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(Stroke. 1995;26:2298-2301.)
© 1995 American Heart Association, Inc.
Articles |
Transcranial Color-Coded Duplex Sonography in Cerebral Arteriovenous Malformations
From the Departments of Neurology (C.K., P.B.) and Neuroradiology (H.H., H.C.N., D.K.), Alfried-Krupp-Hospital, Essen, Germany.
Correspondence to Christof Klötzsch, Department of Neurology, Alfried-Krupp-Hospital, 45117 Essen, Germany.
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Abstract |
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 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
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Background and Purpose It is well known that significant changes in cerebral hemodynamics may occur during the treatment of cerebral arteriovenous malformations with the complication of intracerebral hemorrhage and parenchymal edema. We used transcranial color-coded duplex sonography to study alterations in blood flow velocities during staged embolization.
Methods Forty-one patients aged 40±13 years (mean±SD) with angiographically proven cerebral arteriovenous malformations were studied. The blood flow velocities of the anterior, middle, and posterior cerebral arteries were measured in 16 patients with supratentorial arteriovenous malformations, both before the first and then after each successive embolization (three to seven treatments).
Results In 29 of 41 patients (71%), transcranial color-coded duplex sonography satisfactorily revealed the malformations and their main feeders. After the final embolization, we found a reduction in the peak flow velocity in treated feeders of 23±28% compared with the values before the first embolization. The untreated feeders showed an increase in peak flow velocities of 12±23% as an expression of increased collateral flow. After the treatment of the supplying feeders, we observed a reduction in flow velocity of 25±13% in seven patients, with cross-filling of the arteriovenous malformation through the contralateral anterior cerebral artery and the anterior communicating artery.
Conclusions The technical advantage of transcranial color-coded duplex sonography compared with transcranial Doppler sonography is that it allows the exact identification of different feeding arteries in arteriovenous malformations. Repeated measurements during stepwise embolization with corrected insonation angle are easily achieved, and noninvasive quantification of hemodynamic changes is possible. The method may be helpful in the planning of the different steps of embolization.
Key Words: cerebral arteriovenous malformation • duplex scanning • embolization, therapeutic • ultrasonics
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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During the last decade, the technique of staged embolization1 2 3 4 of AVM has become established. It is a useful method for size reduction of large AVMs, thus making surgical resection or radiosurgery5 possible. A few earlier studies have investigated hemodynamic changes before and after embolization or surgical resection with TCD6 7 8 9 10 11 12 and xenon single photon emission computed tomography.13 14 15
However, the reasons for the development of severe collateral edema and intracerebral hemorrhage after these treatments remain a subject of controversy.9 10 13 Large AVMs in particular may present with contralateral and ipsilateral neurological deficits that are probably caused by hemodynamic steal phenomena.15 16 17 18
The new method of TCCD allows intracranial vascular structures to be visualized directly.19 20 21 22 23 24 25 Additionally, it is possible to quantitatively measure blood flow velocity with the integrated pulse-wave Doppler device.20 We used this new method to study, as a first step, the assessability of AVMs with different size and location. As a second step, we investigated the capability of TCCD in estimating hemodynamic changes during stepwise embolization.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Assessment of AVMs
Forty-one patients (23 men, 18 women) with angiographically proven supratentorial or infratentorial AVMs were examined with TCCD. The patients were referred consecutively to one of the authors (D.K.) for embolization of the AVM. The mean±SD age of the patients was 40±13 years (range, 16 to 69 years). Using a color-coded ultrasound device with a 2/2.25-MHz probe (Acuson XP 128/10v), we investigated the AVMs through the temporal bone window (Fig 1
) with transversal and coronal
sections. For patients in whom the AVM was located infratentorially, an
additional nuchal approach through the foramen magnum was used. The
flow velocities were investigated with an integrated, range-gated,
2-MHz pulse-wave Doppler with acoustic focusing and
real-time spectral analysis. The feeding arteries and
draining veins were previously established with four-vessel
digital-subtraction angiography. Seven AVMs were located in the
frontal lobe, 7 in the temporal lobe, 10 in the parietal lobe, 3 in the
occipital lobe, 6 in the basal ganglia, and 5 in the central gyrus.
