(Stroke. 1997;28:1311-1313.)
© 1997 American Heart Association, Inc.
Articles |
From the Department of Neuroscience and Neurorehabilitation, University of Genova (Italy).
Correspondence to Massimo Del Sette, MD, Department of Neurosciences and Neurorehabilitation, University of Genova, Via De Toni 5-16132 Genova, Italy.
| Abstract |
|---|
|
|
|---|
Methods We evaluated 90 consecutive patients admitted for their first hemispheric TIA or ischemic stroke within 72 hours of onset. All of them underwent 30-minute bilateral transcranial Doppler monitoring of middle cerebral arteries, within 72 hours of onset. The monitoring was repeated after an additional 24 hours and after 7 days. We then classified the episodes in the following etiologic categories: cardioembolic, atherothrombotic, small-vessel disease, mixed cases, unknown origin, and other causes.
Results We included 75 patients, with a mean interval of registration of 32.04±19.39 hours. There were 9 patients with MES (12%). All MES were recorded only on the symptomatic middle cerebral artery, and the majority were recorded during the first or the second registration. No statistically significant difference was found in risk factors and hematologic parameters. Five patients (56%) had atherothrombotic episodes, 3 patients (33%) had cardioembolic episodes, and 1 patient (11%) had a protein S deficit. No patient with MES had small-vessel disease (P=.01).
Conclusions MES are an infrequent finding in patients with TIA or ischemic stroke within 72 hours of onset, but they can be recorded more easily with serial registration. In our patients, MES were found only on the symptomatic middle cerebral artery and were present in atherothrombotic and cardioembolic episodes but not in small-vessel disease.
Key Words: cerebral ischemia, focal embolism transcranial Doppler
| Introduction |
|---|
|
|
|---|
| Subjects and Methods |
|---|
|
|
|---|
| Results |
|---|
|
|
|---|
|
|
Five patients with MES (56%) were classified in the atherothrombotic group, 3 patients (33%) were cardioembolic, and 1 patient (11%) had a protein S deficit. No patient with MES was classified as having small-vessel disease. All of the 5 patients classified as having had atherothrombotic episodes had ipsilateral carotid stenosis of >60% or carotid occlusion; the other 4 patients classified in other diagnostic categories had normal carotid duplex or slight atherosclerotic changes without stenosis.
The comparison between patients with small-vessel disease and patients
with cardioembolic or atherothrombotic episodes showed a significant
difference (P=.01) (Table 3
).
|
| Discussion |
|---|
|
|
|---|
Some authors have already reported a higher prevalence of MES in atherothrombotic or cardioembolic stroke compared with lacunar syndromes or lacunar infarctions.2 4 Grosset et al,4 studying 45 patients within 48 hours of onset, did not find MES in 8 patients with small-vessel disease. Daffertshofer et al2 reported 4.5% of MES in patients with small-vessel disease, as opposed to 14.2% in large-vessel disease; moreover, none of the patients with lacunar infarction on CT scan showed MES. Our findings are in agreement with these data and suggest that a cardiac or artery-to-artery embolic event might be necessary to develop local particles to be recorded, whereas in small-vessel disease a different process may lead to the small-artery occlusion, without any signal in the main MCA trunk.
In all of our patients, MES were recorded only on the symptomatic side, irrespective of the etiologic categories of the single patient. Some authors reported that MES in acute stroke can be recorded ipsilaterally to carotid stenosis or bilaterally, in patients with cardioembolic stroke.4 In our 3 patients with cardioembolic stroke, MES were recorded only on the symptomatic MCA. Sliwka et al10 reported a unilateral occurrence of MES in 8 (62%) of 13 patients with cardioembolic stroke. Other authors reported a hemispheric side preference of cardiac valvular emboli in individual patients, suggesting a possible explanation of the clinical observation of lodging preferences of recurrent cardiac embolism.11 12 An alternative explanation of the unilateral presence of MES in the acute phase of TIA or stroke could be a local spontaneous clotting and thrombolysis phenomenon,13 14 but it needs to be confirmed by larger samples.
In our patients, MES are not related to a previous clinical event
or silent brain infarctions, in disagreement with Tong and
Albers,1 who have reported MES to be correlated with a
previous recent event. Our different findings might be due to the
larger number of patients and to the serial registration we used. MES
were not related to 30-day prognosis nor to therapeutic regimen (Table 2
), in agreement with other findings, even if the therapeutic
implication of MES is not yet clarified.2 15
In conclusion, our data confirm that MES are an infrequent finding in patients with acute TIA or stroke within 72 hours and that serial registrations may increase the sensitivity of the recording. MES recorded in the acute phase of ischemic episodes may have a pathophysiological meaning, being correlated to the embolic origin of the event and, possibly, to local clotting phenomena.
| Selected Abbreviations and Acronyms |
|---|
|
| Acknowledgments |
|---|
| Footnotes |
|---|
Received February 10, 1997; revision received April 18, 1997; accepted April 28, 1997.
| References |
|---|
|
|
|---|
2.
