1737

Anterior Cerebral Artery Velocity Changes inDisease of the Middle Cerebral Artery Stem

L.M. Brass, MD, D.L. Duterte, MD, and J.P. Mohr, MD

Transcranial Doppler ultrasonography can map the changes in blood velocity that resultfrom stenosis or occlusion of the middle cerebral artery. To evaluate patterns of collateralblood flow in disease of the middle cerebral artery stem, we used both cerebral angiographyand transcranial Doppler ultrasonography to study the systolic blood velocities in bothanterior cerebral arteries in 10 consecutive patients with middle cerebral artery stenosis orocclusion. Five patients had no evidence of hemodynamically significant carotid disease andgood-quality measurements of systolic velocity in each anterior cerebral artery. Two of thefive patients had middle cerebral artery stem stenosis and the other three had occlusion. Theratios of mean blood velocity in the normal compared with the abnormal side for the fivepatients (mean 1.34±0.23, range 1.15-1.74) were significantly higher than ratios for 10controls (mean 1.04±0.12, range 0.76±1.19) using an unpaired t test (f=3.492,0.0005 <p< 0.005). Our results suggest that transcranial Doppler ultrasound measurementsof anterior cerebral artery blood velocity may be a useful index of collateral blood flow fromthe anterior cerebral artery territory into the middle cerebral artery territory. Changes inmean velocity ratio may document the evolution and adequacy of collateral blood flow overthe cerebral convexity in middle cerebral artery stem disease. In addition, the changes inanterior cerebral artery blood velocity appear to be an important corroborative finding formiddle cerebral artery stem occlusion. (Stroke 1989;20:1737-1740)

Documentation of middle cerebral artery(MCA) disease has, until recently, beenlimited largely to angiographic examina-

tion. Transcranial Doppler ultrasonography (TCD)allows for insonation of the basal cerebral arteriesthrough an intact cranium.1 Stenosis of the proximalMCA is easily recognized as a focal increase in bloodvelocity.2 An absence of the MCA signal may indi-cate an MCA occlusion but can also be due totechnical factors.3 With the possibility of hyperacutetherapies for acute MCA occlusion (i.e., within thefirst few hours after onset), there is a need for a safe,rapid, and reliable technique to determine the pres-ence of MCA disease. We sought to develop associ-ated TCD measurements that would assist in theultrasonic diagnosis of MCA stem occiusion.

From the Stroke Service, Neurological Institute of New York,Columbia-Presbyterian Medical Center (J.P.M., D.L.D), NewYork, New York, and the Stroke Service, Yale-New HavenHospital (L.M.B.), New Haven, Connecticut.

Supported in part by a gift from the Horace W. GoldsmithFoundation, National Institute of Neurological and Communica-tive Disorders and Stroke Clinical Neuroscience Training Pro-gram Contract NS-07155 and Contract NS-2-2079, and the YaleStroke Program.

Address for correspondence: Lawrence M. Brass, MD, YaleStroke Program, Department of Neurology (LCI-700), Yale-New Haven Hospital, 333 Cedar Street, New Haven, CT 06510.

Received August 5, 1988; accepted July 25, 1989.

Though anatomic variations are common in theanterior cerebral arteries (ACAs), the Al segmentswill be normal in 87-98% of individuals.4-5 In casesof MCA occlusion or hemodynamically significantstenosis, the majority of blood flow from the distalinternal carotid artery (ICA) will be into the ACAand the posterior communicating artery. We exam-ined the blood velocity in these arteries to docu-ment the changes seen in patients with severe MCAdisease. These changes could be useful in the diag-nosis of MCA occlusion and may also provideinformation about the changes in collateral bloodflow from the ACA territory into the MCA territory.

Subjects and MethodsWe reviewed the TCD examinations performed at

Columbia-Presbyterian Medical Center over 6 monthsand identified 10 patients in whom there was evi-dence of MCA stenosis or occlusion. From thisgroup, we selected patients who had a technicallyadequate TCD examination that included both ACAand angiographic confirmation of their MCA stenosisor occlusion with no evidence of stenosis or hypopla-sia of the ACA. Five patients met these criteria(three with MCA stem occlusion and two with ste-nosis). Ten additional patients with normal MCA

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1738 Stroke Vol 20, No 12, December 1989

velocities on TCD examination were selected toserve as controls.