Three cerebellar AVMs were additionally examined. Angiography revealed
that AVM diameter was less than 5 cm in 14 patients but greater in the
remaining 27 patients.
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Hemodynamic Studies
Sixteen of the 41 patients (7 women, 9 men; aged 40±14 years),
exclusively with supratentorially located AVMs,
were examined before the first embolization and then within 2.5±2 days
after each embolization. Each patient received 5±2 treatments, with a
time interval of 7±4.5 days between the embolizations. Five AVMs were
located in the frontal lobe, 4 in the temporal lobe, 3 in the central
region, 2 in the parietal lobe, 1 in the basal ganglia, and 1 in the
occipital lobe. The angiographically determined volume of the insonated
AVMs ranged from 5 to 78 cm3, with a mean value of
30±25 cm3. Angiography revealed a single feeding artery in
3 AVMs, with 2 or more feeders in the remaining 13 AVMs. The feeding
artery was in 15 cases the MCA, in 11 cases the ACA, and in 13 cases
the PCA. Seven of the 16 patients showed cross flow (Fig 2) from the contralateral hemisphere
through the anterior communicating artery. Two others had collateral
flow from the posterior circulation through the posterior communicating
artery. Peak flow velocities of the ACA, MCA, and PCA were measured on
both sides using pulse-wave Doppler at the same depth with an
identical angle correction. The peak flow velocity values before the
first treatment were taken as baseline values (=100%). To make flow
velocity changes after treatment comparable, these values were
expressed as percentages of the baseline values. Staged embolizations
were performed with a superselective catheterization
technique using thrombogenic platinum coils,2 4 polyvinyl
alcohol particles,2 4 and bucrylate.3 In two
patients the AVM could be completely occluded, whereas in the other
patients a size reduction before microsurgery or
stereotactic radiosurgery was achieved. Statistical
differences among subgroups were estimated with the unpaired
t test.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Assessment of AVMs
The AVM and the main feeding arteries were demonstrable (Table 1
) in 29 of 41 consecutive patients
(71%). In the remaining 12 patients, it was not possible to
investigate the AVM, the feeders, and the circle of Willis
sufficiently. Six of these patients had an inadequate insonation
window. Neither parieto-occipital localized AVMs nor small
superficial AVMs in the central gyrus could be displayed due to the
anatomic limitations of the temporal bone window. In two small
microfistulous AVMs in the basal ganglia, the tiny feeding arteries and
the nidus were not demonstrable. Cerebellar AVMs were detectable with
TCCD, but the differentiation between the PCA and the superior
cerebellar artery or between the anterior and posterior
inferior cerebellar arteries was not reliable. In 6
patients with adequate insonation conditions, it was not possible to
demonstrate additional meningeal (n=4) or choroidal (n=2) feeders.
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Hemodynamic Studies
In the subgroup of 16 patients treated by endovascular means
(Table 2), we observed decreased peak
flow velocities in treated feeders (n=25) after embolization of
-23±28% (mean±SD). The decrease amounted to -8±16% per
embolization. Untreated feeders (n=12) showed increased peak flow
velocities of +12±23% due to increased collateral flow velocity. The
peak velocities in untreated main feeders (n=8) increased +3±21% per
embolization and +4.5±20% in cortical feeding arteries (n=4).
Differences between these two subgroups were not statistically
significant (P=.85). In three ipsilateral nonfeeding
arteries, peak flow velocities increased +43±8% (an increase of
+14±25% per embolization). In 7 patients with cross-filling of
the AVM via the contralateral ACA through the anterior communicating
artery, we observed a velocity reduction in the contralateral ACA of
-25±13% after embolization of the supplying ACA or MCA feeder
(a reduction of -7±8.5% per embolization). No significant
hemodynamic changes (-0.5±17%) occurred in
contralateral nonfeeding vessels (n=32).
