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(Stroke. 1995;26:1024-1027.)
© 1995 American Heart Association, Inc.
Articles |
Transcranial Doppler Ultrasonography in Cerebral Arteriovenous Malformations
Diagnostic Sensitivity and Association of Flow Velocity With Spontaneous Hemorrhage and Focal Neurological Deficit
From Columbia Presbyterian Medical Center, New York, NY.
Correspondence to H. Mast, MD, The Neurological Institute of New York, Stroke Unit, 710 W 168th St, New York, NY 10032.
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Abstract |
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 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
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Background and Purpose We sought to investigate (1) the sensitivity of transcranial Doppler ultrasonography (TCD) for diagnosis of cerebral arteriovenous malformations (AVMs) and (2) the association of feeding artery flow velocity profiles with spontaneous hemorrhage and focal neurological deficit in AVM patients.
Methods We examined 114 consecutive AVM patients prospectively by TCD; 22 non-AVM patients with acute cerebral hemorrhage and 52 normal subjects served as controls. To estimate the association of blood flow velocity patterns in feeding arteries with spontaneous hemorrhage and focal neurological deficit, the total group of AVM subjects was divided into patients with and without a history of bleeding and also into those with and without clinical signs of "steal" (focal deficit unrelated to hemorrhage).
Results Sensitivity for large and medium-sized AVMs was high (>80%), whereas 62% of small AVMs were missed. TCD was also highly sensitive (80%) in a group of five AVM patients with acute hemorrhage. Flow velocity profiles were not related to spontaneous hemorrhage (mean velocity, 111 cm/s in patients with hemorrhage versus 114 cm/s in patients without hemorrhage; P=.65) or clinical signs of steal (mean velocity, 111 cm/s versus 113 cm/s in patients with and without steal, respectively; P=.89).
Conclusions We concluded that (1) TCD is highly sensitive for large and medium-sized AVMs; (2) in acute cerebral hemorrhage TCD may help to differentiate AVM from non-AVM bleeds; (3) the predictive value of TCD findings for clinical sequelae of AVMs remains undetermined; and (4) the concept of hemodynamic steal in AVMs is not supported by TCD data.
Key Words: blood flow velocity • cerebral arteriovenous malformations • hemorrhage • transcranial Doppler
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The sensitivity of transcranial Doppler ultrasonography (TCD) and the association of flow velocity profiles with clinical sequelae (spontaneous hemorrhage, "steal") of cerebral arteriovenous malformations (AVMs) has thus far only been tested in small samples of 40 patients or fewer.1 2 3 4 5 Two of these investigations reported that AVM patients with a history of hemorrhage had significantly lower flow velocities than those without hemorrhage.3 4 Some authors have also claimed that in AVM patients who have focal neurological deficits assumed to be induced by "misery perfusion," the velocities measured by TCD in feeding arteries are higher than in AVM patients without steal.1 3 However, other studies were unable to replicate this observation.4
The Columbia Presbyterian Medical Center AVM Data Bank offered the opportunity to investigate these questions in a larger sample of 114 prospective subjects with cerebral AVM.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The AVM Data Bank is a prospective database for patients with AVMs of the central nervous system. It was established to document information from patient history, neurological examination, TCD, cerebral angiography, brain imaging, neurological outcome, and treatment by interventional neuroradiological, neurosurgical, and radiotherapeutic procedures. Seventy-eight embolizations and 31 operations were performed on the 70 patients referred in 1994.
For the present investigation 114 consecutive cerebral AVM patients
with complete TCD investigation were analyzed from January 1993 through
November 1994 (Table 1
). TCDs were performed with the
use of a TC 2020 (Pioneer by Nicolet) instrument. The examiners were
unaware of AVM location and size. Peak and mean flow velocities and
pulsatility indexes of the middle, anterior, and posterior cerebral
arteries were recorded through transtemporal windows (depth of
insonation, 45 to 50 mm, 60 to 70 mm, and 65 mm, respectively). Basilar
and vertebral arteries were insonated through the suboccipital window
(depth of insonation, 80 to 90 mm and 65 to 70 mm, respectively). The
measured flow parameters were later matched to the main arterial feeder
defined by angiography; ie, in patients with a multiunit AVM fed
predominantly through the middle cerebral artery, TCD recordings were
taken from this vessel. Accordingly, if AVMs were fed through only one
major pial artery, TCD recordings from this vessel were analyzed. AVM
size classification followed the scheme proposed by Stein and
Kader6 : maximum diameters of 
2.5 cm in any plane defined
small AVMs, AVMs with diameters of 2.6 to 5 cm were classified as
medium sized, and AVMs with diameters of >5 cm were classified as
large. Twenty-two consecutive, prospectively encountered non-AVM
patients with acute hemispheric hemorrhage and 52 normal subjects
served as control groups for specificity calculations.
