(Stroke. 1999;30:897-899.)
© 1999 American Heart Association, Inc.
Letters to the Editor |
Advantages of Transcranial Power Duplex Imaging After Contrast Injection to Detect Low Flow in a Moyamoya Syndrome
Department of Neurology, CHUV, Lausanne, Switzerland
Department of Neurology, Hôpital de Jolimont, La Louvière, Belgium
To the Editor:
We read with great interest articles recently published in Stroke by Nabavi et al,1 Goertler et al,2 and Postert et al,3 who reported an increasing interest for the diagnostic value of contrast-enhanced transcranial color-coded duplex sonography in ischemic cerebrovascular disease. To the best of our knowledge, however, transcranial power duplex imaging (TPDI) after contrast injection has not yet been evaluated in stroke patients.
TPDI is one of the most recent development in neurosonology. Distinct from color duplex flow imaging (CDFI), PDI produces intravascular color signals based on the reflected echo amplitude, depending mainly on the amount of red blood cells within the sample volume. The consequence of this principle, associated with the use of special filter systems for blood/tissue discrimination, is an increased signal-to-noise ratio. PDI provides a more useful diagnosis in complicated, high-grade stenoses of internal carotid arteries (ICAs) than does CDFI,4 but it has not yet been studied in stenoses of intracranial arteries, even though a superiority of PDI over CDFI has been suggested regarding the depiction of central as well as peripheral segments of intracranial vasculature.5 Injection of contrast agent for ultrasound results in a significant signal enhancement of the cerebral arteries and improves the diagnostic usefulness6 of transcranial duplex imaging, but it has not yet been evaluated specifically in severe stenoses of intracranial vasculature. However, a recent study7 suggests a strong interest in using ultrasound contrast with CDFI in the differential diagnosis between subocclusion and occlusion of ICA, allowing the depiction of slow flow in large vessels. We would like to share our interesting experience of combining these 2 new duplex imaging modalities—TPDI with contrast injection—to improve cerebral artery delineation and to image low flow in a case of moyamoya syndrome.
In October 1996, a 42-year-old man without previous medical history was
admitted because he presented with 5 recurrent transient
ischemic attacks (TIAs), manifested each time by an isolated
left-sided hemiparesis. The motor deficit was completely resolved each
time within 24 hours. Brain MRI showed multiple small ischemic
lesions without leukoencephalopathy in the white matter of both
hemispheres. Conventional cerebral angiography revealed bilateral
stenosis of the supraclinoid ICA (left>right), subocclusion of
the right middle cerebral artery (MCA), severe stenosis at the
origin of the left MCA and of the anterior cerebral artery (ACA), and
collateralization by the external carotids (middle meningeal/temporal
arteries) as well as pial collaterals arising from the branches of the
posterior cerebral arteries (PCAs). According these radiological
findings and the absence of any other demonstrated cause of TIAs
despite an extensive search, we concluded that it was moyamoya
syndrome and instaured antiplatelets (300 mg/d of aspirin) as
treatment. Three months later, the patient continued to present
with TIAs, exhibited as left-sided hemiparesis, and stopped working. At
this time, we discussed the opportunity of surgical
revascularization because of his poor response to
the medical therapy, but the patient refused surgery. In October 1997,
he noticed a slight regression of TIA occurrence—always characterized
by a left hemiparesis—and continued to take aspirin. He rejected
conventional angiography because he was still opposed to surgery, and
we performed MR angiography (MRA) as well as a transcranial
color Doppler flow imaging (TCDFI) and a TPDI without and after
contrast injection (c-TPDI). MRA was performed using both 3D
time-of-flight and phase contrast techniques without contrast agent
injection on a 1.5-T system. Maximum intensity projection images
disclosed severe stenosis of the supraclinoid ICA on both sides
(left>>right) and absence of detectable flow within the proximal
segment of the 2 MCAs and the left ACA (Figure 1
).
Slow flow reappeared distally in the left MCA, and a marked
collateralization from external carotids arteries and PCAs was observed
(Figure 1). The conventional TCD showed peak systolic
velocities of 175 and 259 cm/s on the right and left terminal ICAs,
respectively, with no Doppler signal recorded on both MCAs and
on the left ACA. TCDFI (Figure 2, panel
1)
showed a mosaic-like pattern of changing red and blue effects
(aliasing) in the region of both terminal ICAs (left>>right),
suggestive of stenoses of the terminal ICAs, and no depiction
of the 2 MCAs and left ACA. TCDFI detected enlargement of the PCA on
both sides and small collateralizing vessels. TPDI without Levovist
enhanced (panel 2) the detection of small, atypical collateralizing
vessels and showed some signals on both MCAs. TPDI after contrast
injection (panel 3) considerably improved the diagnostic
usefulness of TPDI: both MCAs were well distinguished by c-TPDI in
contrast with previous modalities. Moreover, c-TPDI revealed multiple
collateralizing vessels. In our case, we assume that both the
neurosonographer and neuroradiologist who performed the MRA were
informed of the results of the former conventional angiography (in
which patency of intracranial vessels was found) at the moment of their
examination. Thus, we believe that the knowledge of the previous
intracranial vascular status of the patients as reported by
conventional angiography could not logically influence one more than
the others.
