattle HP, Schroth G. Transcranial color-coded duplex sonography in the evaluation of collateral flow through the circle of Willis. AJNR Am J Neuroradiol. 1997;18:127–133.[Abstract]
23.
Kaps M, Damian MS, Teschendorf U, Dorndorf W.
Transcranial Doppler ultrasound findings in middle
cerebral artery occlusion. Stroke. 1990;21:532–537.
24. Lindegaard KF, Bakke SJ, Grolimund P, Aaslid R, Huber P, Nornes H. Assessment of intracranial hemodynamics in carotid artery disease by transcranial Doppler ultrasound. J Neurosurg. 1985;63:890–898.[Medline] [Order article via Infotrieve]
25.
Seidel G, Kaps M, Gerriets T. Potential and limitation
of transcranial color-coded sonography in stroke patients.
Stroke. 1995;26:2061–2066.
26. Von Büdingen HJ, Staudacher T. Evaluation of Vertebrobasilar Disease. New York, NY: Raven Press; 1992.
27. Baumgartner RW, Baumgartner I, Schroth G. Diagnostic criteria for transcranial colour-coded duplex sonography evaluation of cross-flow through the circle of Willis in unilateral obstructive carotid artery disease. J Neurol. 1996;243:516–521.[Medline] [Order article via Infotrieve]
28. Snedecor GW, Cochran WG. Statistical Methods. Ames, Iowa: Iowa University Press; 1989.
29.
Kaps M, Seidel G, Bauer T, Behrmann B. Imaging of the
intracranial vertebrobasilar system using color-coded ultrasound.
Stroke. 1992;23:1577–1582.
30. Martin PJ, Evans DH, Naylor AR. Transcranial color-coded sonography of the basal cerebral circulation. Stroke. 1994;25:390–396.[Abstract]
31.
Schöning M, Jochen W. Evaluation of the
vertebrobasilar-posterior system by transcranial color
duplex sonography in adults. Stroke. 1992;23:1280–1286.
32.
Baumgartner RW, Arnold M, Gönner F, Staikow I,
Herrmann C, Rivoir A, Müri RM. Contrast-enhanced
transcranial color-coded duplex sonography in
ischemic cerebrovascular disease. Stroke. 1997;28:2473–2478.
33.
Nabavi DG, Droste DW, Kemeny V, Schulte-Altedorneburg
G, Weber S, Ringelstein EB. Potential and limitations of
echocontrast-enhanced ultrasonography in acute stroke patients.
Stroke. 1998;29:949–954.
34. Alexandrov AV, Bladin CF, Norris J. Intracranial blood flow velocities in acute ischemic stroke. Stroke. 1994;25:1378–1383.[Abstract]
35.
Ringelstein EB, Biniek R, Weiller C, Ammeling B,
Nolte PN, Thron A. Type and extent of hemispheric brain infarctions and
clinical outcome in early and delayed middle cerebral artery
recanalization. Neurology. 1992;42:289–298.
36.
Landwehr P, Schindler R, Heinrich U, Dölken W,
Krahe T, Lackner K. Quantification of vascular stenoses with
color Doppler flow imaging: in vitro investigations.
Radiology. 1991;178:701–704.
37.
Mast H, Mohr JP, Thompson JLP, Osipov A, Trocio SH,
Mayer S, Young WL. Transcranial Doppler ultrasonography
in cerebral arteriovenous malformations: diagnostic
sensitivity and association of flow velocity with spontaneous
hemorrhage and focal neurological deficit. Stroke. 1995;26:1024–1027.
38.
Schneider PA, Ringelstein EB, Rossmann ME, Dilley RB,
Sobel DF, Otis SM, Bernstein EF. Importance of cerebral collateral
pathways during carotid endarterectomy.
Stroke. 1988;19:1328–1334.
39. Sorteberg W. Cerebral Artery Blood Velocity and Cerebral Blood Flow. New York, NY: Raven Press; 1992.
40. Baker AB, Iannone A. Cerebrovascular disease, I: the large arteries of the circle of Willis. Neurology. 1959;9:321–333.
41.
Bogousslavsky J, Barnett HJM, Fox J, Hachinski VC,
Taylor W. Atherosclerotic disease of the middle cerebral artery.
Stroke. 1986;17:1112–1120.
42. Pessin M, Kwan E, Dewitt LD, Hedges DR, Gale D, Caplan LR. Posterior cerebral artery stenosis. Arch Neurol. 1987;44:85–89.