The device used was the Model TC2-64 (EME,Ueberlingen, F.R.G.). It is a microcomputer-controlled directional Doppler device operating at 2MHz pulsed ultrasound, using a 64-point fast-Fourier transform spectrum analyzer. The transcra-nial probe is 22 mm in diameter and uses a focusedbeam operating at depths of 25-155 mm electroni-cally adjustable in 5-mm steps. The pulse repetitionfrequency was 5-10 KHz, with a sound intensityrange of 10-100 mW/cm2, a pulse length of 13 /usec,a gate width of 13 ^isec, a vessel wall filter of 150Hz, and a low-pass filter of 10 kHz. The output isdisplayed as a time versus Doppler shift plot on acathode ray terminal. A hard copy of the output wasmade on an Epson RX-80 dot matrix printer (Tor-rance, California) using a customized program devel-oped by one of us for the Tandy Model 100 laptopcomputer (Fort Worth, Texas).

The technique has been described.1 All studieswere performed with the patient in bed, at rest, withthe head elevated no more than 30°. TCD record-ings were made along both MCAs and both ACAs.The arithmetic mean of the systolic blood velocitiesin each ACA (MOSV) was calculated for eachsubject and used in all analyses.

In the patients, ipsilateral MOSV (on the side ofthe MCA disease) was divided by that of the contra-lateral (normal) side to calculate the ACA velocityratio (ACAVR). In the controls, MOSV of the rightside was divided by that of the left side to calculateACAVR. Mean ACAVRs were calculated for eachgroup and compared using the unpaired t test.

ResultsA typical TCD study is illustrated in Figure 1. An

angiogram and a computed tomogram (CT scan) fromone patient are shown in Figures 2 and 3, respec-tively. The posterior communicating arteries were notreliably identified in 40% of the patients, and thesemeasurements were not analyzed further. The twopatients with MCA stenosis had each had 80-90%stenosis with peak velocities of 230 cm/sec (115 cm/sec on the contralateral side) and 160 cm/sec (78cm/sec on the contralateral side) in the MCA stem.

In the patients (mean age 42 years), ipsilateralMOSVs were significantly higher than contralateralMOSV; therefore, ACAVRs were >1.00 (Table 1).Mean ACAVR for the group was 1.34 (range 1.15-1.74); that is, the blood velocities in the ACA on theside of the MCA disease were 35% higher thanthose of the contralateral side. In the control group(mean age 53 years), mean ACAVR was 1.04 (range0.76-1.19); the groups were significantly different(t=3.492, /><0.005).

DiscussionAn increase in ACA blood velocity with MCA

disease has been noted.6-7 Mattle et al7 reported theresults of TCD examination on 61 patients with a

FIGURE 1. Schematic drawing of transcranial Dopplerultrasonograms in patient with middle cerebral artery(MCA) stenosis (shaded area). Blood velocity increasesin region of stenosis; velocities proximal and distal tostenotic region are near normal. Velocity also increasesin ipsilateral Al segment of anterior cerebral artery, animportant corroborative finding in MCA occlusion.

clinical diagnosis of MCA ischemia. Only one patienthad angiographic demonstration of MCA stem occlu-sion with a normal ICA; four patients had MCA stemstenosis demonstrated by angiography and a normalICA, but the degree of stenosis in these four was"less than 75% on average." In addition, the patientswith angiographic demonstration of MCA stem dis-ease were not considered separately in their analysis.

In our patients, the increased velocity in the ipsi-lateral Al segment of the ACA proved to be animportant corroborating sign of MCA occlusion orstenosis. Because of technical difficulties in insonat-ing the MCA in some individuals, the determinationof MCA occlusion should not be based solely on theabsence of a TCD signal. Most often these technicaldifficulties limit insonation of both the MCA and theACA. It is conceivable that the MCA might not beidentified because of a tortuous course, because ithas moved out of the line of the ultrasonic beam, orbecause of variations in the skull contour that allowthe distal Al segment to be insonated, but not theMCA stem. Increased blood velocity in the ipsilat-eral ACA should help in diagnosing MCA occlusion.

