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(Stroke. 1996;27:1347-1349.)
© 1996 American Heart Association, Inc.

Articles

Detection of Microembolic Signals in Patients With Middle Cerebral Artery Stenosis by Means of a Bigate Probe

A Pilot Study

Darius G. Nabavi, MD; Dimitrios Georgiadis, MD; Thorsten Mumme; Peter Zunker, MD E. Bernd Ringelstein, MD

the Department of Neurology, University of Munster (Germany).

Correspondence to Darius G. Nabavi, MD, Department of Neurology, University of Munster, Albert-Schweitzer-Straße 33, 48129 Munster, Germany.

	Abstract

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Background and Purpose Middle cerebral artery (MCA) stenosis is a relatively rare occlusive disease with an annual stroke risk of approximately 7% to 8%. However, the frequent coincidence of cardiac or ipsilateral carotid artery disease may lead to difficulties in identifying the relevant embolizing source in symptomatic patients. We undertook this study to evaluate the prevalence of microembolic signals (MES) as well as the potential and limitations of bigate monitoring in patients with MCA stenosis.

Methods Fourteen patients aged 33 to 87 years with angiographically demonstrated symptomatic (acute, n=2; chronic, n=8) or asymptomatic (n=4) MCA stenosis were examined. Six patients (43%) had additional cardiac (n=3) or carotid artery (n=3) disease. By means of a bigate probe, simultaneous insonation of prestenotic and poststenotic vessel segments was attempted.

Results In 10 patients (71%), MES detection could be performed sufficiently at target vessel sites. In the remaining patients, either prestenotic (n=3) or poststenotic (n=1) monitoring was not satisfactory due to insufficient transtemporal bone window or the great length or extent of MCA stenosis. Poststenotic MES were detectable in 2 acutely symptomatic and 1 asymptomatic patient (prevalence, 21%). In the latter case, the sequential appearance of MES in both prestenotic and poststenotic channels excluded MCA stenosis but strongly favored coexisting carotid artery stenosis as the active embolic source.

Conclusions MES are detectable in patients with MCA stenosis. Bigate monitoring in this setting is feasible and allows identification of the active source among "competing" embolizing conditions.

Key Words: cerebral embolism • middle cerebral artery • stenosis • ultrasonics

	Introduction

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Middle cerebral artery stenosis is a rare occlusive disease^{1 2 3 4} with an annual stroke risk of approximately 7% to 8%.⁴ The fact that stroke incidence is not reduced in these patients after extracranial-intracranial bypass surgery despite poststenotic hemodynamic improvement strongly argues for an embolic stroke mechanism.⁵ This concept is further supported by clinical,^{1 6} imaging,⁷ and autopsy studies.⁸ To date, stroke-preventive therapy in patients with symptomatic and asymptomatic MCA stenosis is empirical because prospective trials and prognostic markers are still lacking. A recent retrospective study of 151 symptomatic patients with intracranial artery disease including 39 patients with MCA stenosis suggested a superiority of oral anticoagulation compared with antiplatelet therapy.⁹ The coincidence of potential embolic diseases of the ipsilateral ICA or the heart⁴ could lead to further difficulties in evaluating the true pathogenetic role of MCA stenosis in symptomatic cases. Detection of MES by means of TCD has been described in various stroke-prone patients with extracranial carotid^{10 11} and cardiac^{12 13} embolic sources. We investigated the prevalence of MES in patients with MCA stenosis and evaluated the feasibility and relevance of bigate monitoring in these patients.

	Subjects and Methods

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Fourteen consecutive patients with moderate (n=10) or severe (n=4) MCA stenosis were enrolled in this study. Eight patients with known MCA stenosis and a history of TIA (n=3) or ischemic stroke (n=5) that occurred 14±3 months (mean±SD) previously were examined parallel to their routine follow-up Doppler examination. Additionally, 4 neurologically asymptomatic patients in whom MCA stenosis was diagnosed during routine ultrasound cerebrovascular screening were examined. Finally, 2 patients presenting with acute onset of neurological symptoms attributable to the MCA territory in whom MCA stenosis was primarily diagnosed were also monitored. MCA stenosis was diagnosed on the basis of typical TCD findings¹⁴ and subsequently confirmed by intra-arterial digital subtraction angiography in all cases. Quantification of the MCA stenosis was performed on the anteroposterior views of the angiograms. According to previous reports,⁴ severe MCA stenosis was defined as 70% to 99% and moderate stenosis as >50% to 69% reduction of vessel diameter. Neurological history, focused on the occurrence of ischemic events, and a neurological examination were performed by an experienced neurologist. In all cases, the type of stroke-preventive therapy was recorded, and blood was drawn to evaluate the actual international normalized ratio in patients receiving oral anticoagulants.

TCD examination was performed with a pulsed Doppler machine (TC 4040, EME). Length and extent of MCA stenosis were determined to define the target depths of prestenotic and poststenotic monitoring with the bigate probe. This probe, consisting of one transmitting and two receiving channels, is capable of simultaneously insonating at two different depths of the same vessel. One channel harvested flow signals from the proximal MCA segment or distal carotid siphon and the second one from the distal MCA segment. The aim was to simultaneously insonate prestenotic and poststenotic MCA segments (Figure). If this could not be achieved, sample volume was placed at the greatest possible distance from the stenosis center. Thus, monitoring was performed over (1) prestenotic and poststenotic, (2) prestenotic and intrastenotic, or (3) intrastenotic and poststenotic MCA segments. The values of the sample volumes were set as low as possible to avoid overlap. Data from both channels were recorded on digital audiotapes with a two-channel recorder (Sony 59ES). MES detection was performed for 45 minutes at the two insonation depths. The visual and acoustic criteria used to identify MES have been described elsewhere.¹⁵ The 2 patients with acute stroke symptoms were monitored on the day of admission, ie, before initiation of anticoagulation, as well as 24 hours, 1 week, and 3 months after initiation of anticoagulant treatment (international normalized ratio values, 2.5 to 4.0 on all monitoring sessions). The other patients were monitored on only one occasion while on antiplatelet (n=5) or anticoagulant (n=7) therapy.