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Normal TCD values for peak and mean flow velocities and pulsatility indexes were derived from the literature. The values used were from the studies that most closely matched our sample in terms of age.7 For sensitivity/specificity calculations,8 TCD values were considered pathological when they exceeded the normal values from the literature by more than 1 SD.
Two further analyses were undertaken. The first compared velocities and pulsatility indexes among AVM patients with and without a history of hemorrhage. The second compared the same parameters among patients with and without possible steal. For the latter analysis patients with a history and/or neurological examination of a focal neurological deficit that was unrelated to AVM hemorrhage were classified in the possible steal category. Any clinical course (progressive, stable, or reversible) of such a syndrome was accepted in this category.
We used t tests for statistical comparisons of continuous
variables; 
2 tests were applied to frequency
analyses.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Feeding artery peak and mean velocities as well as pulsatility indexes of all AVMs; the subgroups of small, medium-sized, and large AVMs; and the main pial feeding arteries are shown in Table 2
. The velocities fell with decreasing AVM size,
reaching the normal range in small AVMs. Pulsatility indexes rose with
decreasing AVM size. High velocities with low pulsatility indexes were
found in five patients insonated within 8 days from an acute
hemorrhage. Sensitivity was high for medium-sized and large AVMs, but
more than 50% of small AVMs were missed (Table 2). Velocities and
pulsatility indexes of non-AVM patients with an acute hemispheric
hemorrhage and of normal control subjects showed a specificity of TCD
of 89% or more (Table 2).
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No statistically significant differences of velocities and pulsatility
indexes were found between AVM patients with and without a history of
hemorrhage (Table 3). Similarly, patients with focal
neurological deficits unrelated to hemorrhage did not differ in their
TCD pattern when compared with AVM patients without possible steal
(Table 3).
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Our data suggest that TCD is highly sensitive for medium-sized and large AVMs but does not detect most of those that are small.
TCD appears to be sensitive for an AVM even in the acute phase after hemorrhage. It may therefore be a useful adjunct to imaging in this setting. Another analysis of a small sample of patients with acutely bleeding AVMs found significantly lower flow velocities than we have reported.1 It remains unclear whether differences in timing of the TCD investigation and/or extent of the hemorrhages can account for this discrepancy. Larger numbers of patients are needed to settle this issue.
We were unable to confirm the hypothesis that AVM patients with a history of hemorrhage show significantly lower velocities than those without hemorrhage. Previous work was confounded by differences in AVM size between the two groups.3 4 Since blood flow velocities decrease with malformation size and in these samples the bleeding AVMs were smaller than the nonbleeding AVMs, they were more likely to show lower velocities in feeders. No conclusion can be drawn from this finding. The morphological characteristics that may separate high- from low-risk AVMs (in terms of bleeding) are yet to be defined, and the hypothesis that hemorrhages occur more often in smaller AVMs has been questioned.9 10 Thus far it remains unclear whether the reported higher proportion of small malformations among bleeding AVMs reflects a lower frequency of other modes of presentation or a higher absolute risk. Our data do not even support a strong association between AVM size and hemorrhage. A search for other determinants of hemorrhage is in order: preliminary data suggest that aneurysms on AVM feeders11 and deep venous drainage10 may be such risk markers.
Our results also raise doubts as to the validity of the notion of hemodynamic steal in AVMs. This pathophysiological concept rests on the assumption that high flow volumes shifted through AVM fistulas lead to misery perfusion in surrounding brain tissues when a critical threshold is exceeded. In principle, such a mechanism would explain chronic, progressive focal neurological deficits and also syndromes with a stable or reversible course. Some authors have extended the steal hypothesis still further to account for the occurrence of seizures.12 Velocity and vessel diameter are both part of the blood flow volume equation. Hence, they have been used to estimate flow volumes in AVMs.3 In our study velocities (and pulsatility indexes) were not determinants of focal neurological deficits unrelated to hemorrhage. The proportion of patients meeting clinical criteria for steal (9%) was rather small, and literature reports on this feature vary widely, from 1% to 40%.13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 The investigation by Manchola et al,3 which proposed a positive association between high flow volumes and progressive focal syndromes, showed a surprisingly large proportion (25%) of such cases, and their results may be confounded by differences in AVM sizes between groups with and without steal. Larger AVMs display higher flow velocities than smaller ones. Our data suggest that any claims for the effect of flow velocities on focal deficits should only be made after AVM size is controlled. The steal hypothesis has also been challenged by a positron emission tomography study28 that found diminished blood flow but no increase in substrate extraction fractions in brain tissues adjacent to AVMs, a finding that denied misery perfusion. In aggregate, both clinical data and the evidence emerging from pathophysiological studies suggest that the steal notion is at the least weakly founded and should be called into question.
In summary, TCD is a sensitive tool in large and medium-sized AVMs. Its use in predicting clinical sequelae of AVMs is yet to be defined. Neither clinical nor sonographic evidence supports the concept of misery perfusion or steal as an important factor in AVM presentation.
Received December 6, 1994; revision received February 14, 1995; accepted March 7, 1995.
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References |
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