The ability to determine MCA occlusion will beimportant in addressing the natural history of MCAdisease. This occlusive state has a poor prognosis,with as few as 20% of patients having a goodoutcome.8-9 MCA occlusion can mimic lacunarsyndromes10 and has a wide range of clinicalpresentations.11-12 Neither the clinical syndromesnor CT scans can reliably diagnose MCA disease,and until now angiography has been the requireddiagnostic step.

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Brass et al ACA Blood Velocity in MCA Stem Disease 1739

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FIGURE 2. Angiogram of patient with mid-dle cerebral artery stenosis. Note that bloodfrom anterior cerebral artery fills vessels overlateral part of hemisphere.

With the promising results of tissue plasmino-gen activator13 and some renewed interest in

TABLE 1. Anterior Cerebral Artery Blood Velocity Ratios byTranscranial Doppler Ultrasonography

Subject

1

2

3

4

5

6

7

89

10

Mean±SEM

Patients

1.741.151.221.271.33

1.34±0.23*

Controls

1.050.941.111.001.151.021.071.080.761.19

1.04±0.12

Data are ratio of mean systolic blood velocity in contralateraldivided by that in ipsilateral side for patients, right divided bythat in left side for controls. Blood velocity increases in proximalanterior cerebral artery ipsilateral to diseased middle cerebralartery.

*p<0.005 different from control by unpaired / test.

embolectomy,14-16 TCD may prove useful in screen-ing patients with acute cerebral ischemia in theMCA distribution without the risks associatedwith angiography.

The changes in ACA blood velocity at the time ofocclusion, or over time, may reflect the degree ofcollateral blood flow. The prognosis of patients withMCA occlusion depends on their age, location ofthe occlusion, and the collateral circulation.8

The degree of collateral blood flow also appearsto correlate with the clinical outcome in patientswith surgical revascularization.15 Siato et al8 mea-sured collateral blood flow by timing the conductionof contrast material through the ACA into the M2segment of the MCA. These authors correlated theextent collateral blood flow in the ACA with thesize of the infarction. It may be possible to obtainsimilar information by TCD examination of theACA blood velocity or pulsatility.

In animal models, it appears that collateral circu-lation may evolve over the first month after a MCAocclusion.17'18 Changes in the ACA blood velocity,and vascular reactivity, over time could provide

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1740 Stroke Vol 20, No 12, December 1989

FIGURE 3. Noncontrast computed tomogram of patientin Figure 2. Radiodensity in middle cerebral artery ishighly suggestive of thrombosis there.

information on similar changes on humans. Ultra-sonic studies of the ICA suggest that end-diastolicblood velocity may correlate more closely withblood flow.19 These studies were performed withpatent ICAs and may not hold true with TCDexamination of the MCA, especially when the ves-sels are highly stenotic or occluded. Diastolic bloodvelocities were not routinely recorded in our labo-ratory at the time of this study. Studies are cur-rently underway to investigate the relation betweenTCD and cerebral blood flow measurements.

TCD will allow us to expand our understanding ofMCA disease and may prove useful in identifyingpatients with MCA disease and may assist in deter-mining their prognosis. Our data suggest that a 20%difference in ACA blood velocities is associatedwith severe MCA stem disease. The ACAVR maybe affected by other factors (such as the duration ofMCA disease), and the finding of ACA blood veloc-ity asymmetry should be interpreted in light of theclinical information and the technical quality of theTCD examination. An ACAVR of 1.19 (asymmetryof almost 20%) occurred in one of our controls andcould conceivably occur in other settings, such as anarrowed Al segment of the ACA. None of our

patients had hemodynamically significant ICA ste-nosis. The effect that occlusive carotid artery dis-ease would have on ACAVR in patients with MCAstem disease is unknown.

