Table 2 gives specific data of the study group and shows the relationship between clinical data and the presence or

absence of cerebral embolism. Table 2 shows that cerebral embolism in this patient cohort was associated with a high-grade internal carotid artery stenosis. Retinal events and aphasia were more frequently seen in patients who experienced cerebral embolism. Table 3 shows the epidemiology of cerebral embolism. It showed a wide range of frequencies of emboli during the 30 min monitoring. Most emboli were short lasting, low intensity events that occurred in the diastolic phase of the cardiac Decitabine purchase cycle. The emboli had a very prominent musical sound expressed by the low zero-crossing index. The most prominent source of the embolus was an internal carotid artery stenosis. In most patients the internal carotid artery stenosis was located at the origin of the vessel. In two out of eleven patients the stenosis was located at the level of the carotid syphon. The embolic activity decreased after therapeutical interventions such as carotid surgery, angioplasty and a drug switch from aspirin to clopidogrel. Table 4 shows the outcome of the study protocol in relation to positive and negative embolism. Table 5 shows the outcome of both the control and study group. Table 4 shows that the diagnosis and treatment of

patients with positive cerebral embolism was performed much faster than the diagnosis and treatment of patients without cerebral embolism. Stroke and TIA

recurrence rate in both groups were very low (respectively 0.0% and 3.2%). In the study PD-1/PD-L1 inhibitor cancer group, one patient experienced a stroke recurrence in the ipsilateral posterior cerebral artery resulting in a permanent hemi-anopsia. In the control group four recurrent strokes were observed. All these events occurred in the ipsilateral middle cerebral artery territory; two of these events occurred in the post-operative phase of carotid surgery. One of these Cepharanthine events was classified as a possible cerebral hyperperfusion syndrome. Spencer was the first investigator who showed that detection of cerebral embolism was possible with TCD [8]. His initial study describes the ongoing cerebral embolism in patients scheduled for carotid surgery. Soon after his publication the first reports appeared about MES signals in TIA and stroke patients. In the last ten years a number of studies showed unequivocal that ongoing cerebral embolism in carotid artery disease is a strong independent predictor of stroke [1] and [2]. The current clinical study tried to explore the potential of embolus detection to enhance the outcome of patients with symptomatic carotid artery disease. Briefly summarized this study revealed a non-significant reduction in recurrent events in the study group. Probably sample size in this pilot study was insufficient to detect a significant decline.