View larger version (12K): [in this window] [in a new window]   Figure 1. Principle of prestenotic and poststenotic bigate monitoring in MCA stenosis.

All patients additionally underwent extracranial color-coded duplex sonography of the brain-supplying arteries (Sonos 2000, Hewlett-Packard) as well as transthoracic echocardiography.

	Results

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Fourteen patients aged 64±14 years (mean±SD; range, 33 to 87 years) were examined in this study. Their clinical and angiologic details are summarized in the Table. TCD examinations of the patients with MCA stenosis revealed mean (±SD) flow velocities of 154±43 cm/s, with a mean (±SD) length of 9.8±4.0 mm (range, 6 to 18 mm). In 6 patients an additional potential embolic source was identified in either the ipsilateral ICA (n=3) or the heart (n=3) by extracranial color-coded duplex sonography or transthoracic echocardiography, respectively (Table).

View this table: [in this window] [in a new window]   Table 1. Clinical, Angiologic, and Monitoring Details of Patients With MCA Stenosis

A satisfactory insonation of prestenotic and poststenotic MCA segments was possible in 10 patients (71%). In these patients, the mean (±SD) distance of the two centers of sample volumes was 15.8±1.8 mm, while the mean (±SD) value of sample volumes was 8.3±1.3 mm (range, 6 to 10 mm) (Table). In the remaining 4 patients, either the proximal (n=3) or distal (n=1) channel could not be sufficiently insonated because the peripheral extent was too great (patient 11), the MCA stenosis was too long (patients 9 and 12), or the transtemporal bone window was insufficient (patient 3). The bigate probe mounting procedure took 12±3 minutes (mean±SD). Because of the high susceptibility of bigate monitoring to movement disturbances, interruption of the monitoring session with correction of the position of the probe was required in 8 patients (57%).

MES were detected in 3 patients (overall prevalence, 21%). Two and 3 poststenotic MES were detected in the 2 acutely symptomatic patients on initial examination. Their purely poststenotic appearance confirmed MCA stenosis as the embolic source. Additionally, 3 MES were detected in an asymptomatic patient with a coexisting ipsilateral ICA stenosis. Two microemboli sequentially appeared in both channels with a time delay of 0.01 and 0.02 seconds, and the third was visualized solely in the prestenotic channel. This observation excluded MCA stenosis and strongly favored ipsilateral ICA stenosis as the embolizing source. No MES were detected in the remaining patients and on follow-up monitoring of the 2 acutely symptomatic patients while they were receiving oral anticoagulants.

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Since TCD has been validated as a screening method for MCA stenosis,^{16 17} this diagnosis has been made noninvasively in a considerable number of symptomatic and asymptomatic patients.^{14 18 19 20} At present, no valid data concerning their individual prognosis and defining the appropriate treatment are available. Furthermore, the coexistence of potential embolic disorders of the ipsilateral ICA and/or the heart, which may be as high as 67% in patients with MCA stenosis,⁴ leads to further difficulties in identifying the relevant embolic source in symptomatic patients.

Our results suggest that detection of MES distal to MCA stenosis is feasible and bears potential clinical relevance. Use of the bigate probe in this setting, originally applied to distinguish true MES from artifacts,²¹ further helps to localize the origin of microemboli. Simultaneous monitoring of prestenotic and poststenotic MCA segments, which was achieved in 71% of our patients, enables differentiation of MES originating from MCA stenosis itself (ie, MES detectable only in the poststenotic channel) or from a more proximal source (ie, MES detectable only in the proximal or in both channels). The latter was observed in a patient with a tandem ICA stenosis. The appearance of one MES solely in the prestenotic channel in the same patient could be due to its passage through a small branch of the proximal MCA segment or insufficient time overlap of the Doppler machine. The additional time expense for exact bigate probe positioning and mounting seems acceptable with respect to the additional diagnostic information.

MES originating from the MCA stenosis occurred only in the two acutely symptomatic patients before initiation of anticoagulant treatment. Presumably, this low prevalence is the result of successful suppression of microemboli by antihemostatic treatment in the other patients²² or lack of symptoms and a long-lasting event-free interval in the previously symptomatic patients. Furthermore, the relatively short monitoring time of 45 minutes may also explain the negative TCD findings.

To the best of our knowledge, this is the first study of microemboli detection in patients with MCA stenosis. Our results demonstrate its applicability and the additional diagnostic potential of prestenotic and poststenotic bigate monitoring in this particular setting.

	Selected Abbreviations and Acronyms

 

ICA = internal carotid artery MCA = middle cerebral artery MES = microembolic signals TCD = transcranial Doppler sonography TIA = transient ischemic attack

Received February 15, 1996; revision received April 9, 1996; accepted April 11, 1996.

	References

Top Abstract Introduction Subjects and Methods Results Discussion References

 

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