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Dramatic changes in cerebral hemodynamics occur during treatment of AVMs with microsurgical resection and/or embolization.12 13 In AVMs with more than one feeding artery, for example, the malformation is capable of recruiting blood flow from another untreated feeding artery. Petty et al12 have reported a few cases of steal effects in ipsilateral nonfeeding arteries after treatment.
In addition to increased perfusion of untreated feeders and steal effects, intracerebral hemorrhage or perifocal edema may develop as a result of an imbalance of arterial inflow and venous drainage. A noninvasive monitoring system for follow-up examinations during stepwise treatment of AVMs is thus useful. Although some studies have made use of TCD6 7 8 9 10 11 12 for this task, no study has used TCCD previously for follow-up examinations. During treatment, feeders and draining veins change their flow characteristics, which makes a repeated identification of the vessels with TCD both difficult and unreliable.
TCCD enables monitoring of hemodynamic changes during stepwise embolization of AVMs. Repeated measurements after each embolization with corrected insonation angle are easily performed. Angle correction for distorted arteries raises problems for TCCD because one needs a straight arterial segment of approximately 2.5 cm to perform reliable angle measurements concerning the three-dimensional course of arteries.26 However, in contrast to TCD, TCCD offers the ability to insonate a vessel under visual control repeatedly at the same depth and under the same angle. In the present study, we compared flow velocity changes after embolization with baseline values acquired before treatment and thus evaluated percentage changes as opposed to absolute values.
A decrease of flow velocity in treated feeders and an increase in untreated feeding arteries as a result of collateral flow have been reported in a previous TCD study.12 These changes can be hemodynamically explained, as can the observation of reduced cross-filling through the anterior communicating artery after embolization of ACA and MCA feeders. The alterations in flow velocity showed a large interindividual variability that depended on the number of feeders, the size of the AVM, and the volume of embolized lumen. The increase in flow velocity in ipsilateral nonfeeding arteries may be a result of reduction of steal effects in the circle of Willis,15 with consecutive normalization of flow velocities in nonfeeding arteries.16 TCCD is capable of detecting an increase in flow velocity in untreated feeders or newly recruited feeders. This information could influence the decision of which feeder should be treated next. While this decision has up to now depended on angiographic criteria such as changes in the angioarchitecture of the AVM, it could be possible to perform TCCD examinations between two treatments and decide the moment and extent of the following embolization on the basis of TCCD criteria. TCCD could be especially useful for follow-up examinations in outpatients who have been discharged from the hospital after incomplete embolization of their AVMs.
The technical limits of TCCD were revealed by inadequate bone windows. In AVMs located in the posterior fossa, the differentiation of feeding arteries was unreliable because of the close proximity of the vessels. In patients with additional meningeal or choroidal feeders, these vessels could not be visualized as a consequence of small diameter or close location to the skull. The examination of small microfistulous AVMs was impaired by the low shunt volume and slightly elevated peak flow velocities in the feeding arteries. Because of anatomic limitations of the temporal bone window with limited insonation angles, parieto-occipital or superficial localization of AVMs were further hindrances in achieving sufficient visualization of the malformation.
As a noninvasive bedside test, TCCD is suitable as a quickly applicable screening method for AVMs in patients with cryptogenic intracranial hemorrhage or in patients with frequent monomorphic migraine attacks, but it should be clear that a negative TCCD examination does not exclude AVMs. If all feeding vessels of an AVM are identified angiographically, TCCD offers the possibility of quantitative evaluation of the hemodynamic changes that occur after treatment of cerebral supratentorial AVMs. Further studies may be helpful for a better understanding of the hemodynamic changes caused by the embolization.
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Selected Abbreviations and Acronyms |
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Received May 1, 1995; revision received September 5, 1995; accepted September 5, 1995.
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References |
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