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We agree with Morgenstern et al,8 who observed in two
moyamoya patients that TPDI visualized parts of the intracranial
collateral network not possible with TCDFI and allowed a better
diagnosis of intracranial vascular pathology than TCDFI. In our case,
TPDI also improved the detection of the intracranial collateral network
and noted color signals on both MCAs, which was not possible with
TCDFI. Meairs and Hennerici9 recently concluded that
although TPDI was an interesting approach, allowing imaging of small
vessels (the anterior and posterior communicating arteries, for
instance) as well as identifying low flow after intracranial
stenoses or occlusions, clinical evaluation of TPDI was still
underway. C-TPDI considerably enhanced the ability to evaluate
collateralization as well as low flow in a subocclusive
stenosis of intracranial vasculature in our case, just as
described by Hennerici7 for extracranial large arteries.
This case report suggests that PDI with contrast could be superior to
3D and phase-contrast MRA to identify very low flow consecutive to a
proximal intracranial artery stenosis, but no definite
conclusions can be drawn for these single case report findings. Further
clinical studies are required to address this issue. It is well known
that MRA can overestimate the degree of brain arterial
stenosis, particularly in high-grade stenoses, which
are visualized as a loss of signal and, in consequence, erroneously
interpreted as an occlusion. c-TPDI associated with 3D reconstruction
(Figure 2
, panel 3) allows a better visualization of the supply from
PCA to MCA. With 3D imaging, the small, atypical collateralizing
vessels are, in fact, loops or branches of the vessels equivocally
identified as vessels or artifacts with TCDFI, TPDI, and c-TPDI.
However, despite the fact that no false-positive diagnosis of a
nonoccluded intracranial artery by TPDI with contrast has been reported
(series have included too few patients), we should take this
possibility into account for the following reasons. First, a short
application period (10 to 15 seconds) of the echo-contrast agent as
applied in our study and others could lead to an increased color
"blooming" artifact that could be erroneously interpreted as
residual poststenotic flow, even if "blooming" was reduced
by decreasing the color Doppler gain. The use of a slower
administration of the echo-contrast agent (at least 3 minutes) may
reduce color artifacts but has not yet been specifically compared with
the short application period. Second, as described by Baumgartner et
al,3 a deep middle cerebral vein that drains toward the
insula and the basal vein of Rosenthal provides color Doppler
signals showing the same flow directions as those of the MCA and PCA,
respectively. Consequently, it is very difficult to discriminate slow
arterial flow (poststenotic) from venous flow by
means of TPDI without spectral Doppler analysis. This point
is still more crucial for TPDI with or without contrast because this
duplex modality, by principle, cannot provide information concerning
the flow's direction. Even if TPDI and c-TPDI essentially provide a
"map" of the intracranial circulation without
hemodynamic data about flow velocity and direction (the
reason we feel that these techniques must be combined with conventional
TCD), we believe that these 2 modalities, particularly c-TPDI,
represent a promising technique by which to diagnose
subocclusive stenosis of brain arteries characterized by low
flow. Further investigations in larger series will be required to
establish the reliability of c-TPDI to diagnose low flow in brain
circulation.
References
1.
Nabavi DG, Droste DW, Kemény V,
Schulte-Altedorneburg G, Weber S, Ringelstein EB. Potential and
limitations of echocontrast-enhanced ultrasonography in acute stroke
patients. Stroke. 1998;29:949–954.
2.
Goertler M, Kross R, Baeumer M, Jost S, Grote R, Weber
S, Wallesch C-W. Diagnostic impact and prognostic relevance
of early contrast-enhanced transcranial color-coded duplex
sonography in acute stroke. Stroke. 1998;29:955–962.
3.
Postert T, Federlein J, Braum B, Köster O,
Börnke C, Przuntek H, Büttner T. Contrast-enhanced
transcranial color-coded real-time sonography: a reliable
tool for the diagnosis of middle cerebral artery trunk occlusion in
patients with insufficient temporal bone window. Stroke. 1998;29:1070–1073.
4.
Steinke W, Ries, Artemis N, Schwarz A, Hennerici M.
Power Doppler imaging of carotid artery stenosis:
comparison with color Doppler flow imaging and angiography.
Stroke. 1997;28:1981–1987.
5. Postert T, Meves S, Börnke C, Przuntek H, Buttner T. Power Doppler compared to color-coded duplex sonography in the assessment of the basal cerebral circulation. J Neuroimaging. 1997;7:221–226.[Medline] [Order article via Infotrieve]
6. Ries F. Clinical experience with echo contrast-enhanced transcranial Doppler and duplex imaging. J Neuroimaging. 1997;7(suppl 1): S15–S21.
7. Hennerici M, on behalf of the Carotid Echocontrast Duplexsonography vs Arteriography Study (CEDAS). Echocontrast duplexsonography is as effective and valid as angiography for the diagnosis of high-grade carotid obstruction. Cerebrovasc Dis. 1998;8(suppl 4):18. Abstract.
8. Morgenstern C, Griewing B, Müller-Esch G, Zeller JA, Kessler C. Transcranial power-mode duplex ultrasound in two patients with moyamoya syndrome. J Neuroimaging. 1997;7:190–192.[Medline] [Order article via Infotrieve]
9. Meairs SP, Hennerici M. Cerebrovascular ultrasound. In: Ginsberg MD, Bogousslavsky J, eds. Cerebrovascular Disease II. Oxford, UK: Blackwell Science; 1998:1318–1336.
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