43. Baumgartner RW, Mathis J, Sturzenegger M, Mattle HP. A validation study on the intraobserver reproducibility of transcranial color-coded duplex sonography velocity measurements. Ultrasound Med Biol. 1994;20:233–237.[Medline] [Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  M. Nedelmann, E. Stolz, T. Gerriets, R. W. Baumgartner, G. Malferrari, G. Seidel, M. Kaps, and for the TCCS Consensus Group Consensus Recommendations for Transcranial Color-Coded Duplex Sonography for the Assessment of Intracranial Arteries in Clinical Trials on Acute Stroke Stroke, October 1, 2009; 40(10): 3238 - 3244. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Schreiber, M. Serdaroglu, F. Schreiber, M. Skalej, H.-J. Heinze, and M. Goertler Simultaneous Occurrence and Interaction of Hypoperfusion and Embolism in a Patient With Severe Middle Cerebral Artery Stenosis Stroke, July 1, 2009; 40(7): e478 - e480. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Nedeltchev, S. Bickel, M. Arnold, H. Sarikaya, D. Georgiadis, M. Sturzenegger, H. P. Mattle, and R. W. Baumgartner Recanalization of Spontaneous Carotid Artery Dissection Stroke, February 1, 2009; 40(2): 499 - 504. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Seidel, H. Cangur, T. Albers, A. Burgemeister, and K. Meyer-Wiethe Sonographic Evaluation of Hemorrhagic Transformation and Arterial Recanalization in Acute Hemispheric Ischemic Stroke Stroke, January 1, 2009; 40(1): 119 - 123. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Valaikiene, G. Schuierer, B. Ziemus, J. Dietrich, U. Bogdahn, and F. Schlachetzki Transcranial Color-Coded Duplex Sonography for Detection of Distal Internal Carotid Artery Stenosis AJNR Am. J. Neuroradiol., February 1, 2008; 29(2): 347 - 353. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Arnold, R. W. Baumgartner, C. Stapf, K. Nedeltchev, F. Buffon, D. Benninger, D. Georgiadis, M. Sturzenegger, H. P. Mattle, and M.-G. Bousser Ultrasound Diagnosis of Spontaneous Carotid Dissection With Isolated Horner Syndrome Stroke, January 1, 2008; 39(1): 82 - 86. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Ois, E. Cuadrado-Godia, J. Jimenez-Conde, M. Gomis, A. Rodriguez-Campello, J. E. Martinez-Rodriguez, E. Munteis, and J. Roquer Early Arterial Study in the Prediction of Mortality After Acute Ischemic Stroke Stroke, July 1, 2007; 38(7): 2085 - 2089. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. J. del Zoppo and J. A. Koziol Recanalization and Stroke Outcome Circulation, May 22, 2007; 115(20): 2602 - 2605. [Full Text] [PDF]
|
|
|
|
 |
|
 C.-H. Lu, H.-W. Chang, C.-C. Lui, C.-R. Huang, and W.-N. Chang Cerebral haemodynamics in acute bacterial meningitis in adults. QJM, December 1, 2006; 99(12): 863 - 869. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Kunz, G. Hahn, D. Mucha, A. Muller, K.M. Barrett, R. von Kummer, and G. Gahn Echo-Enhanced Transcranial Color-Coded Duplex Sonography in the Diagnosis of Cerebrovascular Events: A Validation Study AJNR Am. J. Neuroradiol., November 1, 2006; 27(10): 2122 - 2127. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Weimar, M. Goertler, L. Harms, H.-C. Diener, and for the German Stroke Study Collaboration Distribution and outcome of symptomatic stenoses and occlusions in patients with acute cerebral ischemia. Arch Neurol, September 1, 2006; 63(9): 1287 - 1291. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Mazighi, R. Tanasescu, X. Ducrocq, E. Vicaut, S. Bracard, E. Houdart, and F. Woimant Prospective study of symptomatic atherothrombotic intracranial stenoses: The GESICA Study Neurology, April 25, 2006; 66(8): 1187 - 1191. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. H. Benninger, D. Georgiadis, J. Gandjour, and R. W. Baumgartner Accuracy of Color Duplex Ultrasound Diagnosis of Spontaneous Carotid Dissection Causing Ischemia Stroke, February 1, 2006; 37(2): 377 - 381. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Kern, W. Steinke, M. Daffertshofer, R. Prager, and M. Hennerici Stroke recurrences in patients with symptomatic vs asymptomatic middle cerebral artery disease Neurology, September 27, 2005; 65(6): 859 - 864. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. A. Ringleb, E. I. Strittmatter, M. Loewer, M. Hartmann, J. B. Fiebach, C. Lichy, R. Weber, C. Jacobi, K. Amendt, and M. Schwaninger Cerebrovascular manifestations of Takayasu arteritis in Europe Rheumatology, August 1, 2005; 44(8): 1012 - 1015. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S.-C. Tang, J.-S. Jeng, P.-K. Yip, C.-J. Lu, B.-S. Hwang, W.-H. Lin, and H.-M. Liu Transcranial Color-Coded Sonography for the Detection of Middle Cerebral Artery Stenosis J. Ultrasound Med., April 1, 2005; 24(4): 451 - 457. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C Kremer, T Schaettin, D Georgiadis, and R W Baumgartner Prognosis of asymptomatic stenosis of the middle cerebral artery J. Neurol. Neurosurg. Psychiatry, September 1, 2004; 75(9): 1300 - 1303. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Blaser, W. Glanz, S. Krueger, C.-W. Wallesch, S. Kropf, and M. Goertler Time Period Required for Transcranial Doppler Monitoring of Embolic Signals to Predict Recurrent Risk of Embolic Transient Ischemic Attack and Stroke From Arterial Stenosis Stroke, September 1, 2004; 35(9): 2155 - 2159. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Ghosh, D. Tampieri, and D. Melancon Immediate Evaluation of Angioplasty and Stenting Results in Supra-Aortic Arteries by Use of a Doppler-Tipped Guidewire AJNR Am. J. Neuroradiol., August 1, 2004; 25(7): 1172 - 1176. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. A. Sloan, A. V. Alexandrov, C. H. Tegeler, M. P. Spencer, L. R. Caplan, E. Feldmann, L. R. Wechsler, D. W. Newell, C. R. Gomez, V. L. Babikian, et al. Assessment: Transcranial Doppler ultrasonography: Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology Neurology, May 11, 2004; 62(9): 1468 - 1481. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. du Mesnil de Rochemont, B. Turowski, M. Buchkremer, M. Sitzer, F. E. Zanella, and J. Berkefeld Recurrent Symptomatic High-Grade Intracranial Stenoses: Safety and Efficacy of Undersized Stents-- Initial Experience Radiology, April 1, 2004; 231(1): 45 - 49. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. W. Baumgartner, C. Sidler, M. Mosso, D. Georgiadis, and L. R. Caplan Ischemic Lacunar Stroke in Patients With and Without Potential Mechanism Other Than Small-Artery Disease * Editorial Comment Stroke, March 1, 2003; 34(3): 653 - 659. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Devuyst, J. Bogousslavsky, R. Meuli, J. Moncayo, G. de Freitas, and G. van Melle Stroke or Transient Ischemic Attacks With Basilar Artery Stenosis or Occlusion: Clinical Patterns and Outcome Arch Neurol, April 1, 2002; 59(4): 567 - 573. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M Goertler, T Blaser, S Krueger, K Hofmann, M Baeumer, and C-W Wallesch Cessation of embolic signals after antithrombotic prevention is related to reduced risk of recurrent arterioembolic transient ischaemic attack and stroke J. Neurol. Neurosurg. Psychiatry, March 1, 2002; 72(3): 338 - 342. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Klotzsch, A. Bozzato, G. Lammers, M. Mull, and J. Noth Contrast-Enhanced Three-Dimensional Transcranial Color-Coded Sonography of Intracranial Stenoses AJNR Am. J. Neuroradiol., February 1, 2002; 23(2): 208 - 212. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. W. Baumgartner, A. Frick, C. Kremer, E. Oechslin, E. Russi, J. Turina, and D. Georgiadis Microembolic signal counts increase during hyperbaric exposure in patients with prosthetic heart valves J. Thorac. Cardiovasc. Surg., December 1, 2001; 122(6): 1142 - 1146. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. W. Baumgartner, M. Arnold, I. Baumgartner, M. Mosso, F. Gonner, A. Studer, G. Schroth, B. Schuknecht, and M. Sturzenegger Carotid dissection with and without ischemic events: Local symptoms and cerebral artery findings Neurology, September 11, 2001; 57(5): 827 - 832. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Krejza, Z. Mariak, E. R. Melhem, and R. J. Bert A Guide to the Identification of Major Cerebral Arteries with Transcranial Color Doppler Sonography Am. J. Roentgenol., May 1, 2000; 174(5): 1297 - 1303. [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||