The changes in ACA blood velocity provide impor-tant confirmatory evidence in cases of MCA occlu-sion. These same changes may also prove to be auseful index of collateral circulation from the ACAterritory and may help predict the extent of infarc-tion in patients before the CT scan becomes positive.

References1. Aaslid R, Markwalder TM, Nornes H: Noninvasive trans-

cranial Doppler ultrasound recording of flow velocity inbasal cerebral arteries. J Neurosurg 1982;57:569-574

2. Kirkham FJ, Neville BGR, Levin SD: Bedside diagnosis ofstenosis of the middle cerebral artery. Lancet 1986;l:797-798

3. Bruno A, Biller J, Silvidi JA: A reason for failure to obtaintranscranial Doppler flow signals: Hyperostosis of the skull(letter). Stroke 1988;19:274

4. Alpers BJ, Berry RG: Circle of Willis in cerebral vasculardisorders. Arch Neurol 1963;8:398-402

5. Fisher CM: The circle of Willis: Anatomic variations. VaseDis 1965;2:99-105

6. Brass LM, Mohr JP: Transcranial Doppler evaluation ofcollateral flow from the anterior to the middle cerebral arteryterritory in MCA stem disease (abstract). Neurology 1988;38(suppl 1):343

7. Mattle H, Grolimund P, Huber P, Sturzenegger M, ZurbruggHR: Transcranial Doppler sonographic findings in middlecerebral artery disease. Arch Neurol 1988;45:289-295

8. Saito I, Segawa H, Shiokawa Y, Taniguchi M, Tsutsumi K:Middle cerebral artery occlusion: Correlation of computer-ized tomography and angiography with clinical outcome.Stroke 1987;18:863-868

9. Yoshimoto T, Ogawa A, Seki H, Kogure T, Suzuki J:Clinical course of acute middle cerebral artery occlusion. JNeurosurg 1986;65:326-330

10. Adams HP, Damasio HC, Putman SF, Damasio AR: Middlecerebral artery occlusion as a cause of isolated subcorticalinfarction. Stroke 1983;14:948-952

11. Hinton RC, Mohr JP, Ackerman RH, Adair LB, Fisher CM:Symptomatic middle cerebral artery stenosis. Ann Neurol1979;5:152-157

12 Aoki N: Caudate head hemorrhage caused by asymptomaticocclusion of the middle cerebral artery. Surg Neurol 1987;27:173-176

13. The tPA-Acute Stroke Study Group: An open multicenterstudy of the safety and efficacy of various doses of r-tPA inpatients with acute stroke: Preliminary results (abstract).Stroke 1988;19:134

14. Meyer FB, Piepgras DG, Sundt TM, Yanagihara T: Emer-gency embolectomy for acute embolic occlusion of themiddle cerebral artery. Clin Neurosurg 1985;32:155-173

15 Meyer FB, Piepgras DG, Sundt TM Jr, Yanagihara T:Emergency embolectomy for acute occlusion of the middlecerebral artery. J Neurosurg 1985;62:639-647

16. Risberg J, Smith P: Prediction of hemispheric blood flow fromcarotid velocity measurements. Stroke 1980;ll:399-402

17. Coyle P, Heistad DD: Blood flow through cerebral collateralvessels one month after middle cerebral artery occlusion.Stroke 1987;18:407-411

18. Coyle P: Diameter and length changes in cerebral collateralsafter middle cerebral artery occlusion in the young rat. AnatRec 1984;210:357-364

19. Diaz FG, Ausman JI, Mehta B, Dujovny, De Los Reyes RA,Pearce J, Patel S: Acute cerebral revascularization. J Neu-rosurg 1985;63:200-209

KEY WORDSultrasonics

• cerebral arteries • collateral circulation

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L M Brass, D L Duterte and J P MohrAnterior cerebral artery velocity changes in disease of the middle cerebral artery stem.

Print ISSN: 0039-2499. Online ISSN: 1524-4628 Copyright © 1989 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Stroke doi: 10.1161/01.STR.20.12.1737

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