Daffertshofer M, Ries S, Schminke U, Hennerici
M. High-intensity transient signals in patients with cerebral
ischemia. Stroke. 1996;27:1844-1849.
3.
Forteza AM, Babikian VL, Hyde C, Winter M, Pochay
V. Effect of time and cerebrovascular symptoms on the prevalence
of microembolic signals in patients with cervical
carotid stenosis. Stroke. 1996;27:687-690.
4. Grosset DG, Georgiadis D, Abdullah I, Bone I, Lees KR. Doppler emboli signals vary according to stroke subtype. Stroke. 1994;25:382-384.[Abstract]
5.
Consensus Committee of the IXth International Cerebral
Hemodynamics Symposium. Basic identification criteria
of Doppler microembolic signals. Stroke. 1995;26:1123.
6.
Adams HP, Bendixen BH, Kapelle LJ, Biller J, Love BB,
Gordon DL, Marsh EE III, and the TOAST Investigators. Classification of
subtype of acute ischemic stroke: definitions for use in a
multicenter clinical trial. Stroke. 1993;24:35-41.
7. Bamford JL, Sandercock PAG, Warlow CP, Slattery J. Interobserver agreement for the assessment of handicap in stroke patients. Stroke. 1989;20:828. Letter.[Medline] [Order article via Infotrieve]
8. Droste DW, Decker W, Siemens HJ, Kaps M, Schulte-Altedorneburg G. Variability in occurrence of embolic signals in long term transcra- nial Doppler recording. Neurol Res. 1996;18:25-30.[Medline] [Order article via Infotrieve]
9. Takada T, Moriyasu H, Oita J, Minematsu K, Yamaguchi T. Detection of embolic signals in acute ischemic stroke. Cerebrovasc Dis. 1996;(suppl 2):32-178. Abstract.
10.
Sliwka U, Lingnau A, Stohlmann WD, Schmidt P, Mull M,
Diehl RR, Noth J. Prevalence and time course of
microembolic signals in patients with acute stroke: a
prospective study. Stroke. 1997;28:358-363.
11. Kaps M, Sedel G, Berg J. Is there a hemispheric side preference of cardiac valvular emboli? Ultrasound Med Biol. 1995;21:735-756.
12. Gates PC, Barnett HJM, Silver MD. Cardiogenic stroke. In: Barnett HJM, Mohr HP, Stein BM, Yatsu FM, eds. Stroke: Pathophysiology, Diagnosis and Management. New York, NY: Churchill Livingstone; 1986;2:1085-1109.
13. Diehl RR, Sliwka U, Rautenberg W, Schwartz A. Evidence for embolization from a posterior cerebral artery thrombus by transcranial Doppler monitoring. Stroke. 1993:24:606-608.
14. Del Sette M, Finocchi C, Angeli S, Conti M, Gandolfo C. Transcranial Doppler detection of microemboli in a stroke patient with polycythemia rubra vera. Cerebrovasc Dis. 1995;5:208-211.
15. Georgiadis D, Hill M, Zunker P, Stogbauer F, Ringelstein EB. Anticoagulation monitoring with transcranial Doppler. Lancet. 1994;344:1373-1374.
This article has been cited by other articles:
![]() |
H. Poppert, S. Sadikovic, K. Sander, O. Wolf, and D. Sander Embolic Signals in Unselected Stroke Patients: Prevalence and Diagnostic Benefit Stroke, August 1, 2006; 37(8): 2039 - 2043. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. H. Rapp, X. M. Pan, B. Yu, R. A. Swanson, R. T. Higashida, P. Simpson, and D. Saloner Cerebral Ischemia and Infarction From Atheroemboli <100 {micro}m in Size Stroke, August 1, 2003; 34(8): 1976 - 1980. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. L. Stork, K. Kimura, C. R. Levi, B. R. Chambers, A. L. Abbott, and G. A. Donnan Source of Microembolic Signals in Patients With High-Grade Carotid Stenosis Stroke, August 1, 2002; 33(8): 2014 - 2018. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Kelly, B.J. Hunt, A. Rudd, and R.R. Lewis Should patients with lacunar stroke and severe carotid artery stenosis undergo endarterectomy? QJM, May 1, 2002; 95(5): 313 - 319. [Full Text] [PDF] |
||||
![]() |
Z. Kaposzta, E. Young, P. M. W. Bath, and H. S. Markus Clinical Application of Asymptomatic Embolic Signal Detection in Acute Stroke : A Prospective Study Stroke, September 1, 1999; 30(9): 1814 - 1818. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Brey and M. Carolin Detection of cerebral microembolic signals by transcranial Doppler may be a useful part of the equation in determining stroke risk in patients with antiphospholipid antibody syndrome Lupus, January 1, 1997; 6(8): 621 - 624. [PDF] |
||||
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1997 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |