(Stroke. 1995;26:1517-1519.)
© 1995 American Heart Association, Inc.
Articles |
From the University Department of Neurology, King's College Hospital School of Medicine and Dentistry and the Institute of Psychiatry (H.S.M.), and the Rita Lila Weston Institute of Neurological Studies, University College London Medical School (M.J.H.), London, UK.
Correspondence to Dr Hugh Markus, University Department of Neurology, Institute of Psychiatry, De Crespigny Park, London, SE5 8AF, UK.
Key Words: carotid artery diseases embolism heart valve prosthesis ultrasonics cerebral ischemia
| Introduction |
|---|
The principles underlying ultrasonic detection of cerebral emboli are
relatively simple. Being both larger than the surrounding red blood
cells and of a different material with different acoustic impedance
than the surrounding blood, the incident ultrasound beam is both
reflected and scattered at the interface between the embolus and blood.
This results in an increase in the intensity of the received signal
which, as the embolus is in the sample volume for a short time only, is
of short duration. It has been clearly demonstrated in both animal
models3 4 and flow models5 that platelet,
thrombus, atheroma, and fat emboli result in the expected
short-duration, high-intensity signal, usually within the Doppler
flow spectrum. In these experimental studies, emboli smaller than 200
to 400 µm could not be reliably introduced, but it is likely that
much smaller emboli can be detected using this technique. The intensity
increase tends to be unidirectional, and frequency or velocity focused.
In contrast, artifact results in predominantly bidirectional signals
that can usually,
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