Advantages of transcranial power duplex imaging after contrast injection to detect low flow in a moyamoya syndrome.

Abstract

HomeStrokeVol. 30, No. 4Advantages of Transcranial Power Duplex Imaging After Contrast Injection to Detect Low Flow in a Moyamoya Syndrome Free AccessOtherPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessOtherPDF/EPUBAdvantages of Transcranial Power Duplex Imaging After Contrast Injection to Detect Low Flow in a Moyamoya Syndrome G. Devuyst N. Cals, V. de Borchgrave, P. Bara and M. Vandooren G. DevuystG. Devuyst Department of Neurology, CHUV, Lausanne, Switzerland Search for more papers by this author N. CalsN. Cals Department of Neurology, Hôpital de Jolimont, La Louvière, Belgium Search for more papers by this author , V. de BorchgraveV. de Borchgrave Department of Neurology, Hôpital de Jolimont, La Louvière, Belgium Search for more papers by this author , P. BaraP. Bara Department of Neurology, Hôpital de Jolimont, La Louvière, Belgium Search for more papers by this author and M. VandoorenM. Vandooren Department of Neurology, Hôpital de Jolimont, La Louvière, Belgium Search for more papers by this author Originally published1 Apr 1999https://doi.org/10.1161/01.STR.30.4.897Stroke. 1999;30:897–899To 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.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.Download figureDownload PowerPoint Figure 1. MR angiogram using time-of-flight (TOF) technique and maximum intensity projection image reconstruction algorithm showing severe stenosis of the distal segment of the ICAs, reduced flow in the M2 segment of the left MCA, and absence of detectable flow within the M1 segment of both MCAs as well as within the left ACA. These features led to a presumptive diagnosis of moyamoya disease. (Through the courtesy of Dr T. Duprez and Prof G. Cosnard, Department of Radiology, Université Catholique de Louvain, UCL, Bruxelles, Belgium.)Download figureDownload PowerPoint Figure 2. Panel 1, No color signal depicted on the right MCA while an aliasing phenomenon is observed on the right terminal internal carotid artery; small collateralizing vessels and large right PCA observed on TCDFI. 2, In comparison to TCDFI, appearance of small color signals on the right MCA and better visualization of both collateralizing vessels and right PCA with TPDI. 3, TPDI after contrast injection (c-TPDI) reveals the right MCA and a very developed collateral network that converges toward the territory of MCA; the right MCA is clearly visualized, and parts of vessels equivocally interpreted as vessels or artifacts appear as branches or loops of colateralizing vessels on c-TPDI with 3D reconstruction (fourth panel). 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.CrossrefMedlineGoogle Scholar2 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.CrossrefMedlineGoogle Scholar3 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.CrossrefMedlineGoogle Scholar4 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.CrossrefMedlineGoogle Scholar5 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.MedlineGoogle Scholar6 Ries F. Clinical experience with echo contrast-enhanced transcranial Doppler and duplex imaging. J Neuroimaging. 1997;7(suppl 1): S15–S21.Google Scholar7 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.Google Scholar8 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.CrossrefMedlineGoogle Scholar9 Meairs SP, Hennerici M. Cerebrovascular ultrasound. In: Ginsberg MD, Bogousslavsky J, eds. Cerebrovascular Disease II. Oxford, UK: Blackwell Science; 1998:1318–1336.Google Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Bacigaluppi S, Dehdashti A, Agid R, Krings T, Tymianski M and Mikulis D The contribution of imaging in diagnosis, preoperative assessment, and follow-up of moyamoya disease, Neurosurgical Focus, 10.3171/2009.01.FOCUS08296, 26:4, (E3) April 1999Vol 30, Issue 4 Advertisement Article InformationMetrics Copyright © 1999 by American Heart Associationhttps://doi.org/10.1161/01.STR.30.4.897 Originally publishedApril 1, 1999 PDF download Advertisement