[Circulating cerebral microembolisms. Detection with transcranial Doppler ultrasound]

Ischaemic stroke is predominantly caused by cerebral emboli which may originate from cardiac sources or atherosclerotic lesions of the cerebral arteries. The diagnosis is primarily based on clinical symptoms and may be confirmed by typical patterns in cranial computed tomography. Echocardiography, ultrasonography of the supraaortic vessels, and angiography are additional diagnostic tools and helpful in clarifying the pathogenesis. Circulating cerebral emboli can be detected using transcranial Doppler sonography (TCD). Emboli are characterised by short-term, high-intensity ultrasonic signals with characteristic audible "chirps". Because of their acoustic impedance, gaseous emboli reflect the ultrasonic beam with a higher intensity than do formed particles. The differentiation between true embolic signals and artifacts (probe dislocation, electrocautery) requires an experienced observer. With recent developments in automatic detection systems, monitoring will become more feasible for clinical applications. During cardiovascular surgery, TCD signals implying cerebral emboli have been registered in various studies. The incidence of embolic signals during cardiopulmonary bypass varies with stage (before, after aortic declamping) and type of surgery (coronary, valve replacement) and the perfusion regime (bubble, membrane oxygenator). For carotid surgery, embolic signals are most likely to occur with carotid clamping, during shunt insertion, and after declamping. There are some studies suggesting a relation between intraoperative embolic signal count and post-operative neurologic state, but the prognostic significance of these signals is still under debate. Strictly controlled prospective studies including a large number of patients have to be conducted to answer the question whether embolic signal count indicates an increased stroke risk. The high number of patients after valve replacement showing up to 30 embolic signals per minute without suffering from neurologic symptoms raises the question whether continuous, predominantly gaseous microembolisation may cause cumulative brain damage. At present, the nature of emboli (gaseous vs. solid) cannot be easily identified by TCD in clinical settings. Future technical improvement of ultrasonic devices may solve this problem, since detection of solid rather than gaseous emboli seems more likely to be clinically relevant.