From the Stroke Unit, Section of Neurology, Hospital Universitari Doctor
Josep Trueta, Girona, Spain.
Correspondence to Antoni Dávalos, MD, Section of Neurology, Hospital Universitari Doctor Josep Trueta, C/Francia, s/n, 17007 Girona, Spain. E-mail adavalose{at}meditex.es
Abstract
Background—Middle cerebral artery (MCA) stenosis is a
rare occlusive disease in western populations, with a high risk of
stroke recurrence. An artery-to-artery embolic mechanism has
been argued. We report the detection of a new pattern of
microembolic signals (MES) in the MCA
poststenotic segment in a patient with multiple recurrent
transient ischemic attacks.
Case Description—A 75-year-old man was admitted to our hospital
with a transient leg monoparesis on the left side. Right MCA
stenosis was detected by transcranial Doppler
ultrasonography (TCD). In spite of aspirin treatment, the patient had a
recurrent right hemispheric transient ischemic attack, and
anticoagulant therapy was started. A new, similar event happened after
correct anticoagulation. The bigated TCD monitoring study of both MCAs
disclosed clusters of MES at the poststenotic MCA segment. Each
cluster contained between 12 and 45 embolic signals. The patient became
asymptomatic and clusters of MES disappeared, coinciding
with the combination of ticlopidine and oral anticoagulants.
Conclusions—We describe a new presentation of MES,
ie, grouped in clusters of signals, that may be associated with a high
risk of stroke recurrence.
Stenosis of the MCA
causes less than 5% of the ischemic strokes in western
populations.1 2 Ischemic events in the
hemisphere distal to the stenosis could occur because of
hemodynamic insufficiency or by embolic
artery-to-artery mechanism, but the fact that stroke recurrence
is not reduced in these patients after extracranial-intracranial bypass
surgery strongly suggests the latter.3 4
We report the case of a patient with recurrent TIAs and MCA
stenosis in whom TCD monitoring showed several clusters of MES
at the poststenotic segment of the affected MCA.
Case Report
A 75-year-old man was admitted to our hospital because of sudden
lower left limb paresis. On the previous day, the patient had suffered
two events of acute transient paresthesia, each lasting for about 30
minutes in the same zone, but he did not consult his general
practitioner. His medical history was remarkable only for
arterial hypertension and mild
hypercholesterolemia. On admission he was
alert, oriented, and with normal speech; mild paresis in the leg and a
Babinski sign were observed. Arm strength, sensitivity, and cerebellar
functioning were normal. Results of chest x-ray and ECG and biochemical
and hematologic parameters were normal. Ten hours after
admission the patient became asymptomatic. Cranial CT
showed a right lenticular hypodensity that was interpreted as an old
lesion. Cervical color-coded duplex sonography revealed a low-grade
(<30%) bilateral carotid artery stenosis, and there were no
ulcerated plaques. The patient was treated with aspirin (300 mg/d). The
day after admission, the TCD study showed a high-grade right MCA
stenosis, with a mean velocity of 272 cm/s. The
stenosis was confirmed through cranial helical CT angiography
(Fig 1
Discussion
It has been shown during the last 7 years that TCD can detect
cerebral microemboli.5 6 These microemboli were
originally identified during monitoring of carotid and cardiac
surgery7 and described as HITS over the
background blood flow Doppler signal. Subsequently, studies with in
vitro models8 9 suggested that these signals
could be caused by air bubbles and fat or platelet-fibrinogen
embolic particles. There has been considerable discrepancy between
different investigators about the frequency of MES in the different
pathologies. To address this problem, the Consensus Committee of the
9th International Cerebral Hemodynamic Symposium
established as embolic signals only the HITS that are unidirectional,
high intensity, of short duration, and accompanied by a characteristic
"clicking" sound.10 Any MES should be
recorded as HITS in TCD monitoring. Although the definition of HITS
did not mention the temporal profile of the signal distribution, our
own experience and previous reports11 12 found
HITS with an aleatory but homogeneous distribution over the
monitoring time. MES have been detected in a variety of conditions,
including prosthetic valve replacement,13
high-grade carotid stenosis,14 atrial
fibrillation,15 and acute cerebral
ischemia,16 but only a few
studies17 18 have reported MES in relation to
intracerebral artery stenosis. MCA
stenosis is a relatively rare disease in the Caucasian
population, but it is strongly associated with a high rate of stroke
recurrence.19 An embolic artery-to-artery
mechanism has been suggested for stroke in these patients, and it is
supposed that the emboli spring from the stenotic segment to
reach the distal field of the artery. Navabi et
al18 found MES in the poststenotic
segment in 14% (2 of 14) of MCA stenoses but all occurred in
the acute phase of stroke in patients not treated with anticoagulants.
However, Sliwka et al20 could not detect any MES
in 58 patients with chronic stenosis who received different
treatments. This could result either from MES never having been
present or from their disappearance during the natural course of
symptomatic MCA stenosis.
In this article we describe a new pattern of clusters of MES at the
poststenotic segment of the MCA in a patient with ipsilateral
recurrent ischemic events, a finding that to the best of our
knowledge has not been previously reported. In our patient, the
disappearance of clusters of MES in the early acute phase may reflect
the natural course of the MCA stenosis or a treatment effect of
the acenocoumarol and ticlopidine combination. Although at present
the best treatment for intracranial artery stenosis remains
uncertain, it seems that there is a favorable risk-to-benefit ratio for
anticoagulant compared with aspirin therapy for prevention of major
vascular events in symptomatic
patients.21 We think that MES detection in the
acute phase of symptomatic MCA stenosis is probably
a marker for partial recanalization and speculate
that the new form of MES presentation we describe is due to
the release of multiple particles of microaggregates owing to turbulent
flow at the level of the stenosis. Our results suggest that
clusters of MES could be associated with a high risk of
recurrence and that anticoagulant along with antiplatelet
drugs could be a treatment option in these cases.
Selected Abbreviations and Acronyms
Received October 16, 1997;
revision received December 5, 1997;
accepted December 5, 1997.
References
© 1998 American Heart Association, Inc.
Case Reports
Clusters of Microembolic Signals: A New Form of Cerebral Microembolism Presentation in a Patient With Middle Cerebral Artery Stenosis
Key Words: cerebral embolism • middle cerebral artery • stenosis • ultrasonography
). Forty-one hours after admission
the patient suffered a new TIA with left brachiocrural hemiparesis that
lasted for 8 hours; anticoagulant therapy was started with sodium
heparin. Five days after admission the patient had a new, brief TIA
recurrence (only 5 minutes), in spite of correct
anticoagulation (activated partial thromboplastin time was
three times the control value). TCD monitoring of both MCAs was
performed for 1 hour with a pulsed-Doppler machine (DWL Multidop
X4) provided with two bigated probes and special software for the
detection of MES. These probes, which are capable of
simultaneous insonation at two different depths of the same
vessel, were placed over each MCA. We placed one gate receiving flow
signals from the stenotic segment at the right artery and the
second gate at the greatest possible distance from the center of
stenosis. The sample volume of probe insonation was only 5
mm because only a short poststenotic segment of the right MCA
was detected in the same plane. Data from both channels was
recorded on digital audiotape (Sony SLV-425) to confirm visual and
acoustic criteria for MES. During the monitoring we detected MES only
on the right side. Grouped MES were detected at the rate of eight
clusters per hour, and each cluster contained between 12 and 45 embolic
signals (Fig 2). Only about 50% of the
proximal MES could also be recognized at the distal gate, probably as a
result of a partial lumen insonation at the depth of 40 mm;
alternatively, MES could have escaped from the second gate by traveling
through lenticulostriate branches. A further study with the two gates
located in the prestenotic segment did not disclose MES.
Ticlopidine (250 mg/12 h) was added to the anticoagulant treatment.
Forty-eight hours later the patient remained asymptomatic
and a new TCD monitoring did not show clusters of signals, although
there were 18 ungrouped MES per hour. The patient was discharged 4 days
later, free of TIA recurrences and on a regimen of ticlopidine
and acenocoumarol (INR 2.6). Three months later, the TCD study showed a
high-grade MCA stenosis with a mean velocity of 226 cm/s, but
again no MES were detected. At the last check-up, 5 months after
discharge, the patient was still healthy and receiving acenocoumarol
(INR 2.5) and ticlopidine. A new helical CT did not reveal new cerebral
infarcts, and the degree of the stenosis was similar to that of
the first examination.
View larger version (73K):
[in a new window]
Figure 1. Helical CT angiography of the intracranial
arteries. The arrow indicates a high-grade right MCA stenosis.
The CT image is a multiprojection volume reconstruction.
View larger version (101K):
[in a new window]
Figure 2. Example of a cluster of MES. The upper panel shows
a sequence of MES in a very high time resolution spectral display. In
each spectral window, the calculated transit distance (lower right),
the absolute dB value (lower left), and the depth of insonation (upper
left) are displayed. The relative dB level and the time are given under
the spectrum. Nearly thirty MES can be identified in a 3-second period
of time. The lower panel shows a raw Doppler signal of one of the
individual microemboli. The time delay of the episode at each
insonation depth is displayed in milliseconds. The TCD software uses
the delay in the detection of particles to automatically distinguish
between emboli (particles in movement) and artifacts.
HITS
=
high-intensity transient signals
INR
=
international normalized ratio
MCA
=
middle cerebral artery
MES
=
microembolic signals
TCD
=
transcranial Doppler ultrasonography
TIA
=
transient ischemic attack
This article has been cited by other articles:
 |
|
 |
|
  M Goertler, T Blaser, S Krueger, K Hofmann, M Baeumer, and C-W Wallesch Cessation of embolic signals after antithrombotic prevention is related to reduced risk of recurrent arterioembolic transient ischaemic attack and stroke J. Neurol. Neurosurg. Psychiatry, March 1, 2002; 72(3): 338 - 342. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Segura, J. Serena, M. Castellanos, J. Teruel, C. Vilar, and A. Davalos Embolism in acute middle cerebral artery stenosis Neurology, February 27, 2001; 56(4): 497 - 501. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. V. Alexandrov, R. A. Felberg, A. M. Demchuk, I. Christou, W. S. Burgin, M. Malkoff, A. W. Wojner, and J. C. Grotta Deterioration Following Spontaneous Improvement : Sonographic Findings in Patients With Acutely Resolving Symptoms of Cerebral Ischemia Stroke, April 1, 2000; 31(4): 915 - 919. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||