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We read with great interest Markus' overview of transcranial Doppler (TCD) ultra- songraphy.1 Markus highlighted the new aspects of such clinical applications of this technology in cerebral haemodynamics and detection of emboli. Although the application of TCD in acute stroke was briefly discussed, we point out some of the recent and exciting findings in the acute stroke setting.
There is increasing evidence that intravenous tissue plasminogen activator (TPA) is an effective therapy for ischaemic stroke.2 However, the impact of this therapy has been limited by several factors. Clearly TPA is not efficacious for all eligible patients, with about 50% of treated patients left dependent or dead. Explanations for this incomplete effect include poor recanalisation rate, completed infarction before reperfusion, no reflow phenomenon, and haemorrhagic complications. New strategies must be adopted to both improve our understanding of how and when thrombolysis treatment works to improve our approach to achieving benefit from these therapies. Vascular neuroimaging in the acute setting of ischaemic stroke is an important step in this direction. The technique of TCD is inexpensive, portable, and non-invasive, and is well suited to the acute stroke setting and readily accessible at many centres. Several recent studies have shown that TCD can define arterial obstruction in acute cerebral ischaemia with a high degree of sensitivity and specificity compared with magnetic resonance (MRA) or conventional angiography.2-4
It is able to confirm the presence of arterial occlusion, determine site and extent of obstruction, and uniquely monitor for signs of recanalisation.2-7 Previous studies have shown that early TCD studies can predict outcome. Arterial patency or early recanalisation predicts neurological improvement with TPA whereas persistent occlusion is associated with poorer outcome.5-6
Hence,TCD could become the ideal modality to assist the clinician in the emergency room with patient selection for intra-arterial therapy. If the middle cerebral artery stem occlusion can be confirmed or ruled out in a matter of minutes by bedside TCD, the need for angiography could be reduced to a minimum in this setting.3 Obtaining continuous information about the status of an arterial occlusion during intravenous thrombolysis has the potential to be very helpful in further decision making. Dramatic clinical recovery can be achieved during TPA infusion if early complete recanalisation of the middle cerebral artery occurs.7 Microembolic signals have also been described during monitoring of thrombolysis or spontaneous recanalisation and may signify clot dissolution.7-8 On the other hand, persisting arterial occlusion may identify patients at high risk of worsening or recurrent stroke who may require aggressive measures of secondary stroke prevention.
Although TCD can offer a wealth of interesting information, its use is still limited due to many factors, including operator dependency and the need for in depth knowledge of cerebrovascular pathophysiology. Standardisation and prospective validation of TCD methodology is necessary to broaden its application for this exciting new setting. If TCD can be shown to be both valid and reliable for diagnosing occlusion among a group of clinicians we expect broader acceptance of this modality.
We view TCD as a neurological “stethoscope” of the brain (as Camilo Gomez described it) in the acute setting and utilise this technique to compliment our clinical findings in the emergency room. We encourage others to consider TCD for this application.
I agree with Barber and colleagues that transcranial Doppler (TCD) may well have important applications in selection of patients with acute stroke for thrombolysis. It is an appealing hypothesis that it may allow the identification of patients in whom recanalistion has already occurred, and in whom thrombolysis is not indicated, therefore sparing them treatment with thrombolysis and possible complications. This could increase the risk-benefit equation when giving thrombolysis. It is possible, however, that patients in whom the middle cerebral artery is patent may also benefit from thrombolysis. For example, patients with middle cerebral artery branch occlusions, which are not detectable by TCD, may also benefit. In addition, it is unclear from the thrombolysis trials whether patients with lacunar stroke may also benefit. Stroke subtyping was not sufficiently rigorous to answer this question. Despite these provisos I would agree with Barber and colleagues that this hypothesis needs testing. I would strongly encourage any future thrombolysis trials to include assessment of middle cerebral artery patency by transcranial Doppler at the time of patient recruitment. The advent of new small easily portable TCD machines which are considerably cheaper than the previous PC based models, will greatly facilitate such a study.
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