Assessment of >50% and <50% Intracranial Stenoses by Transcranial Color-Coded Duplex Sonography

Ralf W. Baumgartner, MD; Heinrich P. Mattle, MD; Gerhard Schroth, MD

Background and PurposeA 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. MethodsProspectively 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. ResultsTCCS 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). ConclusionsTCCS may reliably assess 50% and 50% basal cerebral artery narrowing and prove useful for noninvasive management of patients with symptomatic intracranial stenoses. (Stroke. 1999;30:87-92.) Key Words: anticoagulants aspirin stenosis ultrasonography, transcranial
therosclerotic 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 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

Patient Recruitment and Inclusion and Exclusion Criteria
Between November 1992 and December 1996, 310 consecutive patients (102 women, 208 men; meanSD age, 5616 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

Received August 18, 1998; final revision received October 1, 1998; accepted October 1, 1998. From the Department of Neurology, University Hospital of Zu rich (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 Zu rich, Switzerland. E-mail Strusbmg@neurol.unizh.ch 1999 American Heart Association, Inc. Stroke is available at http://www.strokeaha.org

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Figure 1. TCCS ndings obtained by transtemporal insonation with axial (top 2 color images) and coronal (bottom 2 color images) scanning planes in a patient with an angiographically proven 50% stenosis of the ACA. The corresponding schemes are on the right side. Both images on the left side show intrastenotic color and spectral Doppler ndings with increased velocities and high-intensity, low-frequency signals. Both images in the middle show poststenotic color and spectral Doppler ndings with normal velocities and high-intensity, low-frequency signals in the top panel.

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, highintensity 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 Ro ther 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 Bu dingen 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 (512512 matrix; since December 1993, 10241024 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 diameterresidual lumen/normal lumen diameter). Finally, each intracranial artery was graded separately as follows: no stenosis, stenosis 50%, stenosis 50%, occlusion.

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Figure 2. TCCS ndings obtained by transtemporal insonation with an axial scanning plane in a patient with an angiographically proven 50% stenosis of the MCA. The top image gives the color Doppler road map, which shows a focal color abnormality composed of red, orange, yellow, and green related to increased velocities, aliasing, and/or reversed ow and suggests that the MCA is straight for 20 mm, enabling the use of an angle indicator. The bottom images also show the corresponding Doppler spectra: on the left normal prestenotic velocities, in the middle increased intrastenotic velocities with high-intensity, low-frequency signals, and on the right normal poststenotic velocities with high-intensity, low-frequency signals.

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.

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

Results

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 falsepositives; 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

TABLE 1. Ultrasonic Detection of >50% Intracranial Stenoses (n31) With Angiography as Standard of Reference
Ultrasound PSV Cutoff, cm/s ACA MCA PCA BA VA 155 220 145 140 120 Sensitivity, % 100 100 100 100 100 Specificity, % 100 100 100 100 100 Positive Predictive Value, % 100 100 100 100 100 Negative Predictive Value, % 100 100 91 100 100 Angiography MeanSD Degree (Range) 608 (5271) 6711 (5080) 637 (5072) 6714 (5385) 6914 (5584)

No. 4 11 10 3 3

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TABLE 2. Ultrasonic Detection of <50% Intracranial Stenoses (n38) With Angiography as Standard of Reference
Ultrasound PSV Cutoff, cm/s ACA* MCA PCA BA VA 120 155 100 100 90 Sensitivity, % 100 94 100 100 100 Specificity, % 99 100 100 100 100 Positive Predictive Value, % 73 95 100 100 100 Negative Predictive Value, % 100 100 100 100 100 Angiography MeanSD Degree (Range) 3812 (2047) 368 (2248) 2912 (1341) 334 (2937) 326 (2539)

No. 5 18 5 4 5

*One stenosed anterior cerebral artery was missed because of an inadequate temporal bone window.

because they were not found to be as sensitive and accurate as the PSV values for the assessment of stenoses.

range, 30% to 80%) additional 70% to 100% carotid obstruction.

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 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 (r0.93, P0.0001).

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 falsenegative 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.

Discussion
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 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.

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 (meanSD, 17424 cm/s; range, 157 to 215 cm/s) compared with MCAs without (meanSD, 23773 cm/s; range, 172 to 400 cm/s) additional 70% to 100% carotid obstructions (P0.05). The degree of narrowing showed a nonsignificant trend to be lower in MCAs with (meanSD, 394%; range, 36% to 41%) compared with MCAs without (meanSD, 5516%;
TABLE 3.

PSVs in Intracranial Arteries With >50% Stenoses, <50% Stenoses, and No Stenoses at Angiography
Degree of Stenosis at Angiography 50% 50% 12815 (109145) 17624 (141217) 12717 (112154) 11917 (109139) 1004 (94104) 0% 8118 (33135) 10020 (58151) 6312 (36100) 6416 (28100) 4714 (2089) 50% vs 50% .05 .0001 .01 .05 .05

P
50% vs 0% .0001 .0001 .0001 .01 .01 50% vs 0% .0001 .0001 .0001 .001 .001

ACA MCA PCA BA VA

18934 (155227) 30149 (221400) 19917 (176228) 19446 (144248) 19166 (123256)

Values are meanSD PSV (range).

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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 falsenegative 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 (P0.05). 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 malforma-

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tions 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 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 wellknown 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

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17. Sitzer M, Fu rst G, Fischer H, Siebler M, Fehlings T, Kleinschmidt A, Kahn T, Steinmetz H. Between method correlation in quantifying internal carotid stenosis. Stroke. 1993;24:15131518. 18. Von Bu dingen 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;27:101104. 20. Giller CA. Is angle correction correct? J Neuroimaging. 1994;4:5152. 21. Baumgartner RW, Mattle HP, Kothbauer K, Schroth G. Transcranial color-coded duplex sonography in cerebral aneurysms. Stroke. 1994;25: 2429 2434. 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;18:127133. 23. Kaps M, Damian MS, Teschendorf U, Dorndorf W. Transcranial Doppler ultrasound findings in middle cerebral artery occlusion. Stroke. 1990;21: 532537. 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. 25. Seidel G, Kaps M, Gerriets T. Potential and limitation of transcranial color-coded sonography in stroke patients. Stroke. 1995;26:20612066. 26. Von Bu dingen 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. 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: 15771582. 30. Martin PJ, Evans DH, Naylor AR. Transcranial color-coded sonography of the basal cerebral circulation. Stroke. 1994;25:390 396. 31. Scho ning 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, Go nner F, Staikow I, Herrmann C, Rivoir A, Mu ri RM. Contrast-enhanced transcranial color-coded duplex sonography in ischemic cerebrovascular disease. Stroke. 1997;28: 24732478. 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. 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;42:289298. 36. Landwehr P, Schindler R, Heinrich U, Do lken W, Krahe T, Lackner K. Quantification of vascular stenoses with color Doppler flow imaging: in vitro investigations. Radiology. 1991;178:701704. 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;9:321333. 41. Bogousslavsky J, Barnett HJM, Fox J, Hachinski VC, Taylor W. Atherosclerotic disease of the middle cerebral artery. Stroke. 1986;17: 11121120. 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;20:233237.

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.

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